What is M.E.?

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. In search engine popularity, it was second only to the very factually-deluded Chronic Fatigue Syndrome Wikipedia page. I personally have no idea why the site is no longer available, but since the information was collected from reputable sources and donated by fellow people with ME, I thought it would be appropriate to scout down an old cache of the page and post it here so our efforts wouldn’t disappear entirely.
There was no existing data for “comorbid conditions” or “severity,” which is why those sections appear to be missing, but in the Severity section I’ve added a list of resources for those with severe myalgic encephalomyelitis. The last version of the original page was updated sometime in 2009, so developments such as the introduction of the International Consensus Criteria of 2011, or the introduction of SEID in 2015, were not referenced.
This page is popular, so if you’d like to help by contributing a reference-based update on anything important that has happened since 2009, please contact me. Update: The new global activist movement #MEAction has chosen to use the following information as the template for its MEpedia page on Myalgic Encephalomyelitis, so desires to add edits should be directed there. (For the time being I still recommend this version, because all click-through links and references were removed in the process of creating the template, which is still in progress.)
The information I’ve contributed is highlighted in maroon, and points that I believe to be of particular importance have been bolded.

Myalgic Encephalomyelitis (ME)

from Disapedia.com

Myalgic Encephalomyelitis (abbreviated ME) is a chronic, inflammatory, post-viral, primarily neurological disease that is multisystemic, i.e. affecting the central nervous system (CNS), immune system, cardiovascular system, endocrinological system, and musculoskeletal 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 fatiguability, 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 (1).

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, United States, and New Zealand while symptoms persist.

Myalgic encephalomyelitis is usually 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. A consistently-progressive form is possible, although rare.

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 (-itis) of the brain (encephalo-) and spinal cord (myel-). accompanied by muscle pain (myalgic).

See more in History.

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 (1). 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 verbalization (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.

Differential Diagnosis

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.

See symptom comparison lists of some of the illnesses most commonly misdiagnosed.

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 (3).

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 heterogeneous 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.

Kerr et al proposed 7 different subsets for “CFS” as it is defined today (4):

  • Subtype 1 * This is one of the more severe subtypes. Effects are cognitive, musculoskeletal, sleep-related and anxiety/depression.
  • Subtype 2 * This is one of the more severe subtypes. Effects are musculoskeletal, pain and anxiety/depression.
  • Subtype 3 * This subtype has the mildest symptoms.
  • Subtype 4 * This subtype is dominated by cognitive issues.
  • Subtype 5 * Effects are musculoskeletal and gastrointestinal.
  • Subtype 6 * This subtype is dominated by post-exertional malaise (extreme crash after exercise or exertion.)
  • Subtype 7 * This is one of the more severe subtypes. Effects are pain, infections, musculoskeletal, sleep-related, neurological, gastrointestinal, neurocognitive and anxiety/depression.


Resources for Severe Myalgic Encephalomyelitis

Factors triggering a relapse

ME relapses are often a result of over-activity, 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 postpartum 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 co-morbid 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 led 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 led 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 Coxsackie-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 Chlamydophila pneumoniae. Protein findings relating to several infections have seen found in the oligoclonal bands ME patients. Research has shown that, much like the relationship between HIV and 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, and reducing relapses.

Mitochondrial cocktail

  • Acetyl-L-carnitine
  • Coenzyme q-10
  • D-ribose
  • Magnesium


  • L-glutathione

Disease-modifying treatments (in trial):.

  • Ampligen
  • Imunovir
  • Valcyte


  • Pacing
  • Switching
  • Avoiding relapse triggers
  • Maintaining good hydration
  • Dietary modification


  • Neurontin (pain control and neuroprotection)
  • EPA fatty acid
  • Saline infusions
  • Midodrine


The prognosis (the expected future course of the disease) for a person with myalgic encephalomyelitis depends on severity; chronicity of the disease; initial symptoms; 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.

Currently, there are no clinically established laboratory investigations available that can predict prognosis or response to treatment.


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. M.E. outbreaks are still happening even though the epidemics are no longer being recorded or studied. Cort Johnson wrote that Dr. Byron Hyde mentioned having “reports of over sixty” M.E. outbreaks from just 1988 to 2003, which were “no longer figured in the literature” and “were not given any mention in the [International Consensus Criteria].” Epidemics have a penchant for enclosed communities such as schools and hospitals, although not all of the outbreaks have occurred in enclosed communities.

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

See first: The Parts of M.E.: How did we get here?

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 liability 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 review, in which no actual patients were examined: “…Epidemic hysteria is a much more likely explanation” (2). Interest dropped, to be rekindled only after a similar outbreak at Incline Village, Lake Tahoe, Nevada in the mid-1980s.

CDC Intervention

In 1987, researchers from the US Centers for Disease Control & Prevention (CDC) decided to treat the Lake Tahoe outbreak of M.E. as well as other M.E. outbreaks from the mid-1980s as an entirely new illness, yet another decision based on a complete lack of patient examination. It was only after the doctors managing the epidemics used over $200,000 of their own money to fund MRIs, that they found their patients had brain lesions indistinguishable from those found in people with AIDS.

Nonetheless, these findings were dismissed because they were not present in all patients, and in 1988 the CDC christened the illness chronic fatigue syndrome (CFS) instead of M.E., effectively because three M.E. experts left the committee meeting early due to (1) a lack of patient information and (2) the remaining members’ preoccupation with Epstein-Barr Virus, which was biologically incapable of causing the outbreaks due to the virus’s extensive latency period. CFS is a highly contentious concept to patients and specialists alike. Because of the similarity in terminology, CFS is often confused with “chronic fatigue”; many believe this to have been intentional for the benefit of disability insurance companies (Osler’s Web, Hillary Johnson, pp 217 – 219).

In 1993 the term Chronic fatigue syndrome (CFS) was added to the alphabetic list of the WHO ICD classification under R53.82 “Symptoms, signs and abnormal clinical and laboratory findings, not elsewhere classified.”

Although neither chronic fatigue syndrome nor its criteria were developed to replace myalgic encephalomyelitis, many, particularly in the psychiatry field, falsely promoted that ME was synonymous with CFS. The first CFS criteria published in 1988 by Holmes (5) were in fact created as to provide a rational basis for evaluating patients who have chronic fatigue of undetermined cause.

Vilified but Vindicated

Research increased after the CFS criteria were further relaxed in 1994, but it was criticized for its over-inclusiveness. With all objective signs now expunged, the obvious possibility of misdiagnosis bedeviled clinical and research work. Lacking a diagnostic laboratory test of any kind, CFS is frequently misdiagnosed in patients presenting symptoms to other similar biological conditions, infections such as Lyme disease (for which standard testing produces an extremely high rate of false-negatives) or Epstein-Barr (the cause of glandular fever/infectious mononucleosis), or psychological conditions.

A lack of information and awareness has led to both ME and CFS patients being stigmatized, sometimes as hypochondriacs or lazy, yet at other times as over-active and perfectionist. Because immune-related symptoms are common, the immune system was suspected of being dysfunctional or responding inappropriately to specific viruses, leading to the proposal of the alternative name, “chronic fatigue and immune dysfunction syndrome” (CFIDS).

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 appropriateness of physical rehabilitation programmes.

ME Redux

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 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 [listed] ME as a differential diagnosis on their website [until 2011], reflecting the incompatibility of the traditional definitions by stating the following

“Various terms are often used interchangeably with CFS. CFS is the preferred term because it has an internationally accepted case definition that is used in research and clinical settings. The name chronic fatigue and immune dysfunction syndrome (CFIDS) was introduced soon after CFS was defined; there is no case definition for CFIDS, and the name implies an understanding about the pathophysiology of CFS that does not currently exist. Chronic active Epstein-Barr virus (EBV) infection (chronic mononucleosis) was thought to be the cause of CFS during the 1980s, and this association is now known to be rare. However, post-infection fatigue syndromes have been associated with EBV and other infectious agents. The name myalgic encephalomyelitis (ME) was coined in the 1950s to clarify well-documented outbreaks of disease; however, ME is accompanied by neurologic and muscular signs and has a case definition distinct from that of CFS” (Centers for Disease Control and Prevention).

Patients and specialists alike have 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–several of whom were present in the 1980s outbreaks–agreed that “CFS downplays the severity of the disease and is hurtful to patients” and publicized their deliberation that CFS should now be termed ME. However, no statement was made on definition, and considering the slew of misdiagnosed individuals accrued within the “CFS” umbrella since 1988, other doctors, researchers, and ME experts insist that the CFS illness described by the CDC and Oxford Criteria in the UK, no longer represents ME. There are historical reasons for choosing myalgic encephalomyelitis as the name, however the acute post-viral onset, brain inflammation, neurological damage, and extremely specific pattern of muscle fatigue inherent in ME are not a required part of any CFS diagnosis. Multiple studies from Jason et al. show most people with a CFS diagnosis do not have myalgic encephalomyelitis. 

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. However, there is no ICD code for “ME/CFS” or “CFS/ME.” Although M.E. remains under ICD G93.3 as “benign myalgic encephalomyelitis,” Professor Malcolm Hooper (6) explains: “The word ‘benign’ was used because it was thought at the time that the disorder was not fatal (as poliomyelitis could be, with which it had some similarity), but it was quickly realised by clinicians that ME was not a benign condition, as it has such high morbidity… By 1988 clinicians had stopped using the word ‘benign’ and referred to it as ME, the first to do so being Dr. Melvin Ramsay.” 

The ICD-10-CM officially states that M.E. and CFS are two separate entities, each mutually exclusive of the other. M.E. is listed as subset of G93.3 Postviral Fatigue Syndrome under Diseases of the nervous system, while CFS is listed under R53.82 as a subset of Malaise and fatigue. Both entities have “a type 1 exclusion” listed for the other, which is “used when two conditions cannot occur together.” The World Health Organization’s International Classification of Diseases (ICD) page for M.E. explicitly states R53.82 Chronic Fatigue Syndrome as a type 1 exclusion that “should never be used at the same time as G93.3. A type 1 excludes note is used when two conditions cannot occur together.”

M.E. vs CFS Resources

ME CFS SEID criteria-only

Note: Because of thirty years of confusion, some information labeled under CFS may be relevant to M.E., since some researchers use additional characteristics to select for different subsets of patients; for example, selecting the most severely affected (which through no coincidence tend to be those with M.E., often due to years of being told to exercise when this leads to disease progression and premature death), those with an acute viral onset, and those who met diagnostic criteria which required muscle fatigue on exertion. Likewise, not all information labelled “M.E.” is actually referring to the specific disease of myalgic encephalomyelitis, and may only be borrowing the name while in fact the data therein describe general CFS or “ME/CFS.”



  1. Ramsay, A. (1988). Myalgic encephalomyelitis and postviral fatigue states: The saga of Royal Free Disease. (2nd ed.). London: Gower Medical Publishing.
  2. McEvedy, C. P., & Beard, A. W. (1970). Royal Free Epidemic of 1955: A Reconsideration. British Medical Journal, 1(5687), 7–11. PMCID: PMC1700894
  3. Hyde, B. (1992). The Clinical and scientific basis of myalgic encephalomyelitis/chronic fatigue syndrome. Ogdensburg, N.Y.: Nightingale Research Foundation.
  4. Kerr, J., Burke, B., Petty, R., Gough, J., Fear, D., Mattey, D., … Nutt, D. (2007). Seven genomic subtypes of chronic fatigue syndrome/myalgic encephalomyelitis: A detailed analysis of gene networks and clinical phenotypes. Journal of Clinical Pathology, 730-739.
  5. Holmes, G. (1988). Chronic Fatigue Syndrome: A Working Case Definition. Annals of Internal Medicine, 387-387.
  6. The Terminology of ME & CFS by Professor Malcolm Hooper
  • Wallis AL, “An investigation into an unusual illness seen in Epidemic and Sporadic Form in a General Practice in Cumberland in 1955 and subsequent years”, M.D. Thesis, Edinburgh University, 1957.
  • Acheson E (1959). “The clinical syndrome variously called benign myalgic encephalomyelitis, Iceland disease and epidemic neuromyasthenia.”. Am J Med 26 (4): 569-95. PMID 13637100.
  • Goldstein JE, Hyde BM (1992). The Clinical and scientific basis of myalgic encephalomyelitis/chronic fatigue syndrome. Ogdensburg, N.Y: Nightingale Research Foundation, 628-633. ISBN 0-9695662-0-4.
  • Carruthers BM, Jain AK, De Meirleir KL, Peterson DL, Klimas MD, Lerner AM, Bested AC, Flor-Henry P, Joshi P, Powles ACP, Sherkey JA, van de Sande MI (2003). “Myalgic encephalomyelitis/chronic fatigue syndrome: Clinical working definition, diagnstic and treatment protocols”. Journal of Chronic Fatigue Syndrome 11 (1): 7-36. DOI:10.1300/J092v11n01_02.
  • 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.
  • Jason, LA, et al., “Chronic Fatigue Syndrome: The Need for Subtypes.” Neuropsychology Review, Vol. 15, No. 1, March 2005, pp. 29-58 [PDF Format]
  • Crowhurst G, “Supporting people with severe myalgic encephalomyelitis.” Nursing Standard. 19, 21, 38-43. 2005
  • Goudsmit E, Stouten B, Howes S, Illness Intrusiveness in Myalgic Encephalomyelitis An exploratory study [1]

External links & Organizations


10 thoughts on “What is M.E.?

  1. Rainbow at night,

    I just wanted to pass along a few words of support. I read parts of your blog (sorry not all of it) and felt the need to let you know how loved you are by Jesus. It seems you may have had some bad experiences with folks who may or may not have been Christians? I myself have Lymes,Bartonella, Babesia, and more issues going on that complicate treatments. My desire is to encourage you to really spend time in the Gospels (Mathew,Mark, Luke, and John) and to truly ask Jesus to reveal himself to you in a powerful way. He loves you more than you can comprehend. I pray that Jesus himself will reveal his love for you in such a way that you will not only trust him with your eternal life but also trust him to heal and take care of you during this difficult time in your life. Jesus has wonderful plans for you, plans to give you a hope and a future. Plans to use what he does in your life to glorify his name and to bring others to the knowledge of his saving grace.

    Sometimes folks think Christianity is judgmental, and maybe sometimes it may have been presented that way. One thing to realize though, the Kingdom of God does have rules, just like your parents house may have had rules when you were growing up. The rules against sin are not to punish us. You see, sin separates us from God. God does not want to be separated from us, he wants to have an intimate relationship with him, where we cast all our anxieties and worries on him. He loves us so much!!!!! Jesus came that we have life more abundantly, he is faithful and will forgive our sins if we turn from them. All of us have sinned and fallen short of his will, that is why he died. He died to take away our sins so that we can have eternal life with him.

    Lord bless you!!

    JCB-a follower of Jesus


    1. Hi JCB,

      Thank you for taking the time to write and wish me well. God HAS revealed Himself to me in the most powerful way, and I’m sorry if it scares you that I can be full of Love, Peace, Joy, and Compassion, without any influence of Jesus; I know your religion doesn’t teach that this is possible without Jesus, and I’m sorry. To use an analogy from a film I recently saw, if someone stood up and said “we should only get our nutrition from pudding!” then another person stood up and said, “No! We should only get our nutrition from potatoes!” we would know clearly that this was wrong. It’s the same for religion.

      I am a Universalist which means I believe all of our spiritual practices, with their many names and ways of connecting to our divinity, are directing us toward the same place, whether you call it God (I do), The Universe, The Source of All, etc. This is a beautiful earth with endless paths to help us find our way back to the soul within us. It doesn’t make any sense for any one religion to claim it is the only way.

      Our God has nothing BUT Love for me, just as He does for you–God IS Love, to me. The origin of all our collective positive energies. He has given me peace NOW, joy NOW, and through following what the Universe has planned for me, I have had more amazing experiences in the past year than possibly all of my life. And I will continue to have them because what God has for me, it is for me, and nothing can change that.

      I would hope people who have read my blog at all in the past year would pay attention and see what is possible when you follow your intuition, live for the present moment, and not view illnesses or death as punishments, because they aren’t. “Culturally and religiously, all of us are heir to the idea that you die as a consequence of disobedience, and in that sense, it’s a punishment.” (Stephen Jenkinson, grief counselor. Film, “Griefwalker”) We need to wake up to how we’ve been taught to view sickness and death. You didn’t do anything wrong, JCB. You don’t need to strive to be “okay one day” because you already are. Sickness and death are part of everyone’s life, at some point; all things will die and move on to their next journey, and it will not be a punishment. You, too, will die, and it will be the natural process of Life, not an absence of God’s love and protection. I believe, as I think you do, also, that our souls will return to our place of origin. You are going to be okay.

      Wishing you Peace,



  2. Kit,

    Thanks for your kind words. I respect you views and opinions. I guess what I am hoping for is that you do not close yourself off from Jesus because of some bad experiences. We humans sometimes do a poor job showing his love to others. His love for us truly cannot be measured. Just because we do not agree on spiritual matters at this time does not mean we cannot love each other. It seems from your words that you agree with this statement.

    In Christs love,



  3. This article is really fascinating to me. There are many similarities to MS, and not just the broad and obvious (vitamin D deficiency, CNS inflammation and deterioration, etc). A section I noticed was regarding HHV-6 and -7 as being possible causes or triggers. I recently read an article stating basically the same thing about MS, and people with MS are often prone to shingles outbreaks even though many people with MS, particularly those who have Relapsing-Remitting and are still relatively healthy and high functioning, are not immune compromised. I had my first shingles outbreak when I was 25 or 26, long before my MS diagnosis. So the idea of viruses in the system being complicit in these disorders (particularly, I have to point out, viruses that are stored in the friggin spine!) seems like something the medical community should follow up on a bit more. :p
    It’s a bit sickening how often misunderstood and invisible disorders are immediately socked away under a mental health label. Of course it’s almost always done by people who aren’t actually mental health professionals, too. Doctors seem to think that psychology and psychiatry are just simple follow ups to physical medicine, and while my GP has told me outright that she won’t treat my MS because she doesn’t know enough about it, she has no problem treating my mother’s depression.
    There is widespread discrimination against people with mental health diagnoses, and since these other disorders (MS, ME, and similar such) so strongly affect the CNS they often cause all manner of mood or behavioral issues that aren’t necessarily psychiatric, but likely were the first thing a person noticed, like lack of interest in activities that they enjoy, or irritability, or even just the fatigue, which has now moved over from being a medical issue to a psychological issue. Once a person is openly being treated for a psych issue (and we shouldn’t have to hide it, honestly, this isn’t the dark ages), Drs often just assume all further complaints can be attributed to that. I had been experiencing intermittent loss of motor control in my entire right side, but since I was being treated for depression I was told it was psychosomatic! Unbelievable. It took them finding lesions in my brain to take me seriously. I guess they were psychosomatic lesions, too. :p
    There’s actually an article about it if you’re interested. http://mobile.nytimes.com/2013/08/11/opinion/sunday/when-doctors-discriminate.html?pagewanted=all&_r=0
    Also, I seriously love the conversation in the comments section here. <3


    1. There are a LOT of similarities between M.E. and MS–there’s even a list, here, to showcase it even more.

      I can understand that completely! I was actively dying from (a host of things, really, but mainly) an infection of bartonella that had spread to my brain and heart, and the first neurologist I saw told me to take 100mg of Zoloft because it was just stress-induced. The scary thing? This man SAW that I had brain lesions, didn’t even tell me, and still only recommended psychiatric treatment! I didn’t find out until two years later when I ended up in the hospital for a week, had another brain scan, and found out my last TWO scans (the first of which was done by that “neurologist”) had evidence of a significant lesion on my pons. Honestly, the lesion location coupled with my extensive symptom presentation would have been enough for a diagnosis of MS (which the hospital put as a differential diagnosis, were my symptoms not found to be related to my current predicament), so not only did he miss a chance to further investigate me for a WELL KNOWN neurological disease for which I had all of the presentation requirements, but because he didn’t even do THAT he missed the severe disease that was actually killing me. All because he thought it was stress.

      I usually have a lot of compassion for doctors, but this fellow has been well known for doing this–he has a 1 out of 5 star rating on every site, and the only reason he’s been able to stick around is due to being the only neurologist in my city for over a decade. If your negligence reaches the point that it PROMOTES suffering in 80% of the people that see you, you need to stop what you’re doing.

      So there’s my similar story! Thank you for your words, and the link. I’ll be keeping up with your blog, and after I finish my next post (should be within the day, or tomorrow), I really want to comment on your recent post about grief and chronic illness! I already shared it to Twitter! ♥



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