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Encephalomyelitis, Myalgic

Chronic fatigue syndrome (CFS), also known as myalgic encephalomyelitis (ME), post-viral fatigue syndrome (PVFS) and various other names, is a syndrome of unknown and possibly multiple etiology, affecting the central nervous system (CNS), immune, and many other systems and organs. Most definitions other than the 1991 UK "Oxford", require a number of features, the most common being severe mental and physical depletion, which according to the 1994 Fukuda definition is "unrelieved by rest", and is usually made worse by even trivial exertion (controversially the Oxford and Fukuda require this to be optional only). more...

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However patients usually contend that they have many, often severe symptoms which are far more onerous, such as pain, muscle weakness, loss of brain function, hypersensitivity, orthostatic intolerance, immune and in some cases life-threatening cardiac and respiratory problems, and it is these symptoms exacerbated by extremely low stamina that cause greatest suffering, not "fatigue", which more properly describes a normal state of recovery unrelated to pathology. Some cases resolve or improve over time, and where available, treatments bring a degree of improvement to many others.

History

Originally studied since the late 1930s as an immunological neurological disorder under the medical term "myalgic encephalomyelitis" (ME), CFS has been classified by the World Health Organization (WHO) as a disease of the central nervous system since 1969. In 1992 and early 1993 the terms "post-viral fatigue syndrome" (PVFS) and "chronic fatigue syndrome" (CFS) were added to ME under the exclusive ICD-10 designation of G93.3.

Nomenclature

There are a number of different terms which have been at various times identified with this organic neuroimmune disorder.

Myalgic encephalomyelitis (ME, "inflammation of the brain and spinal cord with muscle pain") as a disease entity has been recognized and described in the medical literature since 1938, with the seminal paper being that by Wallis in 1957; Sir Donald Acheson's (a former Chief Medical Officer) major review of ME was published in 1959; in 1962 the distinguished neurologist Lord Brain included ME in his textbook of neurology, and in 1978 the Royal Society of Medicine accepted ME as a distinct clinical entity. In 1988 both the UK Department of Health and Social Services and the British Medical Association officially recognized it as a legitimate and potentially distressing disorder. Opponents to the term ME maintain there is no inflammation and that not all patients report muscle pain. United Kingdom and Canadian researchers and patients generally use this term in preference to CFS.
Chronic fatigue syndrome (CFS); this name was introduced in 1988 by a group of United States researchers based at the Centers for Disease Control and Prevention, and is used increasingly over other designations, particularly in the United States.
Chronic fatigue immune dysfunction syndrome (CFIDS); many people, especially patients in the United States, use the term CFIDS (pronounced ), which was originally an acronym for the above or "Chronic Fatigue & Immune Dysregulation Syndrome". This term was introduced by patients current with the biomedical research in an attempt to reduce the psychiatric stigma attached to "chronic fatigue", as well as the public perception of CFS as a psychiatric syndrome.
Post-viral syndrome (PVS or PVFS); this is a related disorder. According to original ME researcher Dr. Melvin Ramsay, "The crucial differentiation between ME and other forms of post-viral fatigue syndrome lies in the striking variability of the symptoms not only in the course of a day but often within the hour. This variability of the intensity of the symptoms is not found in post-viral fatigue states" (Ramsay 1989).
Chronic Epstein-Barr virus (CEBV) or Chronic Mononucleosis; the term CEBV was introduced by virologists Dr. Stephen Straus and Dr. Jim Jones in the United States. The Epstein-Barr virus, a neurotropic virus that more commonly causes infectious mononucleosis, was thought by Straus and Jones to be the cause of CFS. Subsequent discovery of the closely related human herpesvirus 6 shifted the direction of biomedical studies, although a vastly expanded and substantial body of published research continues to show active viral infection or reinfection of ME/CFS patients by these two viruses. As these viruses are also found in healthy controls, however, it is uncertain what role they play in CFS.
Low Natural Killer cell disease; this name is used widely in Japan. It reflects research showing a reduction in the number of natural killer cells in many CFS patients.
Yuppie Flu; this was a factually inaccurate nickname for CFS, first published in a November 1990 Newsweek article. It reflects the belief that CFS mainly affects the affluent ("yuppies"), and implies that it is a form of malingering or burnout. CFS, however, affects people of all races, genders, and social standings, and this nickname is inaccurate and considered offensive by patients. It is likely that this article contributed to the damaging public (and even medical) perception of CFS as a psychiatric or even psychosomatic condition.
Uncommonly used terms include Akureyri Disease, Iceland disease (in Iceland), Royal Free disease (after the location of an outbreak), raphe nucleus encephalopathy, and Tapanui flu (after the New Zealand town Tapanui where a doctor who investigated the disease lived).

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Red Blood Cells & CFIDS - chronic fatigue immune deficiency syndrome
From Townsend Letter for Doctors and Patients, 11/1/01 by Jule Klotter

According to an article by Maryann Spurgin, PhD, New Zealand researcher Dr. L.O. Simpson has theorized that myalgic encephalomyelitis (ME), also known as chronic fatigue immune deficiency syndrome (CFIDS), results from "insufficient oxygen availability due to impaired capillary blood flow." Simpson attributes the impaired capillary blood flow to smaller-than-usual capillaries and to the presence of abnormal red blood cells (nondiscocytes).

In healthy people, most red blood cells are smooth-surfaced and concave-shaped with a donut-like appearance. These discocytes have extra membranes in the concave area that give them the flexibility needed to move through capillary beds, delivering oxygen, nutrients, and chemical messengers to tissue and removing metabolic waste, such as carbon dioxide and lactic acid. Abnormal red blood cells lack flexibility that allow them to enter tiny capillaries. These nondiscocytes are characterized by a variety of irregularities, including surface bumps or ridges, a cup or basin shape, and altered margins instead of the round shape found in discocytes.

When people become ill or physically stressed, a higher percentage of discocytes transform into the less flexible nondiscocytes. Simpson says that the blood samples of marathon runners show a higher percentage of cup-shaped nondiscocytes (somatocytes) after a race. This higher percentage soon reverts to pre-race, normally-low levels of abnormally-shaped cells. Similarly, researchers found that the percentage of nondiscocytes in people with a viral head cold peaked on the fifth day and declined by the tenth day.

Simpson found that people with ME/CFIDS have higher percentages of nondiscocytes than people with other chronic illnesses, such as Lupus, multiple sclerosis, Huntington's disease, malaria, and diabetes. In addition, the percentages of cup-shaped somatocytes in ME/CFIDS patients can remain high for months, inhibiting blood flow. Simpson believes that, in ME/CFIDS, either the mechanism whereby red blood cells revert to the discocyte form is hampered for some reason or that whatever triggered the red blood cells to transform into nondiscocytes remains in effect, albeit unidentified. Ms. Spurgin notes that red blood cell morphology is also affected by toxic chemicals, providing a possible link between ME/CFIDS, environmental illness and multiple chemical sensitivity, and Gulf War Syndrome.

Simpson found that vitamin B12 injections reduced nondiscocyte levels in some ME patients. These patients also experienced symptomatic improvement. Patients whose nondiscocyte levels remain unaffected by the B12 injections noticed no improvement. Research with diabetic patients found that omega-3 fatty acids can also reduce nondiscocyte levels and improve capillary flow; and omega-6, in the form of evening primrose oil, has improved blood filterability in cigarette smokers.

"The Role of Red Blood Cell Morphology in the Pathogenesis of ME/CFIDS" by Maryann Spurgin, PhD, The CFIDS Chronicle, Summer 1995 discocytes have extra membranes in the concave area that give them the flexibility needed to move through capillary, beds, delivering oxygen, nutrients, and chemical messengers to tissue andremoving metabolic waste, such as carbon dioxide and lactic acid. Abnormal red blood cells lack flexibility that allow them to enter tiny capillaries. These nondiscocytes are characterized by a variety of irregularities, including surface bumps or ridges, a cup or basin shape, and altered margins instead of the round shape found in discocytes.

When people become ill or physically stressed, a higher percentage of discocytes transform into the less flexible nondiscocytes. Simpson says that the blood samples of marathon runners show a higher percentage of cup-shaped nondiscocytes (somatocytes) after a race. This higher percentage soon reverts to pre-race, normally-low levels 'of abnormally-shaped cells. Similarly, researchers found that the percentage of nondiscocytes in people with a viral head cold' peaked on the fifth day and declined by the tenth day.

Simpson found that people with ME/CFIDS have higher percentages of nondiscocytes than people' with other chronic illnesses, such as Lupus, multiple sclerosis, Huntington's disease, malaria, and diabetes. In addition, the percentages of cup-shaped somatocytes in ME/OFIDS patients can remain high for months, inhibiting blood flow. Simpson believes that, in ME/OFIDS, either the mechanism whereby red blood cells revert to the discocyte form is hampered for some reason or that whatever triggered the red blood cells to transform into nondiscocytes remains in effect, albeit unidentified. Ms. Spurgin notes that red blood cell morphology is also affected by toxic chemicals, providing a possible link between ME/OFIDS, environmental illness and multiple chemical sensitivity, and Gulf WarSyndrome.'

Simpson found that vitamin B12 injections reduced nondiscocyte levels in some ME patients. These patients also experienced symptomatic improvement. Patients whose nondiscocyte levels remain unaffected by' the B12 injections noticed no improvement. Research with diabetic patients found that omega-3 fatty acids can also reduce nondiscocyte levels and improve capillary flow; and omega-6, in the' form of evening primrose oil, has improved blood filterability in cigarette smokers.

"The Role of Red Blood Cell Morphology in the Pathogenesis of ME/OFIDS" by Maryann Spurgin, PhD, The CFIDS Chronicle, Summer 1995

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