A Hummingbirds' Guide to M.E.

Testing for Myalgic Encephalomyelitis

Testing for Myalgic Encephalomyelitis provides a basic overview of some of the series of tests which can be done to help confirm a suspected M.E. diagnosis (and also contains further information on many other aspects of diagnosis).

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Testing for Myalgic Encephalomyelitis: Summary

Many articles on Myalgic Encephalomyelitis (M.E.) in the mainstream media (and even some medical texts) unequivocally proclaim that not only are there no tests which can be utilised to help confirm a M.E. diagnosis, but that despite extensive testing no objective or quantifiable abnormalities have ever been found in any patients with M.E. whatsoever. Despite their popularity, these are simply absurd claims.

The reality is that objective evidence of quantifiable organic abnormalities in Myalgic Encephalomyelitis patients has existed since the 1950s. Not only are there a series of tests which readily allow a M.E. diagnosis to be confirmed, but more than a thousand medical studies have shown a variety of measurable and in some cases extremely severe abnormalities in many different bodily systems of M.E. patients. Various other abnormalities are also visible on physical exam, and have been confirmed by autopsy. Tests will only all be normal in M.E. patients – as with all illnesses – if completely the wrong tests are done, or if those tested do not in fact have M.E. in the first place.

As with a wide variety of illnesses; Lupus, multiple sclerosis, and ovarian cancer for example, there is as yet no single test which can diagnose M.E. in all patients. Therefore, along with these other illnesses, M.E. must instead be diagnosed by a combination of: taking a detailed medical history (to rule out other possible causes of symptoms), noting the type and severity of symptomatology and other characteristics of the illness, the type of onset of the symptoms (an acute or sudden onset of symptoms is always seen in M.E. If present this characteristic rules out a wide variety of other illnesses associated with gradual onset) and looking for some of the physical signs of illness. A series of tests may also then be necessary both to rule out other illnesses, and/or to help confirm a suspected M.E. diagnosis.

What is true however, is there are no tests which can be used to diagnose ‘Chronic Fatigue Syndrome.’ But despite popular opinion, M.E. and ‘CFS’ are not at all the same thing. 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. In a nutshell:

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.

There is also no such disease/s as ‘CFS/ME,’ ‘CFIDS,’ ‘ME/CFS’ or Myalgic Encephalomyelitis. These are in effect just other terms for ‘CFS’ or refer to texts which unscientifically mix together facts about M.E. and ‘CFS’ and thus only contribute to the confusion between the two which causes so much harm. For more information see: Who benefits from 'CFS' and 'ME/CFS'?, What is Myalgic Encephalomyelitis? A historical, medical and political overview and The Terminology Explained, plus Why the bogus disease category of ‘CFS’ must be abandoned.

Contrary to much of the propaganda surrounding the illness, it is also not ‘fatigue’ or ‘tiredness’ that is the one essential characteristic of M.E. but central nervous system (CNS) dysfunction. As M.E. expert Dr Byron Hyde explains: ‘The one essential characteristic of M.E. is acquired CNS dysfunction, [not] chronic fatigue. A patient with M.E. is a patient whose primary disease is CNS change, and this is measurable. We have excellent tools for measuring these physiological and neuropsychological CNS changes: SPECT, xenon SPECT, PET, and neuropsychological testing.’ 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.

Some of the series of tests which can (in combination) help to confirm a M.E. diagnosis include:

SPECT and xenon SPECT scans of the brain

SPECT scans have demonstrated decreased cerebral blood flow most frequently in the frontal, parietal, temporal, occipital and brain stem areas of the brain. These abnormalities have also been shown to correlate with clinical status. Dr Byron Hyde adds that, ‘I do not describe a patient as having M.E. unless there is an abnormal SPECT. If the SPECT is normal, I often repeat it along with xenon SPECT. If the brain scans remain normal, I conclude that it is [not] M.E.’

MRI scans of the brain

Punctate, subcortical areas of high signal intensity consistent with edema or demyelination were identified by MRI in over 78% of M.E. patients (similar to those seen in MS). Research has shown that an estimated 80% of M.E. patients will have abnormal MRI scans. M.E. patients with abnormalities on MRI have been reported as being more severely impaired than those without such abnormalities.

PET scans

PET scans have shown decreased metabolism of glucose in the right mediofrontal cortex and generalised hypoperfusion of the brain with a particular pattern of decreased neuronal metabolism in the brain stem.

Neuropsychological testing

Of the CNS dysfunctions that make up M.E., cognitive dysfunction is easily one of the most disabling characteristics of the illness. Neuropsychological testing can be used to identify cognitive dysfunction and/or to confirm a M.E. diagnosis. It should focus on the abnormalities known to differentiate M.E. from other causes of organic brain dysfunctions. Dr Byron Hyde explained that:

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. Neuropsychological changes must be measured in relation to estimates of prior achievement. This feature may improve over a period of years in patients with adequate financial and social support and can be made worse by chronic stressors. The neurophysiological changes are those observed by a qualified Neuropsychologist with experience in examining this type of disease spectrum. Some of the deficits that a Neuropsychologist should consider examining include: (a) word finding problems, (b) Subtle problems with receptive and expressive aphasia, (c) Decreased concentration, (d) Distractibility and the decreased ability to process multiple factors simultaneously, (e) Dyscalculia, (f) Decreased fine and gross motor problems, (g) Dysfunction of spatial perception, (h) Abstract reasoning, (i) Compromised visual discrimination, (j) Sequencing problems. In Cochran’s Q Neuropsychological tests there is an increased observation of significant problems in both immediate and delayed verbal recall. In Dr Sheila Bastien’s investigations, over 50% of M.E. patients have delayed visual recall, TAP dominance, TPT N-Dominance and 40% or more have abnormalities of Immediate visual recall, Tap N-Dom, Grip N Dominance, & grip dominance problems.

EEG brain maps and QEEG brain maps

95% of M.E. patients have been found to have abnormal cognitive-evoked EEG brain maps. But Dr Byron Hyde argues that QEEG brain maps are even more accurate and that they, ‘have been able to demonstrate not only lack of normal activity in M.E. patients but migration of the normal activity centers from injured areas to different parts of the brain.’

Neurological examination and the Romberg or tandem Romberg test

Most M.E. patients have abnormal neurological examination. The Romberg test is a useful test of brain stem function, Professor Malcolm Hooper explains that, ‘Dr Paul Cheney found that 90% of patients have an abnormal Romberg versus 0% of controls.’

Tests of the immune system

The immune system abnormalities in M.E. patients fit the immune pattern seen in viral infections. Specific findings include (but are not limited to): Increased numbers of activated cytotoxic T cells (most patients have evidence of T-cell activation), Low natural killer cell numbers/percentage and function (cytotoxicity), Elevated immune complexes, Atypical lymphocyte count, Significantly reduced CD8 suppressor cell population and increased activation marker (CD38, HLA-DR) on CD8 cells, Abnormal CD4/CD8 ratio, Elevations of circulating cytokines and Immunoglobulin deficiencies (most often IgG 1 and IgG 3)

Erythrocyte Sedimentation Rate (ESR)

An unusually low sedimentation rate of <5mm/hr is common in M.E. ESR rates as low as 0 have been documented in M.E. patients, and levels of 1 and 2 are very common. Dr Byron Hyde reported in 1989 that, "To my knowledge, there are only five diseases that have a pathological low sedimentation level: Myalgic Encephalomyelitis, sickle-cell anemia, hereditary sperocytosis, hyper-gammaglobulinemia and hyper-fibrogenemia.’

Insulin Levels and Glucose Tolerance Tests

Derangement of insulin response is a frequent finding in M.E. patients. Glucose tolerance curves are often abnormal.

24 Hour Holter Monitor

A 24 hour Holter monitor (a type of heart monitor) may show repetitively oscillating T-wave inversions and/or a flat T-wave may be found. Holter monitors may also show heart rates as high as (or higher than) 150 beats per minute as an immediate or delayed response to the patient maintaining an upright posture, or at rest. Heart rates as low as 40 beats per minute may also be observed (during sleep).

Tilt Table Examination

Orthostatic intolerance is very common in M.E. patients and may manifest as one of, or a combination of the following: Neurally mediated hypotension (NMH): Postural orthostatic tachycardia syndrome (POTS) or Delayed postural hypotension. If a tilt table is not available, doctors may prefer to do a ‘poor man’s tilt table test’ (as described in the full-length version of this text).

Dr Byron Hyde explains that testable vascular and cardiac dysfunction is the most obvious set of dysfunctions when looked for and is probably the cause behind a significant number of M.E. complaints, and that all moderate to severe M.E. patients have one or more or multiple of the following vascular dysfunctions:

Severe postural orthostatic tachycardia syndrome (POTS)
Cardiac irregularity on minor positional changes or after minor physical activity
Raynaud’s phenomenon (vasoconstriction of small arteries or arterioles of extremities, with change in colour of the skin, pallor and cyanosis),
Circulating blood volume decrease (up to 50%)
Bowel dysfunction caused by vascular dysfunction (vascular dysfunction may be the most significant causal basis of the multiple bowel dysfunctions occurring in M.E.),
Persantine effect in M.E. patients
M.E. associated clotting defects
Anti-smooth muscle antibodies (This is an antibody to the muscle tissue in the arterial bed. It is elevated in about 5% of M.E. patients)
Cardiac dysfunction (There are a large number of cardiac dysfunctions that can regularly appear in M.E.).

Note however that the primary vascular change in M.E. is seen in abnormal SPECT brain scans.

Exercise testing and chemical stress tests

Cardiopulmonary exercise testing is widely used for the diagnosis (and functional assessment) of various cardiac and metabolic disorders and can also be used in the diagnostic evaluation of M.E. patients. Heart rate and blood pressure responses during the exercise test may reveal abnormalities specific to ME including: lower cardiovascular and ventilatory values at peak exercise (patients only being able to attain half the expected maximal workload and oxygen uptake compared to sedentary controls), elevated resting heart rates and an inability to reach maximum age-predicted heart rates. As exercise tests are not appropriate for many M.E. sufferers, Dr Byron Hyde writes: ‘Patients with ME frequently cannot do exercise tests, and so I then do chemical testing as a second best.’

Physical Exam

There are also a variety of abnormalities visible on physical exam in M.E. patients. These abnormalities are not usual in healthy patients but they are also found in people with other organic illnesses (so they are not specific to M.E.). The post-exertional paralytic muscle weakness unique to M.E. should also be tested for; a diagnosis of M.E. should never be made without this characteristic being present. Physical signs of illness commonly observed in M.E. patients include:

Nystagmus; nystagmus is jelly-like and variable (15% of M.E. patients will have nystagmus)
Sluggish visual accommodation and unequal pupils and contrary pupil reaction to light
A labile blood pressure (sometimes as low as 84/48 in an adult at rest)
Shortness of breath (particularly on exertion)
Subnormal temperature
Cogwheel movement of the leg on testing, and muscular twitching or fasciculation
Hyper-reflexia without clonus
Destruction of fingerprints is sometimes seen (atrophy of fingerprints is due to perilymphocytic vasculitis and vacuolisation of fibroblasts)
Ghastly pallor of face with frequent lupus-like submaxillary mask or facial vasculoid rash
Parkinsonian rigidity of facial expression
Scanning, disjointed speech, or speech reversals
Nasal passage obstruction and inflamed areas around tonsillar pillars
Sicca syndrome of conjunctiva and mucous membranes
Frequent equivocal Babinski/plantar reflex on one side

In conclusion

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.

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 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.

M.E. is a distinct neurological illness which has a well-documented and unique set of characteristics, symptoms, physical signs and diagnostic (and other) abnormalities which may be tested for. Contrary to popular belief, M.E. is a distinct, recognisable entity that can be diagnosed relatively early in the course of the disease, providing the physician has some experience with the illness.

The new Nightingale Definition of M.E. created by the worlds leading M.E. expert Dr Byron Hyde MD also makes diagnosis easier than ever before even for those with no prior experience in diagnosing M.E. This is a pure M.E. definition and, most importantly, it is a TESTABLE M.E. definition and so is essential reading for all doctors with an interest in correctly diagnosing M.E.

Whilst various ‘fatiguing conditions’ with a variety of different aetiologies may be made up of vague and mild ‘everyday’ type symptoms, have no physical signs and no tests which have shown abnormalities or that can aid diagnosis; Myalgic Encephalomyelitis shares none of these characteristics.

Myalgic Encephalomyelitis is a distinct organic neurological disorder which can occur in both epidemic and sporadic forms and is severely disabling and sometimes fatal. It bears no relationship to any unrelated, vague and hard to diagnose ‘fatiguing illnesses’ or to any of the definitions of ‘CFS.’

For more information:

Please see the more comprehensive full-length Testing for M.E. text for more information on this text as well as on all other aspects of diagnosis (and for references).
See What is M.E.? for more information on all medical and political aspects of M.E.
See The misdiagnosis of CFS for information on what a diagnosis of ‘CFS’ based on any of the CFS definitions actually means.
See Smoke and Mirrors for a discussion of why the disease category of 'CFS' must be abandoned.

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References:

All of the information concerning Myalgic Encephalomyelitis on this website is fully referenced and has been compiled using the highest quality resources available, produced by the world's leading M.E. experts. More experienced and more knowledgeable M.E. experts than these – Dr Byron Hyde and Dr. Elizabeth Dowsett in particular – do not exist. Between Dr Byron Hyde and Dr. Elizabeth Dowsett, and their mentors the late Dr John Richardson and Dr Melvin Ramsay (respectively), these four doctors have been involved with M.E. research and M.E. patients for well over 100 years collectively, from the 1950s to the present day. Between them they have examined more than 15 000 individual (sporadic and epidemic) M.E. patients, as well as each authoring numerous studies and articles on M.E., and books (or chapters in books) on M.E. Again, more experienced, more knowledgeable and more credible M.E. experts than these simply do not exist.

This paper is merely intended to provide a brief summary of some of the most important facts of M.E. It has been created – by a well-read layperson purely for the benefit of those people without the time, inclination or ability to read each of these far more detailed and lengthy references created by the world’s leading M.E. experts. The original documents used to create this paper are essential additional reading however for any physician (or anyone else) with a real interest in Myalgic Encephalomyelitis: see the full-length text or the References page.

"People in positions of power are misusing that power against sick people and are using it to further their own vested interests. No-one in authority is listening, at least not until they themselves or their own family join the ranks of the persecuted, when they too come up against a wall of utter indifference.’ Professor Hooper 2003

‘Do not for one minute believe that CFS is simply another name for Myalgic Encephalomyelitis (M.E.). It is not. 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’ Dr Byron Hyde 2006

The term myalgic encephalomyelitis (means muscle pain, my-algic, with inflammation of the brain and spinal cord, encephalo-myel-itis, brain spinal cord inflammation) was first coined by Ramsay and Richardson and has been included by the World Health Organisation (WHO) in their International Classification of Diseases (ICD), since 1969. It cannot be emphasised too strongly that this recognition emerged from meticulous clinical observation and examination. Professor Malcolm Hooper 2006

M.E. 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. It has an UNIQUE Neuro-hormonal profile. .Dr Elizabeth Dowsett

M.E. appears to be in this same family of diseases as paralytic polio and MS. M.E. is less fulminant than MS but more generalized. M.E. is less fulminant but more generalized than poliomyelitis. This relationship of M.E.-like illness to poliomyelitis is not new and is of course the reason that Alexander Gilliam, in his analysis of the Los Angeles County General Hospital M.E. epidemic in 1934, called M.E. atypical poliomyelitis. Dr Byron Hyde

Dr Melvin Ramsay on Myalgic Encephalomyelitis: "The degree of physical incapacity varies greatly, but the [level of severity] 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."

The vested interests of the Insurance companies and their advisers must be totally removed from all aspects of benefit assessments. There must be a proper recognition that these subverted processes have worked greatly to the disadvantage of people suffering from a major organic illness that requires essential support of which the easiest to provide is financial. The poverty and isolation to which many people have been reduced by ME is a scandal and obscenity. Professor Malcolm Hooper 2006

‘Thirty years ago when a patient presented to a hospital clinic with unexplained fatigue, any medical school physician would search for an occult malignancy, cardiac or other organ disease, or chronic infection. The concept that there is an entity called chronic fatigue syndrome has totally altered that essential medical guideline. Patients are now being diagnosed with CFS as though it were a disease. It is not. It is a patchwork of symptoms that could mean anything’ Dr Byron Hyde 2003

A one-page summary of the facts of Myalgic Encephalomyelitis

Myalgic Encephalomyelitis is a disabling neurological disease that is very similar to multiple sclerosis (M.S.) and polio (poliomyelitis). Earlier names for M.E. were ‘atypical multiple sclerosis’ and ‘atypical polio.’
Myalgic Encephalomyelitis is a neurological disease characterised by scientifically measurable post-encephalitic damage to the brain stem. This is always damaged in M.E., hence the name M.E. The term M.E. was coined in 1956 and means: My = muscle, Algic = pain, Encephalo = brain, Mye = spinal cord, Itis = inflammation. This neurological damage has been confirmed in autopsies of M.E. patients.
Myalgic Encephalomyelitis has been recognised by the World Health Organisation’s International Classification of Diseases since 1969 as a distinct organic neurological disease with the ICD code G.93.3.
Myalgic Encephalomyelitis is primarily neurological, but also involves cognitive, cardiac, cardiovascular, immunological, endocrinological, metabolic, respiratory, hormonal, gastrointestinal and musculo-skeletal dysfunctions and damage. M.E. affects all vital bodily systems and causes an inability to maintain bodily homeostasis. More than 64 individual symptoms of M.E. have been scientifically documented.
Myalgic Encephalomyelitis is an acute (sudden) onset, infectious neurological disease caused by a virus (a virus with a 4-7 day incubation period). M.E. occurs in epidemics as well as sporadically and over 60 M.E. outbreaks have been recorded worldwide since 1934. There is ample evidence that M.E. is caused by the same type of virus that causes polio; an enterovirus.
Myalgic Encephalomyelitis can be more disabling than MS or polio, and many other serious diseases. M.E. is one of the most disabling diseases there is. More than 30% of M.E. patients are housebound, wheelchair-reliant and/or bedbound and are severely limited with even basic movement and communication.
Why are Myalgic Encephalomyelitis patients so severely and uniquely disabled? For a person to stay alive, the heart must pump a certain base-level amount of blood. Every time a person is active, this increases the amount of blood the heart needs to pump. Every movement made or second spent upright, every word spoken, every thought thought, every word read or noise heard requires that more blood must be pumped by the heart.

     However, the hearts of M.E. patients only pump barely pump enough blood for them to stay alive. Their circulating blood volume is reduced by up to 50%. Thus M.E. patients are severely limited in physical, cognitive and orthostatic (being upright) exertion and sensory input.

     This problem of reduced circulating blood volume, leading to cardiac insufficiency, is why every brief period spent walking or sitting, every conversation and every exposure to light or noise can affect M.E. patients so profoundly. Seemingly minor 'activities' can cause significantly increased symptom severity and/or disability (often with a 48-72 hour delay in onset), prolonged relapse lasting months, years or longer, permanent bodily damage (eg. heart damage or organ failure), disease progression or death.

     If activity levels exceed cardiac output by even 1%, death occurs. Thus the activity levels of M.E. patients must remain strictly within the limits of their reduced cardiac output just in order for them to stay alive.

    M.E. patients who are able to rest appropriately and avoid severe or prolonged overexertion have repeatedly been shown to have the most positive long-term prognosis.
Myalgic Encephalomyelitis is a testable and scientifically measurable disease with several unique features that is not difficult to diagnose (within just a few weeks of onset) using a series of objective tests (eg. MRI and SPECT brain scans). Abnormalities are also visible on physical exam in M.E.
Myalgic Encephalomyelitis is a long-term/lifelong neurological disease that affects more than a million adults and children worldwide. (Causes of death in M.E. include heart failure.)

For more information, and to read a fully-referenced version of this text compiled using information from the world’s leading M.E. experts, please see: What is Myalgic Encephalomyelitis? Extra extended version. Permission is given for this unedited document to be freely redistributed, please redistribute this text widely.

Information on the neurological disease Myalgic Encephalomyelitis