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Myalgic Encepahalomyelitis is not fatigue, or 'CFS' 
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The new paper Myalgic Encephalomyelitis is not fatigue, or 'CFS' explains why M.E. is not defined by mere 'chronic fatigue' and why M.E. and 'CFS' are not synonymous terms, as well as why a diagnosis of CFS based on any of the definitions of CFS can only ever be a misdiagnosis.
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Myalgic Encepahalomyelitis is not fatigue, or 'CFS'
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Copyright © by Jodi Bassett June 2007 on www.ahummingbirdsguide.com
This version updated February 2008
Myalgic Encephalomyelitis (M.E.) is not synonymous with being tired all the time. If a person is very fatigued for an extended period of time this does not mean they are having a ‘bout’ of M.E. To suggest such a thing is no less absurd than to say that prolonged fatigue means a person is having a ‘bout’ of multiple sclerosis, Parkinson’s disease or Lupus. If a person is constantly fatigued this should not be taken to mean that they have M.E. no matter how severe or prolonged their fatigue is. Fatigue is a symptom of many different illnesses as well as a feature of normal everyday life – but it is not a defining symptom of M.E., nor even an essential symptom of M.E.
There are a number of post-viral fatigue states or fatigue syndromes which may follow common infections such as mononucleosis/glandular fever, hepatitis, Q fever, Ross river virus and so on. M.E. is an entirely different condition to these self-limiting fatigue syndromes however (and is not caused by the Epstein Barr virus or any of the herpes or hepatitis viruses), the science is very clear on this point. People suffering with any of these post-viral fatigue states or fatigue syndromes do not have M.E. M.E. is also not the same condition as Lyme disease, athletes over-training syndrome, burnout, depression, somatisation disorder, candida, multiple chemical sensitivity syndrome or Fibromyalgia, or indeed any other illness. M.E. is a distinct neurological illness with a distinct; onset, symptoms, aetiology, pathology, response to treatment, long and short term prognosis – and World Health Organization classification (G.93.3) (Hyde 2006, 2007, [Online]) (Hooper 2006, [Online]) (Hooper & Marshall 2005, [Online]) (Hyde 2003, [Online]) (Dowsett 2001, [Online]) (Hooper et al. 2001, [Online]) (Dowsett 2000, [Online]) (Dowsett 1999a, 1999b, [Online]) (Dowsett 1996, p. 167) (Dowsett et al. 1990, pp. 285-291) (Dowsett n.d., [Online]).
M.E. is also not defined by ‘fatigue following exertion which can last up to 24 hours’ as the bogus definitions of ‘CFS’ describe. Fatigue following activity (or post-exertional fatigue or malaise) is a common symptom of a large number of different illnesses – but what is happening in M.E. is quite different. Overexertion does not cause fatigue in M.E. but instead a worsening of the severity of the illness generally and of various neurological, cognitive, cardiac, cardiovascular, immunological, muscular and gastrointestinal (and other) symptoms. The severity of these symptoms can range from mild to severe to life-threatening. The effects of overexertion can last for hours, days, weeks or even many months in M.E., or can even be permanent. The onset of these post-exertional effects are very often significantly delayed so that very often the worsening of the illness caused by overexertion has not even begun within 24 hours in M.E., let alone been completely resolved in that time.
The reaction people with M.E. have to physical and mental activity, sensory input and orthostatic stress not only has nothing to do with mere fatigue (or ‘malaise’) but is in fact unique to M.E. in a number of ways. This reaction is so abnormal in fact that exercise testing is one of the series of tests which can be used to help confirm a M.E. diagnosis, as are various tests which measure the abnormal responses to orthostatic stress seen in M.E. This is simply not the case in post-viral fatigue syndromes, Lyme disease, Fibromyalgia and so on. These patient groups do not exhibit the same measurable pathological abnormalities as M.E. patients in these (and other) tests. Recent research has also shown that postural stress exacerbates cardiac insufficiency in M.E. and that this cardiac insufficiency is the cause of many of the symptoms and much of the disability of M.E. This pathology is also not seen in any of those illnesses causing fatigue after exertion which are commonly misdiagnosed as ‘CFS.’ The way people with M.E. respond to physical and mental activity, sensory input and orthostatic stress is profoundly different than in these other illnesses; it is an entirely different problem, of a much greater magnitude (Cheney 2006, [video recording]) (Hooper & Marshall 2005, [Online]) (Hyde 2003, [Online]) (Dowsett 2001, [Online]) (Hooper et al. 2001, [Online]) (Dowsett 2000, [Online]) (Dowsett 1999a, 1999b, [Online]) (Dowsett et al. 1990, pp. 285-291) (Ramsay 1986, [Online]).
What does define Myalgic Encephalomyelitis?
What defines M.E. is not ‘chronic fatigue’ but a specific type of acquired damage to the brain. Myalgic encephalomyelitis is an acutely acquired illness initiated by a virus infection with multi system involvement which is characterised by post encephalitic damage to the brain stem; a nerve centre through which many spinal nerve tracts connect with higher centres in the brain in order to control all vital bodily functions – this is always damaged in M.E. (Hence the name Myalgic Encephalomyelitis.) Central nervous system (CNS) dysfunction, and in particular, inconsistent CNS dysfunction is undoubtedly both the chief cause of disability in M.E. and the most critical in the definition of the entire disease process.
Myalgic Encephalomyelitis is a loss of the ability of the CNS (the brain) to adequately receive, interpret, store and recover information which enables it to control vital body functions (cognitive, hormonal, cardiovascular, autonomic and sensory nerve communication, digestive, visual auditory balance etc). It is a loss of normal internal homeostasis. The individual can no longer function systemically within normal limits. This dysfunction also results in the inability of the CNS to consistently programme and achieve normal smooth end organ response. There is also multi-system involvement of cardiac and skeletal muscle, liver, lymphoid and endocrine organs. Some individuals also have damage to skeletal and heart muscle.
This diffuse brain injury is initiated by a virus infection which targets the brain; M.E. represents a major attack on the central nervous system (CNS) by the chronic effects of a viral infection. M.E. is an infectious and primarily neurological disease process which occurs in epidemic and sporadic forms. There is a history of recorded outbreaks of M.E. going back to 1934, when an epidemic of what seemed at first to be poliomyelitis was reported in Los Angeles. A review of M.E. outbreaks found that clinical symptoms were consistent in over sixty recorded epidemics of M.E. spread all over the world. M.E. has been linked to Poliomyelitis (Polio) since 1934 and for a number of years M.E. was referred to as ‘atypical Polio.’ A significant number of the world’s leading M.E. experts believe that M.E., like Polio, is caused by an enterovirus. The evidence which exists to support this theory is compelling, for example: M.E. epidemics very often followed Polio epidemics, M.E. resembles Polio at onset, serological studies have shown that communities affected by an outbreak of M.E. were effectively blocked (or immune) from the effects of a subsequent polio outbreak, evidence of enteroviral infection has been found in the brain tissue of M.E. patients at autopsy, and so on. (See: The outbreaks (and infectious nature) of M.E. and for more information.)
M.E. is primarily neurological, but because the brain controls all vital bodily functions virtually every bodily system can be affected by M.E. Again, although M.E. is primarily neurological it is also known that the vascular and cardiac dysfunctions seen in M.E. are also the cause of many of the symptoms and much of the disability associated with M.E. – and that the well-documented mitochondrial abnormalities present in M.E. significantly contribute to both of these pathologies. There is also multi-system involvement of cardiac and skeletal muscle, liver, lymphoid and endocrine organs in M.E. Some individuals also have damage to skeletal and heart muscle. Thus Myalgic Encephalomyelitis symptoms are manifested by virtually all bodily systems including: cognitive, cardiac, cardiovascular, immunological, endocrinological, respiratory, hormonal, gastrointestinal and musculo-skeletal dysfunctions and damage.
M.E. is an infectious neurological disease and represents a major attack on the central nervous system (CNS) – and an associated injury of the immune system – by the chronic effects of a viral infection. There is also transient and/or permanent damage to many other organs and bodily systems (and so on) in M.E. M.E. affects the body systemically. Even minor levels of physical and cognitive activity, sensory input and orthostatic stress beyond a M.E. patient’s individual post-illness limits causes a worsening of the severity of the illness (and of symptoms) which can persist for days, weeks or months or longer. In addition to the risk of relapse, repeated or severe overexertion can also cause permanent damage (eg. to the heart), disease progression and/or death in M.E.
M.E. is not stable from one hour, day, week or month to the next. It is the combination of the chronicity, the dysfunctions, and the instability, the lack of dependability of these functions, that creates the high level of disability in M.E. It is also worth noting that of the CNS dysfunctions, cognitive dysfunction is one of the most disabling characteristics of M.E.
There is just no other illness that is even remotely like M.E. M.E. is a distinct, recognisable disease entity which contrary to popular belief is not difficult to diagnose and can in fact be diagnosed relatively early in the course of the disease (within just a few weeks) – providing that the physician has some experience with the illness. Although there is (as yet) no single test which can be used to diagnose M.E. there are a series of tests which can confirm a suspected M.E. diagnosis. If all tests are normal, if specific abnormalities are not seen on certain of these tests (eg. brain scans), then a diagnosis of M.E. cannot be correct (Hyde 2006, 2007, [Online]) (Hooper 2006, [Online]) (Hooper & Marshall 2005, [Online]) (Hyde 2003, [Online]) (Dowsett 2001, [Online]) (Hooper et al. 2001, [Online]) (Dowsett 2000, [Online]) (Dowsett 1999a, 1999b, [Online]) (Hyde 1992 p. xi) (Hyde & Jain 1992 pp. 38 - 43) (Hyde et al. 1992, pp. 25-37) (Dowsett et al. 1990, pp. 285-291) (Ramsay 1986, [Online]) (Dowsett n.d., [Online]) (Dowsett & Ramsay n.d., pp. 81-84) (Richardson n.d., pp. 85-92).
What are some of the real hallmark symptoms and characteristics of Myalgic Encephalomyelitis?
What characterises M.E. every bit as much as the individual neurological, cognitive, cardiac, cardiovascular, immunological, endocrinological, respiratory, hormonal, muscular, gastrointestinal and other symptoms is the way in which people with M.E. respond to physical and cognitive activity, sensory input and orthostatic stress, and so on. In other words, the pattern of symptom exacerbations, relapses and of disease progression.
The way the bodies of people with M.E. react to these activities/stimuli post-illness is unique in a number of ways. Along with a specific type of damage to the brain (the central nervous system) this characteristic is one of the defining features of the illness which must be present for a correct diagnosis of M.E. to be made. The main characteristics of the pattern of symptom exacerbations, relapses and disease progression (and so on) in Myalgic Encephalomyelitis include:
- People with M.E. are unable to maintain their pre-illness activity levels. This is an acute change; M.E. patients can only achieve 50%, or less, of their pre-illness activity levels post-M.E.
- People with M.E. are limited in how physically active they can be but they are also limited in similar way with; cognitive exertion, sensory input and orthostatic stress.
- When a person with M.E. is active beyond their individual (physical, cognitive, sensory or orthostatic) limits this causes a worsening of various neurological, cognitive, cardiac, cardiovascular, immunological, endocrinological, respiratory, hormonal, muscular, gastrointestinal and other symptoms.
- The level of physical activity, cognitive exertion, sensory input or orthostatic stress needed to cause a significant or severe worsening of symptoms varies from patient to patient, but is often trivial compared to a patient’s pre-illness tolerances and abilities.
- The severity of M.E. waxes and wanes throughout the hour/day/week and month.
- The worsening of the illness caused by overexertion often does not peak until 24 - 48 hours (or more) later.
- The effects of overexertion can accumulate over longer periods of time and lead to disease progression, or death.
- The activity limits of M.E. are not short term, a gradual (or sudden) increase in activity levels beyond a patient’s individual limits can only cause relapse, disease progression or death in patients with M.E.
- The symptoms of M.E. do not resolve with rest. The symptoms and disability of M.E. are not just caused by overexertion, there is also a base level of illness which can be quite severe even at rest.
- Repeated overexertion can harm your chances for future improvement in M.E. M.E. patients who are able to avoid overexertion have repeatedly been shown to have the most positive long-term prognosis.
- Not every M.E. sufferer has ‘safe’ activity limits within which they will not exacerbate their illness, this is not the case for the very severely affected.
When a person with M.E. is active beyond their individual post-illness limits, the result is not tiredness, fatigue or even exhaustion – nor is ‘malaise’ an accurate word to describe what occurs. There simply is no one symptom caused by overexertion in M.E. What does happen is that there is a worsening of all sorts of different symptoms and of the severity of the illness generally with overexertion. (Repeated or severe overexertion can also cause disease progression, permanent damage, or death in M.E.) It is an entirely different problem of a much greater magnitude.
Overexertion causes an exacerbation of all sorts of combinations of neurological, cognitive, cardiac, cardiovascular, immunological, endocrinological, respiratory, hormonal, muscular, gastrointestinal and other symptoms which can be mild, moderate, severe, or even life threatening (eg. seizures and cardiac events). Many of the symptoms involved are present at a lower level at rest, but overexertion causes them to worsen. (Although some patients may also have some symptoms that only appear after overexertion.) Anywhere from one symptom to a large cluster of symptom can be made worse, or produced, by overexertion. The cluster of symptoms made worse by excessive exertion or stimulus is often very similar from patient to patient, as generally it is a worsening of the most common symptoms of the illness. M.E. patients commonly experience a combination of the following:
Profound cognitive dysfunctions (and various other neurological disturbances), muscle weakness (or paralysis), burning eye pain or burning skin, subnormal temperature or low-grade fever, sore throat or painful lymph nodes (and/or other signs of inappropriate immune system activation), faintness, weakness or vertigo, loss of co-ordination, dyspnoea, an explosion of sensory phenomena (low level seizure activity), cardiac and/or blood pressure disturbances, facial pallor and/or a slack facial expression, widespread severe pain, nausea or feeling as if ‘poisoned,’ feeling cold and shivering one minute and hot and sweating the next, anxiety or even terror (as an organic part of the attack itself rather than as a reaction to it) and hypoglycaemia. Often the patient will feel an urgent need to retreat from all homeostatic pressures. The types of symptoms triggered vary widely from patient to patient, but some combination of these is common. There may also be an accompanying exacerbation of other symptoms. These symptoms often combine to create an indescribable and overwhelming experience of terrible illness that is unique to M.E, and can be profoundly incapacitating. At its most severe, the patient feels as if they are about to die.
Each of the symptoms caused or exacerbated by overexertion can be clearly articulated without difficulty whether they be; seizures, cardiac events, labile blood pressure, tachycardia, shortness of breath, muscle pain, muscle weakness or muscle paralysis, facial paralysis, black outs, flu-like symptoms, nausea, inability to speak or to understand speech, problems with memory, and so on. It makes no scientific or logical sense to subsume these very specific symptoms, and very specific and varied combinations of symptoms, under a vague and inaccurate label of mere ‘fatigue.’ To say that all of these very different and very specific – and in some cases very serious – symptoms can be accurately summarised as being a problem of mere ‘fatigue,’ ‘malaise’ or ‘exhaustion’ is absurd.
Repeated or severe overexertion can also cause disease progression, permanent damage (eg. to the heart), or death in M.E. patients. Again, to suggest that these very serious and long-term effects – including fatalities – could be accurately summarised as being a problem of mere ‘fatigue’ is clearly absurd (Hyde 2006, 2007, [Online]) (Hooper 2006, [Online]) (Cheney 2006, [video recording]) (Hooper & Marshall 2005, [Online]) (Hyde 2003, [Online]) (Dowsett 2001, [Online]) (Dowsett 2000, [Online]) (Dowsett 1999a, 1999b, [Online]) (Dowsett 1996, p. 167) (Hyde 1992 p. xi) (Hyde & Jain 1992 pp. 38 - 43) (Hyde et al. 1992, pp. 25-37) (Dowsett et al. 1990, pp. 285-291) (Ramsay 1986, [Online]) (Dowsett n.d., [Online]).
What is ‘Chronic Fatigue Syndrome'?
CFS was created in a response to an outbreak of what was unmistakably M.E., but this new name and definition did not describe the known signs, symptoms, history and pathology of M.E. It described a disease process that did not, and could not exist. All each of these flawed CFS definitions ‘define’ is a heterogeneous (mixed) population of people with various misdiagnosed psychiatric and miscellaneous non-psychiatric states which have little in common but the symptom of fatigue (a symptom seen in many illnesses but not a defining feature of M.E. nor even an essential symptom of M.E.). The disease category ‘CFS’ has undoubtedly been used to impose a false psychiatric paradigm of M.E. by allying it with various unrelated psychiatric fatigue states and post-viral fatigue syndromes (etc) for the benefit of various (proven) financial and political interests (Hyde 2006, [Online]) (Hooper 2006, [Online]) (Hyde 2003, [Online]) (Hooper 2003, [Online]) (Dowsett 2001, [Online]) (Hooper et al. 2001, [Online]) (Dowsett 2000, [Online]) (Dowsett 1999a, 1999b, [Online]).
The fact that a person qualifies for a diagnosis of CFS (a) does not mean that the patient has Myalgic Encephalomyelitis, and (b) does not mean that the patient has any other distinct and specific illness named ‘CFS.’ A diagnosis of CFS – based on any of the CFS definitions – can only ever be a wastebasket diagnosis, in other words, a misdiagnosis. Despite popular opinion, M.E. and CFS are not synonymous terms. All a diagnosis of ‘CFS’ actually means is that the patient has a gradual onset fatigue syndrome which is usually due to a missed major disease. As Dr Byron Hyde M.D. explains, the patient has:
a. Missed cardiac disease, b. Missed malignancy, c. Missed vascular disease, d. Missed brain lesion either of a vascular or space occupying lesion, e. Missed test positive rheumatologic disease, f. Missed test negative rheumatologic disease, g. Missed endocrine disease, h. Missed physiological disease, i. Missed genetic disease, j. Missed chronic infectious disease, k. Missed pharmacological or immunization induced disease, l. Missed social disease, m. Missed drug use disease or habituation, n. Missed dietary dysfunction diseases, o. Missed psychiatric disease (2006, [Online]).
The only groups which gain from this ‘CFS’ confusion are insurance companies and other organisations and corporations which have a vested financial interest in how these patients are treated, including the government. Under the cover of ‘CFS’ these vested interest groups have assiduously attempted to obliterate recorded medical history of Myalgic Encephalomyelitis; even though the existing evidence has been published in prestigious peer-reviewed journals around the world and spans over 60 years. This is clearly unscientific, and unethical. The only way forward for M.E. patients and all of the diverse patient groups commonly misdiagnosed with ‘CFS’ (both of which are denied appropriate support, diagnosis and treatment) is that the bogus disease category of ‘CFS’ must be abandoned.
People with M.E. must be diagnosed with Myalgic Encephalomyelitis, and treated for M.E. based on information gained solely from studies involving authentic M.E. patients. People with depression must be diagnosed and treated for depression. People with cancer must be diagnosed with cancer and then treated as appropriate for the type of cancer they have, and so on. Physicians who diagnose ‘CFS’ in any patient experiencing fatigue without looking and testing for the true cause of the symptoms (and who choose not to familiarise themselves with the scientific facts about Myalgic Encephalomyelitis) do their patients – and themselves – a great disservice. Some of the conditions commonly misdiagnosed as CFS are very well defined and well-known illnesses and very treatable – but only once they have been correctly diagnosed. Some conditions can become very serious or can even be fatal if not correctly diagnosed and managed, including Myalgic Encephalomyelitis.
Every patient deserves the best possible opportunity for appropriate treatment for their illness, and for recovery and this process must begin with a correct diagnosis if at all possible. A correct diagnosis is half the battle won (Hyde 2006, 2007, [Online]) (Hooper 2006, [Online]) (Hyde 2003, [Online]) (Hooper 2003, [Online]) (Dowsett 2001, [Online]) (Dowsett 2000, [Online]) (Dowsett 1999a, 1999b, [Online]) (Dowsett n.d., [Online]).
In conclusion
All of this is not simply theory, but is based upon an enormous body of mutually supportive clinical information which has been published in prestigious peer-reviewed journals all over the world and spans over 60 years. Confirmation of this hypothesis is supported by electrical tests of muscle and of brain function (including the subsequent development of PET and SPECT scans) and by biochemical and hormonal assays. Newer scientific evidence is increasingly strengthening this hypothesis. M.E. is neither ‘mysterious’ nor ‘medically unexplained. Many aspects of the pathophysiology of the disease have, indeed, been medically explained in volumes of research articles. These are well-documented, scientifically sound explanations for why patients are bedridden, profoundly intellectually impaired, unable to maintain an upright posture and so on.
Myalgic Encephalomyelitis is a debilitating autoimmune disease which has been recognised by the World Health Organisation (WHO) since 1969 as an organic neurological disorder. M.E. is similar in a number of significant ways to illnesses such as multiple sclerosis, Lupus and Polio. M.E. affects all races and socio-economic groups and has been diagnosed all over the world with a similar strike rate to multiple sclerosis. Children as young as five can get M.E., as well as adults of all ages. M.E. can be extremely disabling, and is not a self-limiting or short term illness. 25% of M.E. sufferers are severely affected and housebound and bedbound. In some cases Myalgic Encephalomyelitis can also be progressive, or fatal. Governments around the world are currently spending $0 a year on M.E. research.
The name and authentic definition of Myalgic Encephalomyelitis must be fully restored (to the exclusion of all others) and the WHO classification of M.E. must be accepted and adhered to in all official documentations and government policy. People with M.E. must be diagnosed with M.E. and treated for M.E. again, finally. There were sound medical reasons for the creation of the name in 1956, and for the classification of the illness as a distinct organic neurological disorder by the WHO in 1969; neither of which has changed in the interim (Hyde 2006, 2007, [Online]) (Hooper 2006, [Online]) (Cheney 2006, [video recording]) (Hyde 2003, [Online]) (Dowsett 2001, [Online]) (Hooper et al. 2001, [Online]) (Dowsett 2000, [Online]) (Dowsett 1999a, 1999b, [Online]) (Hyde 1992 p. xi) (Hyde & Jain 1992 pp. 38 - 43). As Professor Malcolm Hooper explains:
The term myalgic encephalomyelitis (means muscle pain, my-algic, with inflammation of the brain and spinal cord, encephalo-myel-itis, brain spinal cord inflammation) was first coined by Ramsay and Richardson and has been included by the World Health Organisation (WHO) in their International Classification of Diseases (ICD), since 1969. The currently version ICD-10 lists ME under G.93.3 - neurological conditions. It cannot be emphasised too strongly that this recognition emerged from meticulous clinical observation and examination (2006, [Online]).
Myalgic Encephalomyelitis is a distinct infectious neurological disease of extraordinarily incapacitating dimensions that affects virtually every bodily system – not a problem of medically unexplained ‘fatigue.’
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For more information:
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Additional notes on this text:
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A note on the quality of the references used to compile this paper: This paper has been compiled using the highest quality resources available. More experienced and more knowledgeable M.E. experts than these – Dr Byron Hyde MD. and Dr. Elizabeth Dowsett MD. in particular – simply do not exist. Not everyone was taken in by the ‘CFS’ insurance scam thankfully! A small but dedicated group of M.E. experts have made many remarkable discoveries about the pathology of M.E. – as well as confirmed many times over what was already known about M.E. prior to 1988, before M.E. research became tainted by ‘fatigue’ and ‘CFS.’ Legitimate unbiased M.E. experts and researchers do exist, and their numbers continue to grow – albeit far more slowly than is needed, unfortunately.
A final additional note on ‘fatigue’: Just as some M.E. sufferers will experience other minor and non-essential symptoms such as vomiting or night sweats some of the time, but others will not, the same is true of fatigue. The diagnosis of M.E. is determined upon the presence of certain neurological, cognitive, cardiac, cardiovascular, immunological, endocrinological, respiratory, hormonal, muscular, gastrointestinal and other symptoms (and so on) – the presence or absence of mere ‘fatigue’ is irrelevant. In addition to these other (far more serious) symptoms, some M.E. sufferers may also suffer with mild, moderate or severe fatigue some of the time, while others will not. Thus the symptom of fatigue is not an essential symptom of M.E. and does not define M.E. (Although the symptom of fatigue is essential to qualify for a misdiagnosis of ‘CFS’). The point to be most aware of is not that M.E. is ‘more than fatigue’ – but that M.E. ISN’T FATIGUE AT ALL.
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Downloads and printer-friendly versions
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The full-length (7 page) version of this text can be downloaded in a printer friendly Word format, PDF format, or as a Large Print PDF.
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Reference (and recommended reading) list
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This paper is merely intended to provide a brief summary of some of the most important facts of M.E. It has been created – by a well-read layperson – purely for the benefit of those people without the time, inclination or ability to read each of these far more detailed and lengthy references created by the world’s leading M.E. experts. The following papers are essential additional reading however for any physician (or anyone else) with a real interest in Myalgic Encephalomyelitis:
The papers by Dr Byron Hyde M.D. and Dr. Elizabeth Dowsett M.D. in particular are very highly recommended. Between Dr Byron Hyde M.D. and Dr. Elizabeth Dowsett M.D. – and their mentors the late Dr John Richardson M.D. and Dr Melvin Ramsay M.D. (respectively) – these four doctors have been involved with M.E. research and M.E. patients for well over 100 years, collectively; from the 1950s to the current day. Between them they have examined more than 14 000 individual (sporadic and epidemic) M.E. patients, as well as each authoring numerous studies and articles on M.E., and books on M.E. Again; more experienced, more knowledgeable and more credible M.E. experts than these simply do not exist. For more information see the References page.
- Cheney, Paul M.D. 2006, The Heart of the Matter [video recording], Available: http://www.ahummingbirdsguide.com/wcheney.htm
- Dowsett, Elizabeth MBChB. 2001, THE LATE EFFECTS OF ME Can they be distinguished from the Post-polio syndrome? [Online], Available: http://www.ahummingbirdsguide.com/wdowsett.htm
- Dowsett, Elizabeth MBChB. 2000, Mobility problems in ME [Online], Available: http://www.ahummingbirdsguide.com/wdowsett.htm
- Dowsett, Elizabeth MBChB. 1999a, Redefinitions of ME [Online], Available: http://www.ahummingbirdsguide.com/wdowsett.htm
- Dowsett, Elizabeth MBChB. 1999b, Research into ME 1988 - 1998 Too much PHILOSOPHY and too little BASIC SCIENCE!, [Online], Available: http://www.ahummingbirdsguide.com/wdowsett.htm
- Dowsett, Elizabeth MBChB. n.d., Differences between ME and CFS, [Online], Available: http://www.ahummingbirdsguide.com/wdowsett.htm
- Dowsett, Elizabeth MBChB. in: Colby, Jane 1996, ME: The New Plague, Ipswitch Book Company, Ipswitch.
- Dowsett E. & Ramsay, A.M. n.d., ‘Myalgic Encephalomyelitis: Then and Now' The Clinical and Scientific Basis of Myalgic Encephalomyelitis / CFS, B. Hyde (ed.), The Nightingale Foundation, Ottawa, pp. 81-84.
- Dowsett E., Ramsay A.M., McCartney A.R., & Bell E.J. 1990, ‘Myalgic Encephalomyelitis: A persistent Enteroviral Infection?' in The Clinical and Scientific Basis of Myalgic Encephalomyelitis, B. Hyde (ed.), The Nightingale Foundation, Ottawa, pp. 285-291.
- Hooper, M 2006, Myalgic Encephalomyelitis (ME): a review with emphasis on key findings in biomedical research J. Clin. Pathol. published online 25 Aug 2006; doi:10.1136/jcp.2006.042408 Available: http://jcp.bmjjournals.com/cgi/content/abstract/jcp.2006.042408v1 and http://www.ahummingbirdsguide.com/Other/ME_A_Review_by_Hooper.pdf
- Hooper, M. & Marshall E.P. 2005, Illustrations of Clinical Observations and International Research Findings from 1955 to 2005 that demonstrate the organic aetiology of Myalgic Encephalomyelitis [Online], Available: http://www.ahummingbirdsguide.com/wmarwillhoopgibsonenqui.htm [Note: This paper is 174 pages]
- Hooper, M. 2003 The MENTAL HEALTH MOVEMENT: PERSECUTION OF PATIENTS? [Online], Available: http://www.satori-5.co.uk/word_articles/me_cfs/prof_hooper_3.html
- Hooper, M. Marshall E.P. & Williams, M. 2001, What is ME? What is CFS? Information for Clinicians and Lawyers, [Online], Available: http://www.ahummingbirdsguide.com/wmarwillhoopwimewicfs.htm
- Hyde, Byron M.D. 2006, A New and Simple Definition of Myalgic Encephalomyelitis and a New Simple Definition of Chronic Fatigue Syndrome & A Brief History of Myalgic Encephalomyelitis & An Irreverent History of Chronic Fatigue Syndrome [Online], Available: http://www.ahummingbirdsguide.com/whyde.htm
- Hyde, Byron M.D. 2007, The Nightingale Definition of Myalgic Encephalomyelitis [Online], Available: www.ahummingbirdsguide.com/whyde.htm
- Hyde, Byron M.D. 2003, The Complexities of Diagnosis in (ed) Jason, Leonard at et al. 2003 Handbook of Chronic Fatigue Syndrome by Ross Wiley and Sons, USA. Available: http://www.ahummingbirdsguide.com/whyde.htm
- Hyde, Byron M.D. 1992, Preface in Hyde, Byron M.D. (ed) 1992, The Clinical and Scientific Basis of Myalgic Encephalomyelitis, Nightingale Research Foundation, Ottawa.
- Hyde, Byron M.D. & Anil Jain M.D. 1992, Clinical Observations of Central Nervous System Dysfunction in Post Infectious, Acute Onset M.E. / CFS in Hyde, Byron M.D. (ed) 1992, The Clinical and Scientific Basis of Myalgic Encephalomyelitis, Nightingale Research Foundation, Ottawa, pp. 38-65.
- Hyde, Byron M.D., Bastien S Ph.D. & Anil Jain M.D. 1992, General Information, Post Infectious, Acute Onset M.E. in Hyde, Byron M.D. (ed) 1992, The Clinical and Scientific Basis of Myalgic Encephalomyelitis, Nightingale Research Foundation, Ottawa, pp. 25-37.
- Ramsay, Melvin A. 1986 MYALGIC ENCEPHALOMYELITIS : A Baffling Syndrome With a Tragic Aftermath. [Online], Available: http://www.meactionuk.org.uk/ramsey.html
- Richardson, J. n.d., ‘M.E., The Epidemiological and Clinical Observations of a Rural Practitioner,’ The Clinical and Scientific Basis of Myalgic Encephalomyelitis, Hyde, Byron M.D. (ed) The Nightingale Foundation, Ottawa, pp. 85-94.
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