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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 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]) (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, vision disturbances, Raynaud’s phenomena, 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 (Bassett 2007, [Online]).
People with M.E. are made very ill and disabled by this problem with their cells; 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.
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.
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. There is a gross mismatch between the severity and complexity of M.E. and the medical and public perception of the disorder (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.)
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 of the body’s vital 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. 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.
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 disease/s as "CFS.’) It is also important that the only terms which are used are those which do have an official and correct World Health Organization classification.
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.
- 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.
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. For more 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 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.
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 (individually determined) 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.
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.
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.
E. The severity of M.E. waxes and wanes throughout the hour/day/week and month.
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.
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.
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.
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.
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.
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.
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]).
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).
- 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?
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 diagnosis of M.E., although various other types of tests are also useful. The abnormalities visible on physical exam in M.E. patients are not usual in healthy patients but they are also found in people with other illnesses (so they are not specific to M.E.). In cases of severe M.E. there are always definite physical signs indicative of physical illness but virtually all patients will have some abnormality on physical exam (Hyde 2007, [Online]) (Hyde 2006, [Online]) (Hooper 2006, [Online]) (Hooper & Marshall 2005a, [Online]) (Hyde 2003, [Online]) (Dowsett 2001a, [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).
While various ‘fatiguing conditions’ with a variety of different aetiology’s may be made up of vague and mild ‘everyday’ type symptoms, have no physical signs and no tests which can aid diagnosis, this is not the case with M.E. M.E. is a distinct neurological illness with a distinct list of symptoms, physical signs and diagnostic (and other) tests – it bears no relationship to such unrelated ‘fatiguing conditions.’ New TESTABLE definitions such as The Nightingale Definition of M.E. now also make diagnosis easier than ever before; even for those with no experience with the illness. Again, if all tests are normal then a diagnosis of M.E. cannot be correct.
- See: Testing for M.E. for more information on the various tests which can aid M.E. diagnosis.
- Objective scientific tests are available which can aid in the diagnosis of M.E. (and easily prove the severe abnormalities across many different bodily systems seen in M.E.), but unfortunately many patients are not given access to these tests. Many (probably most) patients with M.E. are only ever given access to the most basic of tests and these tests are normal in 90% of M.E. patients (as they are with many other serious illnesses). Patients are often given only basics tests and when these are pronounced normal, are told that there is ‘nothing wrong with them.’ This is an abuse of science. In short, a political decision has been made that allowing M.E. patients appropriate testing would be ‘inconvenient.’ For more information on the lack of access to appropriate testing for M.E. patients see: The Montague/Hooper Paper
How quickly can Myalgic Encephalomyelitis be diagnosed?
M.E. can commonly be diagnosed within just a few weeks, if the doctor has some experience with M.E. (Chabursky et al. 1992, p.22).
How common is Myalgic Encephalomyelitis? Who get M.E. and how?
Although the illness we now know as Myalgic Encephalomyelitis has existed for centuries, for much of that time it was a relatively uncommon disease. Following the mass polio vaccination programs of the 1960s cases of polio were greatly reduced and outbreaks of M.E. seemed to be similarly affected. It wasn’t until the late 1970s that M.E. began (for reasons as yet not fully understood) its dramatic increase in incidence worldwide. Over 20 years later, M.E. is a worldwide epidemic of devastating proportions. Many people have died from M.E. and there are now many hundreds of thousands of people severely disabled by this epidemic (TCJRME 2007, [Online]) (Hyde 1992, p. xi).
The main period of infectivity of M.E. peaks at the time just before symptoms appear through to the initial acute phase of the illness (which lasts for several months or in some cases years). M.E. appears to be highly infective but also highly selective. The major mode of infectivity is by airborne or respiratory route. Modes of transmission are thought to include: casual contact (respiratory), salivary transmission (eg. kissing), sexual transmission and transmission through blood products. (Hyde et al. 1992, pp. 25 - 37) (A recent study of 752 patients found that 4.5% of them – almost one in twenty – had had a blood transfusion days or a week before experiencing acute onset of M.E., for example) (Carruthers et al. 2003, [Online]). There is also evidence that asymptomatic carrier of the illness may be able to pass the illness on to others for a brief period following their exposure to the illness (Hyde et al. 1992, pp. 25 - 37).
M.E. has a similar strike rate to multiple sclerosis (or possibly somewhat higher), and is estimated to affect roughly 0.2% of the population. Children and teenagers are also susceptible to the illness and children as young as five have been diagnosed with M.E. (M.E. can occur in children younger than five, but this is thought to be rare.) One hundred thousand kids are estimated to have M.E. in the US alone and a recent study in the UK found that M.E. was by far the most common reason for a child’s long term absence from school. (Munson 2000, p. 198) (Dowsett 1997, [Online]) (Hyde 1992, pp. x - xxi)
There appears to be somewhat of an occupational bias towards teachers (students) and health care workers in the incidence of Myalgic Encephalomyelitis cases (and outbreaks). These are jobs which require higher rates of immunisation than others. This relationship with inoculation is often seen in infectious illnesses (Hyde et al. 1992, pp. 25 - 37). All ages are affected but most commonly sufferers are under 45 at onset. Women are affected around three times as often as men, a ratio common in autoimmune disorders (although in children the sexes seem to be afflicted equally). M.E. affects all races and socio-economic groups and has been diagnosed all over the world. There are more than a million M.E. sufferers worldwide (Hooper et al. 2001 [Online]) (Hyde 1992, pp. x - xxi).
Are there any treatments for Myalgic Encephalomyelitis?
Whilst there is no cure as yet, or treatments which can dramatically influence the course of the illness due to the appalling lack of funding into research; intelligent nutritional, pharmaceutical and other interventions can make a significant difference to a patient's life. Appropriate biomedical diagnostic testing should be done as a matter of course (and repeated regularly) to ensure that the aspects of the illness which are able to be treated can be diagnosed, monitored and then treated as appropriate. Testing is also important so that dangerous deficiencies and dysfunctions (which may place the patient at significant risk) are not overlooked. (Hooper at al. 2001 [Online]).
What is known about Myalgic Encephalomyelitis so far?
There is an abundance of research which shows that M.E. is an organic illness which can have profound effects on many bodily systems. These are well-documented, scientifically sound explanations for why patients are bedridden, profoundly intellectually impaired, unable to maintain an upright posture and so on. More than a thousand good articles now support the basic premises of M.E. Autopsies have also confirmed such reports of bodily damage and infection (Hooper & Williams 2005a, [Online]).
Many different organic abnormalities have been found in M.E. patients (in peer reviewed research). Patient advocates Margaret Williams and Eileen Marshall explain that:
- there is evidence of disrupted biology at cell membrane level
- there is evidence of abnormal brain metabolism
- there is evidence of widespread cerebral hypoperfusion
- there is evidence of central nervous system immune dysfunction
- there is evidence of central nervous system inflammation and demyelination
- there is evidence of hypomyelination
- there is evidence that Myalgic Encephalomyelitis is a complex, serious multi-system autoimmune disorder (in Belgium, the disorder has now been placed between multiple sclerosis and Lupus)
- there is evidence of significant neutrophil apoptosis
- there is evidence that the immune system is chronically activated (eg. the CD4:CD8 ratio may be grossly elevated)
- there is evidence that NK cell activity is impaired (ie. diminished)
- there is evidence that the vascular biology is abnormal, with disrupted endothelial function
- there is novel evidence of significantly elevated levels of isoprostanes
- there is evidence of cardiac insufficiency and that patients are in a form of cardiac failure (which is exacerbated by even trivial levels of physical activity, cognitive activity and orthostatic stress)
- there is evidence of autonomic dysfunction (especially thermodysregulation; frequency of micturition with nocturia; labile blood pressure; pooling of blood in the lower limbs; reduced blood volume (with orthostatic tachycardia and orthostatic hypotension. Findings of a circulating blood volume of only 75% of expected are common, and in some patients the level is only 50% of expected.)
- there is evidence of respiratory dysfunction, with reduced lung function in all parameters tested
- there is evidence of neuroendocrine dysfunction (notably HPA axis dysfunction)
- there is evidence of recovery rates for oxygen saturation that are 60% lower than those in normal controls
- there is evidence of delayed recovery of muscles after exercise. (Affecting all muscles including the heart.)
- there is evidence of a sensitive marker of muscle inflammation
- there is evidence that the size of the adrenal glands is reduced by 50%, with reduced cortisol levels
- there is evidence of at least 35 abnormal genes, (these are acquired genetic changes, not hereditary), specifically those that are important in metabolism; there are more abnormal genes in Myalgic Encephalomyelitis than there are in cancer
- there is evidence of serious cognitive impairment. (Worse than occurs in AIDS dementia)
- there is evidence of adverse reactions to medicinal drugs, especially those acting on the CNS
- there is evidence that symptoms fluctuate markedly from day to day and even from hour to hour (2006, [Online])
(Note that this is only a sample of some of the research available, not an exhaustive list.) From Professor Malcolm Hooper:
In M.E. there is evidence of inflammation of the central nervous system (CNS). In some cases of ME, as in multiple sclerosis, there is evidence of oligoclonal bands in the cerebrospinal fluid. It is accepted by the most experienced M.E. clinicians that some degree of encephalitis has occurred both in patients with M.E. and in those with post-polio syndrome: the areas chiefly affected include the upper spinal motor and sensory nerve roots and the spinal nerve networks traversing the adjacent brain stem (which is always damaged) (Hooper et al. 2001 [Online])
Myalgic Encephalomyelitis expert Dr Byron Hyde MD, explains that:
I have some ME patients with a circulating red blood cell volume less than 50% of expected and a very large number with the range of 60% to 70%. What this test means is that blood is pooling somewhere in the body and that this blood is probably not available for the brain. When blood flow to the heart decreases sufficiently, the organism has an increased risk of death. Accordingly, the human body operates in part with pressoreceptors that protect and maintain heart blood supply. When blood flow decreases, pressoreceptors decrease blood flow to noncardiac organs and shunt blood to the heart to maintain life. This, of course, robs those areas of the body that are not essential for maintaining life and means the brain, muscles, and peripheral circulation are placed in physiological difficulty. (Hyde 2003, [Online])
Dr Byron Hyde MD, also explains that the vascular and cardiac dysfunctions seen in M.E. are often the most obvious set of dysfunctions when looked for, and are the cause of a significant number of M.E. symptoms:
The subject of vascular pathology is not new. The fact of the children dying of a Parkinsonian-like vascular injury to the basal ganglia in Iceland during the Akureyri M.E. Epidemic is an obvious indication of the CNS vascular effects in M.E. (2006, [Online])
Dr. Paul Cheney explains that when disabled M.E. patients stand up, they are ‘on the edge of organ failure’ due to extremely low cardiac output as their Q drops to 3.7 litres per minute (a 50% drop from the normal of 7 litres per minute). Without exception, according to Cheney, every disabled M.E. patient ‘is in heart failure’ and the disability level is exactly proportional to the severity of their Q defect, without exception and with scientific precision (Marshall & Williams 2005a, [Online]) (Cheney 2006, [video recording]) (Williams 2004, [Online]).
It is known that Myalgic Encephalomyelitis is:
- An acute onset (biphasic) epidemic or endemic infectious disease process
- An autoimmune disease (with similarities to Lupus)
- An infectious neurological disease, affecting adults and children
- A disease which involves significant (and at times profound) cognitive impairment/dysfunction
- A persistent viral infection (most likely due to an enterovirus; the same type of virus which causes poliomyelitis and post-polio syndrome)
- A diffuse and measurable injury to the vascular system of the central nervous system (the brain)
- A central nervous system (CNS) disease (with similarities to MS)
- A variable (but always, serious) diffuse (acquired) brain injury
- A systemic illness (associated with organ pathology; particularly cardiac)
- A vascular disease
- A cardiovascular disease
- A type of cardiac insufficiency
- A mitochondrial disease
- A metabolic disorder
- A musculo-skeletal disorder
- A neuroendocrine disease
- A seizure disorder
- A sleep disorder
- A gastrointestinal disorder
- A respiratory disorder
- An allergic disorder
- A pain disorder
- A life-altering disease
- A chronic or lifelong disease associated with a high level of disability
- An unstable disease; from one hour/day/week or month to the next
- A potentially progressive or fatal disease (Hyde 2007, [Online]) (Hooper et al. 2001, [Online]) (Cheney 2007, [video recording]) (Ramsay 1986, [Online])
Myalgic Encephalomyelitis affects every cell in the body.
Is there a legitimate scientific debate about whether or not M.E. is a ‘real’ medical condition?
Despite popular opinion, there simply is no legitimate scientifically motivated debate about whether or not M.E. is a ‘real’ illness or not, or whether or not it is ‘behavioural’ or has a biological basis. The psychological or behavioural theories of M.E. are no more scientifically viable than are the theories of a ‘flat earth.’ They are pure fiction. Strong evidence of the biological basis for the illness has existed since the 1930s and 1950s and more than a thousand good articles now support the basic premises of M.E. as a debilitating organic neurological illness. (Hyde 1992 p. xi) (Hyde & Jain 1992 pp. 38 - 43) (Dowsett 2001a, [Online]). M.E. is not ‘medically unexplained’ or ‘unexplainable.’ The reality is that anyone, whether medically qualified or not, who looks at the worldwide published medical evidence on M.E. could not fail to recognise that the psychological or psychiatric theories could not possibly explain the many different and profound physical abnormalities seen in M.E. (nor the many other characteristics of the disease which are not consistent with psychological or behavioural illness). There are only two ways that a person could reach a different conclusion:
- Bias due to vested political or financial (or other) interests
- Lack of access to a truly representative selection of the evidence (ie. an individual has only availed themselves of the pseudo-science provided by financial stakeholders and not a representative selection (or indeed any) of the legitimate and unbiased science.)
What are some of the most common myths about Myalgic Encephalomyelitis?
There are many, many myths about M.E. Unfortunately, it is very common to read government reports and media articles about M.E. (or ‘CFS’) which do not contain even a SINGLE fact. Some of the most common myths include that:
MYTH: It is only recently that researchers have finally shown that M.E. has a physical or organic basis
MYTH: M.E. can be caused by the Epstein-Barr virus, candida, adrenal exhaustion, hepatitis, Q fever, Ross river virus or glandular fever/mononucleosis
MYTH: It is the name CFS itself that is the cause of all the misunderstandings about the illness. If the name Myalgic Encephalomyelitis was renewed (for example) patients would automatically start to get the recognition and respect they deserve, more money for legitimate research and everything else they so desperately need
The truth is that every one of those statements is completely untrue despite how often they have been repeated and presented as 'facts'.
Similar Medical Conditions?
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.
Myalgic Encephalomyelitis does have some limited similarities – to varying degrees – to illnesses such as multiple sclerosis, Lupus, post-polio syndrome, Gulf War Syndrome and chronic Lyme disease, and others. But this does not mean that they represent the same etiological or pathobiological process. They do not. 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, [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]) (Dowsett 1996, p. 167) (Dowsett et al. 1990, pp. 285-291) (Dowsett n.d., [Online]).
What illnesses such as Gulf War Syndrome, Fibromyalgia, multiple chemical sensitivity and chronic low-dose organophosphate poisoning do have in common with M.E. however is that the same bogus psychiatric model applied to M.E. by vested interest psychiatrists and others has also been extended to these other conditions, leaving many sufferers of these illnesses also without the help and support they so urgently need (Hooper & Marshall 2005a, [Online])
How well is research into Myalgic Encephalomyelitis research funded by government?
M.E. is a comparable illness physically to multiple sclerosis and yet M.E. research receives not even a fraction of the government research funding that MS does – this despite the fact that M.E. is at least as common as MS and can also often be far more physically disabling. A recent article explained that:
Breast cancer is diagnosed in 26 women per 100,000 and receive $716 million dollars in government research funds; lung cancer is diagnosed in 63 women per 100,000 and receives $300 million in government research funds; HIV is diagnosed in 125 women per 100,000 and receives $2921 million in government research funds; and CFS is diagnosed in anywhere from 300-540 women per 100,000 and receives $6 million in government research funds. Research funding for CFS [in the US] is about 107th out of 110 diseases funded (SDCD, [Online]).
But even this small amount of money for 'CFS' research does nothing to help people with M.E., nor patients with any other distinct disease. Studying vague and mixed groups of 'fatigue' sufferers is of no benefit to any patient group; particularly as many of those conducting this 'research' are known to have vested interests in certain outcomes – and even to have determined the outcomes of some of this ‘research’ before the actual studies have been conducted (Hooper 2003a, [Online]). In reality, governments around the world are currently spending $0 a year on M.E. research. Considering the brutal severity of the illness, the vast numbers of patients involved worldwide and the number of patient deaths (many of them preventable), this is a worldwide disgrace.
Abuse and Myalgic Encephalomyelitis
Two of the most common interventions people with M.E. are recommended (or coerced or forced) to participate in are cognitive behavioural therapy (CBT) and graded exercise therapy (GET).
However, despite the misleading claims to the contrary made by various vested interest groups, no evidence exists which shows that CBT and GET are appropriate, useful or safe treatments for Myalgic Encephalomyelitis patients. Studies by these groups (and others) involving miscellaneous psychiatric and non-psychiatric ‘fatigue’ sufferers, and their positive response to these treatments |
