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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.
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.
ME is defined by the following diagnostic criteria.
- Generalised or localised muscle fatigue after minimal exercise with prolonged recovery time.
- Neurological disturbance, especially of cognitive, autonomic and sensory functions, often accompanied by marked emotional lability and sleep reversal.
- Variable involvement of cardiac and other bodily systems.
- An extended relapsing course with a tendency to chronicity.
- 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.
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.
- 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.
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. Infections found in ME patients include various herpes and enteroviruses.
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, and by Baraniuk, who measured errors in protein folding affecting several feedback mechanisms. The RNase L fragmentation has been shown to correlate with patient dysfunction and to be useful as a marker for ME.
Okada demonstrated that brain volume, specifically grey matter, is greatly reduced in ME, especially in areas that serve cognitive and autonomous functions. The general outcome was confirmed by Dutch researchers. It is not known yet how this relates to the vascular problems that are also consistently found on scans.
Exercise intolerance has been linked to the cardiac system, and may be the result of mitochondrial dysfunction in the production of ATP (and therefore of kinetic energy). Mitochondrial dysfunction has been found in post-infective fatigue in a population study in Australia.
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.
Common treatments for ME are diets and supplements (incuding hormones and vitamines), physiotherapy, anti-depressants, pain killers, and complementary and alternative medicine. Coping techniques for ME invariably include some kind of energy management, where striking a balance between activity and rest is prominent.
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. The oldest of the documented outbreaks occurred in Los Angeles, 1934. 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.
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). A multitude of, sometimes significantly different, CFS definitions have been designed, but the Fukuda definition of 1994, 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. 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. 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. It compared favourably to the Fukuda definition of CFS.
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. 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.
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. It is believed by some that Nightingale suffered from myalgic encephalomyelitis during the later part of her life, although other diagnoses that could explain her symptoms have also been suggested.
- European Society for ME
- A Hummingbirds Guide to M.E.
- Nightingale Research Foundation
- Centers for Disease Control and Prevention: CFS