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Copyright © by Jodi Bassett 2004 on www.ahummingbirdsguide.com
This version updated September 2007
Myalgic Encephalomyelitis (M.E.) is a debilitating acquired neurological disease which has been recognised by the World Health Organisation (WHO) since 1969 as a distinct organic neurological disorder with the code G.93.3. M.E. can occur in both epidemic and sporadic forms, over 60 outbreaks of M.E. have been recorded worldwide since 1934.
M.E. is similar in a number of significant ways to illnesses such as multiple sclerosis, Lupus and poliomyelitis (polio). M.E. can be extremely severe and disabling and in some cases the disease is fatal.
Is Myalgic Encephalomyelitis a new illness? What does the name M.E. mean?
The illness we now know as Myalgic Encephalomyelitis is not a new illness. M.E. is thought to have existed for centuries. (Hyde 1998, [Online]) (Dowsett 1999a, [Online])
In 1956 the name Myalgic Encephalomyelitis was created. The term was invented jointly by Dr A Melvin Ramsay who coined this name in relation to the Royal Free Hospital epidemics that occurred in London in 1955 - 1957 and by Dr John Richardson who observed the same type of illness in his rural practice in Newcastle-upon-Tyne area during the same period. It was obvious to these physicians that they were dealing with the consequences of an epidemic and endemic infectious neurological disease (Hyde 1998, [Online]) (Hyde 2006, [Online]). The term Myalgic Encephalomyelitis means: My = muscle, Algic = pain, Encephalo = brain, Mye = spinal cord, Itis = inflammation (Hyde 2006, [Online]). As M.E. expert Dr Byron Hyde MD writes:
The reason why these physicians were so sure that they were dealing with an inflammatory illness of the brain is that they examined patients in both epidemic and endemic situations with this curious diffuse brain injury. In the epidemic situation with patients falling acutely ill and in some cases dying, autopsies were performed and the diffuse inflammatory brain changes are on record (2006, [Online]).
In 1957, the Wallis description of M.E. was created. In 1959 Sir Donald Acheson (a former UK Chief Medical Officer) conducted a major review of M.E. (Hooper et al. 2001, [Online]). In 1959 Dr. Donald Henderson (a CDC epidemiologist) and Dr. Alexis Shelakov (a NIH epidemiologist), published a comprehensive review paper in the New England Journal of Medicine describing several outbreaks. Dr. Henderson noted: ‘The pattern of the epidemic, the absence of any common exposure factors and the high incidence among medical and hospital personnel were consistent only with an infectious disease transmitted from person to person’ (McLaughlin 2004, [Online]). In 1962 the distinguished neurologist Lord Brain included M.E. in the standard textbook of neurology. In recognition of the large body of compelling research that was available, M.E. was formally classified as an organic disease of the central nervous system in the World Health Organisation’s International Classification of Diseases in 1969 with the code G.93.3 (Hooper et al. 2001, [Online]). Professor Malcolm Hooper explains that:
The term myalgic encephalomyelitis has been included by the World Health Organisation (WHO) in their International Classification of Diseases (ICD), since 1969. The currently version ICD-10 lists M.E. under G.93.3 - neurological conditions. It cannot be emphasised too strongly that this recognition emerged from meticulous clinical observation and examination (2006, [Online]).
In 1978 the Royal Society of Medicine held a symposium on Myalgic Encephalomyelitis at which M.E. was accepted as a distinct entity. The symposium proceedings were published in The Postgraduate Medical Journal later that same year. The Ramsay case description of M.E. was published in 1981 (Hooper et al. 2001, [Online]).
Since 1956 the term Myalgic Encephalomyelitis has been used to describe the illness in the UK, Europe Canada and Australasia. This term has stood the test of time for more than 50 years. The recorded medical history of M.E. as a debilitating organic neurological illness affecting children and adults is substantial; it spans over 70 years and has been published in prestigious peer-reviewed journals all over the world (Hyde 1998, [Online]) (Dowsett n.d.a, [Online]) (Hooper 2003a, [Online]) (Dowsett 2001b, [Online]).
As microbiologist and M.E. expert Dr Elizabeth Dowsett explains: ‘There is ample evidence that M.E. is primarily a neurological illness, although non-neurological complications affecting the liver, cardiac and skeletal muscle, endocrine and lymphoid tissues are also recognised’ (n.d.b, [Online]).
Myalgic Encephalomyelitis is not defined by mere ‘fatigue’
Myalgic Encephalomyelitis 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.
The terms ‘fatigue’ and ‘chronic fatigue’ were not associated with defining this illness at all until the new name (and definition) of ‘Chronic Fatigue Syndrome’ was created in 1988 in the USA (Hyde 2006, [online]). But M.E. and CFS are not synonymous terms.
‘Fatigue’ and feeling ‘tired all the time’ are not at all the same thing as the very specific type of paralytic muscle weakness or muscle fatigue which is characteristic of M.E. (and is caused by mitochondrial dysfunction) and which affects every organ and cell in the body; including the brain and the heart. This causes – or significantly contributes to – such problems in M.E. as; cardiac insufficiency (a type of heart failure), orthostatic intolerance (inability to maintain an upright posture), blackouts, reduced circulating blood volume (and pooling of the blood in the extremities), seizures (and other neurological phenomena), memory loss, problems chewing/swallowing, episodes of partial or total paralysis, muscle spasms/twitching, extreme pain, problems with digestion, Raynaud’s phenomenon, vision disturbances, breathing difficulties, and so on. These problems are exacerbated by even trivial levels of physical and cognitive activity, sensory input and orthostatic stress beyond a patient’s individual post-illness limits leaving M.E. patients extremely disabled (Bassett 2007, [Online]).
M.E. expert Dr Melvin Ramsay M.D. explained that this unique characteristic: ‘is virtually a sheet-anchor in the diagnosis of Myalgic Encephalomyelitis and without it a diagnosis should not be made’ (1986, [Online]). This intolerance of certain levels of physical or cognitive activity, sensory input and orthostatic stress is one of the many things which separates Myalgic Encephalomyelitis so distinctly from various post-viral fatigue states or other illnesses involving 'chronic fatigue.’ M.E. expert Dr Byron Hyde M.D. also writes that: ‘In MRI spectography it has been shown that because of an abnormal buildup of normal metabolites, the muscle cell actually shuts down to prevent cell death’ (Hyde 2003, [Online]). People with M.E. are experiencing a form of heart failure which can be exacerbated by even relatively low levels of activity. People with M.E. are made very ill and disabled by this problem with their cells (and their mitochondria, and so on), it affects virtually every bodily system, and has also lead to death in some cases. Many patients are housebound and bedbound and often are so ill that they feel they are about to die.
People with M.E would give anything to instead only be severely ‘fatigued’ or tired all the time.
Fatigue or post-exertional fatigue (or malaise) may occur in many different illnesses such as various post-viral fatigue states or syndromes, Fibromyalgia, Lyme disease, and many others – but what is happening with M.E. patients is an entirely different (and unique) problem of a much greater magnitude. These terms are not accurate or specific enough to describe what is happening in M.E. M.E. is a neurological illness of extraordinarily incapacitating dimensions that affects virtually every bodily system – not a problem of ‘chronic fatigue’ (Hyde 2006, [Online]) (Hooper 2006, [Online]) (Hooper & Marshall 2005a, [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]).
If Myalgic Encephalomyelitis and ‘Chronic Fatigue Syndrome’ are not synonymous terms, why do some groups claim that they are? What is CFS?
The disease category of 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.
The new name and case definition for ‘CFS’ was created in the US in 1988 by a board of 18 members, few of which had either looked at an epidemic of M.E. or examined any patients with M.E. Indeed three of the most experienced members of the board refused to sign the final document and withdrew themselves from the (CDC) definitional committee because the proposed new name for the illness and the definition that went with it were just too different from the Myalgic Encephalomyelitis with which they were so familiar (Hooper et al. 2001 [Online]). With very few exceptions the majority of the remaining members never published on M.E. again in their careers (Hyde 1998, [online]).
The UK definition of CFS was also arrived at without the vast majority of those involved having had the benefit of examining either individual patients or an outbreak of the illness. Many of them were also psychologists rather than physicians. It was a similar story worldwide. As M.E. expert Dr Byron Hyde writes, ‘The inclusion of psychiatrists in the defining of an epidemic and [what is] obviously a disease of infectious origin, simply muddies the water for any serious understanding of that disease’ (1998, [Online]).
So why was the renaming and redefining of the distinct neurological disease Myalgic Encephalomyelitis allowed – or indeed designed – to become so muddied? Indeed why did Myalgic Encephalomyelitis suddenly need to be renamed or redefined at all? Money. There was an enormous rise in the incidence of Myalgic Encephalomyelitis in the late 1970s and the 1980s and so it was at this time that certain psychiatrists and others involved in the medical insurance industry (on both sides of the Atlantic) began their campaign to reclassify the severely incapacitating and discrete neurological disorder known as Myalgic Encephalomyelitis as a psychological or ‘personality’ disorder; in order to side-step the financial responsibility of so many new claims (Marshall & Williams 2005a, [Online]). As Professor Malcolm Hooper explains:
In the 1980s in the US (where there is no NHS and most of the costs of health care are borne by insurance companies), the incidence of ME escalated rapidly, so a political decision was taken to rename M.E. as "chronic fatigue syndrome", the cardinal feature of which was to be chronic or on going "fatigue", a symptom so universal that any insurance claim based on "tiredness" could be expediently denied. The new case definition bore little relation to M.E.: objections were raised by experienced international clinicians and medical scientists, but all objections were ignored… To the serious disadvantage of patients, these psychiatrists have propagated untruths and falsehoods about the disorder to the medical, legal, insurance and media communities, as well as to government Ministers and to Members of Parliament, resulting in the withdrawal and erosion of both social and financial support [for M.E. patients]. Influenced by these psychiatrists, government bodies around the world have continued to propagate the same falsehoods with the result that patients are left without any hope of understanding or of health service provision or delivery. As a consequence, government funding into the biomedical aspects of the disorder is non-existent. (2003a, [Online]) (2001, [Online])
For example, the psychiatrist Simon Wessely – arguably the most powerful and prolific author of papers which claim that M.E. is merely a psychological problem of ‘fatigue’ – began his rise to prominence in the UK at the same time the first CFS definition was being created in the USA (1988). Wessely, and his like-minded colleagues – a small group made up mostly but not exclusively of psychiatrists (colloquially known as the ‘Wessely School’) has gained dominance in the field of M.E. in the UK (and increasingly around the world) by producing vast numbers of papers which purport to be about M.E.
Wessely claims to specialise in M.E. but uses the term interchangeably with chronic fatigue, fatigue or tiredness plus terms such as neurasthenia, CFS and ‘CFS/ME’ (a confusing and misleading term they created themselves). He claims that psychiatric states of ongoing fatigue and the distinct neurological disorder M.E. are synonymous. Despite all the existing contradictory evidence, Wessely (and members of the Wessely School) assert that M.E. is a behavioural disorder (with no physical signs of illness or abnormalities on testing) that is perpetuated by "aberrant illness beliefs" and by "the misattribution of normal bodily sensations" and that patients "seek and obtain secondary gain by adopting the sick role" (Hooper & Marshall 2005a, [Online]).
This group have assiduously attempted to obliterate recorded medical history of Myalgic Encephalomyelitis; even though the existing evidence and studies were published in prestigious peer-reviewed journals and span over 70 years. Wessely’s (and his colleagues around the world) claims have flooded the UK (and worldwide) literature to the extent that medical journals rarely contain any factual and unbiased information on M.E. and so most clinicians are effectively being deprived of the opportunity to obtain even the most basic facts about the illness. This group have also driven government policy on M.E. in the UK to an overwhelming extent. (Wessely is adviser to the UK government and his wife (a GP and psychiatrist) is Senior Policy Adviser to the Department of Health.)
For at least a decade, serious questions have been raised (and published) in international medical journals about possible scientific misconduct and flawed methodology in the work of Wessely and his colleagues. It is only relatively recently however that his long-term involvement as medical adviser – and board member – to a number of commercial bodies having a vested interest in how M.E. is managed have been exposed.
Among his 53, largely undeclared, conflicting interests Wessely is a member of the supervisory board of a company named PRISMA. The same company that is being paid many millions of pounds to supply ‘rehabilitation’ programs (such as CBT and GET) to the NHS for use on ‘CFS’ patients. (Mar 2004, [Online])
The government funded research produced by this group continues to be rigorously criticised on the grounds that it is methodologically flawed and biased and that it relies on a highly selective and misrepresentative choice of references, and too often cites their own studies as the sole or primary references. Despite this, and the fact that this coterie of psychiatrists has a number of outrageous conflicts of interest and proven affiliations with corporate industry they have managed to assiduously infiltrate all the major institutions – including government – directing funding for M.E. research into an exclusively psychiatric model of the illness; and which involves studying ‘fatigue’ sufferers instead of those with M.E. (Mar 2004, [Online]) (Hooper 2003, [Online]) (Hooper et al. 2001, [Online]).
This is the sole reason why the charade that M.E. could be a psychiatric or behavioural ‘fatiguing’ disorder or even a ‘aberrant belief system’ continues; not because there is good scientific evidence – or any evidence – for the theory, or because the evidence proving organic causes and effects is lacking – but because such a view is so financially and politically convenient and profitable on such a large scale to a number of extremely powerful corporations and Government departments (Hooper et al 2001, [Online]). Scientifically such theories have been utterly discredited and disproven many decades ago – and literally hundreds of times over since then – and are at this stage are no more scientifically viable than are those of a ‘flat Earth.’ As Dr Elizabeth Dowsett comments, these ridiculous financially motivated theories bear as much relation to legitimate science ‘as Astrology does to Astronomy.’ (1999b [Online])
This large scale deception has been made possible largely because of the fact that holding some of the most powerful advisory positions in government (as some of these vested interest psychiatrists do) does not seem to be mutually exclusive with also having direct ties and allegiances to industry, even if those industries are directly affected by the decisions made by the government department/adviser in question (as the giant chemical, pharmaceutical and insurance industries are in M.E.) (Hooper 2003a, [Online]). As Professor Malcolm Hooper goes on to explain:
Increasingly, it is now "policy-makers" and Government advisers, not experienced clinicians, who determine how a disorder is classified and managed in the NHS: the determination of an illness classification and the provision of policy-driven "management" is a very profitable business. To the detriment of the sick, the deciding factor governing policies on medical research and on the management and treatment of patients is increasingly determined not by medical need but by economic considerations. Given that what Wessely promotes is contrary to the established scientific evidence, how does he manage to maintain such power and control? Many knowledgeable people believe he maintains it by singing the desired political tune; by scientific misconduct; by manipulation of other people’s published work; by flawed methodology; by deception and by the circularity of self-references. Substantial evidence clearly reveals that in pursuit of his personal ideology or, alternatively, that of his corporate masters, Wessely abuses the scientific process. The implementation of his personal philosophy is not based on medical science and has had devastating consequences, not just for sufferers of M.E. but for their families as well. There is a gross mismatch between the severity and complexity of M.E. and the medical and public perception of the disorder, but until Simon Wessely is held to public account, and medical professionals and public alike are informed and educated about the reality of M.E., this will continue (2003a, [Online]).
Members of the "Wessely school’ in the UK including Wessely, Sharpe, Cleare and White (etc.), their counterparts (and sometime collaborators) in the US; Reeves and Straus (etc. of the CDC) in Australia Lloyd and Hickie (etc.) and the clinicians of the Nijmegen group in the Netherlands each support a bogus psychiatric or behavioural paradigm of ‘CFS’ and recommend rehabilitation-based approaches such as cognitive behavioural therapy (CBT) and graded exercise therapy (GET) as the most useful interventions for ‘CFS’ patients. It is important to be aware that none of these groups is studying patients with M.E. Each of these groups has created their own definition of ‘CFS’ (or uses one) which does not select those with M.E. but instead selects various types of psychiatric and non-psychiatric fatigue sufferers.
The creation of the bogus 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 2006a, [Online]) (Hooper 2006, [Online]) (Hyde 2003, [Online]) (Hooper 2003a, [Online]) (Dowsett 2001a, [Online]) (Hooper et al. 2001, [Online]) (Dowsett 2000, [Online]) (Dowsett 1999a, 1999b, [Online]). As Martin J. Walker summarises: ‘This is a period of hidden-interest conflicts in medicine’ (2003).
The resulting ‘confusion’ between the distinct neurological disease M.E. and the man-made bogus disease category of ‘CFS’ has caused an overwhelming additional burden of suffering for those who suffer from neurological M.E. and their families. It's a big huge mess, that is for certain - but it is not an accidental mess - that is for certain too.
What does a diagnosis of ‘Chronic Fatigue Syndrome’ actually mean?
There are now more than nine different definitions of ‘CFS.’ 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.) (Hyde 2006a, [Online]) (Hooper 2006, [Online]) (Hyde 2003, [Online]) (Hooper 2003a, [Online]) (Dowsett 2001a, [Online]) (Hooper et al. 2001, [Online]) (Dowsett 2000, [Online]) (Dowsett 1999a, 1999b, [Online]).
The fact that a person qualifies for a diagnosis of CFS, based on any of the CFS definitions (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 (2006a, [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 70 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, and may also be subject to serious medical abuse) is that the bogus disease category of ‘CFS’ must be abandoned. As M.E. expert Dr Byron Hyde MD explains:
Do not for one minute believe that CFS is simply another name for Myalgic Encephalomyelitis. It is not. The CDC 1988 definition of CFS describes a non-existing chimera based upon inexperienced individuals who lack any historical knowledge of this disease process. The CDC definition is not a disease process. It is (a) a partial mix of infectious mononucleosis /glandular fever, (b) a mix of some of the least important aspects of M.E. and (c) what amounts to a possibly unintended psychiatric slant to an epidemic and endemic disease process of major importance. Any disease process that has major criteria, of excluding all other disease processes, is simply not a disease at all; it doesn't exist. The CFS definitions were written in such a manner that CFS becomes like a desert mirage: The closer you approach, the faster it disappears and the more problematic it becomes. M.E. and CFS should be separated as definitions. They are not the same. (2006, [Online])
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. (This misdiagnosis and mistreatment may also create legal consequences for the physician.)
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 2006a, 2006b, [Online]) (Hooper 2006, [Online]) (Hyde 2003, [Online]) (Hooper 2003a, [Online]) (Dowsett 2001a, [Online]) (Dowsett 2000, [Online]) (Dowsett 1999a, 1999b, [Online]) (Dowsett n.d., [Online]).
- For more information on why the bogus disease category of 'CFS' must be abandoned see: The misdiagnosis of CFS, Why the disease category of ‘CFS’ must be abandoned and Smoke and Mirrors.
- An 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 certainly essential to qualify for a misdiagnosis of ‘CFS.’
What do the terms CFIDS, ME/CFS, CFS/ME, Myalgic Encephalopathy and ME-CFS mean?
When the terms CFS, CFIDS, ME/CFS, CFS/ME, Myalgic Encephalopathy or ME-CFS are used what is being referred to may be patients with/facts relating to any combination of: 1. Miscellaneous psychological and non-psychological fatigue states (including somatisation disorder) 2. A self limiting post-viral fatigue state or syndrome (eg. following glandular fever.) 3. A mixed bag of unrelated, misdiagnosed illnesses (each of which feature fatigue as well as a number of other common symptoms; poor sleep, headaches, muscle pain etc.) including Lyme disease, multiple sclerosis, Fibromyalgia, athletes over-training syndrome, depression, burnout, systemic fungal infections (candida) and even various cancers 4. Myalgic Encephalomyelitis patients (despite the fact none of the CFS definitions describes M.E., many M.E. sufferers are given a ‘CFS’ misdiagnosis by default).
The terminology is often used interchangeably, incorrectly and confusingly. However, the DEFINITIONS of M.E. and CFS are very different and distinct, and it is the definitions of each of these terms which is of primary importance. The distinction must be made between terminology and definitions.
- Myalgic encephalomyelitis
is a systemic acutely acquired illness initiated by a virus infection which is characterised by damage to the brain stem which results in dysfunctions and damage to many vital bodily systems and a loss of normal internal homeostasis. M.E. can occur in both epidemic and sporadic forms and can be extremely disabling and in some cases the disease is fatal. M.E. is a chronic/lifelong disease that affects adults and children. If all tests are normal, then a diagnosis of M.E. cannot be correct.
- Chronic Fatigue Syndrome
is a man-made construct created in the US in 1988. It is not a distinct disease, but a mere diagnosis of exclusion based on the presence of the symptom of fatigue. If serious abnormalities are found on testing, a person no longer qualifies for a diagnosis of ‘CFS.’ In essence, every diagnosis of CFS can only ever be a misdiagnosis. A diagnosis of ‘CFS’ does not mean a person has any distinct disease, including M.E.
Terms such as ME/CFS, CFS/ME and ME-CFS are illogical and misleading and a contradiction in terms. They make about as much scientific sense as terms such as diabetes/Alzheimers, depression/HIV or headache/peanut allergy. They join together two completely opposed entities as if they were synonymous terms, only increasing the present confusion between M.E. and CFS that causes patients (and the community) so much harm. It is undoubtedly true that some of the very best M.E. advocates (unfortunately) use these terms to refer solely to M.E. patients – but it is also true that many other groups and individuals use these same terms to refer solely to CFS patients and that probably the majority use these terms to identify information relating to a ridiculous and unscientific mix of the two. It is also true that much of the very worst ‘CFS’ propaganda that has been produced has used these terms throughout. There no agreed definition for any of these made-up terms, nor any World Health Organization classification whatsoever. These terms mean very different things to different people. There is no good reason for these terms to be used by any legitimate researchers or advocates (etc.); except for vested interest groups who no doubt find they serve their purposes rather well. (The term ‘CFS/ME’ was after all created by the ‘Wessely school’ in the UK.) These terms are unhelpful and misleading to say the least.
The term CFIDS (Chronic Fatigue and Immune Dysfunction Syndrome) was created in the USA with the admirable intention of trying to distinguish between patients with M.E. (who always have measurable immune system abnormalities) and those with psychological fatigue states or syndromes which may be misdiagnosed as CFS. Unfortunately however, although a small number of legitimate M.E. advocates and researchers do still use this term, far more often what is being referred to when the term ‘CFIDS’ is used is CFS (or various subgroups of CFS) yet again. It is also true that much of the very worst ‘CFS’ propaganda that has been produced has referred to the illness as CFIDS. The term CFIDS has no agreed definition, and no World Health Organization classification at all. It is a made-up term that could be taken to mean anything and which means very different things to different people. (M.E. is not defined by ‘fatigue’ and many different non-M.E. illnesses – including depression – have immune system abnormalities, so this term is still very vague and inclusive and non-specific to M.E.). The term CFIDS should not be considered as synonymous with M.E.
The term Myalgic Encephalopathy was created in the UK, for dubious reasons. This term also has no agreed definition, and no World Health Organization classification. Again, this is a made-up term that could be taken to mean anything. It should not be considered as synonymous with Myalgic Encephalomyelitis. The claimed medical justifications for the creation and use of this made-up name are bogus. As patient advocate Gurli Bagnall explains: ‘From a scientific point of view, "opothy" does not hold water’ (2004, [Online]). Patients with authentic M.E. do have the damage to the brain referred to in the name Myalgic Encephalomyelitis, however this damage is of course not found in patients suffering various types of ‘chronic fatigue’ or tiredness. Again and again it can be seen that those favouring the name change to ME’opathy are either not referring to a purely M.E. patient group or else they have a vested political or financial interest in dishonestly ‘repackaging’ M.E. as a psychological fatiguing disorder, or both. Legitimate M.E. experts, advocates and researchers do not support the name change from Myalgic Encephalomyelitis to Myalgic Encephalopathy; do not be fooled by the shared initials and seeming similarity of these terms, they are not synonymous. Patient advocates Margaret Williams and Eileen Marshall write:
Despite the relentless financial, psychosocial and political engineering that seems to underpin the current determination to remove the term "myalgic encephalomyelitis" (ME) from the medical lexicon (where, based on accurate published evidence of the nature of the disorder, it has resided for the last half century), the present proponents of its demise have failed to produce any evidence-base to support their clamour for its removal and its replacement by the less specific term "myalgic encephalopathy" (2004a, [Online])
The Committee for Justice and Recognition of Myalgic Encephalomyelitis also explain that:
None of the contemporaries of Ramsay, such as Dowsett and Richardson, who have been asked to comment on the appropriateness of a change from ME'itis to ME'opathy have found ME'opathy an acceptable explanation. Myalgia means muscle pain. Encephalo - means brain, myelitis has two meanings, some say it refers to inflammation of the spinal chord, others to inflammation of the myelin, the covering of the brain. Both are physical descriptions. Opathy, on the other hand means pathology - which can mean 'the science or origin, nature, and courses of diseases', but another meaning is 'any abnormal state: social pathology' (Delbridge 1998). Hence encephalopathy can mean 'brain abnormal state' and this meaning would therefore endorse treatments such as CBT and GET - which do not work in those with neurological ME (which meets the Ramsay criteria). This change of name to 'opathy' can therefore be seen to endorse psychological therapies as treatment. Muscle pain brain myelin inflammation is not the same as muscle pain brain abnormal state. And the neurological damage which is evident in ME can be explained by myelin inflammation but it cannot be explained by 'brain abnormal state'. Evidence for brain damage has been found in the research of persons such as Casse et al. (2001), Poser (1992) and others. And there is often confusion with MS by persons in the medical profession - where there is myelin damage ([2007, [Online]).
The only thing that makes any sense is for patients with Myalgic Encephalomyelitis, to be studied ONLY under the name Myalgic Encephalomyelitis – and for this term ONLY to be used to refer to a 100% M.E. patient group The only correct name for this illness – M.E. as per Ramsay/Richardson/Dowsett and Hyde, and the 60+ outbreaks of M.E. recorded worldwide, and so on – is Myalgic Encephalomyelitis. M.E. is not synonymous with CFS, nor is it a subgroup of CFS. (There is no such thing as a subgroup of CFS; there is no such disease/s as "CFS.’) M.E. is not a primarily fatiguing condition, nor is it a wastebasket diagnosis or ‘medically unexplained’ as ‘CFS’ is.
It is also important that the only terms which are used are those which do have an official and correct World Health Organization classification. As Professor Malcolm Hooper explains:
There have been persistent and frequently covert attempts by these [vested interest] psychiatrists to subvert the international classification of this disorder, with destructive consequences for those affected. The classification issue is important and correct classification does matter because it impacts on correct referral to an appropriate specialist, correct investigations, correct diagnosis, correct management and / or treatment, correct State benefit support, correct insurance policy payments and, as part of correct management, the provision of home tuition for young people.’ (2003a, [Online]) (Hooper & Marshall 2005a, [Online]).
There is no such disease/s as ‘CFS’ – the name CFS and the bogus disease category of CFS must be abandoned (along with the use of other vague and misleading umbrella terms such as ‘ME/CFS’ ‘CFS/ME’ 'CFIDS' and 'Myalgic Encephalopathy' and others), for the benefit of all the patient groups involved.
It should also be noted that Wessely, Sharpe, Cleare and White (etc.) in the UK, their counterparts (and sometime collaborators) in the US; Reeves and Straus (etc. of the CDC) in Australia Lloyd and Hickie (etc.) and the clinicians of the Nijmegen group in the Netherlands often use the terms ‘fatigue’ ‘chronic fatigue’ ‘CFS’ CFS/ME’ Myalgic ‘Encephalopathy’ (or Myalgic Encephalomyelitis) INCORRECTLY as if they were synonymous. Such obfuscation has greatly hindered research and caused considerable harm to many hundreds of thousands of patients (Hooper n.d., [Online]).
- For more information on the name Myalgic Encephalomyelitis (and the problems with some of these other terms including ME’opathy) see: The definitions of M.E., Meitis? A slender string to our bow, The Terminology of ME & CFS, What is ME? What is CFS?, and ME and CFS, The Definitions. See On the name MEitis for more further articles.
- For more information on why the bogus disease category of 'CFS' must be abandoned, (along with the use of other vague and misleading umbrella terms such as ‘ME/CFS’ ‘CFS/ME’ 'CFIDS' and 'Myalgic Encephalopathy' and others), see: The misdiagnosis of CFS, Why the disease category of ‘CFS’ must be abandoned and Smoke and Mirrors. M.E. and 'CFS' are not synonymous terms, and should not be used interchangeably. The distinction must be made between terminology and DEFINITIONS. The truth about the organic and distinct neurological illness M.E. must not be allowed to be buried under cover of ‘fatigue’ and ‘CFS’ for another 20 years!
- A note on the current ‘CFS’ name change proposal: It is madness to suggest that CFS should be renamed as ME-CFS or CFS/ME, as some US CFS groups are currently advocating. M.E. and CFS are not the same, only a small percentage of those misdiagnosed with CFS qualify for a diagnosis of authentic M.E., the vast majority do not. People with depression, Lyme disease, candida, etc. do not need to be given an additional misdiagnosis of ME-CFS, they must instead be given a correct diagnosis finally. It is unethical to use the name of another patient group to further your own interests, particularly when this causes significant additional harm and hardship to that group (and also when, generally speaking, that group is far more severely ill and vulnerable). People with various non-M.E. disorders misdiagnosed as CFS, have no more right to use the name Myalgic Encephalomyelitis (or any modified version of it) than they have to use terms such as ‘Cancer’ or ‘HIV’ just because they decide that it would suit their own purposes to do so. The suggestion that CFS should be renamed in any way as M.E. is grossly illogical, unethical and unscientific.
It may well be the case that patients with various post-viral fatigue syndromes (caused by glandular fever or mononucleosis, hepatitis, Ross River virus etc.), some of the main groups pushing for this absurd renaming, would benefit from these conditions being renamed in some way, but this new name must be one which is not TAKEN already by an entirely unrelated and already well-defined patient group! (The fact that some of these patients, and others, may fit the Canadian criteria for ‘ME/CFS’ does not mean that these patients can be correctly diagnosed with M.E. – as per Ramsay/Richardson/Dowsett and Hyde – nor that these illnesses are the same or ‘virtually the same’ as M.E. They are not. The Canadian ‘ME/CFS’ guidelines are not a pure/accurate M.E. definition. Read more about the benefits and the limitations of the Canadian Guidelines at: Canadian Guidelines Review and Testing for M.E.) See: Why the bogus disease category of ‘CFS’ must be abandoned for more information.
What does the term ICD-CFS mean?
The definitions of CFS do not define M.E. but because an outbreak of M.E. in the US was labelled as being ‘CFS’ at the time (and for other reasons to do with political considerations), some researchers have produced valuable research into M.E. under the name ‘CFS.’
The vast majority (an estimated 95%) of ‘CFS’ research however, does not involve M.E. patients and is not relevant in any way to M.E. patients. So sometimes the new term ‘ICD-CFS’ is used to refer to those studies and articles which while they use the term ‘CFS’ do relate in some way (in whole or in part) to people with authentic Myalgic Encephalomyelitis – as per the World Health Organization’s classification of M.E. as an organic neurological disorder at G.93.3 in their current International Classification of Diseases (ICD).
- It should be noted however, that virtually all of the research which does relate to M.E. but which uses the term ‘CFS’ (or ME/CFS, or CFIDS etc.) is also contaminated in some way by CFS propaganda. Not all of the statements made in these papers can be taken at face value unfortunately, and so these papers must be read and understood in the political context in which they was written. Most often these papers contain a bizarre mix of facts relating to both M.E. and CFS, and write as if they represented one and the same patient group.
Not all those involved with ‘CFS’ have vested financial and political interests, yet often these non-vested-interest groups still also produce significantly flawed, psychiatrically biased and ‘fatigue’ based information. Unfortunately these other groups have been unduly swayed and manipulated to varying extents by the enormous amount of superficially legitimate information widely disseminated by such powerful vested groups and individuals. Some researchers have seemingly been taken in entirely by such scientifically unsupportable theories, as have the large majority of the worlds journalists and politicians (albeit with some notable exceptions). Even some of the best research on the illness is shrouded in heavy usage of misleading and propagandising language and false statements which often bizarrely contradict the harsh realities uncovered in the studies themselves, unfortunately. For information on some of the most common inaccuracies and ‘CFS’ propaganda included in genuine ‘ICD-CFS’ research see the paper: Putting Research and Articles on Myalgic Encephalomyelitis into Context
What does define Myalgic Encephalomyelitis? What is its symptomatology?
Myalgic encephalomyelitis is a systemic acutely acquired illness initiated by a virus infection 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.) The CNS is diffusely injured at several levels, these include the cortex, the limbic system, the basal ganglia, the hypothalamus and areas of the spinal cord and its appendages. This persisting multilevel 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 represents an acute change in the balance of neuropeptide messengers, and due to this, a resulting 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 problem is one of maintaining systemic functioning within normal limits in the face of a chronic infectious stress. The resulting loss of normal internal homeostasis arises from the fact that a chronic viral infection provokes reactive changes in these peptides with the consequence of pathophysiological changes and autonomic dysregulation. These powerful excitory and inhibitory mechanisms for rapid physiological adjustment work well with short-term stressors. Frequently, these mechanisms shut down the biological system allowing for compensatory adjustments of the homeostatic mechanisms. When the stressor is an infectious agent, the messenger mechanisms stimulate compensating immune reactions to rid the body of this stressor and ultimately return the individual to a normal internal homeostasis. By definition, chronic infections have managed to escape these initial compensatory immune mechanisms. However, the neurochemical homeostatic events continue to be employed uselessly and to the detriment of the organism. This modulatory biochemical complex, biologically derived over the millennium to assist the organism, destabilises the autonomic neuronal outflow and 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.
M.E. is primarily neurological, but because the brain controls all vital bodily functions virtually every bodily system can be significantly 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. (Chabursky et al. 1992 p. 20) (Hyde 2007, [Online]) (Hyde 2006, [Online]) (Hyde 2003, [Online]) (Dowsett 2001a, [Online]) (Dowsett 2000, [Online]) (Dowsett 1999a, 1999b, [Online]) (Hyde 1992 pp. x-xxi) (Hyde & Jain 1992 pp. 38 - 43) (Hyde et al. 1992, pp. 25-37) (Dowsett et al. 1990, pp. 285-291) (Ramsay 1986, [Online]) (Dowsett & Ramsay n.d., pp. 81-84). M.E. expert Dr Byron Hyde MD explains that:
A significant number of the initial and long-term peripheral or body symptoms, as well as clinical and technological body abnormalities in the M.E. patient, are caused by variable changes in the peripheral and CNS vascular system. The vascular system is perhaps the largest of the body’s organs and both its normal and patho-physiological functions are in direct relationship to CNS and peripheral vascular health or injury, to CNS control mechanisms and to the difficulty of the peripheral vascular system and organs to respond to CNS neuro-endocrine and other chemical and neurological stimuli in a predictable homeostatic fashion. Depending upon the degree and extent of the ongoing CNS and peripheral vascular injuries, these patho-physiological changes in turn may give rise to both transient and in many cases permanent systemic organ changes in the patient (2007, [Online]).
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) that 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. (See the sections below for more information.)
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. (Chabursky et al. 1992 p. 20) (Hyde 2007, [Online]) (Hyde 2006, [Online]) (Hyde 2003, [Online]) (Dowsett 2001a, [Online]) (Dowsett 2000, [Online]) (Dowsett 1999a, 1999b, [Online]) (Hyde 1992 pp. x-xxi) (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.a, [Online]) (Dowsett & Ramsay n.d., pp. 81-84) (Richardson n.d., pp. 85-92).
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 70 years. Modern technology has now served to confirm and to detail the meticulous clinical and scientific observations made about M.E. before 1988.
Confirmation of this hypothesis is now supported by electrical tests of muscle and of brain function (CT, MRI, SPECT and PET scans clearly indicate that metabolic dysfunction in the brain stem and the spinal nerve radiations which transverse it, are associated with viral (inflammatory) damage and are the major cause of the cardinal symptoms of M.E.) and by biochemical and hormonal assays, and microbiology (for example PCR – a microbiological technique capable of amplifying and identifying minute fragments of viral genes, hidden away in internal organs (such as brain, heart or muscle). Many aspects of the pathophysiology of the disease have 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 (Hyde 2007, [Online]) (Hyde 2006, [Online]) (Hooper 2006, [Online]) (Cheney 2006, [video recording]) (Hyde 2003, [Online]) (Dowsett 2001a, 2001b, [Online]) (Hooper et al. 2001, [Online]) (Dowsett 2000, [Online]) (Dowsett 1999a, 1999b, [Online]) (Hyde 1992 p. xi) (Hyde & Jain 1992 pp. 38 - 43).
What is Homeostasis? Homeostasis is the property of a living organism, to regulate its internal environment to maintain a stable, constant condition, by means of multiple dynamic equilibrium adjustments, controlled by interrelated regulation mechanisms. Homeostasis is one of the fundamental characteristics of living things. It is the maintenance of the internal environment within tolerable limits.
What are some of the symptoms of Myalgic Encephalomyelitis?
More than 64 distinct symptoms have been authentically documented in M.E. At first glance it may seem that every symptom possible is mentioned, but although people with M.E. have a lot of different minor symptoms because of the way the central nervous system (which controls virtually every bodily system) is affected, the major symptoms of M.E. really are quite distinct and almost identical from one patient to the next. Different people have a lot of different symptoms but the general pattern and evolution of major symptoms are remarkably coherent from patient to patient in M.E. (Hooper & Montague 2001a, [Online]) (Hyde 2006, [Online]) Individual symptoms of Myalgic Encephalomyelitis include:
Sore throat, chills, sweats, low body temperature, low grade fever, lymphadenopathy, muscle weakness (or paralysis), muscle pain, muscle twitches or spasms, gelling of the joints, hypoglycaemia, hair loss, nausea, vomiting, vertigo, chest pain, cardiac arrhythmia, resting tachycardia, orthostatic tachycardia, orthostatic fainting or faintness, circulatory problems, opthalmoplegia, eye pain, photophobia, blurred vision, wavy visual field, and other visual and neurological disturbances, hyperacusis, tinnitus, alcohol intolerance, gastrointestinal and digestive disturbances, allergies and sensitivities to many previously well-tolerated foods, drug sensitivities, stroke-like episodes, nystagmus, difficulty swallowing, weight changes, paresthesias, polyneuropathy, proprioception difficulties, myoclonus, temporal lobe and other types of seizures, an inability to maintain consciousness for more than short periods at a time, confusion, disorientation, spatial disorientation, disequilibrium, breathing difficulties, emotional lability, sleep disorders; sleep paralysis, fragmented sleep, difficulty initiating sleep, lack of deep-stage sleep and/or a disrupted circadian rhythm.
Neurocognitive dysfunction may include cognitive, motor and perceptual disturbances. Cognitive dysfunction may be pronounced and may include; difficulty or an inability to speak (or understand speech), difficulty or an inability to read or write or to do basic mathematics, difficulty with simultaneous processing, poor concentration, difficulty with sequencing and problems with memory including; difficulty making new memories, difficulty recalling formed memories and difficulties with visual and verbal recall (eg. facial agnosia). There is often a marked loss in verbal and performance intelligence quotient (IQ) in M.E. (Bassett 2007, [Online]).
What other features define or characterise 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:
A. 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.
B. 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.
The bodies of people with Myalgic Encephalomyelitis respond inappropriately to anything that forces the body to have to react in some way or work harder in some way, in order to maintain internal homeostasis, including (but not limited to): physical activity, cognitive exertion (including emotional stress), sensory input and orthostatic stress (maintaining an upright posture).
C. 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.
When a person with M.E. is active beyond their individual post-illness limits, there is a worsening of all sorts of different symptoms and of the severity of the illness generally. Overexertion causes an exacerbation of symptoms which can be mild, moderate, severe, or even life threatening (eg. seizures and cardiac events).
The types of symptoms produced in response to certain levels of physical activity, cognitive activity, sensory stimuli or orthostatic stress may or may not vary depending on the type (and severity) of the activity or stimuli involved. But very often the types of symptoms worsened or produced by overexertion are fairly similar regardless of which exertion or input was involved. Overexertion can sometimes cause just one or two symptoms to worsen (eg. cardiac problems) but often a large cluster of symptoms are worsened. 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. Patients commonly experience a combination of the following symptoms:
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.
D. 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.
When there is talk of ‘overexertion’ leading to an exacerbation of symptoms in M.E. what is being referred to is not hard exercise, it is not anything resembling what healthy people would recognise as ‘overexertion.’ This term just refers to any activity which goes beyond a person’s individual post-M.E. limits. Relapses can be very severe and prolonged (or even permanent) even if a person with M.E. has only gone past their individual limits in a seemingly minor way.
E. The severity of M.E. waxes and wanes throughout the hour/day/week and month.
The severity of M.E. is not stable over the course of a day, or even from one hour (or even one minute) to the next: it also isn’t stable from one week or month to the next. This waxing and waning of the severity of the illness can be very unpredictable. The severity of M.E. also waxes and wanes from one minute/hour/day/week etc. due to the acute and delayed effects of overexertion.
Because of the lack of stability in M.E. you simply cannot know a M.E. sufferers usual ability level or severity level unless you have observed them over a very long period of time, or actually asked the person detailed questions about what their average daily activity limits, abilities and symptoms are. Just observing someone with M.E. do a certain task should not be taken to mean; (a) that they can necessarily repeat the task anytime soon, (b) that they would have been able to do it at any other time of day, (c) that they can do the same task every hour, day or even every week, or month, or (d) that they wont be made very ill afterwards for a considerable period because they had to really push themselves (and make themselves ill) to do the task. Most importantly, because the worsening of the illness caused by overexertion very often does not even begin until 48 or more hour afterwards you also can’t tell by looking if a particular activity was so far beyond a M.E. patient’s individual limits that they will end up having made themselves severely or permanently more ill by completing the task.
- There is also a waxing and waning of the physical signs of M.E. throughout the day, as Dr Hyde M.D. and Dr Jain M.D. explain, "A patient examined in the morning might have nystagmus, which would disappear at midday, recur later, disappear later and recur the next day."
F. The worsening of the illness caused by overexertion can be acute, but often does not reach its peak until 24 - 48 hours (or more) later.
The onset of the worsening of symptoms caused by overexertion is sometimes be acute but often will not peak until 48 hours or more afterward (this is particularly true with regard to physical, cognitive and orthostatic exertions). Symptoms will then persist for hours, weeks or many months, or longer. For many M.E. sufferers, the effects from significant overexertion will very often peak on day three.
Sometimes there is a significant worsening of symptoms evident at the time of overexertion. At other times, there may only be a minor worsening of symptoms at the time of overexertion, but the delayed effects will be severe. Sometimes the acute effects and the delayed effects will both be severe. It varies depending on the type and severity of the overexertion involved, and so on.
G. If people with M.E. push past their individual limits too deeply or too often, the effects of overexertion can also accumulate over longer periods of time and lead to disease progression, or death.
In addition to the effects of overexertion commonly being delayed by 48 hours or so, the worsening of symptoms caused by overexertion can also sometimes be delayed (and accumulate) over weeks or even many months at a time until they are realised in a ‘crash.’ This is a period of intense worsening of the overall condition followed by a gradual return to the patient’s base level of illness over weeks, months or even years.
When the body is confronted with activity (or inputs) beyond the patient’s individual limits severely and/or repeatedly over time, these effects can also become cumulative in the long term; the patient becomes unable to return to their base level of illness at all. What this means is that long-term or permanent worsening of the overall severity of the condition is caused. Thus some patients are still dealing with the severe physical effects of inappropriate advice to be more physically or mentally active etc. five, ten, fifteen or more YEARS afterward and for some patients the damage caused is permanent. Overexertion has also resulted in death in some cases of M.E.
Strong evidence exists to show that overexertion can have extremely harmful effects on M.E. patients. Patient accounts of leaving exercise programs much more severely ill than when they began them; wheelchair-bound or bed-bound or needing intensive care or cardiac care units, are common. (Recent research has shown that postural stress and physical and mental overexertion exacerbate cardiac insufficiency in this disease; see the notes below for more information.) In addition to the risk of relapse, permanent damage, and disease progression, there have also been reports of sudden deaths in M.E. patients following exercise. As M.E. expert Dr. Elizabeth Dowsett explains, ‘20% have progressive and frequently undiagnosed degeneration of cardiac muscle which has led to sudden death following exercise. Prompt recognition and advice to avoid over-exertion is mandatory.’
- Recent research shows that there is diastolic dysfunction and reduced stroke volume/low cardiac output in M.E. – and that certain levels of orthostatic stress and physical and cognitive activity etc. exacerbate this cardiac insufficiency. Dr Cheney explained recently that because it takes more metabolic energy for the heart to relax and fill with blood than it does for it to squeeze and pump blood, the hearts of people with M.E. don’t fill with the proper amount of blood before they pump which is what causes the reduced cardiac output and many of the symptoms of M.E. (and much of the disability of M.E.) So the tachycardia – fast heart rate – often seen in M.E. in response to orthostatic stress and so on is actually compensating for low stroke volume to help increase cardiac output. The heart doesn’t fill with enough blood before each beat of the heart so it is forced to beat faster to try to make up some of the shortfall, but people with M.E. are still left with reduced cardiac output leaves them very ill and disabled. If this problem is severe enough it can also result in death. As one M.E. advocate explains: ‘Cardiac output is sometimes too low to meet the demands of movement, and any attempt to exert oneself beyond one's own capacity for cardiac output - that is when demand exceeds cardiac capacity - would indeed result in death. Studies on dogs have shown that when the demands of the body exceed cardiac output by even 1%, the organism dies. M.E. patients [must] reduce demand and reduce their exertion level to stay within the bounds of their low cardiac output to stay alive.’ (MESA)
- An additional note on exercise:
It is sometimes claimed that while exercise programs are not safe or appropriate for the severely affected, that mild or moderately affected M.E. sufferers can benefit from such interventions. But this assertion is NOT supported by the evidence. Recent studies have shown that graded exercise programs are the actual reason many with M.E. are so severely affected in the first place, thus exercise programs should not be considered safe for M.E. sufferers of any severity. Graded exercise cannot improve authentic M.E.; disabled patients who improve with exercise do not qualify for a diagnosis of authentic M.E.
H. 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.
Increasing the activity levels of someone with M.E. beyond their individual limits, can only ever be counterproductive. It really doesn’t matter if you do this gradually or all at once. Raising the limits gradually may well delay the onset of the relapse in some patients, but the end result will still be relapse and/or disease progression, or death.
M.E. is a chronic illness which affects the vast majority of (if not all) sufferers for many years or decades at a time, or for the rest of their lives. A person who has been correctly diagnosed with M.E. will naturally raise their activity levels when/if they have had an improvement in their illness – but it can never work the other way around. See: Smoke and mirrors for more information.
I. 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.
There is a base level of illness that is always present in M.E., even at rest. This is because the metabolic problems of M.E. are only one part of M.E., they are not the only cause of symptoms or of the worsening of the illness.
But even those symptoms which are caused by the metabolic problems of M.E. (and the loss of homeostasis etc.) do not always resolve with rest. For severely affected patients, just keeping the body going at the lowest possible level can count as ‘overexertion’ – not only can the bodies of these people not cope with extra activity, but they also cannot even cope with keeping the bodily systems and organs going at the lowest possible level – at rest.
Virtually all bodily systems are affected in some way by both the damage to the central nervous system and the metabolic problems of M.E. (including the cardiac insufficiency this causes) etc. so it is no wonder people with M.E. feel so terribly ill, have such a reduced level of functioning in so many different bodily systems and have so many restrictions and limits on how active they can be. Even with complete rest – and some people with M.E. can do almost nothing else – many M.E. sufferers are still very ill and disabled.
J. Repeated overexertion can harm your chances for future improvement in M.E. M.E. patients who are given advice to rest in the early stages of the illness (and who avoid overexertion thereafter) have repeatedly been shown to have the most positive long-term prognosis.
Thus it is vital that M.E. patients are never encouraged to be active beyond their individual limits, as this can only ever be counterproductive. People with M.E. must be allowed to determine for themselves how much rest they need and how active they can be. Giving people with M.E. the support they need to limit their activities in this way is actually the best way to ensure that they each get to be as active as possible in the long term. The importance of getting appropriate rest and avoiding overexertion in M.E. cannot be overstated. Encouraging people with M.E. to engage in even low levels of physical and cognitive activity, sensory input and orthostatic stress beyond their individual limits can have catastrophic long-term consequences.
- For more information about the effects of overexertion on M.E. patients, including statements/research from some of the world’s leading M.E. experts about why overexertion is so physically harmful, see: Smoke and Mirrors. (This paper also includes links to many different patient accounts of the effects of overexertion on people with M.E.). If you have M.E. see Treating Myalgic Encephalomyelitis - The Basics and Treating Myalgic Encephalomyelitis - Avoiding Overexertion for more on the importance of avoiding overexertion.
L. 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.
For very severely affected M.E. sufferers there is virtually no ‘safe’ level of physical or mental activity, orthostatic stress or sensory input; no level which does not produce a worsening of symptoms, and perhaps also contribute to disease progression. Even the most basic actions – speaking a few words, being exposed to moderate light or noise for a few minutes, turning over in bed, having hair or body washed in bed by a carer or chewing and swallowing food – cause severe and extended symptom exacerbations in such patients. It is not uncommon to hear of very severely affected sufferers who are unable to bathe themselves (or even be bathed by a carer) more often than once a week, or even once every few weeks, or even less. Some sufferers cannot chew or swallow food any longer and need to be tube fed. Many patients with severe M.E. are no longer able to toilet themselves, and so on. Either sufferers are just too ill to do these things at all, or they cannot tolerate the very long and severe relapses that come after such activities (Bassett 2007, [Online]).
What triggers the onset of Myalgic Encephalomyelitis?
M.E. expert Dr Byron Hyde explains that:
[The] prodromal phase is associated with a usually short onset or triggering illness. This onset illness usually takes the form of either, or any combination, of the following, (a) an upper respiratory illness, (b) a gastrointestinal upset, (c) vertigo and (d) a moderate to severe meningitic type headache. These are only the most common onset illnesses or symptoms of which there are several. The onset illness is associated with either a low grade or subnormal temperature, headaches, sometimes persisting and accentuated by movement with intermittent attacks of vertigo or dizziness. Evidence of a previous immune insult [such as a recent immunisation] is found regularly in both epidemic and sporadic cases. The incubation period of the triggering illness is 4-7 days. The second and third phases of the illness are usually always different in nature from the onset illness and usually become apparent within 1-4 weeks after the onset of the infectious triggering illness (1998 [Online]).
Despite popular opinion (and the vast amount of ‘CFS’ government and media propaganda) there is no link however between contracting M.E. and being a 'perfectionist' or having a ‘type A’ or over-achiever personality. M.E. also cannot be caused by a period of long-term or intense stress, trauma or abuse in childhood, becoming run-down, working too hard or not eating healthily. Myalgic Encephalomyelitis is not a form of ‘burnout,’ nervous exhaustion or nervous breakdown or the natural result of a body no longer able to cope with long-term stress.
Research also shows that it is simply not possible that M.E. could be caused by the Epstein-Barr virus, any of the herpes viruses (including HHV6), glandular fever/mononucleosis, Cytomegalovirus (CMV), Ross River virus, Q fever, hepatitis, chicken pox, influenza or any of the bacteria which can result in Lyme disease (or other tick-borne bacterial infections). These theories have been disproven with regard to M.E. M.E. is also not a form of chemical poisoning.
M.E. is undoubtedly caused by a virus, a virus with an incubation period of 4-7 days – and there is very good evidence to suggest that the culprit is an enterovirus (Hyde 2006, [Online]) (Hyde 2007, [Online]) (Hooper 2006, [Online]) (Hooper & Marshall 2005a, [Online]) (Hyde 2003a, [Online]) (Dowsett 2001a, [Online]) (Hooper et al. 2001, [Online]) (Dowsett 2000, [Online]) (Dowsett 1999a, 1999b, [Online]) (Ryll 1994, [Online]).
What does cause Myalgic Encephalomyelitis? Are there outbreaks of M.E.?
One of the most fundamental facts about M.E. throughout its history is that it occurs in epidemics. This fact conveys, among other things, the infectious and contagious nature of the disease (Hyde 1998, [Online]). The usual incubation period of the virus infection involved is 4-7 days. There is a history of over sixty recorded outbreaks of the illness going back to 1934 when an epidemic of what seemed at first to be poliomyelitis was reported in Los Angeles. As with many of the other M.E. outbreaks the Los Angeles outbreak occurred during a local polio epidemic.
The presenting illness resembled polio and so for some years the illness was considered to be a variant of polio and classified as ‘Atypical poliomyelitis’ or ‘Non-paralytic polio’ (TCJRME 2007, [Online]) (Hyde 1998, [Online]) (Hyde 2006, [Online]). Many early outbreaks of M.E. were also individually named for their locations and so we also have outbreaks known as Tapanui flu in New Zealand, Akureyri or Icelandic disease in Iceland, Royal Free Disease in the UK, and so on (TCJRME 2007, [Online]) (Hyde 1998, [Online]).
A review of early M.E. outbreaks found that clinical symptoms were consistent in over sixty recorded epidemics spread all over the world (Hyde 1998, [Online]). Despite the different names being used, these were repeated outbreaks of the same illness. It was also confirmed that the epidemic cases of M.E., and the sporadic cases of M.E. each represented the same illness (Hyde 2006, [Online]) (Dowsett 1999a, [Online]).
Myalgic Encephalomyelitis is an acutely acquired neurological illness (with systemic effects) initiated by a virus infection. This point of view is supported by history (M.E. epidemics have followed polio epidemics and 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) incidence (correlation with a flu-like prodromic illness), symptoms (swollen lymph nodes, low-grade fever, sore throat), and similarities with other viral ailments (including post-polio syndrome). A large body and a large body of medical research also supports a viral causation for the illness (Gellman & Verillo 1997, p 19) (Dowsett 1999a, [Online]).
Transmission of M.E. to monkeys has been successfully demonstrated and has produced central nervous system and parasympathetic nervous system injury in at least two separate sets of experiments; in 1934 where ‘cross sections of the spinal cord demonstrated numerous minute haemorrhages in the grey matter’ and in 1949-51 in the Adelaide, Australia epidemic of M.E. where a radiculitis of the sciatic nerve was demonstrated with small punctate lesions of the myelin sheath (Hyde & Jain 1992, p. 40).
M.E. is an infectious neurological disease and represents a major attack on the central nervous system (CNS) by the chronic effects of a viral infection. A significant number of the world’s leading M.E. experts believe that M.E., like poliomyelitis, is caused by an enterovirus. (This includes doctors such as A. Gilliam, A. Melvin Ramsay and Elizabeth Dowsett, John Richardson of Newcastle-upon-Tyne, W.H. Lyle, Elizabeth Bell of Ruckhill Hospital, James Mowbray of St Mary’s, Peter Behan and also the brilliant Byron Hyde of Canada.) The evidence which exists to support this theory is compelling (Hyde 2007, [Online]) (Hyde 2006, [Online]).
Enterovirus infections are able to cause:
- a chronic host infection
- major or no cardiac disease depending on the virulence of the subtype
- cardiac injury dependent upon the sex of the patient and of the level of physical activity of the patient during the acute or infectious stage
- cardiac disease depending upon the immunological variability of the host (Hyde & Jain 1992a, p. 40).
An enterovirus would also explain the; age variation, sex variation, obvious resistance of some family members to the infection and the effect of physical activity (particularly in the early stages of the illness) in creating more long-term/severe M.E. illness in the host (Hyde & Jain 1992a, p. 40). There is also the evidence that; 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 (Hyde 2007, [Online]) (Hyde 2006, [Online]) (Hyde 2003, [Online]) (Dowsett 2001a, [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 & Ramsay n.d., pp. 81-84) (Richardson n.d., pp. 85-92) (Richardson 1999, [Online]).
The US Centres for Disease Control (CDC) placed ‘CFS’ on its "Priority One; New and Emerging" list of infectious diseases some years ago; a list that also includes Lyme disease, hepatitis C, and malaria’ (Gellman & Verillo 1997, p. 19). But no real research into transmissibility (or more importantly on reducing infection rates) has been done by any government on patients with M.E. (or ‘CFS’) despite ample evidence that this is an infectious disease. There have been many well-documented clusters or outbreaks of the illness, reports of as many as 4.5% of M.E. sufferers contracting the illness immediately after blood transfusions (or after needle-stick injuries involving the blood of M.E. patients), evidence of the disease spreading through casual contact amongst family members and so on (Johnson, 1996) (Carruthers et al. 2003, p.79). As Dr Elizabeth Dowsett explains: ‘The problem we face is that, in spite of overwhelming epidemiological and technical evidence of an infectious case, the truth is being suppressed by the government and the 'official' M.E. charities as 'too scary' for the general public.’ (b [Online])
This pretence of ignorance on behalf of government worldwide has had enormous consequences; only in the UK are people with M.E. specifically banned from donating blood for example. So it is that the number of people infected with M.E. continues to rise unabated and largely unnoticed by the public (Johnson, 1996).
M.E. expert Dr Elizabeth Dowsett M.D. writes about Myalgic Encephalomyelitis that: ‘This illness is distinguished from a variety of other post-viral states by an unique clinical and epidemiological pattern characteristic of enteroviral infection. Prompt recognition and advice to avoid over-exertion is mandatory’ (Dowsett et al. 1990, pp. 285-291).
- See: The outbreaks (and infectious nature) of M.E. section for more information.
- For more information about the effects of overexertion on M.E. patients, including statements/research from some of the world’s leading M.E. experts about why overexertion is so physically harmful, see: Smoke and Mirrors. (This paper also includes links to many different patient accounts of the effects of overexertion on people with M.E.). If you have M.E. see Treating Myalgic Encephalomyelitis - The Basics and Treating Myalgic Encephalomyelitis - Avoiding Overexertion for more on the importance of avoiding overexertion.
Is the onset of Myalgic Encephalomyelitis gradual or acute?
Again, only being able to achieve 50% or less of your pre-illness activity level immediately upon becoming ill is virtually universal in Myalgic Encephalomyelitis. (Although a small percentage of sufferers may possibly be somewhat less severely affected at onset.) It must be emphasised that this is not a gradual change in ability levels (etc.) which occurs slowly over weeks, months or years; it is an acute (sudden) change.
The onset of M.E. is always acute and is frequently very dramatic; M.E. patients can very often tell you not just the day that they became ill, but the exact hour they became ill (Chabursky et al. 1992, p.22) (Hyde 2007, [Online]) (Hyde 2006, [Online]) (Hyde 2003, [Online]) (Hyde et al. 1992, pp. 25-37) (Hyde & Jain 1992, pp. 38-65).
- M.E. is always an acute onset illness, however it should be noted that: (a) some sufferers will be unsure of their onset type (they may not recall it, or may not recall it accurately, for various reasons) and (b) in some cases, acute onset M.E. is preceded by a series of unrelated minor infectious episodes (in a previously well patient) which may be misinterpreted as being a gradual onset of the M.E. (These minor infectious episodes may be due to the immune system being under temporary or chronic stress from events such as; recent immunisation, repetitive contact with a large number of infectious persons, or the effect of travel; as in exposure to a new subset of virulent infections. This pre-existing temporary or chronic immune system weakness is not seen in all patients and is not what causes M.E., although a compromised immune system will of course make the body more vulnerable to all types of infections, including M.E.)
Is Myalgic Encephalomyelitis difficult to diagnose? What tests are used to diagnose M.E.?
M.E. is a distinct, recognisable disease entity that is not difficult to diagnose and can in fact be diagnosed relatively early in the course of the disease – providing that the physician has some experience with the illness. There is just no other illness that is even remotely like M.E.
As with a wide variety of illnesses; (Lupus, multiple sclerosis, and ovarian cancer for example) there is as yet no single test which can diagnose M.E. in all patients. Therefore, along with these other illnesses, M.E. must instead be diagnosed by a combination of: taking a detailed medical history (to rule out other possible causes of symptoms), noting the type and severity of symptomatology and other characteristics of the illness, the type of onset of the symptoms (a acute or sudden onset of symptoms is always seen in M.E. If present this characteristic rules out a wide variety of other illnesses associated with gradual onset) and looking for some of the physical signs of illness. A series of tests may also then be necessary both to rule out other illnesses, and/or to help confirm a suspected M.E. diagnosis.
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. Virtually every M.E. patient will also have various abnormalities visible on physical exam. 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 2007, [Online]) (Hyde 2006, [Online]) (Hooper et al. 2001, [Online]) (Chabursky et al. 1992, p.22). As M.E. expert Dr Byron Hyde MD explains:
The one essential characteristic of M.E. is acquired CNS dysfunction. A patient with M.E. is a patient whose primary disease is CNS change, and this is measurable. We have excellent tools for measuring these physiological and neuropsychological CNS changes: SPECT, xenon SPECT, PET, and neuropsychological testing (Hyde 2003, [Online]).
Thus it is these tests which are therefore most critical in the diagno |
