M.E.
Today
Is There a Connection Between ME, Polio and the Post-Polio Syndrome?
This is an important question with three fundamental implications for the future research into the diagnosis, prevention and treatment of all three conditions. In the past, because of their potential for producing paralytic disease in a wide scale, polio viruses were the most extensively investigated of all virus groups and study of polio viruses in tissue culture became possible in 1948 and immunisation followed 10 years later, its apparent success seemed to obviate need and the focus of interest was lost. Yet investigation of a polio-like epidemic back in 1948 had already led to the discovery of the Coxsackie viruses, the first of some 69 strains of non-paralytic enteroviruses (NPEVs) with undisputed potentail for producing widespread neurological, cardiac and musco-skeletal disabilities and which will impel us to return to the drawing board on enteroviruses in the 2nd millenium.
Historically, Distinctions Between ME and Polio Have Always Been Blurred
If we accept the drawing of a limping young man on an ancient Egyptian funeral plaque as the late effect of infantile polio, we must assume that the viruses responsible have been circulating silently in human communities for some 3,000 years, with only a rare paralytic event to call attention to their smooth and naturally immunising passage via faecal/oral and respiratory routes from infant to infant. However, the sudden and seemingly inexplicable emergence of polio and other neurological diseases, in clean well ordered communities, on an epidemic and pandemic scale in the twentieth century, requires careful analysis. It was a change in human hygienic behaviour rather than any virus mutation which destroyed an ancient and stable herd immunity to polio and similar virus infections leading in the front line of attack, non-immune adults (who were more susceptible than infants to chronic neurological and cardiac complications).
The Unexpected Consequences of Mass Polio Vaccinations
Before polio immunisation, 75% of all recorded epidemics of ME had been associated seasonally, geographically and sequentially with outbreaks of polio and, in institutions, affected mainly staff caring for polio patients.(1) In fact the name "myalgic encephalo myelitis" had only been bestowed upon this illness in 1956, after subtle clinical differences had been noted between the two disabilities. Mass polio immunisation in the late 1950s brought about the expected decline in polio epidemics and incidence of new cases (apart from vaccine reversions) approached zero within 5 years, while epidemics of ME continued unabated. Nevertheless, there were several unforseen consequences of this immunisation programme.
As polio declined abruptly, the incidence of ME (charted by date of onset after referral to medical clinics) in the UK and Canada(2) increased with mathematical precision to assume the epidemic and pandemic curve so recently vacated by polio.
Further evidence of the phenomenon (unbiased by physician referral) came from studies of enteroviruses isolated from human sewage in East Slovakia(3) between 1963 and 1966 (immediately after polio immunisation). This indicated that the effect of the attenuated virus vaccine was short-lived and that, within 3 months after an initial reduction of all enteroviruses, the number of non-polio enteroviruses rebounded to a high level. Further community studies in the USA and elsewhere, indicated that the shock of polio immunisation could displace former leading NPEVs by more virulent neurotropic or cardiotropic strains. A sequence of these can be traced through papers written between 1940 and the present day, as follows: ECHO 9(4) displaced in the mid 1960s by Coxsackie B5 (not recognised in some countries for the previous 20 years) and finally by Coxsackie B3 (the leading cause of virus associated cardiac failure in the UK today). Changes in this sequence coincided with the peaks in incidence of ME as recorded above.
Polio immunisation brought to our notice the often forgotten potential for some non-polio enteroviruses to attack motor neurons in the anterior horn of the spinal cord, producing acute flaccid paralysis indistinguishable from poliomyelitis. Neurotropic enteroviruses including Coxsackie A7, B5, B3 and Enterovirus 71 have now replaced polio (due to vaccine virus reversion) as the leading cause of acute flaccid paralysis in countries ranging from the USA, to Europe, Russia and South America(5) while in India acute flaccid paralysis due to Coxsackie A7, B3 and Enterovirus 71 co-exists with indigenous polio.
It must be remembered that nature abhors a vacuum and that NPEVs are rapidly filling the ecological niche recently vacated by wild polio viruses.
What can be learnt about ME from a study of Post-Polio Syndrome?
The late effects of polio were first described in 1875, relating to a young man of 19 who had developed new weakness after recovery from polio at the age of 6 months - a curious recapitulation of the ancient Egyptian funeral picture! This description was forgotten until a young man and middle-aged American survivors of the last major polio epidemics some 30 years before, began to present with new symptoms of muscle weakness, decreased physical endurance, pain and overwhelming fatigue. A prompt epidemiological survey indicated that the condition was widespread(6) and that intervening years of apparent stability had concealed the gradual breakdown of previously damaged but healing neurons, often accelerated by physical over-exertion or mental stress. Current information suggests that there are some 2 million sufferers from PPS in the USA and an estimated 130,000 in the UK where facilities for diagnosis and rehabilitation are minimal. Most of our information therefore comes from the USA via research workers of the calibre of Richard Bruno, Nancy Frick(7) and their team who have written a remarkable series of papers delineating the syndrome, its causes and management, over the past 10 years. They have not only described damage to vital centres In the mid brain, which influence practically all activities of the body, but have shown how the most disabling symptom (overwhelming fatigue) arise from a neural network in the brain stem, whose main function is to maintain wakefulness and focuss attention. It is to their meticulous demonstration, via neuroanatomic, neuroendocrine and neuropsychological studies of the close similarity between PPS and ME, that we owe a rationale for correct management of both syndromes.
The Management of PPS has a lesson for ME sufferers
Over exertion and mental stress are the commonest causes of relapse in PPS and ME. Structuring an environment in which the patient can function within the energy capacity of their individual sleep-waking cycle and providing them with mobility aids and other means of living with disability in a sustainable way, will permit stabilisation in some 91% of patients.
For those with additional symptoms, despite conservation of energy, somplification or work and reduction of stress, controlled trials of drugs which can replace or enhance neurotransmitter function (diminished by polio damage) are underway. These presently include drugs which may enhance dopamine production and improve central fatigue and others which improve transmission of acetylcholine and may relieve local muscle fatigue. However, energy conservation is the sheet anchor of management and no drug can replace strict adherence to this well researched regime in a non compliant patient. Careful study of these research papers and an early trial of energy conservation (provided sufficient energy is conserved to enjoy life!) remains the most appropriate reply that one could possibly make to the infamous advice on progressive exercise given in the recent report of the UK Royal College of Physicians.
Summary
The clinical and neuro anatomical findings in ME and PPS are strikingly similar. Overlapping reports suggesting autoimmunity as well as the findings of fragments of mutant polio or non-polio enteroviruses in both conditions require confirmation. Meanwhile it will require the judgment of Solomon to make a differential diagnosis. Fortunately, management remains the same!
References:
1) Acheson ED. The clinical syndrome variously called benign myalgic encephalomyelitis, Iceland Disease and epidemic neuromyasthenia American Journal of Medicine. 1959;26:569-595
2) Hyde B, Cameron B, Duncker A. et al. Epidemiological aspects of myalgic encephalomyelitis/chronic fatigue syndrome/post viral fatigue syndrome. Ottawa, Ontario, Canada. The Nightingale Research Foundation. 1994
3) Tarabcak M. et al. Study of the effect of vaccination with live polio myelitis vaccine on the circulation of enteroviruses in the population. Journal of Hygiene, Epidemiology, Microbiology and Immunology. 1971;15:248-269
4) Lyle WH. An outbreak of a disease believed to have been caused by ECHO 9 virus. Annals of Internal Medicine. 1959;51:248-269
5) Da Silva EE. et al. Role of Enterovirus 71 in accute flaccid paralysis after the eradication of polio virus in Brazil. Emerging Infectious Diseases. 1996;2(3):231-232
6) Dalakas MC. Post Polio Syndrome 12 years leter in the Post-Polio Syndrome - advances in pathogenesis and treatment. Dalakas MC, Barthfield H, Kurland T, eds. Annals of the New York Academy of Sciences. 1995;253:11-18
7) Bruno RL, Frick NM, Creange S. et al. A Brain Model for Post Viral Fatigue Syndromes. ME Today. 1997;5:18-21
(Based on a paper recently prepared for the Newcastle Research Group by Betty Dowsett and Stephen Everett (Microbiologists))
