For several years, the Myalgic Encephalomyelitis page on Disapedia.com was one of the most well-rounded, concise explanations of the disease to possibly exist on the internet. It was second only to the very factually-deluded Chronic Fatigue Syndrome wikipedia page, in popularity on search engines. I personally have no idea why the site is no longer available, or if it will be coming back, but since the collective information was donated by fellow sufferers, I thought it would be appropriate to scout down an old cache of the page and post it here.
Please note, there was no data for “comorbid conditions” or “severity,” which is why those sections appear to be missing. The last version of the page was updated sometime in 2009, so any more recent developments (such as the introduction of the updated international consensus criteria of 2011) are not included.
I have not taken the liberty to add that much information, myself, but my additions, be they text or links, are highlighted in maroon. I have also underlined points that I believe to be of particular importance.
Myalgic Encephalomyelitis (ME)
Myalgic Encephalomyelitis (abbreviated ME) is a chronic, inflammatory, primarily neurological disease that is multisystemic, affecting the central nervous system (CNS), immune system, cardiovascular system, endocrinological system, and muscloskeletal system. ME can cause a wide variety of symptoms, including changes in sensory tolerance, visual problems, exertional muscle weakness, difficulties with coordination and speech, severe fatigability, cognitive impairment, problems with balance, subnormal or poor body temperature control, and pain. ME will cause a degree of impaired mobility and disability in all cases. The degree of impairment and complexity depends on the degree of diffuse brain injury and end organ involvement.
Myalgic Encephalomyelitis affects the brain and spinal cord which control the body and allow thought and sensory processing, causing dysautonomia, impaired thinking, and loss of internal homeostasis, the process whereby the body maintains a consistent internal environment in response to external stressors. Cellular metabolism and communication is disrupted, causing inefficiency in all biological processes. This includes the cellular mitochondria which process fuel to make energy, resulting in a deficiency of adenosine-triphosphate ATP with a chronic, severe, measurable loss of sustainable strength on exertion. A hallmark of ME is intolerance to previously trivial effort and deterioration through persistent or repeated exertion.
Current theory suggests ME results from a persistent viral infection and/or attacks by an individual’s immune system on the nervous system, musculoskeletal system, and blood vessels. It has been classified by the World Health Organisation as an organic brain disease since 1969. There is a controversial view that ME is not a chronic infectious or autoimmune disease, but rather a psychosocial illness triggered by infection or stress. Usually proponents of this school disdain the term ME, claiming it to be inaccurate. Although more than 50 years of research and clinical observation informs knowledge of ME pathology, its exact cause remains unknown and more research is required, particularly for treatment. ME patients are barred from donating blood or organs in the United Kingdom while symptoms persist.
Myalgic encephalomyelitis is a relapse-remitting disease with new symptoms occurring either in discrete relapses (or “crashes”) or slowly accruing over time. Between relapses, symptoms may resolve completely with sufficient rest, but permanent neurologic problems often persist, especially as the disease advances. ME currently does not have a cure, though some treatments such as antivirals are being trialed, which may at least slow the appearance of new symptoms.
ME affects all ages, with peak incidence typically between 20 and 40 years, and is more common in women than in men.
The name Myalgic Encephalomyelitis refers to the inflammation of the brain and spinal cord. accompanied by muscle pain.
In 1988 The US Centres for Disease Control (CDC), for reasons best known to them, dismissed fifty years of research and decided to treat the Lake Tahoe outbreak as a new illness, which they christened chronic fatigue syndrome (CFS). CFS is a highly contentious concept to patients and specialists alike. Because of the similarity in terminology, CFS is often confused with “chronic fatigue”. A study found that while most medical trainees consider the symptom complex of CFS to be a serious illness resulting in poor quality of life, the “chronic fatigue syndrome” name may be regarded less seriously than the name “myalgic encephalopathy”. Another study found that nurses and physician assistants viewed a patient’s CFS symptoms as more severe and disabling if they were told the patient had a more medical sounding diagnosis of “chronic neuroendocrineimmune dysfunction syndrome”.
Patients and specialists alike had long lobbied for a name and definition change or reversal of “CFS”. In January 2007 The American “CFS Name Change Advisory Board” consisting of doctors Bateman, Bell, Cheney, Jason, Klimas, Lapp, and Peterson agreed that “CFS downplays the severity of the disease and is hurtful to patients” and publicised their deliberation that CFS should now be termed ME.
Signs and symptoms
The core symptom of ME is muscle fatiguability following minimal exertion, plus delayed recovery of muscle power. Ramsay, a world authority on ME, referred to a diagnostic triad of muscle fatiguability, central nervous system involvement, and impaired circulation. However, ME affects many bodily systems, and other symptoms include: Increased sensitivity to light and sound (photosensitivity, hyperacusis) and general migraine-like sensory intolerance, changes in sensation (hypoesthesia), muscle spasms (myclonus or fasciculation), or difficulty initiating movement (transient paralysis), difficulties with coordination and balance (ataxia), problems in speech and verbalisation (Dysarthria, Dysphasia), visual problems (Nystagmus, blurred vision), acute or chronic pain, difficulty standing (orthostatic intolerance), cardiopulmonary symptoms (palpitations, dysrhythmia and dyspnea), sleep dysregulation (hypersomnia, insomnia, or sleep reversal), gastroenteric difficulties, cognitive impairment, and emotional symptomatology (emotional lability or depression). What differentiates ME from similar conditions is the close link with exertion and the variability, not only from day to day, but from hour to hour.
ME is diagnosed definitively using case history to look for a distinctive pattern and type of symptoms and signs. Diagnosis necessitates involvement of the CNS and musculoskeletal symptomology.
All descriptions of M.E. diagnostic criteria tend to emphasize muscle fatiguability and central nervous system involvement (Myalgic Encephalomyelitis Case Definitions, 2011). The Canadian Consensus Criteria represents international efforts to standardize the diagnosis of ME using clinical data and laboratory data, but are controversial. The list of symptoms is long and there is therefore a danger of misdiagnosis. Research criteria based on Ramsay’s descriptions have been used in various studies (e.g. Costa et al, 1995).
Generally consistent findings of a novel low molecular weight antiviral protein (Rnase-L) have shown promise as a potential diagnostic test for CFS and may be relevant to ME. Another test which may become important in the future is an assay of genes for the immune system and mitochondria, however, these tests are so far seen as discretionary. Without research criteria for ME, it is not possible to confirm that abnormalities found in people with chronic fatigue syndrome are also generalizable to ME.
The signs and symptoms of ME can be similar to other medical problems, such as multiple sclerosis, Lyme disease, lupus, sarcoidosis, anemia, cancers, and other autoimmune problems. Additional testing may be needed to help distinguish ME from these other problems.
Disease course and clinical subtypes
The initial acute phase illness most often occurs in summer with a 3-5 day incubation period and during this period is said to be highly infectious.
Generally from then, the initial presentation takes one of two forms: a severe, incapacitating prolonged illness, or an apparent remission followed by increasing relapses until the patient is forced to recognise exertional limitation. The most common initial symptoms reported are: Pain in the spine, neck or head; mild fever and ‘flu-like symptoms; nausea or vomiting; flaccid muscle weakness; and muscle pain or tenderness. For some people, ME is triggered by Hepatitis B vaccination [M.E. Association Survey Report, 2010], blood transfusion, or chemical poisoning, although it is now thought organophosphate poisoning is a different illness.
The later course of ME is difficult to predict, and may either become consistently severe, improve to a plateau, or be markedly relapse-remitting. In some, even prolonged severe incapacitation can be relieved by unpredictable remission, although relapse is always possible. The degree of impairment and complexity depends on the degree of diffuse brain injury and end organ involvement.
The evidence for subgroups is strengthened by research using heterogenous CFS criteria, although this artificial heterogeneity also hampers consensus. It is likely that subtypes exist within the ME milieu based on the clinical findings, history, and perhaps gender of patients.
Factors triggering a relapse
ME relapses are often a result of overactivity, but can occur without warning with no obvious inciting factors. Exposure to increased sensory information in light, sound, and movement can provoke a sensory storm which has been termed “The Mall Effect” due to its particular provocation by the stimulus of a busy shopping mall.
Infections, such as the common cold, influenza, and gastroenteritis, also increase the risk for a relapse. Heat and cold can transiently increase symptoms.
Pregnancy can directly affect the susceptibility for relapse. Later pregnancy appears to offer a natural protection against relapses, and there are anecdotal reports of post-partum remission. However, pregnancy does not seem to influence long-term disability.
Although much is known about abnormalities in myalgic encephalomyelitis, the reasons why they occur is not known. There are two ME conferences held in the UK each year attended by international research luminaries, and other conferences held worldwide.
Myalgic encephalomyelitis is a complex disease in which the immune and neurological systems appear dysregulated and in conflict, producing a wide variety of findings.
The problem is that most of the research in recent years has been conducted on people with CFS. This is a heterogeneous population, and includes patients with psychiatric disorders, as well as vitamin and nutritional deficiencies (especially vitamin D) and post-viral states such as ME.
According to a strictly immunological explanation of CFS, the inflammatory processes triggered by T-cells create leaks in the blood-brain barrier (a capillary system that should prevent entrance of T-cells in the nervous system). These leaks, in turn, cause a number of other damaging effects such as swelling, activation of macrophages, and more activation of cytokines and other destructive proteins such as Rnase-L. A reduced ability to move metabolites in and out of cells (channelopathy) has been implicated in this process. This may also be applicable to ME.
Some evidence shows viral infection of muscle and brain in at least a proportion of sufferers. This triggers inflammatory processes, stimulating other immune cells and soluble factors like cytokines and antibodies.A model for late ME has been proposed analogously to post-polio syndrome in which repaired nerve tissue forms inappropriately [The Late Effects of ME: Can they be distinguished from the Post-polio syndrome?]. Radiological research on ME has shown hypoperfusion of the brain stem and an abnormal response to exertion, but research on CFS is often inconsistent and must be interpreted with caution. For example, a reduced volume of grey matter may be a result of a lack of activity and is reversible with cognitive behaviour therapy.
An inquest into the death of Sophia Mirza from ME found inflammation of the dorsal spine ganglia and liver abnormalities. However, she had comorbid disorders.
Hemodynamic abnormalities are widely found, including serum and RBC hypovolemia, NMH, cerebral hypoperfusion. Vascular and endothelial abnormalities have been published by MERUK. However, none of these studies used research criteria for ME so the results may not be applicable to ME.
Some cardiological features such as cardiac insufficiency, inverted T-waves and myofiber disarray have been reported in CFS and recently added to by findings of reduced Q-value. This has lead clinician and researcher Dr. Paul Cheney to posit that CFS is form of partially compensated cardiomyopathy in which orthostatic intolerance and rapid fatiguability are secondary protective mechanisms. Due to the heterogeneity of the population, a single cause is unlikely, but one third of people with ME have abnormalities when tested with Holter monitors.
Although risk factors for myalgic encephalomyelitis have been identified, no single definitive virus has been found in all cases, which has lead to the claim that ME is a common end path of a variety of infectious insults, perhaps most commonly in the retroviral family. It is still possible ME involves some combination of both environmental and genetic factors. Various theories try to combine the known data into plausible explanations. Although most accept an infectious explanation, several theories suggest that ME is an inappropriate immune response to an underlying condition, a theory bolstered by the observation that there is sometimes a family history of autoimmune disease. There is also a shift from the Th1 type of helper T-cells, which fight infection, to the Th2 type, which are more active in allergy and more likely to attack the body.
The most popular hypothesis is that a viral infection or retroviral reactivation primes a susceptible immune system for an abnormal reaction later in life. On a molecular level, this might occur if there is a structural similarity between the infectious virus and some component of the central nervous system, leading to eventual confusion in the immune system.
Since ME seems to be more common in people who live farther from the equator, another theory proposes that decreased sunlight exposure and possibly decreased vitamin D production may help cause ME. This theory is bolstered by recent research into the biochemistry of vitamin D, which has shown that it is an important immune system regulator.
Other theories describe ME as an immune response to a chronic infection. The association between ME and the Cocksackie-B, HHV-6, and HHV-7 viruses suggests a potential viral contribution in at least some individuals. Still others believe that ME may sometimes result from a chronic infection with spirochetal bacteria, such as Lyme disease. Another bacterium that has been implicated in ME is Chlamydia pneumoniae. Protein findings relating to several infections have seen found in the oligoclonal bands ME patients. Research has shown that, much like in AIDS, the immune dysfunction accompanying M.E. can lead to temporary or permanent progression of the disease, no matter what infection or combination of infections the PWME comes into contact with; additionally, PWME are more prone to opportunistic infections.
There is no known definitive cure for myalgic encephalomyelitis. However, several types of therapy have been found helpful by sufferers. Different therapies are used for patients experiencing greater neurological symptoms, for patients who have greater muscle and/or cardiac symptoms, for patients who have greater immune symptoms, for patients with an uncertain diagnosis, and for managing the various consequences of ME. Treatment is aimed at reducing disability, restoring sleep, reducing pain, reducing relapses, and preventing disability.
- Coenzyme q-10
Disease-modifying treatments (in trial):.
- Avoiding relapse triggers
- Maintaining good hydration
- Dietary modification
- Neurontin (pain control)
- EPA fatty acid
- Saline infusions
The prognosis (the expected future course of the disease) for a person with myalgic encephalomyelitis depends on severity and chronicity of the disease and initial symptoms; the age; and the degree of disability the person experiences. In general, 25% are severely disabled, though a number move in and out of categories due to relapse-remission. The life expectancy of people with ME is generally less than that of unaffected people; research done on CFS has suggested this decrease may be 25-30 years. Fatalities are generally rare, with a mortality rate anywhere from 5-10%, and occur mainly due to heart or pancreatic failure, opportunistic infection, neurodegeneration, cancer, and suicide.
ME has been found world-wide, in at least 63 epidemics documented in published papers from the 1930′s to the 1980s. Currently ME is less epidemic and more endemic than in previous decades. Epidemics have a penchant for enclosed communities such as schools and hospitals, although not all of the outbreaks have occurred in enclosed commmunities.
As observed in many autoimmune disorders, ME is more common in females than males; the mean sex ratio is about two to three females for every male. In children the sex ratio is approximately equal.
The Formative Years
The first definitive description of an illness resembling poliomyelitis was by Gilliam after the 1930s Los Angeles outbreak. Careful clinical observation in all the epidemics repeatedly found reproducible signs and a distinctive pattern of CNS and sensory nerve involvement, muscle weakness with pain or tenderness, and emotional lability with a chronic, relapsing course.
In the 1950s, the public eye was caught by several outbreaks of a mysterious illness that incapacitated communities, often in hospitals. In the Iceland epidemic it was noted patients who contracted the illness developed immunity to poliomyelitis, suggesting confirmation of an association.
Autopsy findings on experimentally infected monkeys during the Adelaide epidemic led to the conclusion that the disorder was caused by inflammation of the brain and spinal cord. Accordingly, names such as atypical polio and Akiyuri disease were replaced in 1956 in the UK by the term Benign myalgic encephalomyelitis. However, autopsies on humans have revealed only evidence of infection, notably in the brain, heart, and skeletal muscle.
WHO Classification and Disgrace
ME has been included in the classification of the World Health Organization (WHO) as a disease of the central nervous system since 1969.
In the ICD-10, ME is the only disorder listed in the tabular classification under G93.3, Post-viral fatigue syndrome (PVFS).
Despite the increasing prevalence of non-epidemic cases, the disorder was soon dismissed by some as mass hysteria due to the 1970 McEvedy and Beard speculative research, in which no patients were examined. Interest dropped, to be rekindled only after a similar outbreak at Incline Village, Lake Tahoe, Nevada in the mid-1980s.
In 1987, researchers from the Centers for Disease Control & Prevention (CDC) assumed that the cases they observed during the mid 1980s were not ME, and therefore attached a different name to the phenomenon: Chronic Fatigue Syndrome (CFS). The criteria are broader than those for ME and the assumption that the two disorders are identical requires testing.
The Centers for Disease Control & Prevention published a first working case definition for CFS in 1988,. In 1993 the term Chronic fatigue syndrome (CFS) was added to the alphabetic list of the WHO ICD classification.
Villified but Vindicated
Research increased, more so after the criteria were relaxed in 1994, but was criticised for over-inclusiveness. With all objective signs now expunged, the obvious possibility of misdiagnosis bedevilled clinical and research work. Lacking a diagnostic laboratory test of any kind, CFS has frequently been misdiagnosed, for example, in patients presenting CFS symptoms with similar biological conditions or infections (such as Lyme disease or Epstein-Barr, the latter of which is often the cause of glandular fever, or infectious mononucleosis), or psychological conditions (ranging from depression to hypochondria).
A lack of information and awareness has led to many patients being stigmatised, sometimes as hypochondriacs or lazy, yet at other times as over-active and perfectionistic. Because immune-related symptoms are common in ME patients, their immune system was suspected to be dysfunctional, or responding inappropriately to specific viruses; this lead to the proposal of the alternative name “chronic fatigue immune dysfunction syndrome” (CFIDS).
Researchers in a study of patient perspectives have argued that the earlier failure of Western medicine to demonstrate a viral etiology for ME led to a paradigmatic shift to psychiatric and sociocultural research, which effectively delegitimized ME and later CFS as a biomedical phenomenon. More accurate criteria should help to increase homogeneity and identify pathology. It has also been noted that some journals operate pro-psychiatric editorial policies, resulting in a narrow range of opinions and undermining the physicians’ understanding of the illness. A major recurrent criticism of CFS is that it does not make post-exertional malaise or muscle weakness an essential criteria thus leading to the uncertainty and controversy over the appropriatness of physical rehabilitation programmes.
Recent research on CFS may be relevant to ME. For example, studies have revealed pathologically delayed recovery of muscle strength, cardiac and vascular abnormalities, and defects in cellular metabolism. Neurocognitive dysfunction has been objectively observed; and physiological abnormalities relating to immune activity, gene expression, oxidative stress and the nervous system have also been found, plus many psychological and psychiatric studies have also been done. The U.S. Centers for Disease Control & Prevention (CDC) now recognize CFS as a serious illness, but also list ME as a differential diagnosis on their web site, reflecting the incompatibility of the traditional definitions.
The CFS definition allowed sufficient laxity for US specialists, including those who had preceded the CDC at Lake Tahoe, to customize the definition for those patients they thought most representative of ME.
In 2003 a group of international specialists published the consensus definition of an illness now termed “ME/CFS,” the criteria of which, including CNS and exertional signs, was more like that of ME than CFS. In January 2007 The American “CFS Name Change Advisory Board” publicized their deliberation that CFS should now be called ME, though no statement was made on definition. The CDC continue to widen their CFS definition.
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- Gilliam AG. (1938) Epidemiological Study on an Epidemic, Diagnosed as Poliomyelitis, Occurring among the Personnel of Los Angeles County General Hospital during the Summer of 1934, United States Treasury Department Public Health Service Public Health Bulletin, No. 240, pp. 1-90. Washington, DC, Government Printing Office.
- Jason LA, Helgerson J, Torres-Harding SR, Carrico AW, Taylor RR (2003). “Variability in diagnostic criteria for chronic fatigue syndrome may result in substantial differences in patterns of symptoms and disability.”. Eval Health Prof 26 (1): 3-22. PMID 12629919.
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- A Hummingbird’s Guide
- Memorial List
- Dr Cheney on cardiac involvement
- The HHV-6 Foundation
- United Mitochondrial Disease Foundation
- National Gulf War Resources Center (US)