EXPLANATIONS FOR THE REFERENCES
FOR THE POSTURE THEORY, AND FOR THE VERIFIABILITY OF AN ARTICLE ON DA COSTA’S SYNDROME IN WIKIPEDIA.
The modern word for Da Costa’s syndrome is The Chronic Fatigue Syndrome, although there are some variations with Orthostatic intolerance, and Postural Orthostic Tachycardia Syndrome being in the list of symptoms and types. Nowadays these references represent the history of chronic fatigue syndrome research.
AN INTRODUCTORY NOTE FOR WIKIPEDIA EDITORS
I first saw a four line article on Da Costa’s syndrome in WIKIPEDA in late December 2007 with a general invitation to improve it, so I started adding to it, and soon after that someone else included the heading of “History” to a section of the text. I then added reviews to that section but each time I did two editors consistently deleted them.For example, the most common symptom of Da Costa’s syndrome is the breathlessness which, in 1956, Paul Wood described as affecting 93% of patients, however, when I provided some information about the discovery of the cause in the 1940’s they deleted it on the grounds that it was SYNTHESIS of my theory. As you can appreciate all ideas about cause would need to consider those findings, not just my theory, and it would be impossible to discuss the history of the ailment properly without mentioning the research into the cause of the abnormal breathing pattern. However, my two critics deleted all of that information and the references.
They replaced them with their own choice of references that supported their own point of view, but always claimed that it was for reasons related to sourcing policy, and on the eighth of February 2008 the critic named WhatamIdoing made this suggestion . . .
“Posturewriter, why don’t you put all this up on your own website? It would be a more appropriate home for such specialized material.” WhatamIdoing 20:34, 8 February 2008
here http://en.wikipedia.org/wiki/Talk:Da_Costa%27s_syndrome/Archive_1#WP:SYNTH.3F
I soon noticed that my time spent doing the reviews was being wasted by Wikipedia so I decided to set up a new section of my website called “References” and each deleted item was added below. One of the editors objections was that my reviews were too long for encyclopedia purposes, so I began to add all reviews of all articles onto this reference section first, and included everything that I knew to be relevant. I then periodically read them to decide which ones were relevant to Wikipedia requirements and, if necessary, abbreviated them and loaded them onto Wikipedia.
Since then my two main critics have been trying to mislead all other editors into believing that I was using Wikipedia to promote my own theory and website. I have given them that explanation but they continue to twist the truth and tell the folloing lies;
“he’s adding large verbatim dumps of material from his own website: not neutral stuff, but summaries of papers selectively collated and commented to support Posture Theory. He’s turning the Wikipedia article into an annexe of his own references section, and it needs to stop.” Gordonofcartoon10:55,14 May 2008″
here http://en.wikipedia.org/wiki/Wikipedia:Conflict_of_interest/Noticeboard/Archive_24#Da_Costa.27s_syndrome_take_.232
Note that I didn’t have a reference section on my website before I started on Wikipedia, and although I know a lot about the history of Da Costa’s syndrome, I have not written about it before, and it wasn’t necessary for me to do to promote anything, but now that I have spent 12 months doing the reviews I am not going to waste them. Also note that all reference to my own research and theory were deleted from the Wikipedia article in January 2007 (more than 12 months ago) and haven’t been added since.
(Note also that the 11th edition of my book called “The Posture Theory”, published in the year 2000, had 1000 pages of information about the effect of posture on a large range of ailments, and was supported by 130 references from a much broader range of sources, and a much longer period of history. I have also sent many letters and articles to newspapers and journals in the past, where about one in every four have been accepted for publication, and the others have been routinely rejected without any complaints from me, and without any editor making the ridiculous accusation that I am using their newspaper or journal to promote my ideas. They simply accept the fact that, in a normal situation anyone is entitled to submit an article, and any editor is entitled to reject it if he wishes. My acceptance rate was probably much higher than average so I didn’t bother complaining about such trivial matters of rejection).
You can also see, at a quick glance, by scrolling down this reference list, that it contains too much detail for an encyclopedia article, and needed to be assessed and abbreviated. You can also see that many authors made the same observations and statements, so I generally determined which authors made the best comments about particular aspects. and used their articles to minimise duplication.
For example the topic was based on the 1871 research paper by J.M. Da Costa, so I used it as the basis for the whole history, and I used information provided by MacKenzie in 1916, and Lewis in 1919 as a basis for the early history of the subject, and a good description of the health problems of patients during childhood was made by Caughey in 1939, so I used his rather than dozens of less thorough accounts, and a comprehensive follow up study of the long term outcome of the condition was provided by Edmund Wheeler in 1950, so I mentioned it specifically, and a good overall description was made by Paul Dudley White, so I used his 1951 book often, and a good summary of the history was made by Oglesby Paul in 1987, so I used it as a base for checking and summary. I left the modern history of the topic for my two critics to do, but they spent most of their time criticising me, so I ultimately completed the history to 2008 myself by using more than 20 references to cover the recent period.
Also note that the version that my two critics used as a replacement for the one that I prepared included 7 references that I provided, or were written by the same authors, and some of their others were links to only one sentence or one paragraph of information in lists, dictionaries, or websites, and there is some indication that the editors who were altering the content in Wikipedia were also editing one or more of those sites.
THE REFERENCE LIST
(2) Da Costa, J.M. (January 1871) “On Irritable Heart,” The American Journal of the Medical Sciences, p.18-52; J.M. Da Costa’s research article of 1871 provides the basis for the diagnostic criteria for a set of symptoms, which is why it was later named after him as Da Costa’s syndrome. The symptoms were chest pains, dizziness, breathlessness, palpitations, and fatigue, typically brought on by strenuous exertion, and were associated with a poor physique and a thin chest, and tended to occur during or following such things as viral infections, or the physcial strains of marching at double quick pace, and hard field service, and the waist belt and knapsack had something to do with it. The pulse was influenced by position, stooping, laying on the left and right side in some cases, and the back in others, and the condition was relieved by improved physique. Recommended treatment included not wearing clothing which constricts as it was liable to retard or prevent recovery. He gives the typical case of a man who was on active duty for several months or more and then contracts an annoying bout of diarrhoea or fever and then, after a short stay in hospital, returned to active service and soon found that he could not keep up with his comrades in the exertions of a soldier’s life as previously, because he would get out of breath, and would get dizzy, and have palpitations and pains in his chest, yet upon examination some time later he looked like a man in sound condition”. He also provided the general example of a seizure of distressing palpitations, chest pains, headache, dimness of vision, and giddiness which were . . . “most readily excited by exertion, and might be then so violent, that the patient would fall to the ground insensible”. Although the digestive disturbance which preceded the syndrome usually passed away, the other symptoms, particularly the abnormal response to exertion, would persist, sometimes for a long time afterwards. In his study of up to 300 cases he examined 200 of them in regard to the predisposing cause of this syndrome and he came to the conclusion that many factors seemed to overlap, but close study revealed that it was “Fevers” 17%, “Diarrhoea” 30.5%, “Hard field service, particularly excessive marching” 34.5%, and finally, “Wounds, injuries, rheumatism, scurvy, ordinary duties of soldier life, and doubtful causes” 18%. After the condition had been induced by such factors it tended to prevail in the short term and in some cases for long periods of time, but Da Costa also gives an example of complete recovery; in particular, Case 48 enlisted aged 17 with a thin chest of 27 inches, and suffered dizziness, cardiac pain, shortness of breath, and palpitations while on picket duty, and on one occasion while marching when he dropped out and discarded his knapsack and extra clothing, yet still struggled to keep up with the regiment. He was hospitalised and recovered but recommended for the veteran reserve. When examined in civilian practice 8 years later he was a tall, broad chested man who had spent most of the intervening years working in the open air as a mounted soldier. He only had two bouts of palpitations associated with bilious spells, and occasional colds, and otherwise had perfect health with no other symptoms at all, and could run up and down stairs without getting short of breath. Da Costa added that it was difficult to assess the cause and nature of the ailment and there was room for doubt and difference of opinion, however he concluded that “it enforces the lessons” of not sending troops “just convalescent from fevers, too soon to active work” and the importance of training young recruits in exercise and marching to accustom them to fatigue before they are called upon to undergo the wear and tear of actual warfare and the rapid and incessant manoevering of troops. .” (In a later article by another author the seizures described by Da Costa occurred in recruits at training camps when they were required to sprint along an obstacle course with a fully laden knapsack strapped to their backs, and collapsed to the ground after 50 yards with their hearts pounding, reaching for breath, faintness, dizziness, and extreme restlessness, which persisted for 20 minutes or more, and required several weeks in hospital to recover from – source unknown. M.B).- Such a violent response to that type of sudden or rapid exercise is a diagnostic criteria which can be used to distinguish Da Costa’s syndrome response to effort from the normal response to exertion seen in healthy athletes at the end of a 100 metres race in the Olympics, which involves reaching for breath, rapid but forceful pounding of the heart, partial collapse onto hands and knees for the purpose of resting, and a brief period of recovery. It also explains why most patients avoid exercise althogether, or drop out of inappropreately designed exercise training programmes where they are asked to ignore their symptoms and keep increasing the rate until they reach normal levels.© 27-12-17 & 29-1-08M.B.)
(3) Charles F.Wooley M.D. “Where are the Diseases of Yesteryear? DaCosta’s Syndrome; Soldier’s Heart, the Effort Syndrome; Neurocirculatory Asthenia – And the mitral Valve Prolapse Syndrome,” Circulation, 1976, vol. 53, pp.749-751. This article refers to cases which are associated with thin physique, and “in some the chest is long and narrow, or flattened and associated with a kyphotic curve.”The chest pain was sharp and lancinating, frequently referred to the left side, fatigue was almost universal, and “during exhausting work such as running , patients developed significantly high blood lactate concentration” . . . and “Describing the signs and symptoms as contrasted with those of heart disease” . . . he quotes “‘Lewis T. (Sir Thomas Lewis) who commented ‘it is because these symptoms and signs are largely, in some cases wholly, the exaggerated physiological response to exercise . . . that I term the whole the ‘effort syndrome.'” He also quoted Da Costa regarding what he called seizures of palpitations and chest pains where “The seizures’ were . . . most readily excited by exertion, and might be then so violent, that the patients would fall to the ground insensible.” . . . and . . . “The rapid action was often commented on; but a slow, hard beat of the heart was also spoken of.” Wooley adds “The fits of palpitation were associated with cardiac uneasiness and pain, headache, dimness of vision, and giddiness.” The article also reports that the condition affects sedentary workers, soldiers, especially those who came from sedentary occupations, and athletes, and was more common in women. This author also presented his account of the history of Da Costa Syndrome by commenting on the discussions relating to various chest sounds which were occasionally reported in previous studies, such as “the apical impulse was quick, abrupt or jerky, ‘sometimes the sounds of the heart are split . . . in (one case) the impulse was very irregular; there were double beats and intermissions”, and other odd sounds, and in some cases there were systolic murmurs above the apex. He compared these sounds to the systolic gallop rhythm and systolic clicks which were recently being designated as the nonejection systolic click. These sounds also occurred frequently in young subjects where there was no evidence of heart disease or psychoneuroses, and in nervous people. Wooley had also been involved in another more recent area of study of mitral valve prolapse syndrome and wondered if it was a new disease. He noted that a similar set of symtpoms were involved, namely chest pains, palpitations, breathlessness, and fatigue, and he was able to trace the condition back through reports by Wood, White, and Lewis, to Da Costa where he found that many of those cases involved descriptions of symptoms and sounds that would “certainly” fit the description of mitral valve prolapse syndrome. Ongoing studies showed that some of the heart sounds which were previously interpreted as coming from outside the heart were associated with billowing of the tricuspid leaflets, electrographic ST segment, T-wave changes, abnormal electrographic stress test results, arrhythmias, conduction defects, and abnormal valve motion and ventricular contraction patterns. Wooley’s purpose was “merely to establish the link between DaCosta, Lewis, neurocirculatory asthenia, an mitral prolapse . . . and to recall Lewis’ challenge to bring attitudes of deferred judgment and critical enquiry to our current investigations.”
(4) R.L.Dickinson M.D., Brooklyn (Nov 5th 1887) The Corset Questions of Pressure and Displacement, The New York Medical Journal: Presents a comprehensive review of corset and posture pressure measurements. http://en.wikisource.org/wiki/The_Corset Scroll down to Figure 15 on that webpage, which is related to the impairment of blood flow caused by corsets, postural pressure on the chest and abdominal cavities, and leaning forward in sedentary activities such as writing and sewing, which was up to double, breathing patterns became thoracic, and respiration reduced by one fifth. See also: Valsalva maneuver http://en.wikipedia.org/wiki/Valsalva_maneuver (5) Limner,L., Esq, Madre Natura Versus the Moloch of Fashion, 4th edition, Chatto and Windus, Picadilly, London, 1874, pp. 70-73. A list of more than 60 symptoms and ailments attributed to tight corsets by more than 30 eminent medical men (6) Withington, E.T., Hippocrates with an English Translation, Vol.3, William Heinemann, London, and Hippocrates (460-377 BC): On Joints XL1-XL2. Observations that spinal deformity above the diaphragm disposes to lung disorders and hoarseness, and those below the diaphram dispose to kidney and intestinal disorders. (7) Bulwer John (1650) Anthrompometamorphosis, London, U.K.- For the effects of natural and artificially produced variations in the shape of the human body on health, (8) Kellogg J.H.(1904) The Ladies Guide in Health and Disease, Echo Publishing Co.Ltd. Melbourne. – For a comprehensive review of the effect of tight waisted corsets on womens health in the nineteenth century. The diagram of the internal anatomy of a corseted woman was presented on facing page 244 of this illustrated 690 page book which had an attached booklet of diagrams and was widely available on public distribution in the U.S, the U.K. and Australia, and probably played a significant part in bringing the corset era to an end. (9) Maisel E. (1990) The Alexander Technique: The Essential Writings of F.Matthias Alexander, Thames and Hudson, London – For an account of Alexanders discovery of the postural cause of his voice problem, and how he cured it with a postural improvement tequnique. (10) Edith Sitwell (1930) Alexander Pope (Biography) First published by Penguin Books, Hammondsworth, Middlesex, U.K. in 1948. Describes Alexander Pope’s thin physique, upper and lower spinal deformities and scoliosis, wore a Corset, and wrote in his later years that he was dying of a hundred symptoms, and “writing is becoming very painful to me, if I would write a letter of any length. In bed, or sitting it hurts my breast; and in the afternoon, I can do nothing, still less by candlelight”. also Halsey W.D. (Editorial Director) (1962) Collier’s Encyclopedia Vol.19 p.241-242 The Crowell Collier Publishing Co. U.S.A. – For a summary of Pope’s health problems.
(4a) Wilson, W.D. (1904) Report on the medical arrangements in the South African War. HMSO; London, UK: 1904, p.73. This reference presents evidence that DAH was more likely to effect sodiers who had beem recruited from non-physical occupations, e.g.sedentary occupations, and were not given sufficient physical training prior to being sent on long arduous marches etc. . .“In the latter stages of the war, a large number of small columns were deployed against the Boers so that medical units had long periods of continuous marching to keep up with the widely spread engagements. It was concluded that the prolonged strain of carrying heavy weights and the pressure of straps on the chest had damaged the heart. An official report also argued that ‘cardiac exhaustion cases were much more frequent among men of volunteer companies than the regulars, probably due to the great difference of their usual daily occupation from the life of a soldier on active service”.
(4b)Baker Doris. M. (1955) Cardiac Symptoms in the Neuroses; H.K. Lewis & Co., Ltd. London : This small book describes the symptoms of Da Costa’s syndrome in clear detail and identifies it as a distinct diagnostic entity, and a common condition. Effort syndrome and neurocirculatory aasthenia are used as synonyms, and the symptoms include left-sided chest pain, palpitations, and sighing respiration occurring in response to effort, but also sometimes independently of effort.
(11) Paul Wood, M.D., (May 24th 1941) Da Costa’s Syndrome (Or Effort Syndrome), The British Medical Journal, Vol.1, 1941 p.767-772. . . (Paul Wood was then “Physician to Effort Syndrome Unit, E.M.S ; Physician to Out-Patients, National Hospital for Diseases of the Heart, and the following information is from the first of his three Gaulstonian Lectures to the Royal College of Physicians of London, 1941). The article mentions that the condition has also been called ‘the irritable heart of the soldier’, neurocirculatory asthenia, and ‘autonomic imbalance’. In world war 1 the British Forces had 60,000 cases of which 44,000 received pensions. It notes that it is also common in civilian life, and more common in women than men, and refers to the five classic symptoms of Da Costa’s syndrome, and syncope (fainting) in 34.5% of patients, ‘significant gastro-intestinal symptoms’ in 26%, and nightmares in 23%. The article includes the following information about the cause of the typical left sided chest pain of Da Costa’s Syndrome. “A complete review of the English and American literature, from the heated discussion in the British Medical Journal of 1858 (C.Coote; Inman; Fuller) to the latest remark by Spillane (1940), reveals the astonishing fact that not only the cause but also the site of origin of left inframammary pain is unknown . . . There have been, and still are, four main views as to its origin” namely that it has a cardiac origin, or is referred pain from faulty muscles or ligaments near the spine, or is caused by fatigue of the muscles associated with respiration, or that it is imaginary. He adds “There are three good reasons why the pain is not imaginary”. Firstly the nature of the pain is too uniform, and secondly “medical colleagues who have suffered from it are good witnesses to its reality”, and thirdly it can be abolished by certain injections inserted into the correct location. He also studied the physical possibilities and “Investigated the method of respiration in 150 cases of Da Costa’s syndrome. The cause of left sided chest pain was “elusive” but he found it to be within the muscular and fibrous structures of the anterior chest wall, and, although “very few patients had pain while these measurements were being made” it was related to functional disturbance and poor movement of the diaphragm, especially incomplete expiration, poor expansion of the chest, especially the lower chest, and was often associated with laying on the left side, “a posture which rests the thoracic muscles of respiration on that side at the expense of the diaphragm”. Similar pains sometimes occurred on the right side, and in other parts of the chest wall, and a more severe type of pain was reported in relation to muscular strains such as cranking a lorry engine or lifting a heavy weight. The article also contains a reference to an 1858 report associating the pain to scoliosis (sideways curvature of the spine) with concavity to the left, but Wood was unable to confirm that, and in his final sentence he concludes “it is predisposed to by poor physique in Da Costa’s syndrome; it is maintained and exaggerated by the belief that it arises in the heart. (It can be said that if all of the symptoms of Da Costa’s syndrome were incorrectly regarded as imaginary, and if the real cause of two of them has been investigated and found, then it follows that the real cause of the remaining will eventually be investigated and found, because they are all part of the same ailment, in the same patients, with the same minds, and the same truth in the words they speak. M.B.).
(11a)) Paul Wood, O.B.E., M.D. (Melbourne), F.R.C.P. (London), (revised edition 1956) Diseases of the Heart and Circulation, Eyre & Spottiswoode, London p.937-947 . . . Paul Wood, O.B.E., was Director, Institute of Cardiology, London . . . He wrote . . . “The syndrome is characterised by a group of symptoms which unduly limit the subject’s capacity for effort” . . . ” The cardinal symptoms” . . . of effort syndrome, neurocirculatory asthenia, irritable heart, soldier’s heart, disordered action of the heart (D.A.H.), etc. are “breathlessness (93%), palpitations (89%), fatigue (88%), left inframamary pain (78%), and dizziness (78%), or syncope (fainting) (35%)” . . . (the) Left inframammary pain is commonly described as aching or as sharp and stabbing in quality . . . and arises locally in muscle or fascia . . . It may be initiated . . . by fatigue or strain of respiratory muscles in cases with strain of certain muscular attachments . . . by incessant minimum trauma from . . . faulty posture” . . . and with regard to the breathlessness “It is not only a question of breathlessness on effort, but patients will say they are not able to obtain a satisfying breath, and may take “frequent deep sighs”. This can sometimes occur at night when it “may be confused with bronchial asthma or paroxysmal cardiac dyspnea”. and “A a simple and illuminating test” for the symptom involves forced hyperventilation where “The patient is asked to breath deeply and rapidly for one minute.” When a healthy person is asked to stop he feels breathless for about 20 seconds, but a patient with Da Costa’s syndrome “continues forced breathing, explaining later that he felt breathless.” i.e. there is “Dyspnoea instead of apnoea after forced breathing”, and “Normal subjects have no difficulty holding the breath for at least 30 seconds, but patients with Da Costa’s syndrome usually give up very quickly, 30 per cent of them in less than 10 seconds; moreover, in contrast to controls, they show little distress when the reach the breaking-point.” . . . With regard to the fatigue the patients often do not feel refreshed when they wake up in the morning, as if their sleep has been of no value, and they may “feel tired and listless during the day, and are unduly fatigued by effort. ” . . . (and) . . . Orthostatic dizziness is related to orthostatic hypotension . . . “The effort-tolerance test (for effort-intolerance) consists of stepping on and off a chair ten times, and counting the pulse rate before, immediately after, and subsequently at minute intervals until the resting speed is regained. The deceleration time is abnormal (over 2 minutes) in 33% of these patients.” . . . and . . . “Physical signs of autonomic dysfunction are helpful in . . . assessing the severity of the case.” . . . The photo of a painting of a Da Costa’s syndrome patient, which shows the typical round and sloping shoulders, thin chest, and kyphotic (or stooped) spine, is included on page 941.
Paul Woods Psychological Considerations of cause and effect: Paul Wood also discusses the cause and effect aspect by referring to the similarity of the symptoms of the effort syndrome with those of anxiety in healthy people, and also of the similarity of the symptoms to those of heart disease, and therefore suggests a psychosomatic cause. He advised the doctor not to mistake the left inframammary pain with angina pectoris as that will introduce or aggravate the patients fear of heart disease, which is based on a similar misinterpretation. He suggests that during childhood these patients were timid, and were mollycoddled by their mothers, and that later, in their school years, were protected from the hazards of sport and gymnastics, and developed anxieties about such things into adulthood. He adds “This constant anxiety, operating consciously or subconsciously every second of the day, and night, increases the severity of the psychosomatic symptoms. Under these circumstances the syndrome is maintained long after resolution of the original anxiety” . . . “until finally distressing autonomic reactions are so ingrained and so divorced from conscious thought as to be practically ineradicable”. In his summation he writes “Treatment is never easy, and is the more difficult the longer it is delayed. Failure is certain if any essential factor in the development of the symptoms is overlooked . . . First he must feel that at last he has met a doctor who thoroughly understands his case” . . . “The objective is to convince the patient that the symptoms are emotionally produced. One may point out how sudden fear causes palpitations, sweating, alteration of breathing, and sometimes a fainting attack. He will agree with this, but may object that he feels no such fear. One should then explain that great fear acting for a few seconds may be more than equaled by a tiny remote fear acting over weeks, months, or years, a state called anxiety”. (The advantage of Wood’s observations are that they provide evidence of the physical basis, however his interpretation of psychosomatic cause does not take into account the fact that the symptoms of the effort syndrome sometimes affect individuals who were formerly professional sportsmen or athletes, as was inferred in Charles Wooley’s 1976 essay “Where are the diseases of Yesteryear”, “the syndrome is not peculiarly . . . an athletes malady”, ” as has become more evident since. It is therefore evident that the physically based symptoms are not caused by a fear of exercise, but may result in concerns about the heart in some, but not all cases. M.B). (12) Edwin O.Wheeler, M.D., Paul D.White, M.D., Eleanor W.Reed and Mandel E.Cohen, M.D., Boston (1950), Neurocirculatory Asthenia et.al. (1950) – A Twenty Year Follow-Up Study of One Hundred and Seventy-Three Patients., Journal of The American Medical Association, 25th March 1950 p.870-889 . . . This research and the twenty page report was partially funded by a research grant from the Medical Department of the United States Army, and was produced by medical researchers from the Cardiac Research Laboratory, Massachusetts General Hospital and the Departments of Medicine and Diseases of the Nervous System, Harvard Medical School,.and was read before the section on Internal Medicine at the Ninety-Eighth Annual Session of the American Medical Association, Atlantic City, on June 8th 1949. The article includes references to associated studies which comment on the typical thin physiques, and long, narrow chests of the patients, the vasomotor response to exercise was below normal, with a lag in blood pressure and pulse response to standard exertion, and high blood lactate concentration, low oxygen consumption and low ventilatory efficiency during exhausting work. Most patients completed questionaires, and of the 60 who attended medical examination 11.7% were well, 35% had symptoms, 38.3% had mild disability, and 15% had severe disability. There was less co-morbidity, and longer life expectancy than average, perhaps because they were private patients who probably had above average incomes and sought the advice of a cardiologist, and many of those who reported partial or severe disability led quiet or moderate lifestyles. They reported that they never could do anything strenuous, and that they tired easily and rested often, and they worked slowly, took time off work, changed jobs, or resigned from work, including sedentary work (writing, nursing, teaching), or stopped working at night. In situations of strenuous or sustained activity or lifestyle their health deteriorated, so they resumed their former quiet lifestyle and recovered, and in several cases two or three times throughout their life before recognising and accepting the necessity and value of doing so. Some patients reported that it took several weeks each time, or more than a month, and in one case up to a year to recover from the severe episodes.
Wheeler’s Psychological Survey Conclusions: The study also considered personality aspects of the patients to determine the relevance of psychological factors in relation to the course of the ailment, and Wheeler summarised “from a personal and social point of view they seemed to be reasonably well adjusted citizens” and “Although these patients all have what is called “anxiety” . . . “they did not experience to any conspicuous extent any of the illnesses which are supposed to develop in persons with anxiety . . . such as peptic ulcer, diabetes mellitus, rheumatoid arthritis, asthma, ulcerative colitis, and hypertension.. . . “It is concluded that there is no evidence that anxiety causes these diseases.” However, some patients, when originally consulting a cardiologist, “had a fear of heart disease which played an important role in aggravating their symptoms”, and reassurance “that they had no heart disease . . . was an important factor in making them feel better”, but . . . “It is true that some patients were never convinced that they did not have heart disease”. . . . and there is “no consistent or conclusive evidence that patients treated by . . .(prolonged psychotherapy etc,) ) . . . got along any better than patients who have had little more therapy than simple reassurance and the passage of time.” The other treatments which were reported as not being any more effective than simple reassurance in the long term were adrenal gland denervation, electric convulsive procedure, frontal lobotomy, and sedatives and other medications etc. See that research paper here.
(13a) Sir Thomas Lewis (1918) The Soldiers Heart and the Effort Syndrome, Shaw & Sons, London p. 20-29: A large percentage of soldiers who developed the Effort Syndrome had poor physiques and long, narrow or flat chests associated with a kyphotic curve (hunchback spine) and many came from sedentary occupations. “It is
unquestionable that many men recruited from sedentary occupations
were affected by the condition before joining, although previous to that event in their life-history symptoms had never manifested themselves. The question naturally arises as to the extent to which sedentary work predisposes to the affection; no conclusive answer can be returned from the data at our disposal, though
these strongly suggest sedentary work a a predisposing cause”. Some of those soldiers experienced giddiness when standing up suddenly, or more rarely, even when laying down, and “a number of tested patients complained of equal giddiness when moved on a
swingboard into the lying position” . . . and this . . . “seems to be associated with faulty distribution of the circulating blood during the period of giddiness”.
(13b) T. Lewis (1919) The soldier’s heart and effort syndrome, New York, Paul B.Hoeber. Observations from World War 1. He called it the effort syndrome because in some cases the symptoms were “largely, in some cases wholly, the exaggerated physiological response to exercise . . . that I term the whole the ‘effort syndrome’.” The condition was associated with a thin physique, a long and flattened chest and other chest wall deformities, and a kyphotic curve.
(14a) T. Lewis (1933) Diseases of the heart, New York, The MacMillan Co. p.158-164. Not necessarily a soldier’s or an athletes malady “and is one of the commonest affections of sedentary town dwellers” and “Most of the soldiers came from sedentary occupations and a large percentage of the patients was affected by the condition in civil life many years before joining the Army”, and he considered the possibility that several distinct but similar syndromes were being confused at the time making it difficult to provide useful subdivisions.
(14b) Sir Thomas Lewis (1937) Diseases of the Heart 2nd edition, MacMillan and Co., Limited, London p.97-98 and p.158-164: There is a rare type of postural faintness which is associated with the faulty distribution of blood which tends to accumulated in the abdominal veins. This is closely related to cases where the person feels faint
when they stoop down to lace their boots or lift heavy weights, and it occurs because the mechanical or muscular action compresses the abdomen and
squeezes the blood out of the abdominal veins. When they stand up again the blood takes a few moments longer to fill the veins, and in the meantime blood
(15) Volkov V.S. (1980) Psychosomatic Interrelations and their clinical importance in patients suffering from cardiac type NCD., Soviet Medicine (11) p.9-15, English abstract ( and a translation): A comparative study of exertional capacities of healthy subject in relation to 228 patients with three stages of severity of the effort syndrome which was referred to as neurocirulatory dystony, NCD1, NCD2, and NCD3, where healthy males had an average of 1176 kg/min, and stages 1, 2, & 3 for NCD were 1161, 940 & 591 respectively for males, and for healthy females was 834, and the stages of NCD were 854, 621 & 420 kg/min. respectively, indicating that the severity of the condition was related to the efficiency of circulation and exertional capacity. 87.2% of patients tolerated 600 kg/min. or more, but 14 of the others had to stop because of overwhelming, irradiating heart pain, and would stop because of general fatigue and “fear for their hearts”. 15 other patients stopped their test prematurely because of changes in their heart rates which reached sub-maximal levels.
(16) Banfield M.A. et.al., (Dec. 20th. 1982) SA study matches Russian results, Adelaide “News” p.18: As reported by journalist Diane Beer, Similar findings to Volkov (1980) were made at the South Australian Institute for Fitness research and Training, with regard to the measurements of fitness levels of patients with chronic fatigue. An exercise programme was designed on the basis of the assumption that previous attempts to determine the effects of exercise had been unsuccessful because the organisers had assumed that there was nothing physically wrong with the patients, or that they were simply unfit from lack of exercise, and that they should be able to participate in a normal exercise programme where they were required to gradually improve their fitness to normal levels, and hence return to normal health. The patients were probably reaching a level where they started to get distressing symptoms, and therefore lost faith in the reassurances of the course directors and dropped out of the programmes too soon to get meaningful results. The South Australian programme was designed on the basis of the assumption that the patients could train if they exercised and continued to improve within their own limits. Several programmes were started 3 months apart, and ultimately 80 patients were medically assessed on an ergometric cycle where load was increased over several intervals of rest, and pulse was recorded at each level to produce a graph which provided the standard scientifically reliable estimate of physical exertional capacity which was objectively independent of other factors. In the first year 11 started but did not complete three months training. Four of those were examined six months later and were found to have much the same results. 9 completed three months training for two hours, twice per week, and 5 completed six months or more. Significant improvement was seen in three cases which started below 400 kgm/min, and 3 cases improved but plateaud below 600 kgm after the third month indicating chronicity. One of the initial trainees entered a six mile marathon 12 months later and completed it. The newspaper article and several others between 1982 and 1983 presented a generalised news account of those findings. CFSoriginalResearchIFRT1982-84The study added to the Russian results by measuring the aerobic capacity before commencing a fitness training programme, and again after, to determine the effects of exercise. The study also found that in one group where six people trained for three months in the same class there position on the walking or jogging track corresponded to their measured level of aerobic capacity, and those who reported that they had to restrict their lifestyle before starting the programme were found to have low aerobic capacity, and those whose lifestyle had been unchanged had normal to above average results. It was also noticed that there was some inconsistency in physique where not all of the participants in the programme had the thin and stooped profile sometimes described as typical in the literature.
| The Posture Theory and the Mechanism for Orthostatic Hypotension, Orthostatic Intolerance, Effort Intolerance, and Exhaustion;Evidence and Proof of Concept from 1916 © February 2008According to The Posture Theory, when individuals with stooped spines and flat chests lean toward a desk and bend forward at the waist, they compress the air in their chests and impede the flow of blood from their feet to their hearts. This produces repetitive resistance to blood flow and ultimately strains and stretches the walls of the leg and abdominal veins. In the early stages the person may notice that when they stand up suddenly they feel faint and dizzy for a few seconds. That happens because the sudden weight of blood stretches the weakened walls of the veins so that the blood temporarily pools in them instead of continuing toward the heart and brain at the normal flow rate, and the brain is deprived of its full blood supply until the widened veins fill and full flow starts again. Similarly, when a person suddenly sprints in a race the heart pumps blood out into the arteries with great force and when it enters the veins they stretch abnormally, the blood pools in them, and the return of blood to the right side of the heart is weaker, so it pounds excessively and the person feels suddenly faint, dizzy, breathless, and exhausted, and may feel heart pain, despite the fact that there is nothing wrong with the heart itself. (The heart pounds and races to compensate for the abnormal fall in blood pressure during sudden exertion). The slower flow of blood through the lungs results in an insufficient exchange of oxygen and carbon dioxide which affects the blood chemistry, and doesn’t meet the demands of the exertion, so that an oxygen debt accumulates in the blood until flow stops or a threshold is reached, and the person stops running, falls to the ground and begins forcefully gasping for breath, which probably has the effect of forcing oxygen into the small amount of blood passing through the lungs. The persons heart would continue pounding and racing, and they would continue to be exhausted, faint, and gasping for breath until the blood flow returned to normal levels and sufficient oxygen had been inhaled and transferred into the blood stream. Also, if the blood flow slowed in the early part of the sprint there would be less pressure on the incoming side of the heart valves, which may dispose to temporary functional valve prolapse. These features have all been observed and recorded in research studies, but the forced breathing has generally been regarded as anxiety induced hyperventilation and the changes in blood chemistry has been interpreted as evidence in support of the idea that hyperventilation is the cause, and the mitral valve prolapse has been generally interpreted as the cause of symptoms instead of vice versa, The sense of faintness which a person feels when standing up suddenly is due to the temporary lowering of blood pressure and is therefore called Orthostatic Hypotension, and it can effect healthy people if they don’t drink sufficient water and stand out in the hot sun for long periods of time, or suffer from dehydration. or any factor which reduces the volume of blood in the veins. It can also affect teenagers who grow too tall too quickly, and mild forms of orthostatic hypotention can effect people with varicose veins in the legs, or those who wear tight safety harness straps around their legs which impairs the flow of blood from the feet to the heart. However in more severe forms, where the veins of the legs and the veins of the abdomen are weak or dilated, the person may get the severe symptoms in relation to exertion, which is called Orthostatic Intolerance, Postural Orthostatic Tachycardia Syndrome, or Exertional Intolerance. Such people may feel well while resting, but if they start jogging they may get a sense of uneasiness in the chest, as the flow of blood returning to the heart slows, and that feeling may deter them from running faster, and hence a good way of controlling the condition involves exercising within certain limits, which is called ‘pacing‘. M.B.(17) Wintrobe M.W. et. al. (editors) (1970) Harrison’s Principles of Internal Medicine; 6th edition, McGraw-Hill Book Company, New York. p.106-108 & 225: reference to intra-thoracic pressure – tussive syncope (fainting caused by coughing), and tight collars, tilt table tests, varicose veins and gravitational blood pooling as a cause of orthostatic hypotension, and refers to vasovagal or vasodepressor fainting in relation to conditions which favor vasodilation, and as a symptom of neurocirculatory asthenia. . . . and chronic hypotension as a cause of lethargy, easy fatigueability, presumably due to decreased perfusion of the brain. See also; reference 20, M.A.Banfield April 1980, Hypothetical Shock Mechanisms, Australasian Nurses Journal p.16-18.
(35) Mackenzie, Sir James M.D. (January 18th. 1916) Discussion On The Soldier’s Heart, Therapeutical and Pharmacological Section, Proceedings of the Royal Society of Medicine, Vol.9, p.27 -36; Evidence for the Posture Theory and the relationship to Orthostatic Hypotension and Exertional Intolerance is seen in the following quote from Sir James Mackenzie M.D. in 1916 – regarding the symptom of exhaustion “There is a persistent over-action of vasomotor influences” . . . and sometimes . . . “flushes of heat pass over the body, and warmth may tend to overfilling of the peripheral vessels. This is seen in people who faint when standing in a warm room, or who speedily become exhausted or even faint when exertion is made. In these, the blood tends to accumulate in the peripheral veins of the limbs and in the large abdominal veins, with consequent anaemia of the brain. It is because of this anaemia of the brain that the sense of exhaustion and syncope are provoked”. The author presented this description to show that this type of exhaustion is related to vasomotor disturbance and was not the same mechanism which produced exhaustion of the heart itself. He also referred to the importance of the judicious use of exercise which should involve the simple principle of exercising “so long as it gives him pleasure and causes no distress or discomfort, but to stop or slow down as soon as he experiences the sense of exhaustion, breathlessness and pain.” (The fact that blood accumulates in the abdominal veins is evidence of the posture theory in regard to abdominal vein dystonia M.B.).
(42) Streeten David H.P. (Sept.1998), The Nature of Chronic Fatigue Syndrome (CFS), J.A.M.A. v.280, n.12, 23-9-98, Editorial. (David Streeten is from the Department of Medicine, State University of New York Health Science Section, Syracuse) David Streeten presented an article in the September 23rd edtion of JAMA explaining that the fatigue reported by Da Costa and Lewis were early descriptions of a “newly recognised” delayed form of orthostatic hypotension which is a feature of some types of Chronic Fatigue Syndrome. He stated that “as a working hypothesis”, the fatigue was due to abnormal pooling of blood in the lower limbs which delayed and reduced the flow of blood and oxygen supply to the brain. That effect was compounded by a reduced circulating red blood cell mass. He then emphasised that it is essential to identify these physical abnormalities by repeatedly measuring the patients blood pressure in recumbency and after standing for ten minutes or tilt testing, and that “it is inappropriate to consider that CFS is a manifestation of mental disorder” unless those physical causes are excluded. He added that the expense of these tests was not unreasonable considering that almost every type of work or lifestyle required a person to stand for six hours per day without experiencing the symptoms associated with reduced blood pressure. He then concluded the instigating cause remains unknown, and that effective and safe treatments for the debilitating symptoms are still not available and that further research is required.
(49) Krzysztof Narkiewicz (1998) Chronic Orthostatic Intolerance; Part of a Spectrum of Dysfunction in Orthostatic Cardiovascular Hoeostasis?, Circulation 98:2105-2107. This paper reports on the study of postural orthostatic tachycardia syndrome, and attributes to the gravitational pooling of blood in the lower limbs caused by “impaired venous tone” where “It is generally accepted that autonomic dysfunction is a hallmark of this disorder.” |
| The Posture Theory, Chest Compression, and breathlesness when leaning toward a desk (started 23-6-08)(17a) Banfield M.A. (May 1978) To Breathe or Not to Breathe – Is that the Question?, Australasian Nurses Journal, May 1978. p.5-6.
In one of my essays of 1978 which contributed to The Posture Theory conclusion of June 1980, I considered the effect of leaning toward a desk, with the pressure of the head and shoulders putting downward pressure on the chest, while at the same time wearing a tight waist belt, which would prevent downward movement of the abdominal contents during the inhaling phase of breathing. The combined effect of pressure on the chest from above, and pressure from below, would produce a sandwich effect of increasing the pressure in the chest cavity, and also straining on the thoracic diaphragm (the breathing muscle), and dispose to breathlessness. The problem would be more likely to effect individuals with kyphotic or hunchback spines who bent at the waist, so that their spine bent in the middle, and added to the pressure when they leaned forward, but probably wouldn’t have much effect on individuals with straight spines who bent from the hips so that the back remained straight as they leaned forward. Eating large meals which filled and enlarged the stomach, so that it also compreseed against the chest, would also add to the pressure. In other essays I also suggested how the pressure would also effect blood flow through the chest to cause a Valsalva’s maneuver each time. Those essays were written to explain why a person would feel breathless, and, or faint etc. each time they leaned toward a desk, and how many years of such sedentary activity could cause chronic breathlessness, faintness, and hence fatigue. Many years later, in one of the editons of my book, I included the restricting influence of tight collars which would impair the blood flow to the head, and hence add to the prssure of blood in the chest. The other two references in this section, provide confirmation of the validity of those observations, and add the influence of heavy weights being attached to the tight belts etc, which would also add to the tightness, and hence add to the pressure inside the chest. M.B.
(17b) Myers, A.B.R. (1870) On the etiology and prevalence of diseases of the heart among soldiers. John Churchill & Sons; London, UK: 1870 p.81.“His waist-belt adds to the constriction below the chest, and his tunic collar above it and then, to complete the artificial chest case, the knapsack straps supply all that is requisite, whilst the pouch-belt adds its share to the general compression. The chest, thus fixed as it were in a vice, has little or no power of expansion, and the circulation through the heart, lungs and great vessels is proportionately impeded.
(17c) Maclean W.C (1867) Diseases of the heart in the British Army, the cause and the remedy. Br. Med. J. 1867;1:162.”The pack-straps press on important muscles, arteries, veins and nerves to a degree which only those who have carried the loaded pack can appreciate. The weight, especially when the greatcoat is strapped on, falls, to a great extent, without the line of the centre of gravity You can well imagine how impossible it must be to make severe exertion under so many disadvantages without suffering.
(17d) Howell, J.D. (1998) Soldier’s heart: the redefinition of heart disease and speciality formation in early twentieth century Great Britain. In: Cooter R, Harrison M, Sturdy S. , editors. War, medicine and modernity. Sutton Publishing; Thrupp, Stroud, UK: 1998. pp. 85105′ :Late-nineteenth century investigations of DAH (Disorderly Action of the Heart – Da Costa’s Syndrome) identified a mechanical pathology, whether hypertrophy, valvular lesion or aortic dilatation and proposed mechanical causes, commonly an obstruction of the heart’s outflow.
See also: Edgar Jones (April 29, 2006) Historical approaches to post-combat disorders, Philosophical Transactions of the Royal Society of London, Britain, (Biological Sciences), p.533-542
Regarding Palpitations etc
(2) Da Costa, J.M. (January 1871) “On Irritable Heart,” The American Journal of the Medical Sciences: On page 38 of Da Costa’s original paper he writes “Undoubtedly the waist belt, but particularly the knapsack, may have had something to do with aggravating the trouble; but I could find no proof that they had produced it” . . . and on page 37 he described how some healthy soldiers tried to fake the condition “as is well known (they) may keep up a rapid action of the heart by a tight bandage around the upper part of the abdomen and lower part of the chest”, but one way of checking the matter is by “making him lie down after undressing (which) causes the heart to return to its natural beat”. Note that the temporary effect of tight bandages around the chest for a few minutes is not going to have the same chronic effect as marching for 26 miles at fast pace while having poor food, a fever, and tight straps about the chest and carrying a full 60lb knapsack, as was the case with some of Da Costa’s patients, as described in paragraph 2 of page 38, and paragraph 4 on page 39 etc. Note also that the soldiers who developed Da Costa syndrome tended to be those who had previously been sedentary desk workers, and were sent off to war without any physical training,, and were required to keep up the same marching pace as those who had previously been farmers and worked 16 hours a day in the fields as manual laborers. M.B.
For scientific measurements of pressure inside the chest related to tight clothing in 1997 click here
In the seventeenth century Shakespeare wrote in his play Richard 111, “Oh, cut my lace in sunder, that my pent heart (compressed heart) may have some scope to beat, or else I swoon (faint).” |
(18) Banfield M.A. (March 1979) Introduction to Essays on Effort Syndrome, Australasian Nurses Journal, Port Adelaide, South Australia. p.26-27: A commentary on the interrelated subjects of Da Costa’s Syndrome, Hyperdynamic Circulatory State, Neurocirculatory Asthenia, Pono Palmosis, Shell Shock, Battle Fatigue, Traumasthenia, Vasoregulatory Asthenia, Anxiety Neurosis, Cardiac Neurosis, Cardiophobia, War Neurosis, Cardiac Asthenia, Cardiovascular Neurasthenia, Disorderly Action of the Heart (D.A.H.), Functional Cardiovascular Disease, and Irritable Heart.
(19) Banfield M.A. (Dec.1979) Some Hypothetical Mechanisms for the Symptoms of Neuroses During Pregnancy and Exercise, Australasian Nurses Journal, Port Adelaide, South Australia. p.30-31; A theory on postural compression of the chest cavity as a mechanistic Valsalva’s Maneuver with manifestations of dysautonomia.
(20) Banfield M.A. (April 1980) Hypothetical Shock Mechanisms, Australasian Nurses Journal, Port Adelaide, South Australia. p.16-18; A theory presenting a sequel of emotional stress, chest cavity compression, vena caval and peripheral vascular dystonia and abnormal dilatability, gravitational circulatory derangement (orthostatic hypotension), non-hypo volemic shock, ending with manifestations of dysautonomia.
(21) Nixon P.G. (Oct.1993) The grey area of effort syndrome and hyperventilation: from Thomas Lewis to today, Journal of the Royal College of Physicians of London, Oct;27(4);377-83. “Lewis used the diagnosis ‘effort syndrome’ for subjects whose ability to make and sustain effort had been reduced by homeostatic failure”, and he regarded it as a systems disorder with a metabolic element which was important to recognise in order to prevent “the invention of fanciful, unphysiological diagnoses”. His ideas were dismissed at the time because the metabolic abnormality was not apparent at rest and only occurred during physical exertion. Today, effort syndrome is still a useful description for the condition . . . and . . . “it may be a mistake to treat chronic fatigue syndrome and unspecific illness without including it in the differential diagnosis”.
(22) Wolf S. (Nov. 1947) Sustained Contraction of the diaphragm, the mechanism of a common type of Dyspnoea and precordial pain. Journal of Clinical Investigation, Vol. 26, p.1201: These findings were presented at the Proceedings of the Thirty-Ninth Annual Meeting of The American Society For Clinical Investigation held in Atlantic City, N.J. on May 5, 1947: Regarding “respiratory distress characterized by inability to get a full breath”: Flouroscopic observations showed that the diaphragm function was abnormal in patients who were anxious, and others who were not . . . and when some of them were put in discussions of situational conflict the changes in inspiration and expiration were evident, and when the diaphragms contractile state during inspiration was such that adequate inspiration was no longer possible, breathlessness occurred with a feeling of inability to take a full breath. The spasm of the diaphragm was often accompanied by pains in the chest and shoulder, occlusion of the lower end of the esophagus, and difficulty swallowing.
(23) Cohen M.E., Johnson R.E., Consolazio F.C., and White P.D. et.al, (Nov.1946) (from Massacheusetts General Hospital, Harvard Medical School, and the Fatigue Laboratory, Harvard Graduate School of Business Administration): Summary: Low oxygen consumption and low ventilatory efficiency during exhausting work in patients with neurocirculatory asthenia, effort syndrome, anxiety neurosis, v.25 (6) (1946) p.920, and the full article Studies Of Breathing, Pulmonary Ventilation And Subjective Awareness Of Shortness Of Breath (Dyspnea) In Neurocirculatory Asthnia, Effort Syndrome, Anxiety Neurosis. Nov.23 (1946) p.339-342, and Blood Lactate Response During Moderate Exercise In Neurocirculatory Asthenia, Anxiety Neurosis Or Effort Syndrome Dec.23 (1946), Journal of Clinical Investigation: A comparative study of 20 men with N.C.A. and 20 healthy men on a treadmill found that during hard muscular work, “N.C.A.. patients consume less oxygen, have a lower ventilatory efficiency and show a higher blood lactate than do healthy control subjects of comparable age. Some of the tests were conducted on a larger number of patients. The data are all consistent with the idea that aerobic metabolism in hard muscular work is abnormal in N.C.A. and suggests high oxygen debt.” Comparative studies for three minutes running on a treadmill were maximum oxygen consumption per kgm. body weight and minute with an average of 36.8 ml. for N.C.A., and 47 ml.. for healthy patients of the same age. The data was taken each minute for three minutes, and for each minute was 33.8, 40, & 37.7 ml/kgm body weight for N.C.A. and 35.0, 43.9 & 46.5 ml/kgm. for healthy men of the same age, showing a progressively greater difference with the duration of the run. Also, in blood samples taken 5 minutes after the run the average was 1.31 mgm. of blood lactate per 100 ml of blood and second of running for the N.C.A. patients, as compared to 0.60 mgm. for healthy men, and ventilatory efficiency was lower at all times in the N.C.A. patients. However this particular study did not determine if this was due to poor general health, poor fitness, or lack of training, and “An attempt to train some of these men was unsuccessful as the men did not train properly” Studies by other authors concluded that this was “simply a matter of lack of “persistence”” but this study showed that “this lack of persistence is usually associated with a chemical abnormality – that is, increased blood lactate concentration”, and although the exact mechanism cannot be determined yet “our evidence. . . suggests deficient aerobic metabolism and excessive oxygen debt.” (This review was prepared from my references and notes associated with my 1982 research paper; re; “An attempt to train some of these men was unsuccessful as the men did not train properly” . . . and . . . these patients showed “lack of persisence” in physical training; Why?)
(23a) Cohen M.E. and White P.D. (May 1947) Studies Of Breathing, Pulmonary Ventilation And Subjective Awareness Of Shortness Of Breath (Dyspnea) In Neurocirculatory Asthenia, Effort Syndrome, Anxiety Neurosis, Journal of Clinical Investigation, Vol.26(3), May 26th 1947) p.520-529; (Received for publication December 23, 1946: “In neurocirculatory asthenia, anxiety neurosis, or effort syndrome many respiratory symptoms occur in high incidence. This constitutes a characteristic and therefore diagnostic feature of the disorder; the absence of such symptoms makes the diagnosis of N.C.A. improbable. The complete mechanism of these symptoms is unknown but it is of interest that when respiration is investigated objective abnormalities are found, just as when other symptoms of N.C.A. are investigated with objective methods, which demonstrates that the abnormalities are not all in the subjective sphere“. The respiratory abnormalities at rest are few but during exercise the abnormalities become more pronounced; the deviations from the normal becoming greater as the rate and amount of exercise increases. “It is of interest particularly since the patient’s’ disability involves especially hard work.” In their more detailed account of the condition Cohen and White report that the higher incidence of breathing symptoms in N.C.A. is more pronounced in the chronic cases than in acute forms, and when the patient is required to wear a gas mask or when swimming. Respiratory rate is greater but breathing is shallower and sighing is more frequent than normal. “The resting minute respiratory volume, with persons seated and breathing air, is slightly but significantly higher in patients”. . . and “Both the awareness of and outward appearance of shortness of breath are related in N.C.A. to some factor or factors, other than amount of pulmonary ventilation”. During walking there is higher pulmonary ventilation and a lower ventilatory efficiency, and the difference between the total ventilation of patients compared to healthy controls become greater “as the pace of exercise becomes more rapid” . . . and is “more marked after exercise than during exercise”. “Not only do more patients feel shortness of breath but they also report feeling a greater degree of shortness of breath”. The study of respiratory rate and tidal volume showed that there was a difference in minute respiratory volume between healthy controls and N.C.A. which incicated that it was due to the greater respiratory rate. Also subjects awareness of dyspnea and distress as related to ventilation iindex shows that for the same range ventilation index a higher incidence of patients reports shortness of breath or discomfort as compared with controls. “This shows that the incidence and degree of dyspnea in N.C.A. is not only out of proportion to the amount of exercise, but also is out of proportion to the amount of ventilation and ventilation index”. The results of this study showed “that during running ventilation starts higher but ends lower; as the run progresses, ventilatory efficiency is low at all intervals of run for N.C.A. “. In summarising the study of ventilation, it was found to be higher in N.C.A. patients doing moderate work, compared to healthy people, and “it is higher as hard work begins but becomes lower as hard work progresses.” The ventilation was disproportionately high after exercise and “may be related to other evidence of increased oxygen debt in N.C.A. and high blood lactate after exercise.” “The evidence of poor ventilatory efficiency corresponds interestingly, although it may not explain, another symptom which patients have which is that they ‘can’t get in enough air’ or that ‘air doesn’t seem to do as much good as it should'”. The concluding discussion mentioned that if the type of N.C.A. breathlesness is to be studied effectively the definition of the word dyspnea needs to mean the same thing to all who use it and . . . “it should be used uniformly to mean the same thing by all observers”. . . and by implication involve the same response to exertion. (Like many authors, Cohen and White refer to the fact that the study of symptoms needs to be based on clear descriptions of them, so that they are not mixed in with other groups of similar but slighlty different symtpoms, which would make studying them confusing and give inconsistant, variable, and therefore meaningless results.M.B.)
(24) Baker D.M. (1942) Cardiac Symptoms in the Neuroses, H.K.Lewis & Co., London. This small book provides individual chapters on each of the main symptoms of Da Costa’s syndrome.
(25) Fulcher Kathy Y. & White Peter D. (June 7th 1997) (of the National Sports Medicine Institute, St Bartholomew’s, and the Department of Psychological Medicine of the Royal London Medical School, London) Randomised controlled trial of graded exercise in patients with the chronic fatigue syndrome, British Medical Journal, June 7th, 314(7095):1647-52; Criteria for the study . . . The chronic fatigue syndrome related to physical deconditioning, sleep deprivation and psychological distress. The physical deconditioning may result from reduced physical activity, and this may have detrimental physical and psychological effects which can be improved by fitness training. (“A similar programme improved symptoms and physiological findings in an open study of patients with the ‘effort syndrome'”). . . . Results of the study . . . “66 patients with the chronic fatigue syndrome (according to the Oxford criteria) who had neither a psychiatric disorder nor appreciable sleep disturbance” were randomly allocated to 12 weeks of graded aerobic exercise, or flexibility exercises and relaxation therapy. Only five of the original 71 refused to start the trial, and the remaining all gave valid informed consent to participate. The exercise programme was supervised with each patient being prescribed a starting level determined by their existing capacity, and was gradually improved each week “to a maximum of 60% of peak oxygen consumption”, and each patient was provided with an ambulatory heart rate monitor and instructed not to exceed their prescribed heart rate targets. “The main exercise was walking, but patients were encouraged to take other modes of exercise, such as cycling and swimming. Patients were advised not to exceed prescribed exercise during a good phase. If patients complained of increased fatigue they were advised to continue at the same level of exercise for an extra week and increase when the fatigue had lessened”. Four patients doing the exercise programme, and three doing the flexibility training dropped out before completing the course. However, according to the self rating scores of patients who did complete the programmes, “Fatigue, functional capacity, and fitness were significantly better after exercise than after flexibility treatment”, and 32 of 47 patients rated themselves as better three months after completing supervised exercise treatment, and 35 rated themselves better one year after completing the training, and only one patient claimed to be worse off, with the conclusion that “support the use of appropriately prescribed graded aerobic exercise in the management of patients with the chronic fatigue syndrome”. It was noted that the improvement in the aerobic capacity of patients with CFS who trained, was 13%, which was greater than the 5-10% improvement seen in healthy sedentary people who participated in similar courses. Also, in the CFS patients “Both physiological and perceptual improvements occurred at submaximal treadmill stages after exercise treatment . . . This is clinically important as submaximal activities such as walking are functionally more important than maximal activities such as running”. “The only other treatment of the chronic fatigue syndrome to show promise is cognitive behaviour therapy, which improves functional capacity and symptoms more than both standard medical care and relaxation therapy”. The authors end by discussing the problems in comparing the benefits of exercise treatments with other studies because they may include patients with differences in perceived physical incapacity and co-morbid psychiatric factors. This BMJ paper is supported by 32 references, and had been cited by 40 research journal and other articles.
(26) White P.D. (1951), Heart Disease, 4th. edition, MacMillan, New York, N.Y., p.578-591: In 1913 Paul Dudley White was offered a Harvard traveling fellowshipship to study cardiovascular physiology with Thomas Lewis in 1913, and then he had extensive experience working as a military doctor in Word War 1, and was a founding member of the prestigious American Heart Association, and president of that organisation in 1941, and became emeritus professor of Harvard in 1949. In 1951 the fourth edition of his book “Heart Disease” contained a chapter on “Neurocirculatory Asthenia”, because, as he explains, the symptoms are similar to heart disease, but are not the same, and he adds, that they are also similar to, but can occur in the absence of anxiety, and therefore need to be discussed separately. He gives the definition of N.C.A. as the typical group of symptoms of breathlessness, often with sighing, palpitations, precordial aches and pains, exhaustion, and related symptoms such as dizziness and faintness, which are precipitated by excitement or effort, and “it constitutes a kind of fatigue syndrome” . . . and in some cases . . . “it is more or less a chronic condition” . . . and . . . “That such a state of ill health exists there can be no doubt, no matter what its pathogenesis or exciting factors.” “The effort syndrome, though easily induced, might be at first thought to be unworthy of any special discussion” as it is not apparently organic, and may occur in perfectly normal persons, but it is important, because in some individuals “it is very easily induced.” and it can be “completely incapacitating”. . . “and it is not a normal response to effort. Also the symptoms are not exactly like those produced by effort in a normal healthy person. Some of these individuals are “unable to maintain any degree of physical effort, and quickly accumulating respiratory inefficiency and an excess of lactic acid on exercise.” Also, in some patients the neurocirculatory symptoms are prominent but in others it is gastrointestinal or cerebral symptoms, but the reason for those differences “has not been explained”. The general causes of the condition appear to include such strains as worry over business, social, or family matters, emotional conflicts, physical or nervous fatigue, and exhaustion from acute infections or illnesses. The organic basis is not known although it may involve a disorder of the autonomic nervous system. Other possibilities which have been considered in the past 25 years, include thyrotoxicosis, low-grade infection, adrenal hyperactivity, hyperventilation, and lack of salt, but none have been confirmed, and there is no known pathology. However many of the patients have thin physiques with an “unusually vertical position of the heart”, an easily induced oxygen debt on exercise, and “Another interesting finding is abnormality of shape of the capillary loops at the base of the nail”. . . “It is common to find that the close relatives and recent ancestors of patients” have had similar problems, and “Recent studies have suggested that neurocirculatory asthenia belongs to the Mendelian dominant group of inherited disorders.” It was common in World War 1, occurred in civilians as well as soldier’s, and it is generally seen in young adults, but can occur at any age, and is more common in women than men. Regarding the symptoms, the breathlessness is subjectively unpleasant, and sometimes involves abnormally rapid breathing, and another feature is a characteristic type of sighing which occurs occasionally and can be used to distinguish it from heart disease. “The left breast tenderness is distinctive evidence” of the condition and the precordial pain occurs in that area and is sometimes an ache, and on some occasions there may be sudden, brief, sharp, stabbing pains. The fatigue sometimes produces more incapacity than heart disease, and in some cases results in complete disability. “It is a real and not an imaginary incapacity, even though at first glance it may have appeared imaginary in World War 1 (1914-1918) when it was sometimes labelled ‘malingering,’ and even though in civilian practice it has frequently been diagnosed as ‘mere nervouseness’.” It is milder in civilian life than in war and it is so commonly associated with psycho-neurosis of the anxiety type “that the two conditions have sometimes been confused one for the other or considered to be synonymous, the term anxiety neurosis having come to mean for many the same collection of symptoms which identify neurocirculatory asthenia.” The course of the condition is variable, but does not appear to effect life expectancy. Treatment involves rest for days or months or as long as required, and elaborate psychotherapy is generally not needed. “In fact, since this condition is neither heart disease nor mental disorder, both cardiologist and psychiatrist are well kept away after the diagnosis has been established, so that the patient may not develop unnecessary fears about either heart or mental state.” “The condition must be discussed seriously, not lightly as if it was of no importance”, and it is equally wrong to dismiss it as negligible or imaginary, as it is to to regard it as dangerous or serious and a threat to life which demands bed rest. Careless disregard will alienate patients and have them seeking advice from charlatans. “The plan of life for the patient needs to be worked out with care” where usually normal but quiet work and play are required, with the avoidance of late nights, excessive efforts, and long hours of work or taking on new or burdensome tasks. “Often the patient himself is aware of this necessity, but he has perhaps disliked to humor his symptoms or to fall behind his fellows in strenuous living in the business, professional, or social world. With clear medical advice, however, he realizes the wisdom of doing so, and gradually he adjusts himself to suit his symptoms, and is surprised at recapturing a feeling of well being.” (This review of chapter 22 of P.D.W.’s book was prepared from my notes associated with my 1982 research paper, and placed on this web page on 25-1-08. M.B.)
(27) Mandel E.Cohen, M.D., and Paul D.White M.D. (1972), Neurocirculatory Asthenia: 1972 Concept, Military Medicine, April, p.142-144; The classic symptoms of chest pains, breathlessness, palpitations and fatigue were defined with the comment “The symptoms are not identical with the symptoms of fear, effort, thyrotoxicosis, or convalescence, although there are some resemlances.” The condition was also discussed with reference to the history of the subject using the usual terms of Da Costa’s syndrome, effort syndrome, soldier’s heart, etc,. with the added comment “so many terms have been used for conditions featuring these symptoms that the diagnosis may be obscured by too many names. Although many of the diagnostic terms change or even disappear, the syndrome persists and is common in both war and peace.” They noted that the patients generally had thin physiques and were poor athletes and especially poor swimmers, and they mentioned that when they were medically assessed at rest “there are only a few abnormalities” but “in response to a variety of stresses and stimuli, many definite and interesting abnormalities appear” especially during exercise when breathing rate increases and becomes disproportionally shallow . . . and . . .evidence showed that “aerobic metabolism was defective in these patients” . . . and . . . “Attempts to train patients to better performance were not successful in our observation.” Also, “It has been known since World War 1 that these patients have been particularly intolerant to carbon dioxide” and when they rebreath an accumulated mixture there is “a significant increase in sighing respiration . . . and . . . the appearance of ‘anxiety attacks'”. “These ‘anxiety attacks’ did not occur in healthy controls subjected to breathing carbon dioxide” . . . and . . . “pain, cold, muscular effort, carbon dioxide, noise, flash, and ‘anticipation'” produced abnormal physiological responses at low levels. They concluded with the comment that “The Viennese physician who first used the term ‘anxiety neurosis,’ now fairly obsolete, stated that ‘the symptoms of these patients are not mentally determined or removable by analysis” and they referred to a 20 year follow-up study which found that “simple kindly reassurance . . . worked as well as various types of ‘psychotherapy or psychoanalysis.'” In their assessment the condition had two forms with the minor type being referred to as neurocirculatory asthenia, and the more severe type being called “big NCA” because they generally did not respond well to reassurance, and had the additional feature of the symptoms of depression. They noted that “Manic-depressive disease is supposed to show only classic symptoms of ‘psychological’ abnormality”, but with “about one half” of these patients there are “spectacular medical-like symptoms, such as chest pain, shortness of breath, fatigue,” etc. These people “are incapacitated partially or completely even for office work” and have additional “psychological-like complaints” which “include worry, nervousness, indecisiveness, loss of confidence, feelings of guilt, depressed mood, thoughts of suicide and death by suicide. Almost all patients who commit suicide have manic-depressive disease.” and tend to have short stocky physiques, expressionless faces, and “stooped posture”. In such cases treatment involves the use of “sodium amobarbital for mood disturbance and chloral hydrate for sleep.” In some cases they need to be protected from their attempts at suicide by being confined to “a locked ward hospital” and “There are myriad newer, more expensive and more toxic drugs, with almost no good scientific data to recommend them” and “Electrotherapy is often indicated.” In their concluding discussion they reported that “objective abnormalities – clinical, anatomical, physiological, and biochemical – have been observed” . . . and . . . “there is a more realistic way of classifying neurocirculatory asthenia, despite the mixed-up and fictional psychiatric nomenclature with which we are currently saddled.” They also noted that research was continuing in Sweden, Israel, Japan, and other countries, and they emphasised the importance of determining “what provokes an attack, what makes symptoms worse, what disables,” as it “can be crucial” regarding the benefits to be gained by avoiding such factors. “Most patients believe that attacks are precipitated or made worse by emotion-provoking situations, medical illness, unaccustomed or involuntary hard muscular work, pregnancy, and military service”, and the authors added “infection . . . and . . . extremes of heat and cold as probable provoking ‘stresses'”. in their review of their experience, history, and the War of the Rebellion, “we encountered the same stresses; to quote ‘double quick movements of camp, effected under full burden of arms and accoutrements . . . particularly when the individuals were debilitated from . . . diarroea . . .typhoid fever . . . (and) . . . nervous excitement.” (This review the 1972 concept was prepared from my notes associated with my 1982 research paper, re;“Most patients believe that attacks are precipitated or made worse by . . . unaccustomed or involuntary hard muscular work,” . . . and . . . Attempts to train patients to better performance were not successful in our observation.”. Why? and placed on this web page on 27-1-08. – Another reference; source lost, reported “these patients could not or would not train”. Why? M.B.)
(28) Caughey J.L. Jnr., M.D. (April 1939), Cardiovascular Neurosis; A review. Psychosomatic Medicine,Vol.1 No.3, April 1939, p.311-324; This author was from the Department of Medicine, College of Physicians and Surgeons, Columbia University, and the Presbyterian Hospital, New York City, He reviewed the literature of internal medicine on the subject of cardiovascular neurosis which refers to “cases in which symptoms and signs of circulatory origin are present but cannot be explained on the basis of pathological changes in the cardiovascular apparatus”. He mentioned the similarity of previous terms such as effort syndrome and neurocirculatory asthenia and gives a description of each of the symptoms individually, and presents a typical example of the past and present physique, health, and personal history of such a civilian patient. He was generally aged 30, and previously did clerical work but was currently unemployed, who had a thin build and long chest, was never robust, got frequent sore throats and colds as a child, had his tonsils and appendix out, and was “unable to sit and lie quietly”, and had a weak stomach, and had his kidneys damaged by Scarlet fever, and there were frequent fluctuations in the color and volume of his urine. His blood pressure was unstable, and he may show obvious signs of abnormality in peripheral circulation, with pale fingers, toes, ears or nose in cold weather, as in a Raynaud’s-like disease, and have dermatographia (from derma = skin, and graph = write) where dragging the finger nail lightly across the chest will leave a red line due to blood rising just below the skin, enabling the person to literally write their name on their skin. He will also have poor memory, and difficulty concentrating or thinking clearly. “He has always been nervous and easily fatigued”, and he “was never allowed” to take part in competitive sports and has felt physically inferior to others of his own age. In a typical case he contracted a respiratory infection 3 years earlier, but never recovered properly, and since then has had gradually increasing pain in his heart, shortness of breath, dizziness, faintness and weakness. All of his symptoms were “made worse by exertion or nervous strain”. The author states that the breathlessness “is not true air hunger, but literally a ‘shortness of breath’ a feeling that deep breath cannot be achieved. The patient usually localizes this sensation in the chest wall itself, and describes a constant dissatisfaction similar to the transient annoyance which a normal person has after attempting to sigh but not quite attaining the complete expansion desired,” and it accounts for the tendency to sigh and hyperventilate. This author also notes previous exercise tests which indicate “a physiological abnormality in the patient as compared to the normal person”, but he refers to that response to exercise as “no more dependent on the amount of exertion than it is on the emotional reaction he has, the fear he has that the test will injure seriously his already weakened heart.” In describing the lack of stamina he suggests that there are two groups of patients, the first who never developed the ability to persevere against the challenges and adversities of life, and those who tried but gave up, in both cases concluding that “the present is bad, and that the future is to be even more dangerous and difficult”. “He also explains that many theories have been used in the past to explain the cause of the condition, with widely varying opinions which may each have a “fragment of truth” in them. He lists ten which include; “Pressure from clothing . . . prolonged physical strain . . . infections of various sorts . . . hyperirritability of the autonomic nervous system . . . unfavorable environmental influences in childhood . . . and psychic instability.” The author believes that the patients have a basic weakness in their constitution which is added to by the response to some physical effort, or emotional strain or some physiological reaction to a viral infection, which causes an instability of their physical responses in the future, which is then interpreted as having a serious effect on their health or their heart, and they continue to believe that the symptoms are due to disease despite thorough medical examination which eliminates all of those possibilities. He suggests that a normal person forgets such symptoms but the neurosis patient remains concerned as the result of misinterpreting them as serious because of “some instinctive anxiety”, or “some psychological necessity for using the symptoms as a protection against the pressure of environmental forces.” He then discusses the problems which doctors have to consider when dealing with such patients which include the increasingly and economically competitive nature of modern society and the diversification of disability benefits, and the growth in the medical knowledge of patients which is due to health campaigns, and newspaper articles and books written by popular medical authors. He says that such knowledge is small, but enough to create anxieties in the “uncritical audience” about “the integrity of his own vital processes.” He then adds that these factors come to the physician “like a spark into a box of tinder”, where the patient who has noticed some heart symptoms during a physical or emotional event is likely to have his fears accentuated and instilled by the doctors facial expression as he examines blood pressure. He suggests that it is important to discuss the matter carefully. He adds “No less dangerous are physicians who for one reason or another have never accepted the idea that important, sustained and disabling physiological abnormalities may occur in the absence of any organic disease.” He also states “the doctor may contribute to a later cardiovascular neurosis, by failure to limit the patients physical activities during the convalescent period of vasomotor instability”, or by failure to convince the patient that the symptoms are normal or temporary. He then concludes that the syndrome is due to complicated aspects of the total personality of the patient, and that the symptoms need to be thoroughly separated from those of heart disease by medical and laboratory examination, and then reconditioning the patients interpretation.
(29) Nixon P.G. (June 1994), Effort syndrome: hyperventilation and reduction of anaerobic threshold, Biofeedback Self Regulation, June 1994; 19(2): 155-69; “Effort syndrome is an entity in danger of being subsumed into ‘chronic fatigue syndrome’ and lost to sight”. It is a distinct entity insofar as it features a reduction of the anaerobic threshold for exertion due to depletion of the alkaline buffering systems via hyperventilation. “In other forms of chronic fatigue syndrome, the pathogenesis and logic of therapy are unclear.”
(30) Saish S.G., Deale A., Gardner W.N., & Wessely S., (June 1994), of the Department of Thoracic Medicine, Kings College School of Medicine and Dentistry, London, UK; Hyperventilation and chronic fatigue syndrome, The Quarterly journal of medicine, June 1994, 87(6): 373-4; A study of 31 patients with Oxford, and Joint CDC/NHC criteria for CFS who had “profound fatigue and fatigueability associated with minimal exertion” found that 66% developed the condition after an infection. They were tested “by capnograph or mass spectrometer via a fine catheter taped in a nostril at rest, (and) during and after exercise”, and “Twenty two patients (71%) had no evidence of hyperventilation during any aspect of the test”. One had hyperventilation associated with asthma, and four had hyperventilation associated with panic, and only one with agoraphobia had no other obvious cause, and five had borderline hyperventilation. The results of the testing showed that “There was no association between level of functional impairment and degree of hyperventilation.There is only a weak association between hyperventilation and chronic fatigue syndrome.”
(31) Sharpe M.C. (February 1991), A report – chronic fatigue syndrome; guidelines for research, Journal of the Royal Society of Medicine, Vol.84 p.118-121; On the 23rd. March 1990 Professor Anthony Clare, Clinical Professor of Psychiatry, Trinity College, Dublin, chaired a meeting of 27 medical specialists from a variety of fields of study to discuss the problem of researching fatigue, insofar as there were too many definitions being used for too many different ailments which included too many different types of fatigue in their symptomology, so the assessment and comparison of data was becoming confused. The objective of the meeting was to establish the criteria for defining the problems so that research could progress more effectively in the future. They decided that there were two broad groups which could be called “chronic fatigue syndrome” CFS, and a sub-type of “post-infectious fatigue syndrome” PIFS, and specified that . . . “In reporting studies it should be clearly stated which of these two syndromes is being studied”. They set the criteria of CFS for consideration, and added the post-viral aspect to the second criteria. It included “fatigue as the principle symptom” with a definite onset which is not life long and persisted for at least six months. The fatigue should “be disproportionate to exertion” . . . and . . . “represent a change from a previous state” and be categorised as “mild, moderate, or severe” . . . and “it should be stated whether the fatigue is greatly increased by minor exertion and whether it occurs at rest”. . . and “each of the symptoms should be carefully distinguished from one another”. Other related criteria were mentioned and in conclusion it was stated “The contributors hope that these guidelines will provide a basis for fruitful research studies, and for inter-disciplinary collaboration essential for this field of research. The guidelines are preliminary and will undoubtedly require further refinements and revision. The authors would welcome comments and suggestions.” (Most, but not all cases of the Da Costa’s, (also called the Effort Syndrome) fit the criteria of representing a change from a previous state, where the change followed physical strain or a viral infection or scurvy etc., after which there were abnormal impediments to physical exertion which involved four specific symptoms of chest pains, palpitations, breathlessness, and fatigue. Therefore Da Costa’s syndrome, or the Effort Syndrome is a distinct sub-type of the chronic fatigue syndrome which needs to be studied separately with regard to it’s four classic symptom, and exertion specific nature. M.B.) | The Posture Theory and the Mitral Valve Prolapse Syndrome © February 2008 In his 1976 essay “Where are the Diseases of Yesteryear”, Charles Wooley traces the history of Da Costa’s syndrome, the Effort Syndrome, and Neurocirculatory asthenia through to a different area of study of the Mitral Valve Prolapse syndrome. He comments on the observations of J.M.Da Costa, T.Lewis, P.D.White and others on the similarity of the four classic symptoms, and the heart sounds and rhythms, and the physique and lifestyle of the patients who were typically thin, had stooped upper spines, and long, narrow or flat chests, and did sedentary work in civilian life, and later had the symptoms in relation to the strenuous exertions of army life. When the heart pumps the valves, including the mitral valve open to allow forward blood flow, and then shut to prevent back flow. The mitral valve contains two flaps which open and close, and when they balloon back excessively to stop backward blood flow the condition is called prolapse. The cause is not yet known, although there are several theories. One of the recent observations has been x-ray evidence that the distance between the front of the chest and the spine is smaller than usual in many MVP patients, and the side view shows pancaking (or flattening) of the heart. In my 1980 essay “The Matter of Framework” and later Posture Theory essays, I noted the same physique, and reported that some young people get palpitations when they lean back in their bed to go to sleep at night. Their heart begins to palpitate so they try to prevent the problem by laying back very gradually, or by sleeping with their head and shoulders elevated by three pillows, yet despite that aspect they continue to play strenuous sport without getting any troubling heart symptoms. When they get a job as a clerk and sit at a desk all day they find that they get excessively drowsy, and have difficulty concentrating. After a few years they notice that each time they lean toward a desk to read, write, or count coins, they feel aching in their kidneys and stomach, and sometimes feel faint, dizzy, and exhausted, but each time they lean back they get relief. After a few more years of repeatedly leaning toward a desk they become so faint and dizzy and weak, that it affects their capacity for exertion so they have to give up sport. In The Posture Theory I mentioned that when people with a stooped spine and a vertical breastbone lay backwards, the breastbone moves backwards compressing the heart and bringing it in closer contact with the inside wall of the chest so that it’s pounding was more readily perceived, and thereby explaining the symptom of excessive palpitations. Also, when they lean forward the midriff and breastbone buckles backwards and the lower tip of the breastbone also presses downwards and stabs into the stomach, and the lower ribs compress the left and right bends in the colon. It may be that every time the person leans forward the breastbone recedes backwards and compresses and pancakes or flattens the heart, and alters its geometric shape, and the shape and efficiency of the mitral valve to cause the faintness, and ultimately weaken the valve so that it functions less efficiently during exertion. The following two references support that idea and explains why abdominal pain is an additional feature seen in some cases of Da Costa’s syndrome. M.B. © 6-2-08(32) Kumar U.K, & Sahasranam K.V. (1991); Mitral valve prolapse syndrome and associated thoracic skeletal abnormalities, Journal of the Association of Physicians of India, July 1991, Jul;39(7):536-9; Sixty patients with “echocardiographically proven mitral valve prolapse” were studied to determine the association with skeletal abnormalities of the chest. 91.7% had “atypical chest pain, palpitations, exertional dyspnoea and easy fatigueability” as their major symptoms. 67% had thin physiques, 55% had high arched palates, 55% had thoracic scoliosis, 50% had straight back syndrome, 46.7% had flat chests, and 20% had pectus excavatum (receding chests), and 81.7% had one or more of those features. “Lateral chest radiography showed pancaking of heart shadow in 48.3%”. The main auscultatory finding was non-ejection systolic click(s) in 61.7% of cases, and echocardiography showed pansystolic prolapse in 60% of cases, and “Electocardiographic ST-T-U changes in the inferior and /or lateral chest leads” in 46.7% of cases. “16.7% had cardiac arrhythmias” . . . and . . . “None had infective endocarditis, heart failure or cerebral embolic events.”
(33) Johnston C. (1999) DG Dispatch – GASTRO 99: Research Links Irritable Bowel And Mitral Valve Prolapse; At the Gastro 99 Pan American Congress on Digestive Diseases, Dr. Alejandro Navarro, a resident in gastroenterology in the department of gastroenterology and cardiology at the Chilean Air force National Hospital in Valparaiso, “explained that irritable bowel and mitral valve prolapse can both be caused by dysfunctions in the autonomic nervous system”. ‘We’re not saying there is a cause and effect, but . . . We think that both of these conditions are malfunctions of autonomic nerve signalling’. 25 female patients of average age 38 who had Irritable bowel syndrome were examined with ultra sound, and autonomic nerve tests, as well as having “a fully GI work up to rule out any kind of organic cause for their IBS”. Mitral valve prolapse was confirmed in 76 percent of the women. Eighty percent also had scoliosis. He therefore suggested treating patients with IBS in the same way that the mitral valve prolapse — “with exercise, magnesium supplements and clonazepam.
(The effort syndrome, which is nowadays sometimes referred to as part of the Chronic Fatigue category, often follows a viral infection so it may be that some viruses can weaken the mitral valve. M.B.)
(34a) Lewis, R.P.; C.F.Wooley, A.J.Kolibash and H.Boudoulas (1987). “The mitral valve prolapse epidemic: fact or fiction“. Transactions of the American Clinical and Climatological Association 98: 222-236: These authors relate Da Costa’s syndrome or neurocirculatory asthenia to thin physiques with chest wall deformities, scoliosis and other spinal deformities. The patients probably become anxious about their symptoms and not vice versa, and the symptoms are different to those of anxiety or cardiac neurosis. They generally visit their doctors to get an explanation about why their body is reacting the way it does and generally develop methods of controlling their symptoms by modifying their lifestyle etc, without needing to consult a psychiatrist. Many of these individuals are “extremely productive”. In world war 1 “irritable heart” or Da Costa’s syndrome became one of the commonest maladies affecting and disabling soldiers and “So great was the governments fear of having to provide disability pensions that most of the great thinkers in internal medicine and cardiology were recruited so study the problem”. As a result of their findings “patients with ‘neurocirculatory ashenia’ were excluded from military service in World War 11”. There had been controversy about the cause and nature of the symptoms with some researchers concluding that many of the previous cases were described as having an indication of mitral valve prolapse syndrome. In some of these patients “if you push them too hard, sudden death may occur”, so not all patients can be put “into the one waste basket”. There may be “at least two separate conditions to think about”. The occasional murmurs were indicative of mild mitral valve billowing or regurgitation which, in some cases involves actual mitral valve prolapse, particularly in those over sixty years of age, when surgical repair of the valve may be required. The discussion involved the tendency for these patients to have low blood pressure and the possibility that the reduced blood flow returning to the heart may be responsible for the backward billowing or “pouching” of the mitral valve that could be detected. Their discussion concluded with the suggestion that “if we could discover the cause” . . . or . . . “the missing link” . . . “the factor which chronically reduces the blood volume” . . . then they could solve the mystery of the cause of the condition which links everything together.
(I have also suggested that the constant leaning toward a desk in sedentary work compresses the abdomen and squeezes the blood out of the abdominal veins, and probably eventually chronically stretches or weakens those veins to increase their capacity, and hence the blood volume isn’t actually reduced, but the normal volume isn’t enough to fill the stretched viens. That may become more apparent when they are stretched during postural stooping, or physical exertion, to cause an “effort syndrome”. M.B.) |
(34) Oglesby Paul (1987) Da Costa’s syndrome or neurocirculatory asthenia, British Heart Journal, Vol. 58, p.306-315: In 1987 Paul Oglesby from the Bringham and Women’s Hospital, Harvard Medical School presented a ten page account of Da Costa’s syndrome research in The British Heart Journal. He states “Da Costa’s syndrome or neuorcirculatory asthenia has a long and honourable history in the medical literature”. It is rarely mentioned nowadays and is unlikely to have disappeared, and in fact is still a common and distinct disorder with the same four main symptoms, but is more likely to be labeled as “anxiety state” or “anxiety neurosis”. He then writes “What has been forgotten should not remain forgotten” and then begins to outline the controversies of the time. He starts his study by predating Da Costa to 1863 with other sources that deal with similar ailments, and then threads his way through the effort syndrome and neurocirculatory asthenia to the hyperventilation, anxiety state, systolic click and late systolic murmur syndrome, mitral valve prolapse syndrome, and dysautonomia theories. Along the way he describes the typical thin physique of sedentary workers who enlisted in the army and were not given any physical training, and were required to carry their soldier’s field pack weighing over 60 lbs. strapped to their bodies in a manner which “constricted the circulation” as they were marched into military campaigns with “great and prolonged exertion with the most unfavorable conditions possible – privation of rest, deficient food, bad water and malaria”. In attempting to keep up with the other troops they became severely exhausted and were hospitalised with months of fatigue which featured “shortness of breath after moderate exertion and a rapid pulse on slight effort”, “palpitation”, and “intercostal neuralgia” where a small number recovered and returned to full duty, but the majority were put on light service or pensioned off as being physically unfit for military service. Military administrators tried to prevent those problems in subsequent campaigns by altering “the weight and strappings of the soldier’s packs” and by providing physical exercises at training camps to develop the strength and stamina of new recruits to accustom them to the strenuous exertion which would be required later in actual warfare. Da Costa recommended “provision for adequate convalescence for those with acute infections before they returned to duty.” Another typical case was that of a 22 year old man who, since the age of 17 did light bench work and had palpitations and breathlessness on exertion. In 1914 he enlisted in the army and developed the symptoms when “doubling or hurrying” and in 1915 he went to France and developed the same symptoms “all on marching” and was admitted to hospital with no abnormal physical findings, and again returned to full duty 8 months later but was no better. In 1920 Sir James Mackenzie studied 2000 soldiers with the syndrome and found that in 80% “the first onset of their illness began with a complaint of some infectious nature”, and the remainder were due to “want of rest”. However P.D.White found that infective cause did not appear to be responsible for most cases in civilian practice. In 1941 Paul Wood began studying and reporting on Da Costa’s syndrome in the British Medical Journal, and he concluded that the symptoms more closely resembled those of fear than effort, and that the abnormal response to effort was due to a misinterpretation of the normal symptoms of exercise as evidence of heart disease, and a fear of heart disease, or was due to conditioning, and hysteria. He suggested that the syndrome should be regarded “as an emotional reactive pattern peculiar to psychopathic personalities, and to subjects of almost any form of psychoneurosis”. Also, in his opinion, “hyperventilation was not responsible for the symptoms and signs” and that they depended “on central stimulation, not upon hypersensitivity of the peripheral autonomic ‘gear'”, and that the central stimulation was generally caused by the emotion of fear. His views became influential and were significant in reducing the interest in, and use of the term Da Costa’s syndrome during World War 2 where it was replaced by a variety of psychiatric diagnostic terms. In 1966 C.K. Friedberg wrote “The underlying cause appears to be a fundamental ego insecurity arising from psychological problems which began in infancy and childhood”. In 1972 Cohen and White presented a summary of their own findings and concluded that the cause was unknown and that there may be two forms of the disorder where the milder type was called neurocirculatory asthenia, and the more severe type was manic-depressive disease. However some patients with anxiety or depression do not have the four classic symptoms of Da Costa’s syndrome, and vice versa. Also the rebreathing of a mixture of added CO2 reproduced the symptoms and it was stated “The symptoms of neurocirculatory asthenia were considered not to be identical with those of fear alone”. Oglesby also noted that some patients with neurocirculatory asthenia also had mitral valve prolapse, which according to some authors may be the cause, but some MVP patients have no symptoms at all, or if they do the proportions of the four symptoms are different. He concludes that despite there being controversies about cause, and a large and wide variety of physical and psychological concomitants, and despite the label being rarely used and the syndrome being almost lost amongst many other labels, the effort related condition which Da Costa described in 1871 still existsed and was still common, affecting 2-4% of the population, and is usually easy to recognise and diagnose. (This article also refers to the symptom of breathlessness or ‘smothering’ occurring in crowds, without comment, but implying a fear factor – panic attacks – however that would be due to the excess amount of CO2 being exhaled by large numbers of people in a confined space, with the CO2 being responsible for the abnormal respiratory distress in patients with N.C.A.. Some entertainers take oxygen bottles on stage to deal with that problem themselves M.B.).
(35) Mackenzie, Sir James M.D. (January 18th. 1916) Discussion On The Soldier’s Heart, Therapeutical and Pharmacological Section, Proceedings of the Royal Society of Medicine, Vol.9, p.27 -60; part of a series of discussions on Soldier’s Heart; In his study of 400 cases of World War 1 soldiers with cardiac like symptoms Sir James Mackenzie M.D., who opened the discussion, found that only 10% of them had actual heart disease. The remainder had similar symptoms of a different unknown cause. He described the typical patient as having thin physique, vasomotor instability, and cold, red, or blue hands and noses. If they rested and ate they became fat and breathless. They feel unwell, “out of sorts”, or “rotten”, and “a sense of fatigue or exhaustion easily induced is common to all. Breathlessness on moderate exertion is frequent; pain over the region of the heart less frequent”. Heart rate is normal in some but in others it is persistently high, up to 120 beats per minute, and “exertion, sometimes slight, may produce an undue rapidity”, due to excitability of the heart. Various systolic murmurs were frequent, and some of the patients had edema of the legs, and were irritable, depressed, or brooding over their health or woes. The same ailments occur in civilian life where “we find identical conditions for instance, in people recovering from an exhausting illness, such as typhoid fever, or influenza, or after a severe surgical procedure”, or “in people who have suffered a long mental or physical strain, particularly with insufficient sleep, as in a daughter who has for long periods nursed an ailing mother”. Typically the soldiers “will say they were in the trenches and felt well and fit, until one day they felt seedy and ill, and this continued until they were compelled to seek medical advice, when they were found to have a raised temperature”. After a few days rest they returned to the strenuous life in the trenches and soon collapsed with faintness, breathlessness and pain. The preceding illnesses included diarrhoea, measles, or other infections which accounted for most cases, but some, with no history of infection were gradual in onset, and the remainder “give an account of a very strenuous life”. An example was given of a soldier in the trenches suffering “appendicitis”. He had surgery and returned three months later, and spent two weeks in the trenches again being constantly shelled and was always repairing parapets, rarely getting any sleep at night and only a few hours during the day, and often going 24 hours without sleep. One day a shell exploded nearby and knocked him unconscious. After regaining consciousness he kept working until he was too weak and ill to continue due to pain in his heart. It was concluded that a combination of an infection, and physical and mental strain caused the ailment. Another example was that of an officer who spent a few hours each day for several days practising for a foot race and collapsed on the track. When medically examined he reported feeling “rather seedy” and unwell before, and was exercising to shake off the feeling. He was found to have an elevated temperature, attributed to an infective illness, and was advised to rest. He recovered, returned to perfect health, and resumed training. Mackenzie suggested that the chronic type of this ailment may not be caused by the microbial toxins, but be due to the infection causing some changes “in the economy of the blood, central nervous system, or heart muscle”, and that maybe a vaccine could be developed to prevent the problem, and that treatment should include the removal of the infection or toxins, and improving general health and strength with mild enjoyable exercise such as “bowls or quoits or skittles” in the “fresh air”. He referred to the importance of the judicious use of exercise which should involve the simple principle of exercising “so long as it gives him pleasure and causes no distress or discomfort, but to stop or slow down as soon as he experiences the sense of exhaustion, breathlessness and pain.” (As a final matter this article includes some information which is suitable as Evidence for the Posture Theory and the relationship to Orthostatic Hypotension and Exertional Intolerance. This is seen in the following quote – regarding the symptom of exhaustion “There is a persistent over-action of vasomotor influences” . . . and sometimes . . . “flushes of heat pass over the body, and warmth may tend to overfilling of the peripheral vessels. This is seen in people who faint when standing in a warm room, or who speedily become exhausted or even faint when exertion is made. In these, the blood tends to accumulate in the peripheral veins of the limbs and in the large abdominal veins, with consequent anaemia of the brain. It is because of this anaemia of the brain that the sense of exhaustion and syncope are provoked”. The author presented this description to show that this type of exhaustion is related to vasomotor disturbance and was not the same mechanism which produced exhaustion of the heart itself. This type of fatigue often starts following an infective or exhausting illness where the person tends to feel exhausted and giddy. “If they stop, sit, or lie down the sensation speedily disappears. If they attempt a more violent form of effort, such as walking quickly, or up a hill, or running upstairs, they may be pulled up by breathlessness or palpitation”. According to The Posture Theory, many years of postural compression of the chest, impedes the upward flow of blood and damages the abdominal veins. This Mackenzie paragraph provides the evidence that blood is pooling in the abdominal veins during exertion, and he suggests it is the cause of the fatigue symptoms. M.B.)
Dr. R.M.Wilson contributed to the Mackenzie discussion with his statement “a careful study of upwards of 200 cases of the condition has brought me to the same conclusions”, and he “met with what I can only regard as a definite clinical picture, sharply defined and differentiated” with “The cardinal symptoms” of exhaustion, breathlessness and rapid pulse especially on slight exertion, praecordial and left chest pain, vasomotor instability, and also tendencies to giddiness, nervous symptoms, and high blood-pressure. He commented on the history of the disorder with reference to an 1864 British Government committee convened by Earl de Grey, three generals, and two doctors who concluded that “an old form of accoutrement restricted the heart’s action” which caused what they called “irritable heart” where “on the least exertion its action becomes irregular, and the man becomes breathless”. Their recommendation that the accoutrements (in the knapsack) be held to the body by braces instead of waist straps “was later adopted”. In 1864 Henry Harthorne described a condition in “The American Civil War” in the American Journal of the Medical Sciences with emphasis on “the acceleration of the heart’s movements on the slightest exertion” and breathlessness, which he attributed to an injury to the heart caused “by long-continued over-exertion, with deficiency of rest and often of nourishment; and he pointed out that several months of rest and treatment in hospital failed to do more than improve, without really curing, a large proportion of well-marked cases”. Later, in 1870 Dr. Arthur Myers of the Coldstream Guards gave a similar description and “he also regarded accoutrements as the exciting cause of the trouble“, but the best known contribution to the subject was that of J.M. Da Costa who made the same observations from 300 cases. In 1876 Arthur Davy attributed the problem to “‘Setting-up drill’, by over-expanding the chest, caused dilatation of the heart, and so induced irritability”. Although the idea gained support, there were some soldiers who developed the condition without doing any drill, and the change in accoutrements and drill were deemed ineffective in reducing the incidence of the problem. The next theory was that a bacterial agent was causative, followed by the idea of a faulty thyroid gland being responsible, but nothing could be confirmed other than treatment was more effective in a cheerful situation with pleasant activities rather than depressing situations. Dr. Philip Hamill wrote “I think that the more one sees these patients, the more one realizes that the true irritable heart of the soldier is a very definite condition”. . . and . . . “In most cases irritable heart can be traced back to some undue exertion during some febrile attack – it may be called a cold or influenza” . . . and . . . “It is surprising , however, how high a proportion of soldiers with irritable hearts give a history of diarrhoea”. There is usually no evidence of heart disease but the pulse rate is generally elevated . . . “A common rate is 100”. Slight excitement seems to increase the rate, such as the mention of a cardiograph test. Hamill gives the example of a Territorial officer who joined the Regular Army cavalry regiment, and was also a boxer. One day while doing a long march he felt unwell and “fainted by the wayside, and had to lie down” to recover. “The same thing happened on another march” so he was sent to hospital and upon examination nothing but slight dilatation was found so he was found fit for duty, but a senior medic advised him that it would be unwise to continue in the army. He became a medical student but was restless and couldn’t maintain concentration for long and constantly thought about his “discomforts and disability”. He was keen to rejoin the army but when he applied he was rejected on medical grounds because of slight cardiac dullness, a pulse-rate which reached 120, and oedema of the ankles without albuminuria. “This student’s symptoms were greatly accentuated after a bomb from an aircraft fell near his room” . . . and . . . “His pulse-rate readily rose to 140 per minute after moderate exertion, and remained high for a long time”. His symptoms became worse while studying for an examination, so it is unlikely that “a man badly broken down on a march is ever likely to be fit again for heavy duty“, and “however much these men improve, they are always ready to relapse when the favouring circumstances recur”. He concludes that a large proportion of these men probably have permanent heart damage that will impede their capacity for heavy duty in the future but further research is needed by future generations, and in the meantime the best treatment is pleasant moderate exercise in the fresh air and green fields. Similar treatment was recommended for soldier’s with shell shock. Dr.Alexander Morrison contributed to the discussion with his report from a hospital where three wards, or half the beds were allocated to these soldiers, and he dealt with the question of cause by stating about the heart; “one can find nothing amiss with its size, rhythm, or mechanical structure” and he added that despite this these soldiers had an incapacity to undertake those exertions which were formerly undergone without discomfort. Therefore some factor has been introduced which renders these men incapable of their duties as soldiers”. . . and . . . “that there is a valid incapacitation which they evince is undoubted”, although “The heart itself in such cases shows, as a rule, absolutely no evidence whatever, clinically or otherwise, of physiological disturbance”, and was previously regarded as a disorder of the nervous system. He also commented on the possibility that the condition was caused by a cryptic organism, a microbial infection, toxaemia, or diarrhoea, but he found cases with those preceding problems who did not have soldier’s heart and vice versa, although he could not confidently rule out such possibilities. Dr.O. Leyton stated “I believe that the condition is not due to a single cause“, and after stethoscopic examination he believed that some cases arise from an affliction of the heart and others from a disorder of the vasomotor system. Dr. Florence A. Stoney noted the similarity and possible connection between the symptoms of soldier’s heart and thyroid disease. Sir James Mackenzie concluded the meeting with the hope of getting a hospital devoted exclusively to the study of this subject which attracted medical researchers who were specially qualified “to investigate this subject thoroughly”, and that the lines of study had been established and would lead to more definite findings in the future.
(I have highlighted the aspects of the meeting of Sir James Mackenzie in 1916 which provide evidence consistent with The Posture Theory and my views on the subject, with an additional comment that teatment in fresh air and green fields involves maximum oxygen and the absence of excess CO2 which is more prevalent in crowds or closed buildings, and which dsiposes to symptoms in these patients. M.B.)
(36) Jones E. and Weseley S. (December 1999), Case of chronic fatigue syndrome after Crimean war and Indian mutiny, British Medical Journal, December 1999, Vol. 319, p.18-25; This article opens with the following sentence “Chronic fatigue syndrome was first proposed as a diagnostic label in 1988 to classify a disorder characterised by severe fatigue and exhaustion after minimal physical and mental effort accompanied by other unexplained somatic symptoms”. It was introduced to distinguish the condition from myalgic encephalomyetlitis which was similar to an outbreak of illness in the medical and nursing staff of the Royal Free Hospital in 1956. It was widely assumed in the popular media and occasionally in professional journals as a new disease caused by aspects of “modern life, pollution, stress, working practices, and new infections”. However “Attention has recently been drawn to the often striking similarities” between those conditions and the condition formerly known as neurasthenia which was coined independently in 1869 by George Beard and E.Van Deusen, and described as a physical disorder caused by “the selfishness and luxury of modern life, the restlessness and the craving for excitement, the frantic speeding about in motors and other features of industrial society”. However the author believes it can be traced further back to soldiers “who served in the Crimean war and in India at the time of the mutiny”, and, after examining 4000 pension files in the Royal Hospital Chelsea, two examples were chosen. The first soldier enlisted in 1854 at age 18 and spent 6 months in Crimea as a reinforcement, “although apparently without taking part in a major battle”. He then went with this regiment to India for six and a half years and returned to England, where in May 1864 he “suffered from increasing fatigue” with exhaustion, weakness, tremor, and pains in his knees, elbows, and shoulders, visual problems in his left eye, and a persistent cough, and “was eventually discharged from the army in February 1872 with a diagnosis of general debility, imperfect vision, and rheumatism, and was awarded a disability pension. The army physician attributed his condition to 17 years of army life in Turkey, India, and at home, and the general hardships of a soldier’s life during the Indian mutiny. Cold and general exposure in a country where malaria was endemic probably contributed but there was no evidence the he had contracted malaria. His visual problem was diagnosed as iritis and he went blind in his left eye in 1923. His commanding officer described him as a model soldier who had been regularly promoted until he reached the rank of sergeant, and was not a malingerer. After he was discharged by the medical board in 1872, “as being permanently unfit for contributing to his own support” he returned to his occupation as a house painter, but only on a casual basis, and “Later, he worked as a commercial traveller before ill health forced him to give up employment”, and in June 1885 his condition was described as ‘very unsatisfactory indeed’, and three years later his physician remarked “although he was then able to earn a livelihood . . . he . . . ‘is likely at any moment to be quite unable to do so'”., and in April 1900 he was described as being more debilitated and soon after, as feeble. During his life he was a member of the Birmingham Military Veterans Association, was a recruiting sergeant in World War 1, toured convalescent hospitals, and collected money and provided warm clothing to sailors. At age 85 he complained of chronic rheumatism although there was no swelling in his joints, and was “well preserved for his age”, and he died at age 96. Nowadays he would be given “the diagnosis of chronic fatigue syndrome”. After giving another example it was suggested that the conditions of war in India may have contributed to the ailment, where one troop “was reputed to have travelled over 3000 miles in pursuit of rebels, including a forced march of 251 miles in 11 days”. In another example of a military attack on rebel troops it was reported that “So intense had been the heat that “officers and men were so completely exhausted . . . that they could scarcely sit in their saddles, and were for the moment, incapable of further exertion”. It was concluded that the soldiers symptoms were an indication of chronic fatigue syndrome, which might have been diagnosed as “disorderly action of the heart” in 1915, and is similar to the diagnosis of “post traumatic stress disorder” given to Vietnam soldiers, or that the symptoms may have been attributed to exposure to Agent Orange, and that the way disease is interpreted and labelled varies according to circumstances but the condition is still the same and might now be given to “an ambitious graduate manager working for a large business corporation” . . . and that despite advances in medical knowledge . . . “the clinical dilemmas that surround unexplained symptoms remains almost as challenging”. (Although the complete set of four classic Da Costa’s syndrome symptoms were not specifically referred to in this article, the abnormal fatigueability, and the reference to “disorderly action of the heart” or D.A.H., which is a synonym for Da Costa’s syndrome, provides a trace through history to the modern diagnosis of chronic fatigue syndrome. In a general summary the soldier was fit and healthy before joining the army and was able to participate in full and arduous military duties, but after experiencing an infection, and or combined with the extreme exertions or other conditions of military life, he became excessively exhausted. After recovering, he made numerous attempts to return to a normal and full lifestyle, but each time his health deteriorated. He ultimately restricted his activities, which is when his health stabilised and he subsequently led a long and generally healthy life. In the past some physicians would have called his symptoms “just normal tiredness” or “just nerves”, and some doctors would have referred to his recurring health problems as ‘nervous breakdowns’ and some psychiatrists would have diagnosed a series of ‘mental breakdowns’ in an emotionally insecure patient, and attributed the ailment to a protected and mollycoddled childhood, poor character development, and anxieties or fears of various sorts. However it is clear that when the human body is subjected to extreme conditions such as long marches at double quick pace with poor food and water in extreme heat, and the physical limits are exceeded, the person may recover from the exhaustion, but then they may continue to have a reduced capacity for exertion or strain in the future. If they repeat their attempts to surpass their restricted limit they will become exhausted again, and if they lead a more moderated lifestyle within their limits they may remain reasonably healthy. When questioned about their health problems many fatigued patients will report that they are not anxious or depressed, and that the fatigue is not related to such emotions, and that their health does not suddenly “break down” but that fatigue gradually accumulates until it becomes impractical to continue working, and that if they do, it will become predictably impossible any way, so they stop before any so-called “breakdown”. Their sole purpose in seeking treatment is to gain relief or cure of the fatigue so that they can lead a normal lifestyle again, and they don’t like the way diagnostic terminology often seems as if it is being used to misinterpret or misrepresent their condition. They say that treatment is not very effective, so they encourage research on the ailment. Some suggest that they want a treatment which is as effective as that for gastric ulcers, which until the 1990’s was regarded as a stress disorder which many patients suffered from for 10 years or more despite treatment, and then the microbial cause was found and the condition was curable with two weeks of antibiotics in 90% of cases. Some cases of chronic fatigue are associated with preceding infections and rheumatic muscle and joint pains and others are not, so there may be different types of chronic fatigue requiring different treatments. Nowadays chronic fatigue societies are established world wide and are conducting and promoting their own research programmes. M.B.)
(37) Spillane John D. (Nov. 1940), Observations On Effort Syndrome, The British Medical Journal, November 30th. 1940, p.739-741: Military medical officers of 1940 were well acquainted with soldiers presenting themselves with features of the effort syndrome with breathlessness, left sided chest pain, a rapid heart, and dizzy spells which were “only too common”. Previously called soldier’s heart, irritable heart of soldiers, and disorderly action of the heart, it was decided to call it neurocirculatory asthenia because it was not specifically a soldiers condition, or a heart ailment, and the other label of effort syndrome which was probably likely to stay, was not covering all aspects. The similarity to the symptoms of organic heart disease was “a paradox awaiting explanation”. The often bizarre response of untrained civilians to the extreme exertions of military life, and the abnormal reaction of anxiety cases to exercise were quite different to the response seen in the effort syndrome which appeared to fit somewhere in between. In examining the cause the most obvious observation was that the soldiers had stooped spines, flat chests and poorly developed musculature, and they tended to avoid exertion and hence choose and come from sedentary occupations where they are unfit due to a lack of physical activity or training. However the occasional occurrence of more severe cases of effort syndrome in successful soldiers indicates a non-physique related cause. Examination of specific symptoms showed that the circulation time or velocity of blood flow during exercise was within the normal range, but the characteristic sighing respiration was rare in organic heart disease and common in the effort syndrome. Poor breath-holding power, and irregularity of the respiratory rhythm was common, but according to one paper, only one case of true hyperventilation was found, and “it is almost certainly not a causative factor”, but part of several breathing anomalies in general anxiety. Regarding the characteristic left sided chest discomfort it was stated “The cause of this pain is quite unknown”. . . but “was prominent and the pectoral muscles were tender and sensitive”. . . and “Lewis commented on ‘the myotatic irritability of the pectoral muscles’ in the more seriously affected cases”. During the first world war some study of the psychological aspects were made and there was “much scornful talk”, and “from one’s personal experience, the complaints of the neurotic still arouse mistrust and his treatment still tends to be of the hearty ‘smack on the back’ type or else an irritated resort to discipline”. Examinations of the heart tend to cause anxieties in the neurotic patient and should be avoided so as not create psychological problems later, and it was concluded that the symptoms were those of a psychoneurotic response in the cardiovascular sphere. He added that the psychological causes are often masked by the patient, and that “patients often deny the existence of any psychological difficulties, and persistent enquiry may be necessary before their presence is acknowledged”. (Although this author concludes that the symptoms have a psychoneurotic cause he is dismissing the patients report that they are not anxious about anything, with an interpretation of masked anxiety or denial of anxiety, which could be found on persistent enquiry, but that is a speculative assumption rather than a statement of fact. However he also provides evidence that the most common features in effort syndrome patients are a stooped posture, flat chest, and thin physique with a history of avoiding exercise. Such features would place the head and shoulders forward and place constant or repeated abnormal mechanical strains on the chest muscles which would explain their general tenderness and irritability and proneness to pain, which is very similar to the tenderness in the back muscles of patients with stooped physiques. Sideways curvature of the spine would account for the muscle tenderness on one side, and scoliosis is a common, although less obvious, and less noticed accompaniment of kyphosis. This reference therefore provides strong evidence in support of the posture theory in relation the left inframammary pain. M.B.)
(38) Wittkower E. and Spillane J.P. (Feb. 1940), Neuroses in War (the effort syndrome), The British Medical Journal, Feb.17, 1940, p.266. Wittkower was a Halley Stewart Research Fellow, and Spillane was a Rockefeller Research Fellow, both of the Tavistock Clinic, London, and their paper referred to Da Costa’s observations, soldier’s heart, irritable heart, and effort syndrome synonymously “as an abnormal physiological reaction to effort” with the same set of symptoms and a comment on “an undue increase in pulse rate and a delayed return to normal” after exertion. Various previous studies reported that “About one half of these cases began in civil life, under circumstances where physical strain was unimportant”. There were comments on the frequency of cases who had poor physiques, were highly strung or depressed, and came from sedentary occupations, and the ailment was apparent for “12 per cent. during the period of training”. Sir Thomas Lewis previous studies reported that “In 80% of his cases infectious diseases had preceded the onset of the disorder, although it was only in 30 per cent. that they immediately preceded the onset of symptoms”. Other factors discussed as possible causes had been tobacco, alcohol, hyperthyroidism, gas poisoning and shell shock. There were inconsistent opinions about the effectiveness of treatment and “with most authors cases of effort syndrome are highly resistant to any form of treatment. Of 558 cases seen by Lewis about 50% were deemed “unfit for any category of duty”, and of 239 followed up for the next 11 months, “only thirty-nine returned to the firing line”. “These figures do not correspond with those of the official history of the war, in which it is stated that of 13,408 cases of functional disease of the heart 11,403 were finally disposed of by return to duty. Experience of the results of systematic psychological treatment are not available”. A comment on the discrepancy between medical and official army statistics relating to Da Costa’s syndrome (The official statistics on the history of World War 1 show that 85% of cases of effort syndrome recovered and were sent back to the front line, but the factual research studies of Wittkower and Spillane showed that only 16% recovered fully, which is presumably an indication of the extent to which the condition is being misrepresented to medical consumers and the general public, and may be a reflection of similar methods of disguising the frequency and effect of this condition by changing labels, and using obscure esoteric jargon, mixing the condition in with multiple other poorly defined conditions, and understating the evidence of physical cause, and referring to it as a psychological “all in the mind” ailment, and then repeatedly presenting it after each decade or each war, as a surprisingly new, never before seen or known about rare condition, which must be “just tiredness” or “just nerves” related to the peculiar social conditions of modern life. Also note that Wittkower reported that the results of systematic psychological treatment were not available, probably because the results were poor, and the military authorities did not want the soldiers or the general public to know that, so they instructed the psychologists not to publish them. This is something that medical consumer groups should consider seriously when studying the history of the subject and they should maintain their focus on consistent facts rather than on the ever changing interpretations or opinions which often contradict each other and, or lead nowhere. M.B.)
(39) Wittkower E. & Spillane J.P. (Feb. 1940), Medical Problems in War (part 3, Neuroses in War), The British Medical Journal, February 24th. 1940, p.308-310. Towards the end of World War 1 it was realized that it would be an advantage to the military and society if the recruits who had previous indications of neuroses or psychoses in civilian life were culled out at the initial medical examination. Some of those recruits were more suited to contributing to the war effort by their participation in civilian occupations, but if they were accepted as soldiers and were sent off to war and became ill they were likely to require costly and time consuming medical treatment. If they were returned to the front line after recovering they were likely to relapse during transportation, and would be inefficient and unreliable and “almost hopeless so far as permanent fitness for front-line service is concerned”. They would present morale problems for the other soldiers, and if they were returned to civilian life as chronic invalids they would be unable to do any type of work at all. It was also noted that “many of the men who never saw action (had) a more serious aftermath in symptoms than those who were actually in the thick of it”. However many such recruits had been accepted into the army and were sent off to military campaigns and were described as breaking down and being sent to hospital for treatments. The treatment methods were similar to those in civilian practice except for modification related to the more urgent need of regaining health to recover the manpower and fighting capacity needed for a hostile situation. The two choices were “authoritarian and benevolent methods”, and the two aspects were “”covering” and “uncovering” methods””. Covering meant suppressing the symptoms, and uncovering meant finding the actual cause and eliminating it, and the choice of treatment depended on the time and place, “and the personality, training, and psychopathological outlook of the physician”. The over-sympathetic approach was deprecated and new patients were placed in wards where there were improved or cured cases, and the medics, nurses, and visitors were required to present a hopeful but military attitude to recovery. Some medics regarded the symptoms as “”akin to malingering . . . and . . . treatment was a matter of punishment and included such measures as isolation, severe restriction of diet, transfer to “excited wards” . . . application of painful electrical currents, and prolonged baths until recovery””. Kaufmann gave a three phase treatment which involved (1) preparative suggestion where “the patient was told that painful electrical currents would be applied which were certain to cure his condition”, and (2) strong electric currents were applied for one or two hours, and (3) “active military exercises”were combined to give a cure in one session. This treatment became popular until fatalities occurred and the permanency of results became doubtful. Suggestion was also used in “Sham operations carried out under general anaesthesia” and although these were successful in some cases, they were generally rejected on theoretical grounds. Other treatments included boredom, restricted diets, and confinement to darkened rooms. The physicians were advised to avoid giving the impression of punishment and to tell the patients that “these measures were necessary to calm their nerves”. The tics, tremors and deafness of shell shock patients often disappeared after about six weeks of treatment. Other physicians recommended “rest, good food, and firm benevolence, combined with reassuring and encouraging talks about getting well again . . . and . . . an appeal to patriotism and the sense of duty”, and engaging them in interesting paid occupations such as policing the hospital, or farm work, “rather than non-productive mechanical routine work such as mat-making”. Graduated exercise programmes were also used. Psychiatric treatments given for the different forms of neuroses included analytical cathartic hypnosis and dream interpretation to deal with suppressed emotions which were assumed to exist in relation to the fear of war, and difficulties with authority. A treatment regime for anxiety neurotics included sleeping tablets and sedatives, with the Weir Mitchell diet, and absolute rest and quiet for a few days. After the patients recovered from the worst of the fatigue they were offered hydrotherapy and various distractions to get their mind off the fear and horrors of war, and later discussions about the conflict between the fear of being in the firing line and the sense of duty “assisted in the final adjustment”. Where anxiety states did not respond to rest “a modified psycho-analytical method was recommended.” The affect of these ailments on soldiers in World War 1 was significant. “Nearly 66,000 cases were accepted for pension by the Ministry of Pensions on account of functional disorders of the nervous system alone; 29,000 of these still drew pensions in 1938. Wounds and amputations apart, functional nervous disorders ran second in the incidence of disorders for which pensions were being paid. If functional disease of the heart are included they rank first, even exceeding tuberculosis.” A survey conducted in 1919 showed that “little more than half of them were able to earn their living. A great number of anxiety and effort syndrome cases tended to be permanently affected”. Clerks and professional men made the best adjustment and the rural workers the least. In 1924 many had readjusted to civil life but “effort syndrome remained unchanged”. (This article presents the theme that civilians with mental instability (where patients with the effort syndrome were included in that category), were likely to become more unstable and break down in conditions of war, as much on the way to the front line, as did those actually involved in the battle, which leaves the general impression that anxiety in civil life and the fear of battle were the cause of the ailments. However, most of them had evidence of the ailment prior to the war, and the military activities aggravated their condition, and made it permanently worse, and the health status of effort syndrome patients remained unchanged during the five year follow up study between 1919 and 1924, indicating that the treatment methods, including psychotherapy, were essentially inappropriate because they only provided temporary benefits, with no effect on the long term outcome. Moreover, a person with the effort syndrome was equally likely to develop severe symptoms prior to the war if they participated in a foot race at a country picnic on a sunny day, and the brief excessive exertion would aggravate their vasomotor instability and leave them over reactive for a month or more, during which time they would be likely to over-react to the sudden sound from the backfire of a car engine with the same startle effect as a similar patient on the front line reacting to the sudden sound of gun fire. Regardless of whether the person is anxious or not they are able to maintain reasonable health as long as they avoid exercise, or restrict themselves to moderate exertion, which is the basis for the term Effort Syndrome. Note also that this article gives the impression that treatment relieved the tics, tremors, and deafness of shell shock patients, but they tended to disappear spontaneously after about 6 weeks regardless of treatment. The highlighted text in this review may be of interest to military veterans or medical consumer groups. M.B.)
(40) Goetz C.G., Turner C.M. and Aminoff M.J. editors (1993), Handbook of Clinical Neurology, Vol. 19, 63, p.429 – 447. In chapter 19 of this book H.M.Beumer and G.W. Bruyn trace the history of the Hyperventilation syndrome which they relate to Da Costa’s syndrome. They refer to soldiers in the American Civil War who experienced indefinite heart complaints which were attributed to “lack of sleep and bad food”. Earl de Grey presented four reports on British soldiers with these symptoms between 1864 and 1868, and attributed them to “the heavy equipment they carried” in knapsacks, or to “the pressure of straps (of the knapsacks) and the tightness of uniforms” which compressed the chest and constricted the action of the heart. Also in 1864, Henry Harthorme observed soldiers in the American Civil War who had similar symptoms which were attributed to “long-continued over-exertion, with deficiency of rest and often nourishment”, and in 1870 Arther Bowen Myers of the Coldstream Guards” also regarded the accouterments (the heavy military equipment carried in tightly strapped fieldsacks) as the cause of the trouble and called it neurocirculatory asthenia and cardiovascular neurosis. However “the best known contribution to the subject” was J.M.DaCosta’s study of 300 soldiers which reported similar findings and added that the condition often developed and persisted after a bout of fever or diarrhoea. In 1876 surgeon Arthur Davy attributed the symptoms to military drill where “over-expanding the chest, caused dilatation of the heart, and so induced irritability”.
(41) Bazelmans E. et. al. (Oct. 1997), The chronic fatigue syndrome and hyperventilation, Journal of Psychosomatic Research, Oct. 1997, 43 (4). p.371-377. E. Bazelman and his colleagues from the Department of Medical Psychology of the University Hospital Nijmegen, The Netherlands, noted that hyperventilation could cause fatigue so they studied the possible role of hyperventilation in causing the chronic fatigue syndrome. They found that although more people with CFS had physiological evidence of hyperventilation than healthy controls . . . “no significant differences between CFS patients with and CFS patients without hyperventilation were found on severity of fatigue, impairment, number of complaints, activity level, psychopathology, and depression” . . . and they concluded that hyperventilation was, in some cases of CFS, a consequence of CFS, rather than the cause. (If many of the patients with CFS do not have evidence of hyperventilation, then hyperventilation cannot be the cause in those cases, and probably not in the others either, so the respiratory disorder in CFS would presumably be different, as evident from other studies. M.B.)
(42) Streeten David H.P. (Sept.1998), The Nature of Chronic Fatigue Syndrome (CFS), J.A.M.A. v.280, n.12, 23-9-98, Editorial. (David Streeten is from the Department of Medicine, State University of New York Health Science Section, Syracuse) David Streeten presented an article in the September 23rd edtion of JAMA explaining that the fatigue reported by Da Costa and Lewis were early descriptions of a “newly recognised” delayed form of orthostatic hypotension which is a feature of some types of Chronic Fatigue Syndrome. He stated that “as a working hypothesis”, the fatigue was due to abnormal pooling of blood in the lower limbs which delayed and reduced the flow of blood and oxygen supply to the brain. That effect was compounded by a reduced circulating red blood cell mass. He then emphasised that it is essential to identify these physical abnormalities by repeatedly measuring the patients blood pressure in recumbency and after standing for ten minutes or tilt testing, and that “it is inappropriate to consider that CFS is a manifestation of mental disorder” unless those physical causes are excluded. He added that the expense of these tests was not unreasonable considering that almost every type of work or lifestyle required a person to stand for six hours per day without experiencing the symptoms associated with reduced blood pressure. He then concluded the instigating cause remains unknown, and that effective and safe treatments for the debilitating symptoms are still not available and that further research is required.
(43) Rosen S.D., King J.C., Wilkinson J.B. and Nixon P.G.F. (December 1990), Is chronic fatigue syndrome synonymous with effort syndrome?, Journal of the Royal Society of Medicine, December 1990, Volume 83, p.761-764, These authors from the Department of Cardiology, Charing Cross Hospital, London, conducted psychophysiological studies of 100 patients who had “a condition of incapacity for making and sustaining effort, associated with a wide range of symptoms” and had been diagnosed with chronic fatigue syndrome, myalgic encephalomyelitis, and post-viral syndrome. The study method involved recording the breathing pattern and CO2 levels when the patients were at rest, and then after forced hyperventilation (deliberately breathing deeply and rapidly for 3 minutes), and then measuring the levels 3 minutes afterwards to determine the tendency to continue overbreathing, and then, after another 3 minutes had passed, asking the patient to close their eyes and think about previous personal experiences which were “associated with anger, despair, fear, and happiness”. At the end of this “think test” the patient was asked to open his eyes and relax, and raise his hand when he felt that his breathing had returned to normal. The results showed that 93 of the 100 patients had the characteristics of chronic habitual hyperventilation or effort syndrome. They therefore suggested that the other labels “should be withheld until chronic habitual hyperventilation – for which conventional treatment is available – has been definitively excluded”. They also suggested that the symptoms of hyperventilation predated the viral infections which were presumed by some patient groups and researchers to be the cause of the chronic fatigue, and that the viral infection simply made it worse. They suggested that “It has long been recognized that hyperventilation-related illness can appear after or be aggravated by injury or infection”, and they mentioned the opinions of three authors who regarded normal health as being maintained by leading a moderate lifestyle and staying within reasonable boundaries, and that leading an excessively demanding lifestyle beyond those limits may be the cause of the effort syndrome. They also noted that “the physiological disorders of effort syndrome rarely feature in undergraduate education and sponsored postgraduate meetings” and that “many physicians are reluctant to acknowledge the existence of a condition which formerly was considered to be common”, and in the early stages of the ailment “the patients were bitterly resentful at the failure of diagnosis. In the later stages the anger and frustration were replaced by a flat acceptance of disability as the subjects ‘give in’ or ‘gave up’ the struggle to be well, and adapted to infirmity”. They discussed the possibility that the doctors failure to diagnose the condition made the patients anxious and added to the problem of anxiety induced hyperventilation in the manner of a “vicious circle” which sustained or aggravated the condition. The general view of the authors was that hyperventilation itself was not a pathological process but that the chronic fatigue ailments were due to “the physiological consequences of hyperventilation” in people “who overbreath more vigorously and for longer periods of time, and respond to smaller stimuli when they are overtired or anxious”. They suggested that some patient action groups resented the diagnosis of hyperventilation because they assumed that it was synonymous with hysterical overbreathing “which led to hyperventilation being taken as an insulting suggestion that the illness is “all in the mind”.”
(The breathlessness of the effort syndrome or Da Costa’s syndrome was once regarded as just subjective, or imaginary until several studies in 1947 identified abnormal function of the thoracic diaphragm – the main breathing muscle, as the real cause. The symptom is commoner in thin patients with long narrow chests and stooped spines suggesting a mechanical strain, effect, or injury, and nineteenth century women who wore tight corsets had the same problem of rapid shallow breathing which was then, and is still now generally misrepresented as hysterical – psychologically based breathlessness. Emotions and exertion increase breathing rates in healthy people, so it would also alter differently in people with abnormally functioning diaphragms. Da Costa defined healthy physically fit soldiers who carried heavy equipment on long marches where they had poor quality food and drank bad water, and contracted typhoid or diarrhea (food poisoning), and became chronically fatigued and incapable of such exertion afterwards, so the viral cause cannot be disregarded by a modern study that suggests the condition predated the virus. Also, emotional factors may predate this sort of ailment, but that does not equate with emotion being the only cause, and the term “habitual hyperventilaion” implies a behavioural problem (which is just a bad habit), which is a misleading way of describing chronic abnormal function of the thoracic diaphragm. There are other studies which provide evidence that hyperventilation is not present in every case and, is not the cause. It is also readily apparent that the vast majority of patients with any debilitating disease struggle to deal with it at the outset, but give up and except their disability sooner or later, after the medical treatment or their own methods have not achieved a cure. Action groups consist of patients who respond to their doctors failure to recognise or diagnose the condition by studying the problems themselves, and they argue with each other, in much the same manner as medical researchers become involved in heated debates, from one doctor or specialist to another, and labels will keep changing every week, or every year, or every decade, and adding to the already large total until a convincing explanation or cure evolves.M.B.)
(44) Meriam -Webster online Medical Dictionary 5-10-08; This dictionary contains the following definition for “Neurocirculatory asthenia; : a condition marked by shortness of breath, fatigue, rapid pulse, and heart palpitation sometimes with extra beats that occurs chiefly with exertion and is not due to physical disease of the heart — called also cardiac neurosis, effort syndrome, irritable heart, soldier’s heart “
(45) E.M. Goudsmit, Howes S. (2008), Pacing: A strategy to improve energy management in chronic fatigue syndrome, Health Psychology Update (BPS), 2008, 17, 1, 46-52. This article examines the benefits of exerciseing at appropriate levels for each individual.
(46) R.Schondorf & R.Freeman (1999) The importance of orthostatic intolerance in the chronic fatigue syndrome, American Journal of Medical Science 317, p.117-123: This paper examines the laboratory findings related to orthostatic intolerance in patients with chronic fatigue syndrome (CFS) or myalgic encephalomyetitis.
(47) Online ‘Mendelian Inheritance of Man’ (OMIM) Orthostatic Intolerance :604715, http://www.ncbi.nlm.hih.gov/entrez/dispomim.cgi?id=604715, This online website describes one of the causes of orthostatic intolerance as the mutation in the gene encoding the norepinephrine transporter (SLC6A2; 163970) and mentions that the condition has previously been described by Da Costa, and later referred to as ‘soldier’s heart’, ‘neurocirculatory asthenia’, and ‘mitral valve prolapse syndrome’, and as “being similar in many respects” to ‘chronic fatigue syndrome’.
(48) Cohen M.E., White P.D. (1951). “Life situations, emotions, and neurocirculatory asthenia (anxiety neurosis, neurasthenia, effort syndrome)”. Psychosom Med 13 (6): 33557. On page 346, this paper refers to a book which included a report on a twenty year follow up study in which fifty percent of women who had been pregnant believed that “the disorder had been provoked, or made worse by pregnancy”. The comment was attributed to their reference number 36 – Hamilton B.E. and Thomson K.J.(1941) The Heart in Pregnancy and the Childbearing Age, Boston, Little, Brown and Company.
346
(49) Krzysztof Narkiewicz (1998) Chronic Orthostatic Intolerance; Part of a Spectrum of Dysfunction in Orthostatic Cardiovascular Hoeostasis?, Circulation 98:2105-2107. This paper reports on the study of postural orthostatic tachycardia syndrome, and attributes to the gravitational pooling of blood in the lower limbs caused by “impaired venous tone” where “It is generally accepted that autonomic dysfunction is a hallmark of this disorder.”
(50) Fauci, Anthony S.; et al. (February 2008). Harrison’s Principles of Internal Medicine 17th edition. New York U.S.A.: McGraw-Hill Companies Inc., 2703=2704. The text of this summary links the former term “effort syndrome” to the modern condition of “chronic fatigue syndrome” and refers to graded exercise regimes which have “proven” effective in relieving symptoms and improving exercise tolerance.
(51) Hurst, J.W.; R.B.Logue, R.C.Schlant, N.K.Wenber (1974). The Heart 3rd. edition. New York: McGraw Hill Book Co.,, 1552-1555 – The authors of this paper stated “Attempts by Cohen and his associates to alter these abnormalities by physical training were unsuccessful since the patients could not or would not follow the prescribed training programme.” and commented that previous studies of a small number of patients by Holmgren in 1959 and Levander-Lindgren in 1964 has shown that training programmes had shown some benefits. It was the comment that these patients “would not or could not train” that prompted me to design a programme that patients “could and would train” if they were instructed to train within their own limits. The article also refers to Da Costa syndrome and other synonyms and notes that the symptoms occur in response to exertion, and that some of the patients are tired all the time. the condition was ore common in women, and was associated with body build and posture, and that there was low oxygen consumptom and excess blood lactate production during exertion and that the infusion of sodium lactate brought on the symptoms in these patients but not in healthy individuals. The symptoms were more likely to occur in trains buses or crowds (probably because of the abnormal response to excess levels of CO2 which occur in confined spaces M.B.), and they prefer sitting in aisle seats in theaters.
(52) Lewis, T. (1918). “Observations upon prognosis, with special reference to a condition described as the “irritable heart of soldiers””. Lancet i (181-3)
(53) Osler, Sir William (1918). “Graduated exercise in prognosis. Letter.”. Lancet (1): 231. ( I was not aware of any previous success with fitness programmes at the time of designing the research programme at the South Australian Institute For Fitness Research and Training in 1982 – I found the two papers by Lewis, ref.52, and Osler, ref 53, both from 1918, in late 2009).
(54) Kerley, Charles Gilmore, M.D. (January/Dec 1920). The Effort Syndrome in Children, Archives of Pediatrics,Vol. XXXV11 p.449-454. This author observed that the ‘effort syndrome was seen in some children who typically lacked the ability for ‘sustained effort’ in either physical or mental tasks, and that, although they were intelligent they could not apply themselves to being educated. They generally tire easily and preferred to be spectators in sport rather than being active participants. In any activity . . . “Wherever endurance is required, he fails” . . . and this type of individual . . . “is subject to a great deal of unjust criticism. They are accused of being lazy, indifferent, careless and dull. The fact is they are poor types of humans of from 50 to 75 percent capacity” . . . and when they try to play sport in later life they are turned down by the coaches or trainers . . . and . . . in girls this type of problem may be less noticed than in boys for obvious reasons . . . and . . . “It is important not to confuse these young people with those who suffer from bad habits, as regards their sleep, rest, and general hygiene, or from those who are bodily ill” . . . but are due to the childs ‘constitution’.
In a typical case a young boy in whom . . . “Work in the garden produced dizziness. As a young lad he would ride his bicycle down hill 2 miles to the village, and pay some public conveyance to take him and the bicycle home. He suffered from palpitation if he rode up hill on his bicycle. He was a well meaning, well spoken, kindly disposed young man without a trace of initiative.”
In another case he gives the example of a patient that he had known since the age of two and he wrote . . . “She always has been and always will be useless” and he says that she was typical of “Similar cases” . . . “that exist in all communities, and all have one feature in common – a lessened capacity for sustained effort” . . . and . . . From the standpoint of treatment, they constitute a most discouraging group. Rest cures, change of climate, and various supporting measures are of little avail. as these individuals are fashioned, so they remain” . . . “Thus constituted they enter the world and thus they continue throughout perhaps a long life regardless of attempts at improvement”.
The author also discusses the make-up of such individuals with poor ‘constitution’ and the typical reduced capacity to sustain effort in relation to some army recruits . . . “During the late international war, English army surgeons learned, that, when certain recruits were put to prolonged hard work, at drill, hikes, and other exertion, they failed to measure up to the endurance standard required of a soldier in the field. These recruits had passed the various physical tests, and had been put to training. After a time it was found necessary to disqualify the men, because of inability to perform the duties and bear the hardships demanded, which others were able to meet. To this condition Dr. Thomas Lewis applied the term Effort Syndrome.
(55) Rothschild Marcus A. (April 1930), Neurocirculatory Asthenia, The New York Academy of Medicine, Vol.VI, No.4, p.223-242.(Annual Graduate Fortnight, Functional and Nervous Problems in Medicine and Surgery, October 7 to 19, 1929), The introduction to this article mentions several synonyms for the ailment and includes these words “Da Costa during the Civil War wrote a masterly description of this condition and termed it ‘irritable heart’ . . . and . . . Lewis, in his admirable report suggested the name ‘Effort Syndrome’ . . . and This lecture tonight emphasizes the profession’s interest and the importance of this condition”. There were many causes which included ‘various infections’ and ‘constitutional cases’, The infections included influence, typhoid, and dysentery, and other miscellaneous factors included prolonged service, gassing or shell explosion.
The constitutional type occurred in children, youth, and early adult life, and most soldier’s who developed it already had minor symptoms prior to enlistment. This type were generally tall and thin, with long narrow chests and forward curvature of the lower spine which pushed the abdomen forward, and included visceroptosis with the heart, stomach, and liver etc positioned lower in the torso.
Symptoms: The pulse rate changes when they move from the upright to the reclining position, or in response to fear or other emotional stimulus, and they get palpitations with violent effort “such as the usual exercise test of hopping or forward bending”, with the pulse rate taking up to several hours to return to normal. There is soreness in the skin on the left side of the chest in one quarter of cases, and in others there is general sensitivity in parts of the chest, but mainly in one rib space. Giddiness occurs mainly when getting out of bed, or with physical or emotional effort, and tends to become less noticed later in the day. Faintness or sometimes actual fainting occurs with patients reporting from 1 to 100 times, and is brought on by “the cessation of sudden effort, severe coughing attacks, deep breathing, the effort to stool, the sight of blood, a typhoid inoculation,, or a small pox vaccination”. In most cases the patient feels the faint coming on and sits down to avoid falling and injuring themselves. During the faint the pulse may become imperceptible but gradually return to normal after a few seconds or up to five minutes. Dermatographia is the ability to write on the skin where running a fingernail lightly down the skin leaves a red or white line, and according “dermtographia is practically universal”.
Medical tests: “Orthodiography, x-ray, and fluroscopy” have shown “small” hearts which overact and “swings widely” “like a see-saw”. Blood pressure observations correspond to the extreme lability of the entire vascular apparatus”, but cardiograms are normal and there was no evidence of disease of the heart, and it is important to interpret those factors properly so that the patient does not develop cardiophobia (fear of heart disease), as that will not be helpful in treating the problem. The post viral types generally recover, but the ‘constitutional’ types involve “periods of practical recovery and remission”. The author had followed a small number of cases and they were all leading active useful
Treatments: The treatment involved the graduated exercises used by Sir Thomas Lewis which evolved mild pleasant activities including games and sports, and “Overfatigue should be prevented”. Although some returned to normal health, others reached an improved level but it was less than the normal capacity for effort. Also the patient “should be taught proper posture and breathing exercises.
(Note that when this author refers to faintness being brought on with ‘the cessation of sudden effort’, it may be just a case of the faintness being caused by the sudden effort, and then the person stopping the exercise because of the faintness, or, it may be due to the fact that the effort was sudden (and therefore brief), so they only notice the faintness after. Note also that hopping would result in the loose internal organs of visceroptosis moving up and down, and leaning forward would compress and displace them, and hopping would cause intermittent increases and decreases in the pressure inside the abdomen, and leaning forward would increase the pressure for the duration of the lean).
(56) Sir Maurice Cassidy, K.C.V.O., M.D. (April 22, 1941) Proceedings of the Royal Society of Medicine, Vol. XXX1V, p. 37-50 and p.541-553, Section of Medicine, Discussion On The Nature And Treatment Of The Effort Syndrome.
“At least 50%, probably 70% of the civilian population when taken from their secluded, or at least peaceful, routine of life are liable to effort syndrome. Many of these already suffer from it in various degrees . . . and . . . Even the most stable members of the population under certain conditions may develop this disability.”
“The real national problem of this disability is not so much the cure or alleviation of the cases which arise as the result of the war, but the means whereby it may be prevented before any war starts.”
By the end of World War 1 it became known that the incidence of the effort syndrome increased during periods of active warfare “This was certainly the case in America where during the Civil War the troops were badly clothed, badly fed, overtasked and generally neglected.”
“The causation was ascribed largely to the type of accouterments, and the principle of the brace was recommended to take the weight of the pack off the chest while the tunic at the same time was made looser. When one reads the history of the wars of those days, especially those fought in India with tight-fitting tunics, the weight of the accouterments and sometimes of busbies, the diet and the drink, the temperature and the climate, and the extraordinary exertions demanded of the men, it is amazing that any of those hardy soldiers escaped a breakdown”
It is important to note that the effort syndrome is not common in the Navy and . . . “In the Guards, as in the Navy, the physique of a recruit must be first-class and both these Services are exposed to hardships and terrifying experiences. This seems to show that a member of these specially selected Services, possessing a fine physique, is only in rare instances liable to the disability we are discussing.” | From the Cassidy report“I well remember seeing a rare case of effort syndrome, a man who had been in a Guards regiment. He looked as if all the struts had been removed from his once magnificent chest, the contents of which appeared to have dropped into his sagging abdomen. The chest expansion by measurement was as good as before, but the posture of the man had completely changed.” |
In diagnosing the condition . . . Obvious signs of the condition are poor development, thin physique and posture . . . “Frequent sighs” . . . and . . . the deceleration time of the pulse rate after exertion is longer than 2 minutes, and the symptom of left sided chest pain is “produced locally in muscles, fibrous tissue, or fascia of the chest wall” . . . and . . . is associated with tenderness over the area of pain . . . and . . . “is not referred from the heart” . . . “the difference between left infra-mammary pain and angina has been recited again and again.” . . . The constitutional cases had narrower and smaller hearts than average.
The symptoms of respiratory abnormalities include breathlessness on mild exertion, excitement, or at rest, and “Patients also describe choking sensations when they waken suddenly at night, and lie gasping for breath, for some minutes. Difficulty in wearing a gas mask for more than a few minutes because of feelings of suffocation is also very common.” Breathing rates were irregular. They generally breathed more rapidly, and took in less air with each breath, and “the actual air exchange of the effort syndrome patients is less than that of the control group”, and their breath holding capacity was “extremely bad”. The rate of breathing increased abnormally after exercise, while the depth of breathing remained much the same. “breathing exercises did not lead to any marked improvement. Indeed, any ‘treatment’ directed specifically towards the respiratory anomaly, e.g. attempts at slowing a very rapid rate by explanation, re-education, persuasion or suggestion have proved disappointing.”
According to one report about the effort syndrome. . . “When recovery occurs it may take place suddenly, almost abruptly” . . . (note that the effort syndrome is chronic, and graduated exercise can improve some cases gradually, so the rare reports of sudden recovery probably related to misdiagnosed cardiophobia or exercise phobia M.B.).
Regarding the question of malingering . . . “This group of symptoms is too uniform to be fictitious or fantastic.”
“Of course, the soldier is not supposed to see his diagnoses, but, in fact, he always knows it.” | The Cause and Effect Question“Dr. Aubrey Lewis said that the term effort syndrome was not synonymous with anxiety neurosis as it included many other psychiatric conditions. Some patients with effort syndrome suffered from depression or hysteria; others had a psychopathic personality:; there might also be a few schizophrenics or alcoholics among them. Therefore a uniform plan of treatment for all cases could not be successful.”*****The quote above, which is from the Cassidy report, is typical of some authors who see hundreds of cases of effort syndrome with all sorts of psychological features, and become confused and frustrated by the failure of consistency and treatment. He is suggesting that a large range of psychological conditions can cause exactly the same set of physical symptoms??? which is essentially impossible. However, there is nothing confusing about saying that some people are born with, or acquire a condition that reduces their capacity to sustain effort or strain. Various authors have stated that some people learn how to cope with the symptoms and the limitations quite effectively, but most are reported as being anxious, or depressed, or become alcoholics , or disturbed, or psychotic especially where they find themselves in situation that require more intensive levels of exertion etc. M.B. |
(57) John Parkinson M.D. (April 12th, 1941) Effort Syndrome In Soldiers, British Medical Journal, April 12th, 1941: 1: 545-549. “we are well rid of the terms ‘Soldier’s heart’ and D.A.H.” . . . “In effort syndrome we are dealing with men of every degree of non-athleticism . . . and when they undertake more than their low capacity for effort they also fail with exhaustion, dyspnoea, and palpitation – proof enough that their circulatory system cannot cope with the strenuous task of a soldier” . . . “An expression of this idea is seen in the term ‘neurocirculatory asthenia‘ (N.C.A.) applied in the United States to the term we call effort syndrome. Our term is not ideal, for it might suggest in effort lies the origin of the disability, whereas effort merely reveals it”. . . “Tentatively I would define effort syndrome as a functional circulatory disease, most evident on exertion, unmasked or produced by war service”. It was rare in the Navy and Air force but although the explanation isn’t obvious, more of the recruits were volunteers, and those services “do not demand so uniform or so arduous a training of such a multitude of men for the toll of marching with heavy equipment” . . . A fairly large number of cases were due to infection, and the nervous group was smaller than the constitutional . . . “It constituted a big military problem because of the wastage of men it caused” . . .
White P.D. & Donovan Helen (1967),
Hearts: Their Long Follow-up, W.B. Saunders Company, West Washington Square, Philadelphia Pa, 19105 & 12 Dyott Street, London W.C.1, pages 300-308. The following quotes come from that book (Chapter 18 about ‘neurocirculatory asthenia’ ) . . . “Dr. George Denny and I received into our care from the front not far away exhausted British Tommies who had been exposed to the grim French warfare which prevailed in the First World War. They were the most extreme cases of the irritable heart of soldiers (so called at that time, now evidently neurocirculatory asthenia) that I have ever seen . . .
Despite the obvious exhaustion and the crippling symptoms that these men showed, they were labeled as weaklings and
malingerers by the commanding officer, who ordered us to return them to the front after they were found to have no heart disease. Within a few days most of these patients came back to us still exhausted and were soon after sent back to England with a ‘Blighty ticket’ to be studied by Thomas Lewis and his associates at his hospital ”
“Later on in the American Expeditionary Force in Base Hospital 6 (the Massachusetts General Hospital unit), I again encountered a good many cases but none were so marked in degree as those Tommies at Dannes-Camiers. I might add here that these individuals who were candidates for crippling symptoms were largely excluded from service in the Second World War at the time of their examinations in the draft.
(59) Le Fanu James (March 2003),
The Irritable Heart of Soldiers and the Origin of Anglo American Cardiology:
The U.S. Civil War (1861) to World War 1(1918), Journal of the Royal Society of Medicine 2003 March; 96(3) 151-152. This is a summary of Charles Woolley’s 2002 book by the same title, and it refers to “the distinguished roll call” of physicians who continued the study of irritable heart, or soldiers heart that was started by Da Costa, and it included Samuel Levine, Sir William Osler, Sir James MacKenzie, Sir Thomas Lewis, and others.
(60) Gordon Keith (April 1944), Editorial;
Effort Syndrome, Canadian Medical Association Journal, Vol.50 (4) p.362-363 .PMCID: PMC 1581613. This article summarises the “multiplicity of titles” or labels, and the “differences of opinions regarding its true nature”. The author regards ‘Soldier’s heart’ as inappropriate because it also occurs in civilians, and criticises other labels that focus on any one aspect. The author mentions that it should not be difficult to distinguish the symptoms from those of heart disease. It also mentions “the so-called
bent back of soldier’s”.
(61) Dr. Thomas Lewis M.D.(March 30, 1918),
The tolerance of physical exertion, as shown by soldiers suffering from so-called” irritable heart”, The British Medical Journal, p.363-365. This report was made after the use of graded exercises had been applied as a means of treating the condition, and as a method of grading the severity of their ailment. The methods included a system of independent observation, and objective checks, to prevent the possibility of the soldiers simulating the results to avoid duty. The aim was to determine if the individual was suitable to be returned to full duties on the firing line, and one study of 239 soldiers determined that 72 were. Another 47 were deemed likely to be fit enough within three months, and 20 were unlikely to be suitable within three months and placed on light duties. A further 69 were deemed never likely to be fit for general service and placed on light duties, and 32 were placed on sedentary work at home. The soldiers were followed up after 11 months and their capacity for work was found to correspond with the original estimates, and 38 of them were eventually discharged as permanently unfit. The graded system, and it’s results “aroused a good deal of interest” and “a large number of military hospitals both at home and abroad” “adopted it”.
The paper included a section called “Signs and Symptoms after Drill”. That section was followed by another called “Facial Expression and Breathlessness” and it was augmented by a photo of the typical patient which clearly showed that the abnormal response to exertion caused anxiety. The caption underneath read . . . “Photograph or a patient, aged 28, admitted for long-standing and severe ‘D.A.H.’.
The photograph was taken immediately after fifteen minutes of easy exercises . . . and shows the tension of the sterno-mastoid, slightly opened mouth, and dilated nostrils. The eyebrows are depressed, the forehead furrowed (the central furrow is permanent). The face expresses fatigue and the anxiety of early breathlessness.” (end of quote).
My comment. In some cases Da Costa’s syndrome is a physical condition involving physical symptoms, with a physical cause (long marches), where relapses are brought on by physical exertion (drill).
In other words it is a physical disorder that causes anxiety, not an anxiety disorder that causes physical symptoms.
However some cases appear to be brought on by anxiety, which confuses the argument about cause and effect.
Furthermore, the symptoms of palpitations, breathlessness, faintness, and fatigue, although different, are similar enough to the normal effects of exercise, stress, or worry, to cause confusion.
If the conditions could be easily distinguished there would be no confusion, and no disputes about cause. M.B.
((62) Margaret Cicolella, Staci R.Stevens, Christopher R.Snell, J.Mark VanNess (2007), Legal and scientific considerations of the exercise test, Journal of Chronic Fatigue Syndrome, Vol. 14(2) 2007, pages 61-75. “This article examines the legal and scientific bases on which an exercise stress test can provide medically acceptable evidence of disability for the Chronic Fatigue Syndrome (CFS) patient.”
It explains the fact that
the patients actual experience of the illness, and the resulting inability to sustain gainful employment, is not acceptable evidence in a court, and that
the burden of proof is
on the patient to provide
objective scientific evidence of a “medically determinable impairment (MDI).
It reports that a review of legal documents has shown examples of cases where CFS patients have been assessed on the basis of exercise tests, and that most patients
are denied disability benefits by the Social Security Administration and private insurance companies regardless of the results being good or poor, because
good results are used as
evidence of contradiction to the patients claim, and
poor results are used to argue that the patient was a
malingerer who
deliberately failed to exert himself to the maximum level.
The SSA uses the definition of chronic fatigue syndrome provided by the Centers for Diseases Prevention and Control (CDC) which defines it as fatigue that
cannot be attributed to any other physical or mental disorder, and that the patient must prove the existence of medical impairment and “the inability to engage in substantial employment.”
Post-exertional malaise is considered to be
the cornerstone of the four main symptoms of CFS. The SSA policy
‘specifically disallows’ the patients
‘self-reported’ symptoms as evidence, and states that it must be objectively proven.
In one court case the argument used was that . . . “The
treadmill test documented that she is able to walk up hill for nearly 8 minutes at a time”, which they claimed was not objective evidence of long term disability. In another case it was argued that the patients high performance on the treadmill test indicated that she was still capable of light work, but as the authors of the research paper said,
that test did not reveal anything about the residual fatigue after getting off the treadmill. In a further case the “Claimant’s treating physician stated that maximal oxygen consumption was
only 61% of that predicted for sedentary individuals” and that this poor performance showed the inability of the claimant to “sustain work.” However the
opposing lawyers argued that the test was invalid because the patient
did not do the maximal amount of exercise required. They also “used
video-surveillance showing the claimant running errands with his wife, driving a car, attending church, and
carrying two tote bags, etc. This direct observation of the claimant’s activities was
effectively used to contradict the claim that physical limitations precluded work”, and it has been
argued that they should have sufficient capacity to sustain light work such as toll booth operator or car lot attendant,.
However, the authors suggest that a further test 24 hours
after the exercise,
to determine the persistent effects of exercise, is likely to be
a more reliable guide because . . . “If post exertional malaise effectively means that
the patient who works on Monday will then suffer uncompromising fatigue for several days thereafter, then it is reasonable to assert that there can be no reasonable expectation of regular participation in the
national economy“.
They then give an account of the
“Pacific Fatigue Laboratory Study” which used a
“stadardized bicycle protocol” that showed the difference between the exercise test during, and 24 hours afterwards, and
compared them to the results obtained from healthy controls. They stated that “It is the comparison between tests that shows
a disturbing difference between the two groups. Variability from Test1 to Test 2 in Peak VO 2 and VO 2 @ AT values documents impairment in CFS patient but not the controls.” The report further found that the control subjects showed only a 2-3% variability between tests and that the
CFS patients have a 22-27% variability which is objective evidence to confirm their ‘subjective’ descriptions of post-exertional fatigue. The test was conducted on patients with other illnesses but the results showed that
the difference was unique to CFS, and that
further research was required to determine the effects of different type of work, and how that effected the persons ability to sustain the activity. The authors further state that
“It is imperative to distinguish the ability to work a regular job from engaging in daily activities that permit frequent and extended rest periods” and they conclude that “It is clear that the Pacific study is preliminary and begs further review. But the initial data suggests that the test-retest format offers a superior basis on which to establish disability consistent with SSA policy and other relevant case law.
If the preliminary data holds, the contribution to the CFS patient may be immeasurable.”
In the notes at the end of the paper they state that the Social Security Ruling (SSR) 99-2p(1999) diagnosis requires at least four self-reported symptoms which include short-term memory loss or impaired concentration in work or social activities, sore throat, tender lymph nodes in the neck, muscle pain, joint pain without swelling, non refreshing sleep, and post-exertional malaise lasting more than 24 hours. The authors also report on the laboratory findings of elevated antibody titer to
Epstein-Barr virus capsid antigen equal to or greater than 1:5120 or an early antigen equal to or greater than 1:640, and an
abnormal MRI brain scan, and
neurally mediated hypotension as shown by tilt table testing, and
abnormal exercise test results or
abnormal sleep studies.
See
here http://www.name-us.org/MECFSExplainPages/2007CiccolellaLegalStressTest.pdf
My comments: The 2007 report about the Pacific Fatigue Laboratory study shows that it was very similar to the study that I co-ordinated at the South Australian Institute for Fitness and Training in 1982 (25 years earlier), except that the patients were recruited from individuals who had problems with persistent fatigue for which they had not been given a satisfactory medical explanation. The standard ergometric cycle cardiographic studies showed that
most of those patients had abnormally low aerobic capacity on the first test, and were generally lower than patients who had actual heart disease. The exercise programme that followed was based on the ‘obvious’ fact that they had
a real physical impairment that was only going to be successful if the volunteers
trained within their own limits, and the fact that more than a dozen patients continued to train two nights a week for three to nine months was proof that their ailment was
real, physical and measurable, and definitely not just “subjective”, or fake, or due to laziness or the fear of exercise. Their position on the training track was precise and
accurately reflected the scientifically objective aerobic measurements with the highest being first, and the lowest being at the rear of the field. I had been advised that those measurements were
developed by research cardiologists so that they would be
impossible for a malingerer to fake.
My published essays on this subject have clearly identified that some patients can walk for many miles, as long as they do so within their limits, but if they try to run 100 yards to catch a bus they will experience abnormal palpitations in the first 20 yards, and be gasping for breath and feeling faint or falling to the ground before they reach 50 yards. I have also explained how they can keep up the pace on a normal bush walk but when required to proceed up a steep hill they will have to slow down, and be easily overtaken by little old ladies with walking sticks.
I have also clearly explained that some patients are
born with an inability to sustain effort, and that they may be able to do many things for a short time, but if they try to sustain regular part time, or full time employment,
the fatigue will accrue until they have to resign due to extreme exhaustion, or be sacked for not keeping up the work load of other employees. They are also not going to do treadmill exercise to the full extent of healthy people because they can feel the increase in symptoms as the level of exercise increases and are
not going to push themselves to the limit and experience palpitations, and be gasping for breath and falling to the ground exhausted just to prove a point to some
grubby lawyer. That response is well known to the medical profession as
guarding – i.e. All normal patients will naturally refuse to co-operate with doctors who continue to probe them with procedures that cause pain or harm.
Such facts have been on the public record since 1982, and in earlier essays, and in my book from 1994 -2000, and on my website for the past sixteen years from 1994 to 2010.
The information has been readily available on the Google search engine and I am certain that most researchers who are interested in this topic would have seen it, and many of them would have
copied it.
The Pacific Fatigue Laboratory has
slightly different emphasis but has produced
logically predictable results which have been evident since earlier studies of Da Costa’s syndrome in the first world war, and from
20 year follow up studies of patients which show that if they were unemployed or only partly employed because of their ailment at age 20 they will still be the same at 40, with the intervening period showing evidence that they attempted to improve their financial situation by working but became exhausted each time.
There is
nothing new about companies or governments employing lawyers to send
private detectives out to get photos of patients carrying groceries and then
using it as an argument to deny entitlements to insurance payouts or pensions. They also use dirty tricks such as
interpreting both positive and negative results of tests to
argue that the patient is
not entitled to benefits, often for the
deliberate dual purpose of
frustrating and harassing the patient. They also typically create
misleading impressions, for example, by arguing that negative short term test results have some convincing relevance to an
obvious long term problem,
Those organisations simply
don’t want to take responsibility for the costs of such payouts, and so they keep on
justifying their
culture of denial on the grounds that
the existing scientific evidence isn’t good enough, and it apparently won’t matter how much proof is given by the Pacific study, or any other study in the future. I conclude that the only way is for the 200 million patients with the various types of CFS to band together and collect all of the proof that has been around for the past 100 years and
demand it’s official acceptance, and arrange for the sacking of any official employee who resists the process. Also lawyers who are so negligent that they haven’t seen the evidence, or who have, but
pretend that they haven’t, or who use any of their
dirty tricks to obstruct justice, should be prosecuted for perjury, and crimes against humanity, or what ever other laws that are applicable.
Similar prosecutions should be made against any other individual who tries to hide or falsify the history of evidence.
If that doesn’t happen government officials will still be arguing that the new evidence isn’t good enough, and saving money
for the next five hundred years.
At the moment,
ordinary, honest, uneducated patients without any medical or legal knowledge go into such court cases one at a time. They are
loaded with the burden of proof, and are challenged by
teams of lawyers who have had many years of experience at dealing with
medicine, science, and the law, and are being paid
enormous salaries to
win the case regardless of the evidence, so each case is
stacked against the individual. That situation needs to change.
For more information on the 1982 IFRT fatigue research see
here https://theposturetheory.twebexponent.co.uk/chronic-fatigue-syndrome/#anchor130031
For information on tilt table testing see
here https://theposturetheory.twebexponent.co.uk/chronic-fatigue-syndrome/#anchor412109
For my essays on recurrent accruing fatigue details see
here
For a typical example of deletionism see
here https://theposturetheory.twebexponent.co.uk/dacostas-synd-wikiwebpagel/#Deletionediting
For information on a typical attempt to delete everything about me and my research see
here https://theposturetheory.twebexponent.co.uk/dacostas-synd-wikiwebpagel/#DeletionOfEverythingIWrote
(
(63) Cassidy, Sir Maurice (April 22nd 1941) Discussion on the nature and treatment of the effort syndrome, Proceedings of the Royal Society of Medicine, Vol. XXX1V p.541-554. Sir Maurice Cassidy K.C.V.O., M.D. was the president of the Royal Society of Medicine. He reported that the syndrome described in 1864 by Harthorne, was the same as that described by Da Costa in 1871, and defined by Lewis as the effort syndrome. Harthorne attributed the symptoms
“largely” to the
“tight straps” of
the uniform, and “
recommended a brace to take the weight of the pack”, and
“loose clothing”. In 1870 Arthur Myers
“emphasized” the
“blame” which had
“already” been put on the
“tight fitting tunics” and
the weight of the equipment in the back packs.
Cassidy said that the main interest in the disability occurred because of the increased incidence during warfare, and that it was “certainly the case”
during the American Civil War when
“the troops were badly clothed, badly fed, overtasked and generally neglected”, and that the only way that it could be alleviated or cured was by the graduated exercise programmes of Thomas Lewis.
Cassidy also stated
“At least 50% , probably 70% of the civilian poipulation when taken from their secluded, or at least peaceful, routine of life are liable to effort syndrome.” He added that many soldiers already had the condition before enlisting but had managed the symptoms by choosing a particular occupation that didn’t aggravate them, and that even the most stable of civilians could develop the disability if the conditions of war were severe enough.
Cassidy then gives an example of a man who had been in the Guards regiment . . .
“He looked as if all the struts had been removed from his once magnificent chest, the contents of which appeared to have dropped into his sagging abdomen . . . the posture of the man had completely changed”.
However, the paper carries the following statement . . . “I believe the facts show that the condition always results from emotional causes, which may operate in almost any form of psychoneurosis”, and “It was believed that the element of fear was the main causative factor although it was noticed that
a large proportion of the cases had only been two months in France” . . . and “A large number of men developing effort syndrome are below the physical average”.
My comments on Cassidy’s paper: If you have a look at the
objective facts you can see that
the typical patient has a poor physique and was poorly trained, and then sent off to battle
wearing a heavy knapsack strapped to his chest. It compressed his chest which then collapsed, so the spine fell forward into a stoop.At the same time the contents of the chest were pushed down toward the abdomen forcing the belly forward in a conation called visceroptosis. All of those factors can cause the faintness and fatigue which is typically seen in soldiers with the effort syndrome. However, Cassidy dismissed those factors and said that
he “believed” that the condition was a psychoneurosis
caused by fear, even in soldier’s who were not in the battle zone and had nothing to fear???? What Cassidy
believed was that emotional factors caused poor posture???
As a final note I can say that I have described in my book how the struts of the ribcage support the spine, making it easy to hold an upright posture. However some people have a flat chest which doesn’t offer that support, so the chest is much more likely to collapse, and the stoop is more likely to get worse. Nevertheless anyone with any physique who compresses their chest may develop problems if the chest collapses, because the spine will stoop over the top and makes the pressure worse.
For the full reference see
here http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1998120/
(64) Gregory, William K. (1928), The upright posture of man: A review of its origin and evolution, Proceedings of the American Philosophical Society page 339. Here is a quote from that page “Benjamin Franklin, the illustrious founder of this Society, who labored so successfully for the diffusion of useful knowledge, might very well be imagined as approving the suggestion that the Society should devote one or more of its stated meetings to a consideration of the problems relating to man’s
posture; for it will be
obvious to everyone that
the subject has more than an academic interest, especially if it can be shown that the erect posture is not entirely and unmixed blessing, since it has made civilized man liable to fallen arches, to assorted hernias and to
all the unpleasant visceral ptoses, prolapses
and similar ills that flesh is heir to. This aspect of the subject has been very fully and ably dealt with by others, especially Sir Arthur Keith in his lectures before the British Medical Association, in 1923, and can her only be referred to in passing. (end of quote)
My comments – when I wrote The Posture Theory in 1980 it was
obvious that I had identified the supposedly unknown cause of many symptoms and illnesses. However, since then, despite some people referring to it as common sense or brilliant, I have had my critics who have argued that it is unfounded nonsense that no-one takes seriously. Nevertheless, you can see that the fact that
poor posture compresses the chest and abdomen to cause
downward displacement of the abdominal organs etc., is another way of referring to poor posture as causing ‘all the unpleasant visceral ptoses’.
To read that reference from 1928
see here http://www.jstor.org/pss/984249
(65) Keith, Sir Arthur (14th April 1923) On man’s posture: It’s evolution and disorders, British Medical Journal 1923.1.624
I haven’t read this yet but it was mentioned in the previous reference (64), by Gregory K.Williiams, and it looks interesting and relevant.
(66) Phillip A. Low et al, (15th December 1994), Comparison of the postural tachycardia syndrome (POTS) with orthostatic hypotension due to autonomic failure, Journal of the Autonomic Nervous System, Vol. 50, Issue 2, pages 181-188 (Phillip A.Low was from the Autonomic Reflex Laboratory, Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA). This research compares POTS to orthostatic intolerance caused by autonomic failure, and refers to the orthostatic dizziness, and variability of blood pressure. The following words are a direct quote – “Since POTS patients have a marked reduction in pulse pressure on standing,
a major mechanism of their symptoms might be venous pooling. We therefore studied “
the cardiovascular response to head-up tilt, Valsalva maneuver and deep breathing in: control subjects . . . patients with orthostatic hypotension secondary to autonomic failure . . . and patients with POTS” . . . and concluded . . . “These findings suggest that sympathetic arteriolar function remains relatively intact but that sympathetic
venomotor function is selectively impaired. These findings may have “
significant implications for the treatment of patients with POTS.” See
here
(Note that when I was developing the Posture theory between 1975 and 1979 I included information about Valsalva’s maneuver, tilt table testing, damage to the veins, and treatment methods based on those aspects. M.B.)
(67) Cobb, S; Cohen, M.E.; and Badal, D.W. (1946) “Capillaries of Nail Fold in Patients with Neurocirculatory Asthenia (Effort Syndrome, Anxiety Neurosis).” Archives of Neuroogyl and Psychiatry, LVI, 643.
(68) Bedingfield, H. (1930) Visceroptosis and Allied Abdominal Conditions Associated With Chronic Invalidism, Humphrey Milford, Oxford University Press, London.
(69) Limner, Luke Esq. (1874) Madre Natura versus the molloch of fashion, 4th edition, Chatto and Windus, Picadilly, London.
(70) Cameron C. (1930) The Nervous Child, 4th edition, Oxford University Press, London. This book refers to the breathlessness, faintness, palpitations, restlessness, and irritability, and discusses the changes in skin temperature, and the ready exhaustion that is so common in children who have poor postures with curvature of the upper and lower spines. The author suggests that if the same symptoms were seen by cardiologists they would be diagnosed as having “cardio vascular asthenia” or the “effort syndrome”. The author also suggests that the nervousness causes the muscles to weaken and poor posture results, but the evidence in the book indicates that poor posture is the cause of the nervousness. For example exercise programmes designed for army recruits improved their posture, health, and temperament.
However, if the children’s posture was not corrected they were likely to become sick and miserable adults who needed several forms of surgery.
(71) Simon Wessely FRCP (May 2001) Investigating selected symptoms – Chronic Fatigue: Symptoms and syndrome; Annals of Internal Medicine, May 1, 2001, vol.134 no.9 Part 2, p.838-843. The following quote comes from that article “Particularly unclear is the way in which chronic fatigue and the chronic fatigue syndrome relate to each other: Is one the severe form of the other, or are they qualitatively and quantitatively different?”.
here
(72) Lloyd Andrew R. (2004) An editorial: To exercise or not to exercise in chronic fatigue syndrome No longer a question” – “Graded physical exercise is no panacea, but is beneficial”, Medical Journal of Australia: 180 (9): 437-438. This report describes exactly the same principles for an exercise program that I designed for the Institute for Fitness Research and Training in 1982 and reports on its effectiveness.
here
(73) E M Papper (June 1989) The influence of chronic illness upon the writings of Alexander Pope,
Journal of the Royal Society of Medicine Volume 82, June 1989, p.359. This author attributes Alexander Pope’s health problems to vitamin D deficiency and rickets in childhood which caused his hunchback deformity and sideways curvature of the spine. Also mentioned was the involvement of tuberculosis of the spine (called Pott’s disease), due to drinking milk which was infected with the tubercle bacillus. Here is a quote from that paper . . . “Finally, another major and debilitating illness that he had was asthma.
In view of the severe compression of his lungs by the complications and consequences of kyphoscoliosis and Pott’s disease, the asthma may have been due to lung compression and functional impairment of both respiration and circulation with subsequent congestive heart failure.
Difficulty in breathing in individuals with compressed lungs inside of deformed chests is not unusual. The development of signs of heart failure from which Pope suffered was a major contribution to the unfortunate events which probably caused his death. The end result of his major thoracic cage impairments was total cardiac failure masquerading as asthma’.”
See
here http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1292171/pdf/jrsocmed00149-0049.pdf
My comment: According to my theory written between 1975 and 1980, poor posture compresses the lungs and breathing muscles to cause functional impairment to breathing and circulation. My theory has been criticised by rather ignorant and shallow individuals, but as you can see it has a sound logical and factual basis. It is also my view that Pope may have had a functional breathing problem as seen in Da Costa’s syndrome that was misdiagnosed as asthma, but that is an estimate for further consideration.
A lifesize portrait of the typical thin and stooped physique of a Da Costa’s syndrome patient was displayed in the Museum of the Post-Graduate Medical School of London for several decades. See my report
here
(74) J M Shneerson(2000) Letter: Alexander Pope (1688-1744): his spinal deformity and his doctors, European Respiratory Journal 15:1134. This is a quote from that letter . . . “a French physician, PETIT [2], who published a Thesis in France in 1723 which was translated into English in 1726. In this account he attributes breathlessness to the distortion of the spine which alters the disposition of the ribs and respiratory muscles, and to the smallness of the lungs” See
here http://erj.ersjournals.com/content/15/6/1134.full.pdf
(75) Maj Levander-Lindgren (1964) Studies in Neurocirculatory Asthenia (Da Costa’s Syndrome),1V. Course During Common Treatment and Physical Training and Relations Between Symptoms and Signs. Acta Mediaca Scandinavica. Vol, 175, fasc. 6, 1964
This article states that “Physical exercises are sometimes regarded as useless”, but some studies by Lewis, and Holmgren etc. reported diminishing symptoms. 101 patients were divided into acute and chronic cases and followed up for 2 years, and studied in relation to those who did “routine physical training” and those who didn’t, and in relation to work tests (
exercise tests), and orthostatic tests (
changes in pulse rates and blood pressure when the person moves from the laying to standing position), and how they related to the patients subjective reports of the effects of exercise on their symptoms.
This study was first published in 1964, and first put on the internet on 24th April 2009,
three months after I was banned from Wikipedia, and after two editors deleted my study of the response of 80 patients to exercise in 1982 because, in their opinion, it was ‘nonsense and rubbish’? I gave information about the effects of three months, and six months or more of training on up to a dozen patients, which proved that the subjective response to exercise and improvements corresponded exactly to scientific measurements.. I also mentioned “tilt-table tests, which are “orthostatic tests.) See my early contributions to Wikipedia
here.
My theories were based on my experience at an exercise programme in 1975, before I started reading research papers, and on the effects of tilt table movements on my own health when I was being x-rayed for kidney stones some years later. At that time I had been told that there was no physical basis for the problems, and no scientific evidence whatsoever to explain my symptoms.
My scientific research proved a physical cause, and my theories provide the explanations which are in common use nowadays, thirty years later.
(76) B.Biswal, P.Kunwar, B.H.Natelson (2011) Cerebral blood flow is reduced in chronic fatigue syndrome as assessed by arterial spin labeling, Journal of Neurological Science, Feb. 15, 2011, 301(1-2), 9-15. This is the result of the study of the cerebral blood flow (CBF) of 11 CFS patients compared to 10 age matched healthy controls . . . “The patients as a group had significantly lower global CBF than the controls. The reduction in CBF occurred across nearly every region assessed. Nine of the 11 patients showed these reductions compared to the average control data, while two patients showed actual increases relative to the controls. See
here
(77) Julian M.Stewart (2011) Orthostatic Stress Testing and Instrumentation – Head-up or Upright
Tilt Table Testing (HUT, a website report by the “Center for Hypotension” New York Medical College – seen in October 2001. This webpage shows a test for fainting devised in the 1940’s by NASA. It doesn’t test for dysfunction of the autonomic system, but for it’s compensatory responses to some other factor. The bed is tilted many times at angles between 20 and 70 degrees, and patients with “
orthostatic intolerance” tend to get abnormal changes in pulse rate and blood pressure at every angle of tilt. More details, including pictures of the tilt table at different angles can be seen
here
(
In 1979 I wrote a theory in which i stated that postural compression of the air in the chest could slow the blood flow between the feet and brain and stretch or damage the blood vessels below the chest to cause weak blood flow, faintness and fatigue. Soon afterwards, I had the extreme pain of kidney stones, and was sent for x-rays to assess that problem. I was strapped onto a bed which was tilted at about 10 different angles at intervals of several minutes, and given an x-ray each time to see how the fluid was flowing between my kidneys and bladder, and if it was being blocked by a stone. Each time the bed was tilted I felt extremely faint and weak in the chest as if I was going to lose consciousness and die, and I said to the two doctors that they could also attach stethoscopes to my chest, and blood pressure cuffs to my arms, and use that method as a way of diagnosing my symptoms of faintness and chronic fatigue which were a part of Da Costa’s syndrome. I also told them that I had similar symptoms of faintness whenever my body was swirled about, such as when I was a passenger in a car which sped around curves in the road etc. They didn’t comment. Their purpose was to diagnose kidney stones, and I had surgery to remove them soon after.
Many years later I saw a book which described how nineteenth century women wore tight waisted corsets which compressed and displaced the internal organs, such as the stomach, and made them hang loosely in the abdomen. I then wrote a theory which suggested that the faintness might be occurring when the body was swinging in all directions, because the loose internal organs were swinging about and compressing the blood vessels in the left or right of the abdomen etc. and reducing blood flow to the brain.” M.B.)
(78) OMIM Online Mendelian Inheritance in Man – An Online Catalog of Human Genes and Genetic Disorders (Updated 7 October 2011), Orthostatic Intolerance #604715. The following quote comes from this website – “
Orthostatic intolerance is a syndrome characterized by adrenergic symptoms that occur when an upright posture is assumed: the heart rate increases by at least 30 beats per minute, without orthostatic hypotension (Jacob et al., 1997). Most patients with orthostatic intolerance are women between the ages of 20 and 50 years (Low et al., 1995).
This syndrome, first described by Da Costa (1871) has been called soldiers heart (Fraser and Wilson, 1918), neurocirculatory asthenia (Wooley, 1976), and mitral valve prolapse syndrome (Boudoulas et al., 1980).
It is similar in many respects to chronic fatigue syndrome (Schondorf and Freeman, 1999).” see
here
(79) B.S. Oppenheimer (July13 , 1918) The sympathetic nervous system and the “Irritable heart of soldiers”, British Medical Journal 2(3002), p.29. The following words are a quote from this article . . . “it is evident that a certain number of cases of “irritable heart”
have suffered from symptoms of the condition long before enlisting, some dating the onset to the formative period or even to childhood. The question whether some cases are not congenital or even hereditary in character also occurs,, particularly when dealing with soldiers who belong to the group called constitutionally asthenic. Then there is the serious and, in the American army , immediate problem of dealing with recruits with such histories who break down in training.” (end of quote). See
here – what the author is actually referring to with the word “breakdown” is not “mental breakdown”, but that the soldiers with thin physiques get physically exhausted and collapse when carrying a heavy, fully laden knapsack across obstacle courses, at training camps!
(80) Y.Jammes, J. Steinberg, and S. Deliaux (Nov. 24th 2011), Chronic fatigue syndrome: acute infection and history of physical activity affect resting levels and response to exercise of plasma oxidant/antioxidant status and heat shock proteins, Journal of Internal Medicine, Nov,24, 2011, 10.1111/1365-2796. This study reports on a comparison of exercise test results between CFS patients who had previously participated in sport before developing their ailment. This study suggests that excessive exercise, in combination with a viral infection, may have played a part in causing CFS. See
here (apart from the abnormal findings it indicates that CFS is not caused by the lack or exercise, or the avoidance or fear of exercise, as had been suggested in many previous suggestions prior to my research findings between 1982 and 1984)
(81) P.D.White, K.A.Goldsmith, A.L.Johnson et al., March 5th 2011), Comparison of adaptive pacing therapy, cognitive behaviour therapy, graded exercise therapy, and specialist medical care for chronic fatigue syndrome (PACE): a randomised trial, The Lancet, 377(9768), page 823-836. This modern study essentially duplicates the exercise program design principles which I developed and used in a research program between 1982-1984, and has similar results and conclusions. See
here and
here.
(82) Hamilton B.E. and Thomson K.J.(1941), The Heart in Pregnancy and the Childbearing Age, Boston, Little, Brown and Company. I have not read this book, but according to another reference by Cohen and White (1941) it contains a report about a 20 year follow study in which women who had been pregnant believed that “the disorder had been provoked, or made worse” by pregnancy.
(83) Edward D. Frohlich M.D. e. al, (1969) Hyperdynamic Beta-Adrenergic Circulatory State, Archives of Internal Medicine 123(1):1-7. This article discussed patients with significantly higher resting heart rate than usual. “Graded isoproterenol hydrochloride infusion increased heart rate significantly more” than normal, and in 9 of 14 patients there was “an hysterical outburst, almost uncontrollable, which was promptly reversed with propranolol hydrochloride but not placebo.”
here
(Note that ‘hyperkinetic heart is different to Da Costa’s syndrome, but one of the symptoms of Da Costa’s is palpitations (rapid pounding of the heart occurring occasionally at rest, but always abnormally in response to vigorous exertion). See also this definition from the MediLexicon website . . . “a syndrome in which the heart appears to be “overworking”, beating excessively fast and/or causing subjective awareness of continual cardiac activity”.
here (84) John Allen et al (25th January 2012), Chronic fatigue syndrome and impaired peripheral pulse characteristics on orthostasis–a new potential diagnostic biomarker, Physiological Measurements. 33 p.231 . . . This study confirms that a tilt table test with Multi-site PPG pulse measurement technology has the potential to be used to diagnose CFS, because there are clear differences between CFS patients and controls. The full article can be seen here
(85) Keith Gordon (April 1944), Effort syndrome, Canadian Medical Association Journal, Vol.50, p.362-363.The following words are a quote from this editorial . . . “The multiplicity of titles which have been applied to this symptom-complex is an indication of the difference of opinion which exists regarding its true nature, and they are all open to criticism from the standpoint of descriptive terminology. Any term which suggests that it is a syndrome peculiar to soldiers is faulty, for the reason that it also appears in civilians when one learns to recognize it.” (end of quote)
(86) John Parkinson M.D. (April 12th 1941), Effort syndrome in soldiers, British Medical Journal, 1. p.545-549. The following words are a quote from this article “It is true that about a half has similar symptoms in civil life, but these were rarely combined to give a composite picture like that of effort syndrome in the services. It constituted a big military problem because of the wastage of men it caused. The rarety of effort syndrome in the Navy and its infrequency in the Air Force have been much remarked, and the explanation is not obvious. Volunteers are in greater proportion in these services: besides, they do not demand so uniform or so arduous training of such a multitude of men for the toll of heavy marching with heavy equipment.” (end of quote)
(87) T. Troosters et. al. (1999), Physical performance of patients with numerous psychosomatic complaints suggestive of hyperventilation. European Respiratory Journal, 14, p.1314-1319. This author traces the problem back to Da Costa of 1871, and Lewis 1918, whose research papers he used in his reference list as number 1, and 2. He is confusing the symptoms of exercise phobias, and disease phobias, (such as heart phobias), and thinks that they are the same as Da Costa’s syndrome, when in fact, there are many differences in the nature and type of chest pains, breathing abnormalities and fatigue etc. The following quote comes from his conclusion.
This is a quote from his conclusion . . .
“It seems therefore, that the sequence of events responsible for symptoms and breathing abnormalities during exercise in this group of patients is as follows. Firstly, a psychological conditioning process generated by, or linked to exercise, might be the origin of the many symptoms, i.e. the high anxiety level and a peculiar breathing pattern. The symptoms, when marked, result in a tendency to hyperventilate during and following exercise, with production of new symptoms (paresthesias, dizziness). The learned response is then reinforced by every new trial to exercise. Finally, the occurrence of symptoms with the slightest exertion leads to a reduction of physical activity and an ensuing
deterioration of exercise tolerance.” See here
(88) Caroline T, Anderson (2010) “Chronic Fatigue Syndrome: A Novel: A Tale of Bureaucracy, Money, and Belief. Synopsis here. This information is from the Amazon.com website . . . This book examines the research about CFS and the investigation of a reporter and town doctor into an outbreak of CFS. “The pair uncover a decades-old plot by insurance companies to paint ME/CFS as a psychosomatic illness to avoid making billions in payments as the Centers for Disease Control and Prevention closes its eyes to the situation. It results in controversy and violence ass the local citizens discover the truth, and a link between CFS and infectious viruses. “The Novel’ exposes the money motive that has stifled research into the illness, which has ruined the lives of millions of Americans . . . It vividly shows the power of determined people to challenge injustices that have been perpetuated against individuals with CFS,” Leonard A. Jason, Ph.D. Professor, DePaul University.
(89) Sanne Kreijkamp-Kaspers, Ekua Weba Brenu, Sonya Marshall, Don Staines, and Meike L Van Driel (2011 issue 4 – available from July 2012) Treating Chronic Fatigue Syndrome: A study of the scientific evidence for pharmacological treatments. Talking Point; Official Journal of the ME/CFS Australia (SA) Inc. page 8. (originally from the Australian Family Physician 2012). The direct cost of treating CFS in the U.S. with conventional and alternative methods, is calculated at US $2342 to $8675 per patient per year, with indirect cost is $20,000 per year. The inability to work adds to the cost to the patient and the carer, which “equates to a total cost of at least $18 billion per year in the USA alone.”
(90) Simon Wessely (April 1992) “The measurement of fatigue in chronic fatigue syndrome”, Journal of the Royal Society of Medicine Volume 85 p.189-190″ The following quote comes from that article . . .
“Fatigue remains as elusive a human experience as ever. At the turn of the century fatigue was almost an obsession of doctors, scientists, writers and even politicians. The scientists believed they could measure it, the doctors they could treat it, the writers describe it, and the politicians prevent it’. Many confidently expected that fatigue could be eliminated from schools, factories, armies, and even society. That it had to be dealt with was not in doubt, since many authorities believed that if not checked, fatigue, the inevitable consequence of modern life in all its forms, would somehow destroy the nation’s health and its future. Perhaps only the writers achieved their objective2 . . . The inevitable result of this extraordinary interest in all things fatiguing was a reaction, as a sense of disillusionment set in. Scientists couldn’t measure it3, doctors couldn’t cure it4 and politicians couldn’t prevent it’. Fatigue illnesses, once the backbone of any self-respecting medical text, disappeared from theindexes5. Fatigue laboratories closed6, and interest dwindled.” (end of quote) See here.
Note that although the article is “The measurement of fatigue” the article only presents evidence that it couldn’t be measured.
It also gives my readers some indication of the predicament that I was in as a patient in 1975. Namely, nobody could understand it, diagnose it, or treat it properly, so I had to do it myself.
The evidence also indicates that many people at the highest level of society are trying to erase the evidence, hide it, and deny it’s existence.
(91) Jo Nijs, Jessica Van Oosterwijck & Mira Meeus (February 2013) Myalgic encephalomyelitis/chronic fatigue syndrome: Rehabilitation through activity management, stress management and exercise therapy, International Encyclopedia of Rehabilitation..
This is a quote from another website “another study reported that those people with ME/CFS who are able to stay within ‘energy envelope’ show significant improvements (Jason et al. 2009)” . . .
“Pacing self-management aims at stabilizing the patient’s health status. After the initial stabilization phase, a grading phase is initiated and comprises of graded activity or graded exercise therapy (Figure 1). During the grading phase, the same pacing principles are applied to grade both daily activities as well as exercise levels. When determining an appropriate exercise level, a formal, regulated exercise regime that is gentle, graded, flexible and manageable according to each individual’s capabilities is required. Support for this type of ‘grading’ for people with ME/CFS comes from an observational study (Coutts et al. 2001) and a well-designed randomized controlled clinical trial, which reported that paced and individually-tailored graded exercise was superior to relaxation and flexibility training in patients with ME/CFS (Wallman et al. 2004). The use of graded exercise therapy for people with ME/CFS will be further discussed below (section 4.5) . . .
“Benefits associated with graded exercise were first demonstrated in a 12-week randomized, controlled trial by Fulcher and White (1997) that compared the efficacy of graded exercise to flexibility exercises in ME/CFS participants. Since then, a number of studies have examined the effectiveness of graded exercise therapy for ME/CFS (e.g. Weardon et al. 1998, Powell et al. 2001). According to the Cochrane Library, graded exercise therapy is effective in the short term for treating ME/CFS patients (Edmonds et al. 2004). However, it should be acknowledged that graded exercise therapy is not suitable per se for all people with ME/CFS at any stage of their illness. Rather, graded exercise therapy can be one component of an overall rehabilitation approach to ME/CFS . . .
Introduction of exercise that is beyond a participant’s capacity may not only promote a relapse, but can also result in feelings of demoralization and pain, thus reinforcing avoidance behavior (Figure 1). Therefore, Wallman et al. (2004) introduced the pacing approach into graded exercise therapy for people with ME/CFS. They designed a graded exercise program that is flexible, realistic and manageable according to each individual’s needs and abilities. The program schedules rest periods in conjunction with the exercise periods, as this can help in establishing a manageable routine that can assist in promoting a sense of control over one’s life (Pheby 1997, Sharpe et al. 1997) . . . “Cognitive behavioral programs for people with ME/CFS combine a variety of treatment options, some of which are explained above (e.g. education, time-contingent activity management, time-contingent graded exercise therapy, stress management, sleep advice, goal setting, etc.) . . .
When explaining to people with ME/CFS that rehabilitation is not a cure for ME/CFS, it should be explained that conservative strategies will address perpetuating factors of ME/CFS, and hence lead to increased functioning rather than full recovery.” (end of quote) See here
Most of the information in that article, about the physical aspects of CFS, could have been copied from the detailed descriptions in my essays, books, and website. They may have been copied by earlier authors, so that since then the later authors were not aware that the ideas came from me, but nonetheless they are my theories and methods.
However, the authors mention the concept of kinesiophobia (the irrational fear of movement), and exercise phobia, which is a separate issue, and is not the cause of the abnormal response to exercise. They also refer to the “catastrophizing thoughts”, and “hypervigilance of symptoms”, and “somatization”, which refer to imaginary, exaggerated or psychological causes.
I have said many times before that chronic fatigue is a completely different condition to the “fear” of exercise etc, and that those aspects are common to all illness, not just CFS.
I have also explained that the breathing abnormality in CFS is due to some sort of physical problem and has nothing to do with panic induced hyperventilation. See my YouTube video here.
This is some of what that other author says . . .
“decreased lung function (De Lorenzo et al. 1996) . . . a decreased peak oxygen uptake during exercise performance testing (De Becker et al. 2000), and an increased prevalence of hyperventilation (59%) compared to healthy controls (22%) (Bazelmans et al. 1997). Hyperventilation in not a causal factor for ME/CFS, but is likely to be a perpetuating factor for some patients, especially those having difficulties with acceptance (Bogaerts et al. 2007). See here.
| Summary of References: Da Costa’s Syndrome is just Da Costa’s Syndrome, and a horse is just a horseThe references give clear enough evidence that Da Costa’s syndrome is a distinct condition which involves 4 main symptoms, namely lower left sided chest pain, palpitations, breathlessness, and fatigue, occurring exclusively in response to physical exertion. i.e. it is an effort syndrome. Those symptoms are different from other forms of pain or breathlessness, and are not a normal physiological response to exercise. Cases can be found where these core symptoms are associated with a wide range and countless number of other physical and psychological symptoms or sequels, which has resulted in it being given more than a hundred different labels, where the name Da Costa’s Syndrome is rarely used nowadays, but that does not change the basic nature of the problem where the precise physical basis still needs to be researched and found by whoever chooses to take on the continuing challenge. What is the physical cause of the abnormal response to exertion???An analogy can be given that a horse is just a horse, and it doesn’t become anything else just because it is ridden by a jockey, or tows a cart, or if a team of them pulls a wagon, and it doesn’t change if it roams about on the same farm with sheep and cows, or if it is painted with black and white stripes to make it look like a zebra, and it can swim, but that doesn’t make it a fish, and it can be seen at the top of cliffs, but that doesn’t mean that it can fly like an eagle, and if it is given gills, or someone tries to sew wings on its back, it is still just a horse, and if you study the history of the horse you will read a lot about other modes of human transport including camels, elephants, and automobiles, but a horse is still a horse. M.B. |
