Friday, April 15, 2011

From 1978 -- yet STILL not taken seriously!


At a symposium held recently at the Royal Society of Medicine…there was clear agreement that myalgic encephalomyelitis is a distinct nosological entity.   Other terms used to describe the disease were rejected as unsatisfactory for various reasons: the cardinal, clinical features show that the disorder is an encephalomyelitis… the exhaustion and tiredness are similar to that described by patients with multiple sclerosis.  From the patient's point of view the designation benign is also misleading, since the illness may be devastating.  Originally, the term was used because no deaths had been recorded from myalgic encephalomyelitis.  Two patients who had had the disease have now been examined post mortem: one was found to have multiple sclerosis.  The adjective epidemic is correct, since most cases occur in an epidemic, but the disease may be endemic, and sporadic cases may occur.

Some authors have attempted to dismiss this disease as hysterical (McEvedy, C.P and Beard, A.W in BMJ 1970), but the evidence now makes such a tenet unacceptable.  Some purely psychiatric symptoms may well occur, particularly in patients entering the chronic phase.  No doubt too, in an epidemic, some hysterical persons will simulate the symptoms of the disease.  Nevertheless, the organic basis is clear – from the finding that the putative agent can be transferred to monkeys (Pellew, R.A.A and Miles, J.A.R – Medical Journal of Australia, 1955),  the detection of an increased urinary output of creatine (Albrecht, R.M, Oliver, V.L and Poskanzer, D.C, Journal of the American Medical Association 1964), the persistent finding of abnormal lymphocytes in the peripheral blood of some patients (Wallis, A.L, Edinburgh University 1957), the presence of lymphocytes and increased protein concentration in the cerebrospinal fluid of occasional patients (Acheson, E.D. American Journal of Medicine 1959), and the neurological findings. At this symposium more evidence was produced to support the organic nature of the disease. Increased serum concentrations of lactic dehydrogenases and transaminases have been found in several patients examined during the acute attack.  In a recent outbreak in London immunological studies showed a high incidence of serum anticomplementary activity and the presence of ill-defined aggregates on electron microscopy of acute-phase sera (Dillon, M.J et al, BMJ 1974).  A perplexing finding suggesting the possibility of a persistent virus infection, was the ability of lymphocytes from patients to proliferate and survive in vitro for up to 19 weeks.  The results of electroencephalographic studies were also stated to be abnormal, confirming other reports (Ramsay, A.M and O'Sullivan, E, Lancet 1956).

We still know nothing about the nature and cause of epidemic myalgic encephalomyelitis, but outbreaks are still occurring.  Future epidemics should be studied by a collaborative team of neurologists, epidemiologists, virologists and immunologists.  Its findings would be important not only for the study of epidemic myalgic encephalomyelitis but also for other neurological disorders, including multiple sclerosis.

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