The Hummingbirds' Foundation for M.E.

The Hummingbirds' Foundation for M.E. (HFME) is fighting for the recognition of M.E.,
and for patients to be accorded the same basic human rights as those with similar
disabling and potentially fatal neurological diseases such as M.S.

An important note:

Before reading the research/advocacy information given in the links below, please be aware of the following facts:

1. Myalgic Encephalomyelitis and ‘Chronic Fatigue Syndrome’ are not synonymous terms. The overwhelming majority of research on ‘CFS’ or ‘CFIDS’ or ‘ME/CFS’ or ‘CFS/ME’ or ‘ICD-CFS’ does not involve M.E. patients and is not relevant in any way to M.E. patients. If the M.E. community were to reject all ‘CFS’ labelled research as ‘only relating to ‘CFS’ patients’ (including research which describes those abnormalities/characteristics unique to M.E. patients), however, this would seem to support the myth that ‘CFS’ is just a ‘watered down’ definition of M.E. and that M.E. and ‘CFS’ are virtually the same thing and share many characteristics.

A very small number of ‘CFS’ studies refer in part to people with M.E. but it may not always be clear which parts refer to M.E. The
A warning on ‘CFS’ and ‘ME/CFS’ research and advocacy paper is recommended reading and includes a checklist to help readers assess the relevance of individual ‘CFS’ studies to M.E. (if any) and explains some of the problems with this heterogeneous and skewed research.

In future, it is essential that M.E. research again be conducted using only M.E. defined patients and using only the term M.E. The bogus, financially-motivated disease category of ‘CFS’ must be abandoned.

2. The research referred to on this website varies considerably in quality. Some is of a high scientific standard and relates wholly to M.E. and uses the correct terminology. Other studies are included which may only have partial or minor possible relevance to M.E., use unscientific terms/concepts such as ‘CFS,’ ‘ME/CFS,’ ‘CFS/ME,’ ‘CFIDS’ or Myalgic ‘Encephalopathy’ and also include a significant amount of misinformation. Before reading this research it is also essential that the reader be aware of the most commonly used ‘CFS’ propaganda, as explained in A warning on ‘CFS’ and ‘ME/CFS’ research and advocacy and in more detail in Putting research and articles on Myalgic Encephalomyelitis into context.

The definitions of M.E.(and 'CFS')

An overview from 'What is M.E.?'

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 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 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. 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, 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 limits. 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 (Bassett 2009, [Online]).

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.

Why were the renaming and redefining of the distinct neurological disease Myalgic Encephalomyelitis allowed – indeed intended – 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 reported incidence of Myalgic Encephalomyelitis in the late 1970s and 1980s, alarming medical insurance companies in the US. 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])

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 he created himself). 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]).

The Wessely School and collaborators has 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 claims (and those of his colleagues around the world) have flooded the UK (and worldwide) literature to the extent that medical journals rarely contain any factual and unbiased information on M.E. Thus most clinicians are effectively being deprived of the opportunity to obtain even the most basic facts about the illness.

For at least a decade, serious questions have been raised 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 ‘theory’ is so financially and politically convenient and profitable on such a large scale to a number of extremely powerful corporations (Hooper et al 2001, [Online]). As Dr Elizabeth Dowsett comments, these ridiculous financially motivated theories bear as much relation to legitimate science ‘as Astrology does to Astronomy’ (1999b [Online]).

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, their US counterparts Reeves, Straus etc of the CDC, in Australia Lloyd, 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 uses a definition of ‘CFS,’ or has created their own, which does not select those with M.E. but instead selects those with various types of psychiatric and non-psychiatric fatigue. (These inappropriate interventions are at best useless and at worst extremely harmful or fatal for M.E. patients.)

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. 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 (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]).

 

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. 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 misdiagnosis. 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 explains, the patient has:

Missed cardiac disease, b. Missed malignancy, c. Missed vascular disease, d. Missed brain lesion either of a vascular or space occupying lesion, e. Missed test positive rheumatologic disease, f. Missed test negative rheumatologic disease, g. Missed endocrine disease, h. Missed physiological disease, i. Missed genetic disease, j. Missed chronic infectious disease, k. Missed pharmacological or immunization induced disease, l. Missed social disease, m. Missed drug use disease or habituation, n. Missed dietary dysfunction diseases, o. Missed psychiatric disease (2006, [Online]).

Under the cover of ‘CFS’ certain 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. As M.E. expert Dr Byron Hyde 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 (2006, [Online]).

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. 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]).

 

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.

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.

Chronic Fatigue Syndrome is an artificial construct created in the US in 1988 for the benefit of various political and financial vested interest groups. It is a mere diagnosis of exclusion (or wastebasket diagnosis) based on the presence of gradual or acute onset fatigue lasting 6 months. If tests show serious abnormalities, a person no longer qualifies for the diagnosis, as ‘CFS’ is ‘medically unexplained.’ A diagnosis of ‘CFS’ does not mean that a person has any distinct disease (including M.E.). The patient population diagnosed with ‘CFS’ is made up of people with a vast array of unrelated illnesses, or with no detectable illness. According to the latest CDC estimates, 2.54% of the population qualify for a ‘CFS’ (mis)diagnosis. Every diagnosis of ‘CFS’ can only ever be a misdiagnosis.

Myalgic Encephalomyelitis is a systemic neurological disease initiated by a viral infection. M.E. is characterised by (scientifically measurable) damage to the brain, and particularly to the brain stem which results in dysfunctions and damage to almost all vital bodily systems and a loss of normal internal homeostasis. Substantial evidence indicates that M.E. is caused by an enterovirus. The onset of M.E. is always acute and M.E. can be diagnosed within just a few weeks. M.E. is an easily recognisable distinct organic neurological disease which can be verified by objective testing. If all tests are normal, then a diagnosis of M.E. cannot be correct.
     M.E. can occur in both epidemic and sporadic forms and can be extremely disabling, or sometimes fatal. M.E. is a chronic/lifelong disease that has existed for centuries. It shares similarities with MS, Lupus and Polio. There are more than 60 different neurological, cognitive, cardiac, metabolic, immunological, and other M.E. symptoms. Fatigue is not a defining nor even essential symptom of M.E. People with M.E. would give anything to be only severely ‘fatigued’ instead of having M.E. Far fewer than 0.5% of the population has the distinct neurological disease known since 1956 as Myalgic Encephalomyelitis.

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 – 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.

 

What does the term ICD-CFS mean?

The various definitions of ‘CFS’ do not define M.E. Myalgic Encephalomyelitis is an organic neurological disorder as defined at G.93.3 in the World Health Organization’s International Classification of Diseases (ICD). The definitions of ‘CFS’ do not reflect this. The ‘CFS’ definitions are not ‘watered down’ M.E. definitions, as some claim. They are not definitions of M.E. at all.

However, ever since an outbreak of M.E. in the US was given the label ‘CFS,’ the name/definition ‘CFS’ has prevailed for political reasons. ‘CFS’ is widely though wrongly applied to M.E. as well as to other diseases.

The overwhelming majority of ‘CFS’ research does not involve M.E. patients and is not relevant in any way to M.E. patients. However, a very small amount (a minuscule percentage) of research published under the name ‘CFS’ clearly does involve a significant number of M.E. patients as it details those abnormalities which are unique to M.E. Sometimes the term ‘ICD-CFS’ is used in those studies and articles which, while they use the term ‘CFS,’ do relate to some extent to authentic M.E.

 

Problems with ‘CFS’ or so-called ‘ICD-CFS’ research

The overwhelming majority of ‘CFS’ research does not involve M.E. patients and is not relevant in any way to M.E. patients. A small number of ‘CFS’ studies refer in part to people with M.E. but it may not always be clear which parts refer to M.E. Unless studies are based on an exclusively M.E. patient group, results cannot be interpreted and are meaningless for M.E. While it is important to be aware of the small amount of research findings that do hold some value for M.E. patients, using the term ‘ICD-CFS’ to refer to this research is misleading and in many ways just damaging as using terms and concepts like ‘ME/CFS’ or ‘CFS/ME.’

 

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 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.

M.E. is primarily neurological, but because the brain controls all vital bodily functions virtually every bodily system can be affected by M.E. Again, although M.E. is primarily neurological it is also known that the vascular and cardiac dysfunctions seen in M.E. are also the cause of many of the symptoms and much of the disability associated with M.E. – and that the well-documented mitochondrial abnormalities present in M.E. significantly contribute to both of these pathologies. There is also multi-system involvement of cardiac and skeletal muscle, liver, lymphoid and endocrine organs in M.E. Some individuals also have damage to skeletal and heart muscle. Thus Myalgic Encephalomyelitis symptoms are manifested by virtually all bodily systems including: cognitive, cardiac, cardiovascular, immunological, endocrinological, respiratory, hormonal, gastrointestinal and musculo-skeletal dysfunctions and damage.

M.E. is an infectious neurological disease and represents a major attack on the central nervous system (CNS) – and an associated injury of the immune system – by the chronic effects of a viral infection. There is also transient and/or permanent damage to many other organs and bodily systems (and so on) in M.E. M.E. affects the body systemically. Even minor levels of physical and cognitive activity, sensory input and orthostatic stress beyond a M.E. patient’s individual post-illness limits causes a worsening of the severity of the illness (and of symptoms) which can persist for days, weeks or months or longer. In addition to the risk of relapse, repeated or severe overexertion can also cause permanent damage (eg. to the heart), disease progression and/or death in M.E.

M.E. is not stable from one hour, day, week or month to the next. It is the combination of the chronicity, the dysfunctions, and the instability, the lack of dependability of these functions, that creates the high level of disability in M.E. It is also worth noting that of the CNS dysfunctions, cognitive dysfunction is one of the most disabling characteristics of M.E. All of this is not simply theory, but is based upon an enormous body of mutually supportive clinical information. These are well-documented, scientifically sound explanations for why patients are bedridden, profoundly intellectually impaired, unable to maintain an upright posture and so on (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) (Richardson n.d., pp. 85-92).

  • 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. (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 2009, [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:

  1. People with M.E. are unable to maintain their pre-illness activity levels. This is an acute (sudden) change. M.E. patients can only achieve 50%, or less, of their pre-illness activity levels post-M.E.
  2. 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.
  3. 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.
  4. 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.
  5. The severity of M.E. waxes and wanes throughout the hour/day/week and month.
  6. The worsening of the illness caused by overexertion often does not peak until 24 - 72 hours (or more) later.
  7. The effects of overexertion can accumulate over longer periods of time and lead to disease progression, or death.
  8. 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.
  9. 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.
  10. Repeated overexertion can harm the patient’s chances for future improvement in M.E. M.E. patients who are able to avoid overexertion have repeatedly been shown to have the most positive long-term prognosis.
  11. 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 (Bassett 2009, [Online]).

For the full-length version of this text and for a full list of references for this text see: The Ultra-comprehensive Myalgic Encephalomyelitis Symptom List.

 

What causes Myalgic Encephalomyelitis?

M.E. expert Dr Byron Hyde explains that:

[The] prodromal phase is associated with a 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. The usual 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’ or nervous exhaustion, 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). 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. There is also ample evidence that M.E. is caused by the same type of virus that causes polio; 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. 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]).

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. The world’s leading M.E. experts, namely Ramsay, Richardson, Dowsett and Hyde, (and others) have all indicated that M.E. is caused by an enterovirus. The evidence which exists to support the concept of M.E. as an enteroviral disease is compelling (Hyde 2007, [Online]) (Hyde 2006, [Online]). An enterovirus explains 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]).

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.’ (n.d.a, [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).

 

Is Myalgic Encephalomyelitis difficult to diagnose? What tests can be 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 (within just a few weeks) – providing that the physician has some experience with the illness. There is just no other illness that is even remotely like M.E.

Although there is as yet no single test which can be used to diagnose M.E. there are (as with Lupus and multiple sclerosis and ovarian cancer and many other illnesses) 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 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 changes: SPECT, xenon SPECT, PET, and neuropsychological testing (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. 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 (Hyde 2007, [Online]) (Hyde 2006, [Online]) (Hooper & Marshall 2005a, [Online]) (Hyde 2003, [Online]) (Dowsett 2001a, [Online]) (Dowsett 2000, [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).

  • See: Testing for M.E. for more information on the various tests which can aid M.E. diagnosis. See also: Are we just 'marking time?'
  • 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. For more information on the lack of access to appropriate testing for M.E. patients see: The Montague/Hooper Paper



*O*O*
 The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)
by Dr Byron Hyde 2006

Preface

Since the Nightingale Research Foundation's publication in 1992 of its textbook, The Clinical and Scientific Basis of Myalgic Encephalomyelitis / Chronic Fatigue Syndrome, there has been a tendency by some individuals and organizations to assume that M.E. and CFS are the same illness. Over the course of two International Association of Chronic Fatigue Syndrome (IACFS, formerly the American Association of CFS) conferences, there have been suggestions that the name CFS be changed to M.E., while retaining the CFS definitions as a basis for such change. This does not seem to me to be a useful initiative: it would simply add credence to the mistaken assumption that M.E. and CFS represent the same disease processes. They do not.

M.E. is a clearly defined disease process. CFS by definition has always been a syndrome

At one of the meetings held to determine the 1994 U.S. Centers for Disease Control and Prevention (CDC) definition of CFS, in response to my question from the floor, Dr. Keiji Fukuda stated that numerous M.E. epidemics he cited the Los Angeles County Hospital epidemic of 1934, the Akureyri outbreak of 1947-48 and the 1955-58 Royal Free Hospitals epidemics-- were definitely not CFS epidemics. Dr. Fukuda was correct.

The Psychiatric Label

Unfortunately many physicians and some senior persons in governments, including Great Britain, Norway and to a lesser degree the USA and Canada treat CFS as a psychiatric illness. This view has been arrived by some physician's readings of the CFS definitions from CDC. Indeed, despite clear signals in the 1994 CDC definition that CFS is not a psychiatric disease, each of the CDC definitions and their addenda referring to CFS remain open to interpretation as a psychiatric rather than a physical illness. This is not a view to which I subscribe. It is the CFS definitions themselves that give rise to this inaccuracy. Consider the following:

(a) What other physical disease definitions essentially state that if you discover the patient has any physical injury or disease, then the patient does not have the illness CFS? In other words if you have CFS then it does not result in or cause any major illness. What else could CFS then be but any number of various psychiatric, social, hysterical or mendacious phenomena?

(b) The various CDC administrations dealing with the subject have clearly stated that CFS is a physical, not a psychiatric disease. However, is there any other definition of any physical disease that is not provable by  scientific and clinical tests? Only psychiatric diseases are not clearly verifiable by physical and technological tests.

(c) What other physical disease definition requires a six month waiting period before the illness can be diagnosed? Any physician knows that to treat a disease adequately you have to be able to define the disease at its onset and treat it immediately in order to prevent chronic complications from arising. There are simply no other disease definitions that have ever been assembled similar to the CFS definitions.

I believe it essential to define clearly Myalgic Encephalomyelitis. That is what the Nightingale definition of M.E. sets out to do

A simplified definition of Myalgic Encephalomyelitis

Myalgic Encephalomyelitis is:

 

              1  A variable and biphasic acute onset disease

 

              2  Primary Infection Phase: The first phase is an epidemic or endemic infectious disease generally with an incubation period of 4 to 7 days, where in most, but not all cases, an infection is evident.

 

              3  Chronic Phase: The second and chronic phase follows closely on the first phase, usually within two to seven days, and is characterized by a measurable diffuse change in the function of the CNS. This is the persisting disease that most characterizes M.E. and is demonstrated by the following:

 

              4  Testable Brain Changes: This second phase becomes chronic and is characterized by various measurable and clinical dysfunctions of the cortical or cortical and sub cortical brain. If the patient's illness is not persistently measurable using SPECT, PET or QEEG and/or Neuropsychological changes then it is not M.E. These changes can be roughly characterized as to severity:

1. Type 1: where one side of the cortex is involved. These patients have the best chance of spontaneous recovery.

2. Type 2: where both sides of the cortex are involved: These patients have the least chance of spontaneous recovery.

3. Type 3: where both sides of the cortex, and either one or all of the posterior chamber organs, the Pons and Cerebellum, the sub cortical and brain stem structures are involved. Type 3 are the most severely affected patients and the most likely to be progressive or see little or no improvement with time.

 

5  Pain Syndromes: The pain syndromes associated with the acute and chronic phases of M.E. may include (a) severe headaches of a type never previously experienced, (b) often associated with neck rigidity and occipital pain, (c) retro-orbital eye pain, (d) migratory muscle and arthralgia pain, (e) cutaneous hypersensitivity and (f) fibromyalgia type pain. These pain syndromes tend to decrease over time.

 

6  Neuropsychological Changes: There are neuropsychological changes that are measurable and demonstrate short-term memory loss, cognitive dysfunctions, increased irritability, confusion, and perceptual difficulties. There is usually rapid decrease in these functions after any physical or mental activity. This feature may improve over a period of years in patients with adequate financial and social support.

 

7  Major Sleep Dysfunction: including all forms of sleep dysfunction and day time alertness and sleep reversals.

 

8  Muscle Dysfunction: This feature may be due to vascular dysfunction or peripheral nervous or spinal dysfunction and includes both pain and rapid loss of strength of muscle function after moderate physical or mental activity.

 

9  Vascular Dysfunction: This is the most obvious dysfunction when looked for and probably is the cause behind a significant number of the above complaints. Vascular change is most evident in patients with:

a. POTS: severe postural hypotension.

b. Cardiac irregularity: on minor positional changes or after minor physical activity, including inability for the heart to increase or decrease in speed and pump volume in response to increase or decrease in physical activity.

c. Raynaud's Disease: vasoconstriction, blanching, coldness and pain of extremities. This is in part the cause for temperature dysfunctions seen in M.E.

d. Bowel Dysfunction: vascular dysfunction may be the single most causal basis behind bowel dysfunction when it occurs

 

10  Endocrine Dysfunction: This feature is common and tends to be a late appearance and is most obvious in the:

a. Pituitary-thyroid axis: This is common. Changes in serum TSH, FTI, FT4, Microsomal Ab., PTH, Calcium and phosphorus rarely occur until one or more years after illness onset and usually only after several years. This can be followed by ultrasound of the thyroid gland where a steady shrinking of the thyroid gland occurs with or without the development of non-serum positive Hashimoto's thyroiditis (a seeming contradiction of terms) and a significant increase in thyroid malignancy. Serum positive changes occur only after years.

b. Pituitary-adrenal axis changes: this finding is infrequent.

c. Pituitary-ovarian axis changes:

d. Pituitary-Bladder dysfunction: occurs frequently in the early disease in some people. It is unknown if the cause is due to this link.


The Clinical and Scientific Basis of Myalgic Encephalomyelitis Edited by Byron Hyde, M.D. , Nightingale Research Foundation, Ottawa, Canada

‘It is a fact that the majority of M.E. patients are not in high-stress occupations as the popular press frequently suggests, but are teachers, nurses, physicians, and other health care workers. This group represents those most closely related to infectious illness, frequent immunisations and those most frequently immunised.’

‘Up to 1955, recognised M.E. was clearly previously associated with poliomyelitis. The viruses that cause paralytic poliomyelitis are some of the same viruses that cause M.E. But these enteroviruses that are capable of causing paralysis attach to more than one set of tissue receptors. These other receptors are found on different cells in the brain and spine as well as in other body areas. The symptoms described by M.E. sufferers are due to injury to these other cells.’

Note: This book contains an enormous amount of information on the epiemics of M.E. (and many other aspects of M.E.) that is simply not available anywhere else. Each epidemic is listed and many are gone into in great detail, information is given on transmissibility, onset and on the historical facts of each outbreak (for example; the links with Polio and how sufferers of one early outbreak were actually paid to keep silent about what had happened to them!). This book is essential reading for anyone with an interest in M.E.


*O* ME and CFS, The Definitions from the Committee for Justice and Recognition of Myalgic Encephalomyelitis.

[Contains details of many of the different CFS and M.E. definitions]

"The Committee feels there has been a particular effort to confuse the public about Myalgic Encephalomyelitis. Most of this effort has been rooted in the promotion of the term Chronic Fatigue Syndrome to describe this disease, which has been spreading in epidemic fashion worldwide during the last twenty years. Of particular note is the outright effort undertaken since 1988 by the American CDC to eliminate the name and definition of M.E. and replace it with CFS. [But] no CFS definition defines a neurological disease. All definitions which wear the 'f' word (ie. fatigue) in their name are not ME nor neurological. They are definitions of fatigue conditions. And when these definitions were written it was not neurological ME which they were attempting to define."


ME and CFS, The Definitions  A. Melvin Ramsay M.A. M.D.

‘The clinical course of Myalgic Encephalomyelitis is consistent with a virus type of infection. It most commonly commences with an upper respiratory tract infection with sore throat, coryza, enlarged posterior cervical glands and a characteristic low-grade fever with temperatures seldom exceeding 101°F. Alternatively there may be a gastro-intestinal upset with diarrhoea and vomiting. In 10% of the 53 cases we reported between 1955 and 1958 the onset took the form of acute vertigo often accompanied by orthostatic tachycardia.

The prodromal phase is characterised by intense persistent headache, paraesthesiae, blurring of vision and sometimes actual diplopia. Intermittent episodes of vertigo may occur at intervals both in the prodromal and later phases of the disease.’


The Complexities of Diagnosis  by Byron Hyde MD 2003

(Taken from: Handbook of Chronic Fatigue Syndrome by Leonard A. Jason, Patricia A. Fennell and Renée R. Taylor)

‘The term myalgic encephalomyelitis was based on clinical descriptions of an illness that has occurred both sporadically among the general population and in clusters, or epidemics, usually in hospitals or schools. Over 60 such epidemics have been described in the medical literature (Acheson, 1992; Henderson & Shelokov, 1992; Hyde, 1992) since Sandy Gilliam, Assistant Surgeon General of the United States and later Dean of Medicine at Johns Hopkins, first described the 1934 epidemic in the Los Angeles County General Hospital (1938). B. Sigurdsson et al. (1950) in Iceland, D. A. Henderson, and A. Shelokov, in the United States (1959a, 1959b); A. Wallis, in 1955, and A. M. Ramsay, in 1988, and John Richardson, in England (1992); and P. Behan, in Scotland (Behan & Behan, 1988; Behan, Behan, & Bell, 1985), have all added to this growing literature.

Those who are most injured or die are easily recognized at disease onset or shortly after as CNS, cardiovascular, or organ injury. Because of their overwhelming illness and the specificity of the end-organ injury, they are never diagnosed as ME except in epidemic or cluster situations.’


The Late Effects Of M.E. Dr Elizabeth Dowsett

‘WHAT IS THE EVIDENCE THAT THE LATE EFFECTS OF ME AND THE POST-POLIO SYNDROME CAN BE CAUSED BY ENTEROVIRUSES OTHER THAN POLIO VIRUSES 1-3?

In 1948, the year in which polio viruses were first cultured, specimens from 2 children with clinical poliomyelitis, yielded a non- polio enterovirus, (eponymously called Coxsackie after the neighbourhood in which they lived). This finding opened a Pandora's box of some 70 previously undiscovered enteroviruses of which 14 strains were later found to have neurogenic potential equal to that of polio viruses.

From the late 1940s, studies in the USA indicated that outbreaks of major or minor enteroviral illness (eg. Paralytic or non paralytic and non specific summer 'flu") could be caused by varying proportions of virulent and non virulent polio viruses combined with other neurogenic enteroviruses, for example in Akron and Cincinnati, Ohio (1947) Delaware and Connecticut (1949).

In the UK, an outbreak of poliomyelitis affecting an Edinburgh housing estate from August 1961- February 1962 (a period when polio immunisation with the Salk (injectable) vaccine had recently been introduced) provided evidence that a "mosaic" of enteroviruses, including Polio type 3, Coxsackie viruses B2 and B4, Echo viruses 5 and 15 could act in combination to enhance virulence in individual patients, to block the spread of polio virus type 3 and to interfere with vaccine efficiency. Each virus type appeared sequentially until the arrival of Echo virus 5 in November which ended the outbreak by the following February (as indicated by serial sampling of the local school sewer). It has to be remembered that a sudden change in the virulence and spread of enteroviruses in the 20th century has been due to alterations in human hygienic behaviour rather than to viral mutations.’


A New and Simple Definition of Myalgic Encephalomyelitis and a New Simple Definition of Chronic Fatigue Syndrome & A Brief History of Myalgic Encephalomyelitis & An Irreverent History of Chronic Fatigue Syndrome by Dr Byron Hyde MD 2006

‘Do not for one minute believe that CFS is simply another name for Myalgic Encephalomyelitis (M.E.). It is not. Though CFS is based upon a typical M.E. epidemic, in my opinion it has always been a confused and distorted view of reality. The invention of Chronic Fatigue Syndrome has to be one of the most curious cases of inventive American scientific imperialism that one could imagine. It is my opinion that 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.’

M.E. is not caused by the HHV6 virus: 'This virus was not associated with CFS until after the 1990 period. HHV6 is the virus that causes the benign childhood illness, Roseola. By 1986 HHV6 was already known to have an incubation period of 9 days due to human experimentation when the actual virus was injected into several children. See (Gorbac, Second Edition, Infectious Diseases, page 1335). When acquired by random infection, the incubation period of HHV6 Roseola was more like 12 days. So once again anyone with access to a library or a computer would have soon dispelled any view that HHV6 was a cause of M.E. epidemics where the incubation was approximately 7 days or less.'

M.E. is not caused by the Epstein Barr virus (or mononucleosis/glandular fever): 'The Lake Tahoe epidemic that started in August 1984 also started amongst students. In this case the epidemic began in a high school girls' basketball team that was travelling in a bus to play various other teams. The epidemic spread rapidly with an incubation period of approximately a week. As in many of the other epidemics, it then spread to the general community. After the epidemic started it then involved three high schools, both students and teachers and ultimately spread to the community. For some reason it was considered to be an epidemic of infectious mononucleosis. This is an illness caused by a virus Epstein Barr Syndrome. Associating the Lake Tahoe epidemic with Epstein Barr Syndrome was frankly ridiculous and you will see why almost immediately. Anyone who realizes that infectious mononucleosis is caused by the herpes family virus, Epstein Barr Virus (EBV), and that the incubation period of this illness is approximately 40 days, should have realized that you simply cannot have a rapidly spreading viral epidemic with a virus with a latent period of 40 days. Neither Dr Straus nor Dr Holmes, senior government physicians, should have fallen into such a trap. They only had to go to the excellent CDC library to realize that rather than spending half a million dollars or so on a publication that they should have known would not have incriminated EBV. Yet this epidemic somehow spread the myth that this illness was caused by EBV. Today, as I write this short history of M.E. the vast majority of physicians and the public still associate Epstein Barr Virus with [M.E.]. Such is the perseverance of error.'

'The incubation period from time of contact with the infection until the appearance of the illness is approximately 4-7 days. In its epidemic form M.E. was most commonly seen in (a) Health Care Workers, (b) children and older students in residential schools, nurses residences and hospitals, (c) in military barracks where students or soldiers were housed in close proximity further supporting the belief in its infectious nature. Although M.E. was not caused by poliovirus in the Akureyri epidemic, infection with M.E. somehow protected the patients from the polio epidemic that swept though Iceland in the 1950s. Polioviruses represent three of approximately 100 different enteroviruses. This was the reason why many in the UK believed that some of these epidemics were probably caused by a less lethal non-polio form of enteroviruses such as ECHO, Coxsackie, the numbered and new enteroviruses.'

*HIGHLY RECOMMENDED*


Redefinitions of ME - a 20th Century Phenomenon by Dr Elizabeth Dowsett

‘To suggest that ME/CFS is merely one subgroup amongst this heterogenous collection of physiological and pathological states, makes thus making any attempt at differential diagnosis between them impossibly expensive to pursue; to suggest that diagnosis must be delayed for 6 months, vitiates any real attempt at virus investigation, especially among the young. It has to be remembered that these "Fatigue" definitions were devised specifically for research, not clinical purposes; that they exclude variations in children and adolescents and that scientists in the USA (their main country of origin) are now foremost in seeking a more descriptive name than that of "Chronic Fatigue [Syndrome]" for this illness!’


Research into ME 1988 - 1998 Too much PHILOSOPHY and too little BASIC SCIENCE! by Dr Elizabeth Dowsett

‘The term "Myalgic encephalomyelitis" (ME) was henceforth used in the UK, Canada and Australasia to define an illness which, following a virus infection, leads to multisystem involvement of cardiac and skeletal muscle, liver, lymphoid and endocrine organs but which is primarily due to central nervous system dysfunction and subsequent breakdown in bodily homoeostasis. Confirmation of this hypothesis was supported by electrical tests of muscle and of brain function (including the subsequent development of PET and SPECT scans) and by biochemical and hormonal assays.’

‘In the mid 1980’s, the incidence of ME had increased by some seven times in Canada and the UK, while in the USA a major outbreak at Lake Tahoe (wrongly ascribed at first to a herpes virus) led to calls for a new name and new definition for the disease, more descriptive of herpes infection. This definition based on "fatigue" (a symptom common to hundreds of diseases and to normal life, but not a distinguishing feature of myalgic encephalomyelitis) was designed to facilitate research funded by the manufacturers of new anti-herpes drugs. However, a "fatigue" definition (which also omits any reference to children) has proved disastrous for research in the current decade.’


 1970’s ME Epidemic at California Hospital Erich D. Ryll, M.D.

Using his long experience, Dr. Ryll describes Myalgic Encephalomyelitis and the history of a California Hospital Outbreak during the 1970’s. This report is a valuable page in ME history and provides additional perspective about this infectious disease. Further illustrating the continuous trail of ME epidemics and discussion of the diverse complex of symptoms and pathology. Patients often find his description of the illness very realistic.

‘In the spring and summer of 1975 there occurred a major, severe epidemic of a communicable, apparent viral disease at the Mercy San Juan Hospital in Carmichael, a suburb of Sacramento, California. The first two cases became ill in February; the bulk of the cases fell ill between July and November of 1975. Several cases tailed out to 1978. The epidemic spread to all departments of the Hospital. It was equally severe in all departments.’

‘So what causes IVN/ME? A specific viral agent has not yet been identified. It does not appear to be anything common. It could be a viral agent very difficult to cultivate. It could be what is called a partial virus. Could it be due to two viruses? As yet there has been no association with the retrovirus that has been proven. The previous finding of a retrovirus has not been able to be repeated by experiments and is invalid. But suppose that all, or nearly all of us, carry an unknown retrovirus in our genes. And then another viral agent infects and the two in combination produce the disease? Or could this illness be due to a virus that escapes immune surveillance. This is, that our immune system is unable to detect it as a foreign invader?

There is a very interesting illness called the post-polio syndrome. Patients who have had polio 20-30 years before acquire an illness that closely resembles [M/E.]. Could this syndrome be due to a mutant polio virus that escapes immune detection? Earlier I said that the early epidemics of ME/ENM/CFS were always in association with a polio outbreak. And that those who came down with ME/ENM/CFS were immune to polio.

It is very important for you to have a firm diagnosis. If you know what you are up against, it is half the battle won.’


Differences between ME & CFS by Dr Elizabeth Dowsett

ME is a systemic disease (initiated by a virus infection) with multi system involvement characterised by central nervous system dysfunction which causes a breakdown in bodily homoeostasis (The brain can no longer receive, store or act upon information which enables it to control vital body functions, cognitive, hormonal, cardiovascular, autonomic and sensory nerve communication, digestive, visual auditory balance, appreciation of space, shape etc). It has an UNIQUE Neuro-hormonal profile"

‘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.’


A Rose by Any Other Name by Dr Elizabeth Dowsett

Both the earliest definition (HOLMES et al, 1988) and its revision (FUKUDA, 1994) elevated tonsillitis, glandular enlargement and fatigue to unreal importance while overlooking the characteristic encephalitic features of the genuine illness.  These mistakes also inflated the possibility of a psychiatric diagnosis, leading to the incorporation of such a heterogeneous population of psychiatric and non-psychiatric causes later on, that research groups of different persuasions were unable to compare results or evaluate treatment.

The tools we can use today to study the brain offer possibilities which were unimaginable 50 years ago2.  These include Molecular Biology: 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 3) while a test for rapid diagnosis (within five hours) is currently available.  These tests indicate that viruses from the polio group, or related to it, are involved both in the late effects of ME and the Post Polio Syndrome 4.  Brain Imaging: the use of CT, MRI, SPECT and PET scans clearly indicates that metabolic dysfunction in the brain stem and the spinal nerve radiations which transverse it, are initially associated with viral (inflammatory) damage and are the major cause of the cardinal symptoms of ME – central fatigue, stress induced weakness, autonomic nervous dysfunction and the breakdown of homoeostasis over hormonal and other vital functions5.


Time to put the exercise cure to rest? by Dr Elizabeth Dowsett

There is ample evidence that M.E. is primarily a neurological illness. It is classified as such under the WHO international classification of diseases (ICD 10, 1992) although non neurological complications affecting the liver, cardiac and skeletal muscle, endocrine and lymphoid tissues are also recognised. Apart from secondary infection, the commonest causes of relapse in this illness are physical or mental over exertion 1. And, on follow up over decades (rather than weeks or months), the average person so disabled is found to be functioning (as a student, employee or parent for example) dangerously near their energy limits. The prescription of increasing exercise is such a situation (or in the early stage of the illness when the patient desperately needs rest) can only be counter-productive.

[In other words - YES!]


Recent Epidemics: Why are the Epidemics so important The Committee for Justice and Recognition of Myalgic Encephalomyelitis

"We encourage patients to learn about ME, its history and the epidemics and the modern research. Do not be confused by the deceitful propaganda about a "new disease". No CFS definition defines a neurological disease. All definitions which wear the 'f' word (ie. fatigue) in their name are not ME nor neurological. They are definitions of fatigue conditions. And when these definitions were written it was not neurological ME which they were attempting to define.'

'The CDC history and their record with the ME epidemic, and experiences of ME patients, strongly suggests that in order to help save lives the CDC must be prohibited from any further involvement with any decisions about our disease. It is clear to us that there is a fundamental conflict between the interests of the large and growing patient community disabled by ME with their desire for progress, and the program of the CDC, which has been to delay and derail the search for the cause and cure.'

‘ME outbreaks and sporadic disease has been documented for many decades. ME appeared most commonly during local polio outbreaks, and at a high rate among hospital personnel. At onset ME resembles polio, and for many years was considered a variant of polio and classified as Atypical poliomyelitis.

Although Myalgic Encephalomyelitis had been reported in the medical journals many times over the past century it was considered a rare disease. Despite this profile, during the 1980’s ME exploded into an alarming worldwide epidemic. For example during the last 20 years ME progressed from a rare disease to now claim over a million victims in the USA alone.

Upon this background of alarming community outbreaks, pleas from doctors, a contagious pattern and an expanding epidemic spread, the government health agencies did not act in a straightforward manner to determine the nature, cause, and extent of the epidemic, nor to alert and protect the public.

As the leading example, in the USA, the Centers for Disease Control (CDC) is the agency entrusted to actively investigate precisely this type of major health hazard. Rather than fulfilling its mandate, for some reason, the CDC abandoned their duty and proceeded to avoid its investigation. They then proceeded to develop and implement policies designed to disguise the disease, and confuse the medical community and the public. The centerpiece of this program of confusion and distraction was forged by changing the name of ME to CFS, interpreted by all as an innocuous, unexplainable fatigue condition. This instantly cut off the disease from its history and prior medical investigations and reports. Replacing knowledge with ignorance.

These actions rendered doctors ignorant of the history and the established neurological infectious nature of this epidemic disease. This new name distracted doctors and the research investigators with a major effort that proclaimed a "new illness" and focused all attention on fatigue. These policies of concealment even go so far as to advise doctors not to investigate patients for the infectious causes. Many other governments immediately followed the same model. These policies have not diminished this epidemic, or protected the public, or sought to determine the cause of this disease. These policies reveal a clear pattern of malfeasance and disregard for the public’s health.’

Note: This article lists many of the more than 60 individual outbreaks


Canadian Clinical Case Definition for ME/CFS

Read more about the limitations of the Canadian Guidelines at: Canadian Guidelines Review


Comparing the Canadian Clinical Definition and the Fukuda Criteria For Chronic Fatigue Syndrome by Dr. Leonard Jason

"None of the current CFS case definitions have been empirically derived or prospectively contrasted with one another. Studies examining sources of diagnostic unreliability have shown that subject, occasion, and information variance account for only a small portion of diagnostic reliability.  However, criterion variance, differences in the formal inclusion and exclusion criteria used by clinicians to classify patients' data into diagnostic categories, accounts for the largest proportion of diagnostic unreliability.  Case definitions would be improved if more attention was devoted to developing operationally explicit, objective criteria and standardized interviews."


The specificity of the CDC-1994 criteria for chronic fatigue syndrome: comparison of health status in three groups of patients who fulfil the criteria

Authors: Kennedy G, Abbot NC, Spence V, Underwood C and Belch JJF

Conclusions: Differences in simple, easily performed clinical outcome measurements can be observed between groups of patients, all of whom fulfill the CDC-1994 criteria for CFS. It is likely that their response to treatment may also vary. The specificity of the CFS case definition should be improved to define more homogeneous groups of patients for the purposes of treatment and research.


Dr. P.O. Behan, Prof. Neurology, in: Critical Reviews in Neurobiology, 1988, vol 4

'Epidemic myalgic encephalomyelitis has attracted increasing attention during the last 5 years, leading to a clearer definition of its clinical and laboratory features. The illness occurs both sporadically and in epidemics, with cases being reported from all over the US, Europe, Australasia, and South Africa. Single cases may continue to appear after the epidemic has ended. Thus, it is stressed that the syndrome is an endemic disease with periodic outbreaks of epidemic prevalence.'


*O* MYALGIC ENCEPHALOMYELITIS : A Baffling Syndrome With a Tragic Aftermath. By A. Melvin Ramsay M.D., Hon Consultant Physician, Infectious Diseases Dept, Royal Free Hospital. [Published 1986]

Known as Myalgic Encephalomyelitis in the UK... leaves a chronic aftermath of debility in a large number of cases. The degree of physical incapacity varies greatly, but the dominant clinical feature of profound [muscle weakness/paralysis] is directly related to the length of time the patient persists in physical effort after its onset; put in another way, those patients who are given a period of enforced rest from the onset have the best prognosis.


*O* Myalgic Encephalomyelitis (ME): a review with emphasis on key findings in biomedical research by Professor Hooper 2006, printed in the BMJ

‘Undoubtedly the perverse use of chronic fatigue syndrome, to impose a psychiatric definition for ME/CFS by allying it to fatigue syndromes, has delayed research, the discovery of effective treatment(s), and care and support for those suffering from this illness

I would propose that the use of CFS should now be abandoned and that, following the Minister of Health’s assurances, the WHO definition is now accepted and used in all official documentations. The excellent work on the biological aspects of ME, already carried out by several leading research groups, now requires significant funding.’


*O* Are Myalgic Encephalomyelitis and Chronic Fatigue Syndrome Synonymous Terms?

Paper Presented by Byron Marshall Hyde M.D. – Nightingale Research Foundation. New South Wales, February 1998

At the 1998 M.E./CFS conference in Australia, both Myalgic Encephalomyelitis and Chronic Fatigue Syndrome were used to describe a chronic illness. This paper is a discussion on the similarities and differences in these two terms that may lead to scientific difficulties. The author suggests that the definitional criteria and epidemic history of Myalgic Encephalomyelitis (M.E.) and the inclusion criteria are significantly different from the CDC definitions and history. The three typical phases of M.E. are discussed. A brief review of some of the known deaths in phase 2 of M.E. are also mentioned.


Improving the diagnostic criteria and procedures for chronic fatigue syndrome Biological Psychology, Volume 68, Issue 2, Feb 2005, Pp 87-106 Caroline King [a] and Leonard A. Jason [b] [a] 4 June 2004.

Abstract Since the publication of the case definition for chronic fatigue syndrome (CFS) in 1988 the diagnostic criteria have been revised twice in the U.S. None of the case definitions were derived empirically. As a result, there is concern regarding the sensitivity, specificity, and reliability of the criteria. The goal of the present study was to identify methods for improving the diagnostic criteria for CFS. Three groups of 15 participants each were recruited: participants with (1) CFS, (2) major depressive disorder (MDD), and (3) healthy controls. Using statistical procedures, three methods for improving the diagnostic criteria were explored: identification of new diagnostic symptoms, the use of severity ratings for symptomatology, and the identification of standardized measures that differentiate cases of CFS from other conditions. Results of the present study suggest that these three methods hold promise for improving the sensitivity, specificity, and reliability of the diagnostic criteria for CFS.


Usefulness of the Fukuda and Holmes definition in the diagnosis of CFS P De Becker [1], J Nijs [1], N McGregor [2], K De Meirleir [1] Dept. of Human Physiology, Vrije Universiteit Brussel, Belgium Collaborative Pain Research Unit Department of Biological Sciences Faculty of Science University of Newcastle Callaghan, New South Wales Australia

The Holmes and Fukuda criteria are widely used criteria all over the world, yet a specific European study regarding CFS patient symptomatology has not been conducted so far. This study was performed in an outpatient tertiary care setting fatigue clinic in Brussels. 2073 consecutive patients with major complaints of prolonged fatigue participated in the study. Multi-variate analyses were performed to assess the symptom presentation within a fatigued population and the differences between the Fukuda and Holmes definitions compared with an excluded chronic fatigued group in a large cohort of fatigued patients. Of the 2073 patients complaining of chronic fatigue, 1578 CFS patients fulfilling the Fukuda criteria (100% of CFS group) and 951 (60.3% of the CFS group) fulfilled the Holmes criteria. Discriminantfunction analysis revealed that the Fukuda and Holmes definitions can be differentiated by symptom severity and prevalence. The Holmes definition was more strongly associated than the Fukuda definition with the symptoms that differentiated the CFS patients from the patients that did not comply with the CFS definitions. The inclusion of ten additional symptoms was found to improve the sensitivity/ specificity and accuracy for selection of CFS patients. The CFS patients fulfilling the Holmes criteria have an increased symptom prevalence and severity of many of the symptoms that determine the difference between CFS and CF patients. Patients fulfilling the Fukuda criteria were less severely affected patients which leads to an increase in clinical heterogeneity. We can conclude that the use of the Holmes criteria defining symptoms of fatigue, swollen/tender lymph nodes, sore throat, muscle weakness, recurrent flu-like symptoms, postexertional fatgigue, myalgia, memory disturbance, nonrestorative sleep with addition of certain symptoms (hot flushes instead of low-grade fever, attention deficit, paralysis, new sensitivities to food/drugs, difficulties with words, urinary frequency, cold extremities, photophobia, muscle fasciculations, lightheadedness, exertional dyspnea and gastrointestinal distrurbance) to the Holmes definition and removal of others (arthralgia and low-grade fever) would strengthen the ability to select CFS patients, also the incorporation of a severity index would be beneficial for subcategorization of patients.


Idiopathic chronic fatigue and chronic fatigue syndrome: a comparison of two case-definitions. Arpino C, Carrieri MP, Valesini G, Pizzigallo E, Rovere P, Tirelli U, Conti F, Dialmi P, Barberio A, Rusconi N, Bosco O, Lazzarin A, Saracco A, Moro ML, Vlahov D Laboratorio di Epidemiologia e Biostatistica, Istituto Superiore di Sanita, Rome, Italy. [Medline record in process]

The aim of the study was to compare the signs and symptoms of individuals meeting two different definitions of chronic fatigue syndrome (CFS). Ninety-four patients fitting the eligibility criteria for idiopathic fatigue were enrolled into the study. Of the 94 patients, 48 met the 1988 definition of CFS, 20 the 1994 (but not the 1988) definition of CFS, and 26 met neither definition. The 1994 defined cases were more likely than 1988 defined cases, and non-syndromal individuals to be male, married, and high school educated. The 1994 cases were less likely than 1988 cases to present acute onset, self reported sore throat, mild fever lymphadenopathy, pharingitis. In conclusion, the 1994 criteria increased the number of patients classified as CFS; however, those who fit only the 1994 criteria were less likely to have an acute symptomatic onset and signs and symptoms suggestive of an infectious process.


Do the 1988 and 1994 CFS case definitions identify the same illness complex? Lana A. Tierskv, Stacy Weisberg, John DeLuca, and Benjamin H. Natelson

Objective: The decision to modify the original CFS case definition was based more on a perceived need to do so than on empirical data to support the proposition that the 1988 CFS case definition did not identify a distinct group of cases. If it is true that the 1988 criteria do not delineate a distinct group of cases, patients fulfilling these criteria should have the same symptom complexes as those fulfilling the relaxed 1994 case definition. Conversely, if patients fulfilling the 1988 case definition are a distinct group, their symptom pattern should differ from the profile of individuals fulfilling the 1994 CFS case definition. One purpose of this study was to evaluate these possibilities by comparing the symptom presentation of subjects diagnosed according to the 1988 CFS diagnostic criteria to the symptom complexes of subjects diagnosed according to the 1994 CFS diagnostic criteria. Differences in activity reduction and symptom onset were also investigated. Methods: Sixty-two subjects completed a questionnaire that obtained information pertaining to CFS symptomatology as well as illness course. The data collection format of the list allowed subjects to respond if a CFS symptom was present as well as at what severity the symptom was experienced. Based on responses to the questionnaire CFS subjects were divided into two groups:

1) Subjects meeting the 1988 criteria for CFS, and
2) Subjects meeting the 1994 criteria.

Patients meeting the 1988 criteria also all met the 1994 criteria; however none of the patients meeting the 1994 criteria also met the 1988 standards. Thus, we were able to delineate two groups. Results: When subjects who met the 1988 case criteria (n=45) were compared to those who met only the 1994 criteria (n=17), subjects in the 1988 group were found to suffer from a more severe form of the illness. Specifically, subjects in the 1988 group demonstrated more severe symptoms as well as a greater reduction in activity. The latter group also more frequently reported infectious-type symptoms as well as a sudden illness onset. Conclusions: The 1988 and 1994 CFS case definition criteria appear to identify distinct patient groups. Given that the subjects in the 1988 group more frequently endorsed infectious symptoms as well as more frequently reported a sudden flu-like illness onset, an infectious etiology for this group is hypothesized.


Heterogeneity of symptom, onset and biochemical profiles in "defined" CFS patients McGregor NR¹*, Hoskin L², Dunstan RH¹, Clifton Bligh P², Butt HL¹, Fulcher G², Roberts TK¹. Dunsmore J², Zerbes M¹, Klineberg IJ*

Objective: To assess the symptom, biochemical and onset data of patients who comply with the CFS definitions to assess whether they are either homogeneous or heterogeneous. The CFS definition requires the exclusion of other known fatigue-related diseases and compliance with a primarily host-response associated symptom constellation.1,2 The patient set derived by this process is heterogeneous in their psychological presentation, and no single ætiological agent or event has been found using this definition. Methods: Multiple regression analysis and clustering techniques were applied to several CFS study data sets to detect either homogeneity or heterogeneity of the patients symptoms, onset events, urinary amino and organic acid, and serum lipid profiles. Results: CFS patients divided on the basis of host responses, infectious responses, sudden or gradual onset or type of onset, had different symptom and biochemical constellations. The disturbances of urinary amino and organic acid excretion could distinguish CFS patients from controls, but the events associated with fatigue or muscle pain, common to all CFS patients, were not selective for defined CFS. Common fatigue-associated host response changes could not be specifically associated with any onset event or psychological response. However alterations in the excretion of various metabolites could be associated with different onset, symptom and psychological response patterns. In a similar manner, the plasma fatty acids profile could differentiate defined CFS patients from control subjects but the differentiating patterns did not occur in all defined CFS patients. The lipid profiles associated with current viral infections, such as EBV, or post-EBV infection were not distinguishing factors for defined CFS. The major lipid changes distinguishing CFS patients from controls appear to be of genetic or acquired origin. Multiple regression and clustering techniques revealed 5 basic types of CFS lipid profiles, whilst the control group had a high degree of homogeneity. These CFS lipid changes are associated with known lipid disorders and provided evidence of heterogeneity. Conclusion: The current CFS definitions either lack standardization and/or the CFS exclusion criteria are insufficient to determine all additional excludable fatigue disorders. The capacity to group currently defined CFS patients into subsets using objectively derived measurements, many of which may indicate known disease states, represents a major advance in CFS research.


A definition-based analysis of symptoms in a large cohort of patients with chronic fatigue syndrome. De Becker P, McGregor N, De Meirleir K.VUB, Vakgroep Interne Geneeskunde, KRO gebouw niv.-1, Laarbeeklaan 101, 1090 Brussels, Belgium. pdbeck@minf.vub.ac.be

OBJECTIVE: The Holmes and Fukuda criteria are widely used criteria all over the world, yet a specific European study regarding chronic fatigue syndrome (CFS) patient symptomatology has not been conducted so far. This study was performed to answer the need to assess the homogeneity of a large CFS population in relationship to the Fukuda or Holmes definitions and to assess the importance of a symptom severity scale. DESIGN: Multivariate analyses were performed to assess the symptom presentation within a fatigued population and the differences between the Fukuda and Holmes definitions compared with an excluded chronic fatigued group in a large cohort of fatigued patients. SETTING: An outpatient tertiary care setting fatigue clinic in Brussels. MAIN OUTCOME MEASURES: Prevalence and severity of symptoms and signs in a CFS population and in a chronic fatigued population. SUBJECTS AND METHODS: A total of 2073 consecutive patients with major complaints of prolonged fatigue participated in this study. Multivariate analyses were performed to assess the symptom presentation and severity and the differences between the Fukuda and Holmes definitions. RESULTS: Of the 2073 patients complaining of chronic fatigue (CF), 1578 CFS patients fulfilled the Fukuda criteria (100% of CFS group) and 951 (60.3% of the CFS group) fulfilled the Holmes criteria. Discriminant function analysis revealed that the Fukuda and Holmes definitions can be differentiated by symptom severity and prevalence. The Holmes definition was more strongly associated than the Fukuda definition with the symptoms that differentiated the CFS patients from the patients that did not comply with the CFS definitions. The inclusion of 10 additional symptoms was found to improve the sensitivity/specificity and accuracy for selection of CFS patients. CONCLUSIONS: The CFS patients fulfilling the Holmes criteria have an increased symptom prevalence and severity of many symptoms. Patients fulfilling the Fukuda criteria were less severely affected patients which leads to an increase in clinical heterogeneity. Addition of certain symptoms and removal of others would strengthen the ability to select CFS patients.


How to disguise a disease by Cesar Quintero

‘ME has had a long association with Poliomyelitis. It should also be taken into account that when ME and Polio were described as being similar it was done at a time when Drs were often very experienced with polio cases and knew its features.

In 1938 the U.S. Asst. Surgeon General, Dr A Gilliam published a major report about this Polio-like illness detailing the epidemic of 1934 at Los Angeles California. This was a landmark to the understanding of this disease. The primary importance of this work was to alert the medical world that this was a different disease yet polio-like it was not polio. Accordingly it would be difficult for Drs today to acknowledge the similarities to polio, a disease they have never had any experience with.

The question remains today. Is ME a different expression of polio? Were there other viruses that were present along with the wave of the polio epidemics? Did polio and its companions mutate after the polio vaccine?’

‘In the fifties there was an epidemic in Iceland, also associated with a polio outbreak - but again, recognized to be a new disease. It was found that patients who developed [M.E.] became immune to polio. [M.E.] has occurred more or less world-wide. Epidemics have been described in closed, contained populations such as schools, military barracks, convents, monasteries, and especially hospitals.’


Idiopathic chronic fatigue and chronic fatigue syndrome: a comparison of two case-definitions. Arpino C, Carrieri MP, Valesini G, Pizzigallo E, Rovere P, Tirelli U, Conti F, Dialmi P, Barberio A, Rusconi N, Bosco O, Lazzarin A, Saracco A, Moro ML, Vlahov D. Laboratorio di Epidemiologia e Biostatistica, Istituto Superiore di Sanita, Rome, Italy.

The aim of the study was to compare the signs and symptoms of individuals meeting two different definitions of chronic fatigue syndrome (CFS). Ninety-four patients fitting the eligibility criteria for idiopathic fatigue were enrolled into the study. Of the 94 patients, 48 met the 1988 definition of CFS, 20 the 1994 (but not the 1988) definition of CFS, and 26 met neither definition. The 1994 defined cases were more likely than 1988 defined cases, and non-syndromal individuals to be male, married, and high school educated. The 1994 cases were less likely than 1988 cases to present acute onset, self reported sore throat, mild fever lymphadenopathy, pharyngitis. In conclusion, the 1994 criteria increased the number of patients classified as CFS; however, those who fit only the 1994 criteria were less likely to have an acute symptomatic onset and signs and symptoms suggestive of an infectious process.


U.S. Case Definition of Chronic Fatigue Syndrome: Diagnostic and Theoretical Issues Leonard A. Jason, Caroline P. King, Judith A. Richman, Renee R. Taylor, Susan R. Torres, Sharon Song U.S. Case Definition of Chronic Fatigue Syndrome: Diagnostic and Theoretical Issues
Journal of Chronic Fatigue Syndrome, Vol. 5 (3/4) 1999

SUMMARY. In 1994, researchers from the U.S. Centers for Disease Control and Prevention (CDC) developed a revised case definition of chronic fatigue syndrome (CFS) (1), a complex illness characterized by debilitating fatigue and a number of accompanying flu-like symptoms. Although Fukuda and associates intended to resolve complexities surrounding the classification of individuals with CFS stemming from previous definitional criteria (1), significant problems with the revised criteria endure. This article highlights reliability issues and other conceptual and operational difficulties inherent in the current U.S. definition of CFS (1). We employ case studies derived from a community-based epidemiological study of chronic fatigue syndrome (2) to illustrate examples of the potential for misclassification of individuals with CFS using the current U.S. criteria (1). Moreover, we suggest alternative approaches to classification and ways to operationalize specific concepts embedded in the current U.S. criteria (1).


Defining Chronic Fatigue Syndrome: Methodological Challenges Leonard A. Jason, PhD; Caroline P. King, MA; Renee R. Taylor, PhD; Cara Kennedy, BA Journal of Chronic Fatigue Syndrome, Vol. 7(3) 2000, pp. 17-32 DePaul University.

Accurate diagnosis of Chronic Fatigue Syndrome (CFS) is greatly complicated by the vague wording of many of the major diagnostic criteria (i.e., substantial reductions in previous levels of occupational, educational, social, or personal activities) and the absence of guidelines for health care professionals to follow.

The lack of operationally explicit criteria has forced health care professionals to rely heavily on their own clinical judgement, which may be biased by personal and highly idiosyncratic factors. Thus, in the case of CFS, the lack of consensus among clinicians regarding the interpretation and application of the diagnostic criteria has likely produced problems in diagnostic reliability.

Data from a recent community based epidemiologic study are presented to illustrate these problems and provide recommendations for improving criterion reliability.


Comparison of the 1988 and 1994 Diagnostic Criteria for Chronic Fatigue Syndrome  Leonard A. Jason,(1,2) Susan R. Torres-Harding,(1) Renee R. Taylor,(1) and Adam W. Carrico(1)

In summary, participants meeting the 1988 criteria appear to be a more symptomatic and functionally impaired group than those meeting the 1994 criteria only. Furthermore, these differences do not appear to be influenced by psychiatric variables, as they occurred in the absence of differences in rates of psychiatric comorbidity between the two groups. Taken together, these findings indicate that the 1988 criteria may identify a distinct group of individuals who not only have a higher frequency of CFS symptoms, but also experience greater functional disability. Possibly because of the lesser degree of specificity in criteria, individuals in the 1994 group may comprise more heterogeneous patient groups experiencing more variability and wider ranges of illness severity and functional disability.


Improving the diagnostic criteria and procedures for chronic fatigue syndrome. King C, Jason LA. Spinal Cord Injury Service (128), Hines VA Hospital, P.O. Box 5000, Hines, IL 60141-5128, USA. cpking@rcn.com

Since the publication of the case definition for chronic fatigue syndrome (CFS) in 1988 the diagnostic criteria have been revised twice in the U.S. None of the case definitions were derived empirically. As a result, there is concern regarding the sensitivity, specificity, and reliability of the criteria. The goal of the present study was to identify methods for improving the diagnostic criteria for CFS. Three groups of 15 participants each were recruited: participants with (1) CFS, (2) major depressive disorder (MDD), and (3) healthy controls. Using statistical procedures, three methods for improving the diagnostic criteria were explored: identification of new diagnostic symptoms, the use of severity ratings for symptomatology, and the identification of standardized measures that differentiate cases of CFS from other conditions. Results of the present study suggest that these three methods hold promise for improving the sensitivity, specificity, and reliability of the diagnostic criteria for CFS.


Chronic fatigue syndrome: the need for subtypes. Jason LA, Corradi K, Torres-Harding S, Taylor RR, King C. DePaul University, Chicago, Illinois 60614, USA. ljason@depaul.edu

Chronic fatigue syndrome (CFS) is an important condition confronting patients, clinicians, and researchers. This article provides information concerning the need for appropriate diagnosis of CFS subtypes. We first review findings suggesting that CFS is best conceptualized as a separate diagnostic entity rather than as part of a unitary model of functional somatic distress. Next, research involving the case definitions of CFS is reviewed. Findings suggest that whether a broad or more conservative case definition is employed, and whether clinic or community samples are recruited, these decisions will have a major influence in the types of patients selected. Review of further findings suggests that subtyping individuals with CFS on sociodemographic, functional disability, viral, immune, neuroendocrine, neurology, autonomic, and genetic biomarkers can provide clarification for researchers and clinicians who encounter CFS' characteristically confusing heterogeneous symptom profiles. Treatment studies that incorporate subtypes might be particularly helpful in better understanding the pathophysiology of CFS. This review suggests that there is a need for greater diagnostic clarity, and this might be accomplished by subgroups that integrate multiple variables including those in cognitive, emotional, and biological domains.


Identification of ambiguities in the 1994 chronic fatigue syndrome research case definition and recommendations for resolution Bart Stouten Published 13 May 2005 ©

Background A recent article by Reeves et al. on the identification and resolution of ambiguities in the 1994 chronic fatigue syndrome (CFS) research case definition recommended the Checklist Individual Strength, the Chalder Fatigue Scale, and the Krupp Fatigue Severity Scale for evaluating fatigue in CFS studies. To be able to discriminate between various levels of severe fatigue, extreme scoring on the individual items of these questionnaires must not occur too often. Methods We derived an expression that allows us to compute a lower bound for the number of items with the maximum item score for a given study from the reported mean scale score, the number of reported subjects, and the properties of the fatigue rating scale. Several CFS studies that used the recommended fatigue rating scales were selected from literature and analyzed to verify whether abundant extreme scoring had occurred. Results Extreme scoring occurred on a large number of the items for all three recommended fatigue rating scales across several studies. The percentage of items with the maximum score exceeded 40% in several cases. The amount of extreme scoring for a certain scale varied from one study to another, which suggests heterogeneity in the selected subjects across studies. Conclusions Because all three instruments easily reach the extreme ends of their scales on a large number of the individual items, they do not accurately represent the severe fatigue that is characteristic for CFS. This should lead to serious questions about the validity and suitability of the Checklist Individual Strength, the Chalder Fatigue Scale, and the Krupp Fatigue Severity Scale for evaluating fatigue in CFS research.


Comparing the Fukuda et al. Criteria and the Canadian Case Definition for Chronic Fatigue Syndrome  Leonard A. Jason PhD, © Copyrighted by The Haworth Press, Inc

Abstract: Because the pathogenesis of Chronic Fatigue Syndrome (CFS) has yet to be determined, case definitions have relied on clinical observation in classifying signs and symptoms for diagnosis.

The selection of diagnostic signs and symptoms has major implications for which individuals are diagnosed with CFS and how seriously the illness is viewed by health care providers, disability insurers and rehabilitation planners, and patients and their families and friends.

Diagnostic criteria also have implications for whether research based on varying definitions can be synthesized. The current investigation examined differences between CFS as defined by Fukuda et al. (1994) and a set of criteria that has been proposed for a clinical Canadian Case definition.

There were twentythree participants who met the Canadian criteria, 12 in the CFS (Fukuda et al. (7) criteria) group and the 33 from the chronic fatigue (CF)-psychiatric group. Dependent measures included: work status, psychiatric comorbidity, symptoms, and functional impairment (measured by the Medical Outcomes Study). People meeting the Fukuda et al. and Canadian criteria were compared with people who had a chronically fatiguing illness explained by a psychiatric condition. Statistical tests used included binomial logistic regression and analysis of variance.

The Canadian criteria group, in contrast to the Fukuda et al. criteria group, had more variables that statistically significantly differentiated them from the psychiatric comparison group. Overall, there were 17 symptom differences between the Canadian and CF-psychiatric group, but only 7 symptom differences between the CFS and CF-psychiatric group.

The findings suggest that both the Canadian and Fukuda et al. case definitions select individuals who are statistically significantly different from psychiatric controls with chronic fatigue, with the Canadian criteria selecting cases with less psychiatric co-morbidity, more physical functional impairment, and more fatigue/weakness, neuropsychiatric, and neurological symptoms


Research Criteria for Penguins by Peter Kemp


Defining an Illness: A Look at the Text and Philosophies of the 1994 Revised Case Definition for Chronic Fatigue Syndrome

It doesn't take an advanced scientific pedigree to realize that what the authors were crafting was a recipe for confusion and conflicting results. It also doesn't take a rocket scientist to come to the conclusion that this is not subgrouping. Failure to classify patients by distinct symptoms has led to a severe loss of respect for the CFS research community.


Descriptions of M.E.

A study of the earliest recorded outbreak of epidemic M.E. in the UK appeared in the Thesis of Dr. Andrew Wallis, a Scottish physician, in 1957. It discusses an epidemic in Cumberland in Northern England in 1955.


Definitions of ME from 1956 onwards 


The classic 1959 paper by  Sir Donald Acheson, "The clinical syndrome variously called benign myalgic encephalomyelitis, Icelandic disease and epidemic neuromyasthenia". Acheson ED. American Journal of Medicine 1959;569:595." (Reprinted from the American Journal of Medicine, with permission from Excerpta Medica.) from MERGE

A pdf copy of this paper can now be found at
http://www.meresearch.org.uk/melibrary/information/index.html

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Exciting book news!

Click here to purchase the first HFME book!


The book 'Caring For The M.E. Patient' by Jodi Bassett includes a Foreword by international M.E. expert Dr Byron Hyde.

He writes:

"There is so much false information that is picked up and disseminated it is near impossible to hold one’s head above the water and sift through this morass of misinformation. Any attempt to seek the truth is always a major difficulty. Somehow, Jodi Bassett and Hummingbird have managed to plow through this field of weeds."

"This is a book that deserves being read, not only by patients and physicians with an interest in M.E. but the bureaucrats in the USA Centers for Disease Control who have done so much damage to the understanding of M.E. I recommend her book to all and wish it every best success."

Paperback $18.95
Hardcover $22.95