Wikisage, the free encyclopedia of the second generation, is digital heritage

Myalgic encephalomyelitis

From Wikisage
(Redirected from ME)
Jump to navigation Jump to search
Disease classification WHO
G93.3 Postviral fatigue syndrome
Benign myalgic encephalomyelitis

Myalgic encephalomyelitis (ME) is a neurological disorder of the central nervous system (CNS), classified as a post-viral fatigue syndrome (ICD10 code: G93.3) by the World Health Organization (WHO). The name indicates inflammation of the brain and/or spinal cord accompanied by myalgia (muscle pain). The disease affects multiple bodily systems, including the immune, cardiovascular, neuroendocrine and metabolic.[1]

ME is an endemic disease which is subject to periodic epidemics.[2] While the prognosis is poor, recorded fatalities are relatively rare.

Patients experience a multitude of functional problems, such as exercise intolerance, orthostatic intolerance, chronic fatigue, muscle pain and weakness, sensory disturbances, information processing problems of the brain, concentration loss, malaise, emotional disturbances and sleep disturbances.[3]


ME is defined by the following diagnostic criteria.[4]

  1. Generalised or localised muscle fatigue after minimal exercise with prolonged recovery time.
  2. Neurological disturbance, especially of cognitive, autonomic and sensory functions, often accompanied by marked emotional lability and sleep reversal.
  3. Variable involvement of cardiac and other bodily systems.
  4. An extended relapsing course with a tendency to chronicity.
  5. Marked variability of symptoms both within and between episodes.

The CNS inflammation indicated by the name does not show on MRI scans as with multiple sclerosis, but has been observed in autopsies as was the case for Sophia Mirza. Mild chronic inflammation was found in 95% of 165 stomach biopsy specimens of patients selected by CFS criteria by Chia & Chia.[5]

The diagnostic criteria were formulated by ME researcher A. Melvin Ramsay, who had witnessed the epidemic at the Royal Free Hospital in 1955, after an extensive study of the numerous outbreaks that had been documented, as well as sporadic cases.[2]

The 2007 Nightingale Myalgic Encephalomyelitis Definition, following up on evidence given by its founder Byron Hyde to the Gibson inquiry,[6] summarizes ME thus:

  • Primary M.E. is an acute onset biphasic epidemic or endemic (sporadic) infectious disease process, where there is always a measurable and persistent diffuse vascular injury of the CNS in both the acute and chronic phases. Primary M.E. is associated with immune and other pathologies.[7]


While the pathophysiology of ME is not yet completely charted, some 75 years of research have produced a number of results. The general vision remains that, after an initial trigger (typically viral), the body stays in combat mode against reactivated viral infections, which causes inflammation that can eventually affect all organs.[1] Infections found in ME patients include various herpes and enteroviruses.[2][1]

Some indications of why the inflammation is perpetuated have been found by Suhadolnik, who by chance discovered that the enzyme RNase L, which plays a central role in destroying infected cells, is significantly fragmented, a discovery that was subsequently confirmed by other researchers,[8] and by Baraniuk, who measured errors in protein folding affecting several feedback mechanisms.[9] The RNase L fragmentation has been shown to correlate with patient dysfunction and to be useful as a marker for ME.[10]

Okada demonstrated that brain volume, specifically grey matter, is greatly reduced in ME, especially in areas that serve cognitive and autonomous functions.[11] The general outcome was confirmed by Dutch researchers.[12] It is not known yet how this relates to the vascular problems that are also consistently found on scans.[7]

Exercise intolerance has been linked to the cardiac system[13], and may be the result of mitochondrial dysfunction in the production of ATP (and therefore of kinetic energy).[14] Mitochondrial dysfunction has been found in post-infective fatigue in a population study in Australia.[15]


There is no known cure for myalgic encephalomyelitis. Treatment focuses on aspects of the disease, and may reduce individual symptoms. Some management techniques have a reputation of improving the quality of life of ME patients, but trials intended to present evidence have generally been of poor quality.[16]

Common treatments for ME are diets and supplements (incuding hormones and vitamines), physiotherapy, anti-depressants, pain killers, and complementary and alternative medicine.[17] Coping techniques for ME invariably include some kind of energy management, where striking a balance between activity and rest is prominent.[17]


The diagnosis of myalgic encephalomyelitis was introduced in 1956, identifying a number of outbreaks that had received different names in various parts of the world, including atypical poliomyelitis and epidemic neuromyasthenia, but produced the same symptoms and findings. These included signs of damage to the brain and spinal chord, protracted muscle pain with paresis and cramp, emotional disturbances and a course with relapses.[18] The oldest of the documented outbreaks occurred in Los Angeles, 1934.[19] In 1969, the WHO included ME in their classification. The name 'epidemic neuromyasthenia' remained in use for some time alongside ME, primarily in the USA.[20]

A symposium on epidemic neuromyasthenia was held at the Royal Society of Medicine in April 1978, co-chaired by Ramsay. This lead to the formation of the Study Group on the subject of Myalgic Encephalomyelitis, of which Ramsay was a member.

Chronic fatigue syndrome

Research where patients are selected with a diagnosis of ME is relatively rare outside the recorded epidemics. Since the early 1990s, commonly a simplifying working diagnosis is used to select patients, known as chronic fatigue syndrome (CFS).[21] A multitude of, sometimes significantly different, CFS definitions have been designed, but the Fukuda definition of 1994[22], based on the anecdotal experience of the members of a study group, is practiced most frequently. What they all have in common is that they score symptoms.

While intended for research purposes only, CFS criteria became used as a clinical working diagnosis as well. The new diagnosis of CFS rapidly found wide support in the USA, replacing epidemic neuromyasthenia. In Canada and some European countries, the disease entity ME remained the more popular diagnosis.[23] In research, CFS globally became the preferred way to select patients for study.

It is easier to count symptoms than to diagnose the underlying disease, but the CFS populations and patient selections may contain a significant number of patients that would not be diagnosed with ME.[24] In 2003, an attempt was made to devise a clinical working case definition that would minimize this drawback, the Canadian consensus definition of ME/CFS.[3] It compared favourably to the Fukuda definition of CFS.[25]


In the early 21st century, research on CFS produced various breakthroughs regarding the etiology and nature of myalgic encephalomyelitis. A Name Change Advisory Board of leading experts in the USA launched a campaign in January 2007 in favour of the combined term ME/CFS, maintaining CFS primarily for legal reasons.[23] Since then, researchers and their organizations like the IACFS/ME are often denoting their focus as ME/CFS or CFS/ME, as do patient organizations. Actual scientific research still commonly uses CFS patient selections, but with an interest in subgroups within the CFS populations.[26][27][28][29]

ME awareness day

In 1995, the provincial government of British Columbia awarded a petition by the ME Society of British Columbia and named May 12, the birthday of Florence Nightingale, as ME awareness day.[30] It is believed by some that Nightingale suffered from myalgic encephalomyelitis during the later part of her life,[31][32] although other diagnoses that could explain her symptoms have also been suggested.[31]

See also

External links


  1. 1.0 1.1 1.2 Hyde BM (ed.) (1992), "The Clinical and Scientific Basis of Myalgic Encephalomyelitis / Chronic Fatigue Syndrome", Nightingale Research Foundation, Ottawa, Canada with editorial and conceptual advice from Levine P and Goldstein J., 724+23p, ISBN 0-9695662-0-4
  2. 2.0 2.1 2.2 Ramsay AM (1986), "Postviral Fatigue Syndrome. The saga of Royal Free disease", London, ISBN 0-906923-96-4
  3. 3.0 3.1 Carruthers BM, Jain AK, DeMeirleir KL, Peterson DL, Klimas NG, 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 case Definition, Diagnostic and Treatment Protocols", Journal of Chronic Fatigue Syndrome, Vol. 11 (1)
  4. Ramsay AM, Dowsett EG, "Myalgic Encephalomyelitis -- Then and Now: An Epidemiological Introduction", in: Hyde (1992), chapter 4, pp. 81-84
  5. Chia JKS, Chia AY (2008), "Chronic fatigue syndrome is associated with chronic enterovirus infection of the stomach", Journal of Clinical Pathology", Jan;61(1):43-8
  6. Gibson I, e.a. (2006), "Inquiry into the status of CFS / M.E. and research into causes and treatment", Group in Scientific Research into Myalgic Encephalomyelitis (M.E.), Londen, England
  7. 7.0 7.1 Hyde BM (2007), "The Nightingale Myalgic Encephalomyelitis (M.E.) Definition", The Nightingale Research Foundation, Ottawa, Canada
  8. Suhadolnik RJ, Peterson DL, O’Brien K, Cheney PR, Herst CVT, Reichenbach NL, Kon N, Horvath SE, Iacono KT, Adelson ME, De Meirleir K, De Becker P, Charubala R, Pfleiderer W, "Biochemical evidence for a novel low molecular weight 2-5A-dependent RNase L in chronic fatigue syndrome", J Interferon Cytokine Res 17, pp. 377-385
  9. Baraniuk JN, Casado B, Maibach H, Clauw DJ, Pannell LK, Hess S (2005), "A chronic fatigue syndrome – related proteome in human cerebrospinal fluid", BMC Neurology, 5:22, PMID: 16321154
  10. Suhadolnik RJ, Peterson DL, Reichenbach NL, Roen G, Metzger M, McCahan J, O'Brien K, Welsch S, Gabriel J, Gaughan JP, McGregor NR (2004), "Clinical and Biochemical Characteristics Differentiating Chronic Fatigue Syndrome from Major Depression and Healthy Control Populations: Relation to Dysfunction and RNase L Pathway", Journal of Chronic Fatigue Syndrome, Vol. 12, Number 1, pp. 5-35
  11. Okada T, Tanaka M, Kuratsune H, Watanabe Y, Sadato N (2004), "Mechanisms underlying fatigue: a voxel-based morphometric study of chronic fatigue syndrome", BMC Neurology, Oct
  12. De Lange FP, Kalkman JS, Bleijenberg G, Hagoort P, Van der Meer JWM, Toni I (2005), "Gray matter volume reduction in the chronic fatigue syndrome", NeuroImage 26, pp. 777-781
  13. Peckerman A, Lamanca JJ, Dahl KA, Chemitiganti R, Qureishi B, Natelson BH (2003), "Abnormal impedence cardiographic predicts symptom severity in Chronic Fatigue Syndrome", The American Journal of Medical Science, Aug
  14. Myhill S, Booth NE, McLaren-Howard J (2009), "Chronic fatigue syndrome and mitochondrial dysfunction", Int J Clin Exp Med (2009) 2, 1-16
  15. Vernon S, Whistler T, Cameron B, Hickie I, Reeves W, Lloyd A (2006), "Preliminary evidence of mitochondrial dysfunction associated with post-infective fatigue after acute infection with Epstein Barr Virus", BMC Infect Dis. 2006 Jan 31;6 (1):15 16448567
  16. Chambers D, Bagnall AM, Hempel S, Forbes C (2006), "Interventions for the treatment, management and rehabilitation of patients with chronic fatigue syndrome/myalgic encephalomyelitis: an updated systematic review", Journal of the Royal Society of Medicine, 99(10):506-20, PMID 17021301
  17. 17.0 17.1 De Veer AJE, Francke AL (2008), "Zorg voor ME/CVS-patiënten. Ervaringen van de achterban van patiëntenorganisaties met de Gezondheidszorg", NIVEL, Utrecht, December, 20090108 ("Care for ME/CFS patients. Experiences of the supporters of patient organizations with health care.")
  18. Acheson DE (1956), "A New Clinical Entity?", Leading Article, Lancet, May 26, pp. 789-90
  19. 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
  20. Parish JG, "Early outbreaks of 'epidemic neuromyasthenia'" (1978), Postgraduate Medical Journal, Vol 54, 711-717
  21. Holmes G, Kaplan J, Gantz N, Komaroff A, Schonberger L, Straus S, Jones J, Dubois R, Cunningham-Rundles C, Pahwa S (1988), "Chronic fatigue syndrome: a working case definition", Annals of Internal Medicine, 108 (3), 387-389
  22. Fukuda K, Straus S, Hickie I, Sharpe M, Dobbins J, Komaroff A, (1994) "The chronic fatigue syndrome: a comprehensive approach to its definition and study. International Chronic Fatigue Syndrome Study Group", Annals of Internal Medicine 121 (12), 953-959
  23. 23.0 23.1 Campaign For A Fair Name website
  24. Lavrich C, Kenney KK, Lapp C, Herd J, Kahn D, Levine S, Klimas NG, Jason LA (2003), "Recommendations of the Name Change Workgroup Presented to DHSS CFS Advisory Committee", September
  25. Jason LA, Torres-Harding SR, Jurgens A, Helgerson J (2004), "Comparing the Fukuda et al. Criteria and the Canadian Case Definition for Chronic Fatigue Syndrome", Journal of Chronic Fatigue Syndrome, vol.12 p:39-52
  26. Tan EM, Sugiura K, Gupta S (2002), "The Case Definition of Chronic Fatigue Syndrome", J Clin Immunol, Vol. 22, No. 1, pp. 8-12
  27. Siegel SD, Antoni MH, Fletcher MA, Maher K, Segota MC, Klimas N (2006), "Impaired natural immunity, cognitive dysfunction, and physical symptoms in patients with chronic fatigue syndrome: preliminary evidence for a subgroup?", J Psychosom Res. Jun;60(6):559-566, PMID: 16731230
  28. Jason LA, Corradi K, Torres-Harding S (2007), "Toward an Empirical Case Definition of CFS", Journal of Social Service Research; Vol 34 (2) p43-54
  29. Kerr J, Burke B, Petty R, Gough J, Fear D, David M, Axford J, Dalgleish A, Nutt D (2007), "Seven genomic subtypes of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME): a detailed analysis of gene networks and clinical phenotypes", J Clin Pathol. Dec 5
  30. Provincial Government of British Columbia (1995), resolution #941109
  31. 31.0 31.1 McDonald L (ed) (2002), "Florence Nightingale: An Introduction to Her Life and Family", Laurier Press, ISBN 978-0-88920-387-7 [1]
  32. Jason LA, Taylor RR, Plioplys S, Stepanek Z, Shlaes J (2002), "Evaluating attributions for an illness based upon the name: chronic fatigue syndrome, myalgic encephalopathy and Florence Nightingale disease", Am J Community Psychol 30(1):133–48, pmid=11928774