In 1956, the term “myalgic encephalomyelitis” first appeared in the medical literature, to describe a perplexing series of outbreaks that had been observed over the preceding few decades in various locations throughout the world. These included Iceland, Australia, Durban, Los Angeles, upstate New York, Switzerland, England and Denmark.
Regardless of where the outbreaks were located, the illness observed was remarkably consistent. Writing in the Canadian Medical Association Journal, Rosemary Lindan gave a precise description:
The onset resembles that of poliomyelitis with headaches, lassitude, neck stiffness and sore throat accompanied by pains in the limbs and back, and possibly paraesthesiae and palsies. In contrast to poliomyelitis, however, the fever is never very high; the temperature rarely exceeds 100 degrees F and may persist for long periods.
The clinical picture is dominated by the severe muscular pains, accompanied at first by spasms and exaggerated tendon reflexes. These pains are not transient; they often persist long after any local signs have subsided and may be accompanied by an exquisite tenderness, but at no time does any muscular wasting develop.
A further distinguishing feature of the disease is the onset of behavioural changes, such as emotional lability, irritability and depression.
Disturbances of the cranial nerves such as diplopia and nystagmus, facial weakness, deafness or, in some cases hyperacusis, are common. A high proportion of cases show evidence of involvement of the reticuloendothelial system with enlargement of the cervical lymph nodes, particularly those in the posterior triangle, and, in some patients, hepatitis and splenomegaly.
Lindan R. Benign Myalgic Encephalomyelitis. Can Med Assoc J. 1956 Oct 1;75(7):596-7. PMID: 20325349
Over the next three decades, further reports of occasional, scattered outbreaks in various places continued to appear in the medical literature.
The most famous case was associated with the Royal Free Hospital in London in 1955, with over 300 people (mostly nurses) being affected with what was called “benign myalgic encephalomyelitis.”
The outbreak was written up by the Royal Free hospital staff in the British Medical Journal in 1957.
E. Donald Acheson, who went on to serve as Britain’s chief medical officer from 1983-1991, wrote a review article titled “The Clinical Syndrome Variously Called Benign Myalgic Encephalomyelitis, Iceland Disease and Epidemic Neuromyasthenia” in the American Journal of Medicine in 1959.
Medical journal articles throughout the 1960’s and 1970’s provided an increasingly detailed picture of the disease. Although most cases of the illness continued to be seen as part of epidemics, scattered individual cases were found.
The observations that many patients remained quite sick for years and that a few died from the illness led to the word “benign” being dropped from the name. Specific lab findings (including “normal” levels on all ordinary labs) were reported, and hypotheses about the cause of the illness were presented:
In a recent survey of clinical enzymology Wilkinson (1978) discusses the release of enzymes from cells. He concludes that intracellular energy content is important in the control of membrane permeability and instances loss of enzymes resulting from a variety of insults such as anoxia, deprivation of glucose, high potassium concentrations, high energy phosphates and metabolic inhibitors to both rat muscle and human erythrocytes. If the aetiological factor in benign encephalomyelitis impairs the permeability of the muscle cell membrane as a result of changes in the intracellular energy content, this could be followed by a differential loss of intracellular proteins.
Ramsay AM, Rundle A. Clinical and biochemical findings in ten patients with benign myalgic encephalomyelitis. Postgrad Med J. 1979 Dec;55(654):856-7. PMID: 548947
By the mid 1970s, a few observers argued that the epidemics might have been due to mass hysteria. The editors of the British Medical Journal firmly dismissed that idea:
Some authors have attempted to dismiss this disease as hysterical, but the evidence now makes such a tenet unacceptable. Some purely psychiatric symptoms may well occur, particularly in patients entering the chronic phase. Nevertheless, the organic basis is clear — from the finding that the putative agent can be transferred to monkeys; the detection of increased urinary output of creatine; the persistent finding of abnormal lymphocytes in the peripheral blood of some patients; the presence of lymphocytes and an increased protein concentration in the cerebrospinal fluid of occasional patients; and the neurological findings. Increased serum concentrations of lactic dehydrogenases and transaminases have been found in several patients examined during the acute attack.
Epidemic myalgic encephalomyelitis. Br Med J. 1978 Jun 3;1(6125):1436-7. PMID: 647324
In 1984, a particularly severe outbreak matching the characteristics of the other outbreaks occurred in the Lake Tahoe area of northern Nevada and California. Doctors who had published in the medical literature on the disease eventually visited the town and confirmed that the patients there were suffering from M.E.
During the next three years, a number of outbreaks were reported in various locations in the U.S., including California (Sacramento, San Francisco), Nevada (Carson City, Yerington), upstate New York (Lyndonville) and North Carolina.
Outbreaks also occurred in other countries, including New Zealand and England. Hundreds of individual cases matching the descriptions of M.E. in the literature also were reported.
In 1988, the CDC released a description of the illness but decided to put aside both the name “M.E.” and the established descriptions of the disease. It instead presented a much more non-specific picture of the illness, which it called “the chronic fatigue syndrome.”
The CDC’s description became even more nondescript in 1994, when it was adopted as the official definition of the disease and the number of secondary symptoms (in addition to fatigue) needed to qualify was dropped from eight to four.
The CDC’s description of chronic fatigue syndrome immediately almost obliterated the concept of myalgic encephalomyelitis from the literature. Since 1990, M.E. has almost never been mentioned in the medical literature except as an alternative name in papers focusing on CFS.
The main problem here is not that the name “chronic fatigue syndrome” makes the disease that historically has been called M.E. sound more trivial and less complicated than it actually is (although that is true too). The more important issue is that a disease with a very specific presentation and illness course has been redefined by a loose set of criteria that does not accurately distinguish it from many other kinds of conditions.
As a result, although the literature on “chronic fatigue syndrome” includes many hundreds of papers demonstrating a wide variety of medical abnormalities, these should be considered to be an inadequate representation of the health issues that occur in the disease of M.E., since the research samples are almost always highly diluted with patients who are only mildly sick with M.E. or who do not have the illness at all.
-Lisa Petrison, Ph.D.
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