Myalgic encephalomyelitis

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Myalgic Encephalomyelitis (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.[1][2] It has been classified by the World Health Organization (WHO) as a neurological disease since 1969.[3][4] An M.E. Support article The Symptoms of Myalgic Encephalomyelitis covers cardinal symptoms, secondary features, and characterized symptoms.

A hallmark symptom of ME, Post-exertional malaise, is intolerance to previously trivial effort such as walking to the mailbox, running an errand or grocery shopping, taking a shower or brushing teeth, and deterioration of health from persistent or repeated exertion.[5][6][7][8][9][10][11] Myalgic encephalomyelitis is usually a relapsing-remitting disease with new symptoms occurring either in discrete relapses (or “crashes”) or accruing over time.[12] The National Organization for Rare Disorders (NORD) states: "Symptoms and their severity can fluctuate over the course of the illness, even from hour to hour."[13] The US National Institutes of Health notes that sensitivity to noise, light and chemicals may force patients to withdraw from society.[14]

ME does not have a cure, though treatments including the antiviral Ampligen (now approved for use on ME/CFS patients in Argentina) and immune system modulator Rituximab are being trialled.[15] There is a progressive form of ME but it is rarer than the relapsing-remitting type.[16]

A CFS/ME Norwegian study shows the disease affects all ages, with two peak ages of 10-19 years and 30-39 years; it is more common in women than in men.[17] Research by the Open Medicine Foundation cited in its paper, Metabolic features of chronic fatigue syndrome which studied severe CFS, found that the disease is different in men and women but this is not related to testosterone or estrogen. Michael VanElzakker notes there are male and female differences in neuropathic pain. A study of UK and Dutch co-horts found "younger children had a more equal gender balance compared to adolescents and adults."[18]

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 and with a "high attack rate in females compared with males".[19] The BPS model is being applied to ME, CFS and PVFS by psychiatrists in the UK. However, Dr. VanElzakker said, “Everyone here [at Harvard] recognizes that it’s a neuroimmune condition and approaches it that way.”[20]

ME and CFS patients are barred from donating blood or organs in the United Kingdom, United States and New Zealand while symptoms persist.[21][22][23][24]

Name describes disease[edit | edit source]

The name Myalgic Encephalomyelitis describes the disease: Myalgic (muscle pain), Encephalo (brain), myel (spinal cord), itis (inflammation).[25] The patient has muscle pain and the brain and spinal cord are inflamed.

Dr. Melvin Ramsay used the term ME[26] which is now proving accurate due to brain fMRI's that detail the brain inflammation. The NY Times article Brains of People With Chronic Fatigue Syndrome Offer Clues About Disorder by David Tuller has images of a patient diagnosed with ME/CFS that clearly show brain inflammation. Other brain imaging research has been completed. Dr. VanElzakker proposed the Vagus nerve infection hypothesis in which he hypothesizes a Vagus nerve infection causing symptoms of ME/CFS.[27]

A survey by The MEAction Network in 2016 found patients much preferred the name myalgic encephalomyelitis to other names including Chronic Fatigue Syndrome.[28]

Signs and symptoms[edit | edit source]

Over-exertion can make ME worse and the effects are often delayed and may not be seen within 24 hours.[29] [30]

Invest in ME outlines ME symptoms and notes symptoms can range from mild to very severe and can include:

Post-exertional malaise[edit | edit source]

A core symptom, Post-exertional malaise, is used in diagnosing ME, CFS, ME/CFS and SEID.

Diagnosis[edit | edit source]

The International Consensus Criteria (ICC) is thought to be the best tool for diagnosing ME while the Canadian Consensus Criteria (CCC) diagnoses both ME and Chronic Fatigue Syndrome (CFS) and is an ME/CFS diagnostic tool.

The original criteria developed by Melvin Ramsay, the Ramsay definition, is not used for diagnosing ME today.

Other diagnostic criteria[edit | edit source]

The UK Oxford criteria (the US Institute of Medicine report has called for its retirement)[31] and the US CDC Fukuda criteria (used in some research worldwide) are not describing ME but instead describe chronic fatigue (CF). CF should not be confused with CFS. Many patients and ME organizations believe CFS must not be confused with ME nor its diagnostic criteria used to describe, diagnose or research ME.

Differential diagnosis[edit | edit source]

The signs and symptoms of ME can be similar to other medical problems, "such as cancer, multiple sclerosis, lupus, brucellosis, or another condition."[32] Additional testing may be needed to help distinguish ME from these other problems.

Disease course and clinical subtypes[edit | edit source]

Primary Phase

"The first phase is an epidemic or endemic (sporadic) infectious disease generally with an incubation period of 4 to 7 days; in most, but not all cases, an infection or infectious process is evident."[33]

Secondary Chronic Phase

"The second and chronic phase follows closely on the first phase, usually within two to seven days; it is characterized by a measurable diffuse change in the function of the Central Nervous System. This second phase is the persisting disease that most characterizes M.E."[34]


"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 recognize 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."[35] For some people, ME is triggered by Hepatitis B vaccination [36], blood transfusion[37], or chemical poisoning[38][39] (See: Countess of Mar), although it is now thought organophosphate poisoning is a different illness.[40][41]

Later course

"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."[42]


"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."[43]

Subtypes proposed[edit | edit source]

Kerr et al proposed 7 different subsets for “CFS” as it is defined today:[44]

  • 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.

Severity[edit | edit source]

Factors triggering a relapse[edit | edit source]

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.

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.

Pathophysiology[edit | edit source]

Although much is known about abnormalities in ME., the reasons why they occur are not known. There are two ME. conferences held in the UK each year attended by international research luminaries, and other conferences held worldwide.

ME 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 behavior 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, and 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 cardiologic 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.

Causes[edit | edit source]

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.[45][46][47][48] 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.[49][50] 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.[51] 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.[52][53]

Viral cause[edit | edit source]

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[54][55] [56] suggests a potential viral contribution in at least some individuals. Others believe 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.[57] Protein findings relating to several infections have seen found in the oligoclonal bands ME patients.[58]

The Vagus nerve infection hypothesis accounts for why so many different viral onsets could be responsible. The Vagus nerve runs from the brain stem and throughout the body and has an impact on many body systems.

Treatments[edit | edit source]

There is no known cure for ME. Treatments for sleep problems, headaches and pain are utilized by some doctors for some patients although these are treating symptoms and not ME itself. Success of treating symptoms of ME is not well researched or documented.

Ampligen (Approved for ME/CFS in Argentina) and Rituximab are being trialled.

Epidemiology[edit | edit source]

ME has been found world-wide, in at least 63 epidemics documented in published papers from the 1930s to the 1980s.[59] (See: List of myalgic encephalomyelitis and chronic fatigue syndrome outbreaks.) Epidemics often occur in enclosed communities such as schools and hospitals.

As observed in many autoimmune disorders, ME is more common in females than males; the mean sex ratio is approxmately 2-3 females for every male.[60] In children the sex ratio is approximately equal.[61]

Learn more[edit | edit source]

References[edit | edit source]

  1. Myalgic Encephalomyelitis - NORD
  2. Myalgic Encephalomyelitis (ME) and Chronic Fatigue Syndrome (CFS) Medical Abnormalities Research Citations Compiled by Lisa Petrison, Ph.D.Updated April 4, 2016 - PDF
  3. History of chronic fatigue syndrome - International Classifications
  4. The Terminology of ME & CFS By Professor Malcolm Hooper - PDF
  5. ME/CFS - Pathways to Prevention - NIH
  6. Research Descriptions of M.E. - ME Action UK
  7. The Clinical Features of Myalgic Encephalomyelitis Melvin Ramsay, M.D., 1986
  8. What Is Post-exertional Malaise - Very Well - Adrienne Dellwo
  9. Post Exertional Malaise - Very Well - Adrienne Dellwo
  10. Chronic Fatigue Syndrome - Web MD
  11. PEM Series - Solve ME/CFS - Jenny Spotila
  12. Postexertion 'Crash,' not Fatigue per se, Marks Syndrome - MedScape
  13. Myalgic Encephalomyelitis - NORD
  14. ME/CFS - Pathways to Prevention - Advancing the Research on Myalgic encephalomyelitis/Chronic Fatigue Syndrome
  15. Chronic Fatigue Syndrome & Myalgic Encephalomyelitis Experimental Treatments - ProHealth (Ampligen and Rituximab Tabs
  16. Progressive Myalgic Encephalomyelitis (ME) or A New Disease? A Case Report
  17. Two age peaks in the incidence of chronic fatigue syndrome/myalgic encephalomyelitis: a population-based registry study from Norway 2008-2012 - BMC Medicine
  18. Chronic fatigue syndrome (CFS) or myalgic encephalomyelitis (ME) is different in children compared to in adults: a study of UK and Dutch clinical cohorts. BMJ Open - PubMed
  19. Royal Free Epidemic of 1955: A Reconsideration - McEvedy and Beard - NCBI NLM NIH - PMC
  20. Dr VanElzakker: two new ME/CFS studies at Harvard - Jaime S - MEAction
  21. People with ME/CFS to be permanently excluded from giving blood in the UK from 1 November this year – Department of Health announcement - ME Association
  22. American Red Cross Statement on XMRV and Chronic Fatigue Syndrome - American Red Cross
  23. Chronic fatigue patients barred from blood donation - Washington Post - By: Rob Stein - Dec 3, 2010
  24. - NZBlood
  25. The Terminology of ME & CFS By Professor Malcolm Hooper
  26. The Terminology of ME & CFS By Professor Malcolm Hooper
  27. Dr VanElzakker: two new ME/CFS studies at Harvard - Jaime S. - MEAction
  28. MEAction RFI Poll Report (Part 1 of 3)
  29. What is ME - Invest in ME Research
  30. Myalgic Encephalomyelitis - NORD
  31. US NIH Report Calls for UK Definition of ME/CFS to be Scrapped
  32. Dartmouth Hitchock - Myalgic Encephalomyelitis National Organization for Rare Disorders, Inc.
  33. ME Definition - Nightingale - PDF pg. 6
  34. ME Definition - Nightingale - PDF pg. 6
  35. What Is ME? - Disease course and clinical subtypes - A rainbow at night
  36. ME Association Survey Report, 2010
  37. Can Blood Transfusions Cause ME/CFS? - Massachusetts CFIDS/ME & FM Association
  38. Tired or Toxic? Chronic Fatigue Syndrome and Environmental Toxicity - Michael A. Schmidt - ProHealth
  39. Toxic causes of CFS - the more I ask, the more I find! - Dr.
  40. Chronic exposure to organophosphates: background and clinical picture - Robert Davies, Ghouse Ahmed & Tegwedd Freer
  41. What Is ME? - Disease course and clinical subtypes - A rainbow at night
  42. What Is ME? - Disease course and clinical subtypes - A rainbow at night
  43. What Is ME? - Disease course and clinical subtypes - A rainbow at night
  44. Seven genomic subtypes of chronic fatigue syndrome/myalgic encephalomyelitis: a detailed analysis of gene networks and clinical phenotypes - JCP Online
  45. Onset Patterns of Chronic Fatigue Syndrome and Myalgic Encephalomyelitis: A Mixed Method Approach - Meredyth Evans - DePaul University
  46. Vagus nerve infection hypothesis - MEpedia
  47. Chronic Fatigue Syndrome - Cleveland Clinic
  48. Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is associated with pandemic influenza infection, but not with an adjuvanted pandemic influenza vaccine. - PubMed
  49. Myalgic encephalomyelitis, chronic fatigue syndrome: An infectious disease. Myalgic encephalomyelitis, chronic fatigue syndrome: An infectious disease. RA Underhill - PubMed
  50. Genome-wide association analysis identifies genetic variations in subjects with myalgic encephalomyelitis/chronic fatigue syndrome
  51. Klimas ME/CFS Genes Study - Face Book - Video
  52. Cytokine expression provides clues to the pathophysiology of Gulf War illness and myalgic encephalomyelitis - ScienceDirect
  53. Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and the Potential Role of T Cells - Biological Markers and Guided Therapy, Vol. 1, 2014, no. 1, 25 -38 - PDF
  54. Coxsackie B viruses and myalgic encephalomyelitis.
  55. Ramsay Research Team 5 – The Potential Role of HHV-6 in ME/CFS
  56. Association of active human herpesvirus-6, -7 and parvovirus b19 infection with clinical outcomes in patients with myalgic encephalomyelitis/chronic fatigue syndrome.
  57. Chlamydia Pneumoniae - Stanford Myalgic Encephalomyelitis/Chronic Fatigue syndrome Initiative
  58. CSF Oligoclonal Banding - NY Times
  59. Myalgic Encephalomyelitis: The medical facts - What causes Myalgic Encephalomyelitis? Are there outbreaks of M.E.?
  60. Two age peaks in the incidence of chronic fatigue syndrome/myalgic encephalomyelitis: a population-based registry study from Norway 2008-2012 - BMC Medicine
  61. Chronic fatigue syndrome (CFS) or myalgic encephalomyelitis (ME) is different in children compared to in adults: a study of UK and Dutch clinical cohorts. BMJ Open - PubMed

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From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history