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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 follow 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. (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 (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." (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 flow to the heart and brain is diminished. (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.
(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. (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." (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.)
(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". (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. 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. (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". (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". (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". (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". (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) (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. (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. This paper refers to the incidence of symptoms occurring during pregnancy on page 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).
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