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Paper by Dr E.G. Dowsett

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Can they be distinguished from the Post-polio syndrome?

The following is a copy of the presentation made by Dr Betty Dowsett to the All Party Parliamentary Group at the House of Commons 31/01/01.


Few people would dispute that ME (Myalgic encephalomyelitis), an illness which blights the hopes and aspirations of all sufferers, especially the young, is denied equal treatment in respect of diagnostic facilities, medical coverage and welfare provision. Comparable chronic and unpredictably disabling neurological conditions, for example Multiple Sclerosis, which was formerly ascribed to "hysteria" and similarly neglected, now receive government recognition, facilities within the NHS, and more generous research funding - though the potential cost of effective treatment can still arouse bitter debate.

WHAT IS ME? (1,2,3)

a. ONSET:  It is a syndrome (a group of linked symptoms) initiated by one or more of a related group of enteroviruses which circulate annually in the community in summer and autumn in temperate climates, but all the year round in tropical areas.

b MINOR ILLNESS: The majority of encounters with these viruses are asymptomatic but some subjects, more commonly teenagers and adults, suffer a seemingly trivial minor illness, usually described as a non specific summer 'flu accompanied by gastrointestinal upset, sore throat and occasionally by generalised glandular enlargement.

c. SECONDARY PHASE: The minor illness is self-limiting in 90% of adults. However, some 5-10% of all age groups exposed, may progress to a more significant episode ~ severe headaches and vertigo, a stiff neck and back and generalised muscle pain, signifying that the central nervous system has now become involved with a possible progression to viral meningitis and encephalitis(3). Clinical recovery at this stage is normally possible, but does not preclude further effects of the illness in later years. It has to be remembered that ME is a life-long disability where relapse is always possible.

d. FINAL STAGE(1,2) After a variable interval, a multi-system syndrome may develop, involving permanent damage to skeletal or cardiac muscle and to other "end organs" such as the liver, pancreas, endocrine glands and lymphoid tissues, signifying the further development of a lengthy chronic, mainly neurological condition with evidence of metabolic dysfunction in the brain stem. Yet, stabilisation, albeit at a low level, can still be achieved by appropriate management and support. The death rate of 10% occurs almost entirely from end-organ damage within this group (mainly from cardiac or pancreatic failure). It has to be said that suicide in younger patients and in earlier stages of the disability is related to the current climate of disbelief, rejection of welfare support and loss of educational and employment prospects. It is an additional and potentially avoidable factor.


Most doctors with substantial experience of examining these patients would agree that the outlook for any individual is unpredictable. Case records need to be kept up to date for prolonged periods because patients who have remained clinically stable over 40 years or more and have worked normally for most of their lives are still subject to significant late effects. These include: overwhelming fatigue both physical and mental; cognitive disturbances; muscular and joint pain; muscular weakness and wasting; difficulty with breathing; episodes of hypothermia and low blood pressure; problems with swallowing and voice production as well as sudden attacks of breathlessness while sleeping. The similarities of these symptoms to those complained of by sufferers from the Post-polio syndrome are striking and require further explanation.


The majority of ME patients contract their illness in the 3rd and 4th decade (50%) with secondary peak at puberty (18%). The incidence at the extremes of age below 10 years and above 50 years) has, until recently, been low (about 10% in each group). Epidemiological surveys made between 1988 and 1998, in 2 Essex hospital clinics dedicated to ME, indicate that the percentage of patients over 50 years of age attending with new illness has risen from 6% in 1988 to 16% in 1995 and 18% in 1998. Some patients indeed, present with paralysis. Others have a vague past history of illness in childhood. Some years of "weakness" or "growing pains"; recovery, but always poor at sport; possibly a stable work record for 25 years or more, followed by a decline in walking ability; unusual fatigue after simple tasks; problems with climbing stairs, dressing and with short term memory. The current age range of these patients is from 40-92 years, so it is not easy to dismiss their symptoms as due solely to "ageing". Their social and medical problems are especially severe, as they share all the difficulties of access to remedial and support services complained of by other disabled people in the same age group. However, in the UK, there is almost nowhere to refer patients with suspected post-polio symptoms as the medical profession has largely forgotten or never experienced the many manifestations of that disease. Successful immunisation against only 3 polioviruses among some 69 enteroviruses currently in circulation is deemed to have solved all problems!


Poliomyelitis is an acute enteroviral infection with a wide range of clinical manifestations and multi-organ involvement (a fact which was frequently overlooked by physicians dealing with large numbers of dangerously paralysed patients, between 1940 and 1950). 95% of people who contract the infection remain symptom free or suffer only a trivial non-specific respiratory or gastrointestinal illness as in ME.

Some 5% of those contracting the minor illness develop muscle weakness or paralysis before more serious or fatal complications supervene. The diagnostic distinction between "paralytic" and "non paralytic polio" was entirely arbitrary in the days of the big epidemics. In fact, the category of "non-paralytic polio" contained many patients with mild or temporary paralysis and with encephalitis, which occurs in patients reaching the later stages of this illness. Modem studies indicate that overt paralysis in these patients depends entirely on the percentage of spinal nerve cells destroyed. For damage to be visible as weakness or paralysis at least 50%-60% of the nerves controlling muscular action must be damaged or destroyed. Thus, patients with less damage who may only have had a minor illness, and some who were asymptomatic can still present many years later with a classic Post-polio syndrome.

Recent publication(6,8) of this information (originally derived from studies made in 1955) has resulted in a re-definition of the post-polio syndrome and will certainly include many patients currently seen in ME clinics.


a. A history of remote paralytic or non-paralytic polio, or findings on history, physical examination or laboratory and other technical studies compatible with damage to the central nervous system in earlier life.

b. A period of recovery.

c. A period of stable functioning for 10-50 years.

d. New symptoms for which no other explanation can be found. Many patients and research workers point out that the assessment of sufferers will now have to become more holistic, that standard electrical tests of muscle function (EMG) will have to be more widespread (and repeated), and that manual muscle testing must refer to repetitive activity and daily tasks rather than a single examination on the couch(16).


Yes, undoubtedly! This is an important question with fundamental implications for further research into the diagnosis, treatment and prevention of both disabilities.

Modern research published currently in a dedicated supplement of the American Journal of Physical and Medical Rehabilitation by the Editor and 3 leading research teams(6,8) indicates that part of the current difficulty in obtaining a clear diagnosis of the post-polio syndrome lies in the error of dividing acute poliomyelitis into "paralytic", "non-paralytic", "abortive" and "sub clinical" categories. It has to be recognised that there is a wide range of nerve damage in every patient. The Post-polio syndrome may therefore include:

a. Patients whose nervous system damage was not clinically obvious at the time of diagnosis.

b. Those who had minimal paralysis for a short period and were misdiagnosed as non-paralytic polio.

c. Those patients suffering from infection due to non polio enteroviruses with potential to cause nervous system damage and the “Post polio” syndrome, equal to that of polio viruses e.g. Coxsackie viruses A9, A7; Coxsackie B viruses 1-6; ECHO virus 9; Enteroviruses 70, 71 - all of which have been implicated in outbreaks of ME or epidemics clinically identical to paralytic poliomyelitis.

d. Patients with symptoms clinically identical to the "Post-polio" syndrome whose nerve damage arises from some other cause, for example, local muscle problems due to metabolic dysfunction, the effects of persistent virus infection, immune reaction to fragments of viral genetic material etc.

It is essential that patients with clinical symptoms suggestive of Post-polio syndrome should be referred to a Physician to exclude other nervous diseases (e.g.  Motor Neurone Disease), and especially those which are treatable.


Not really, even if it were useful or practicable to do so at present, as the two conditions are clinically identical and similar in respect of neuroanatomical, neuroendocrine, neuropsychological electroencephalographic and other techniques, including brain imaging and molecular biology, as indicated by a remarkable series of research papers published by Bruno and colleagues over the past 20 years.



a. (II) In 1948, the year in which polio viruses were first cultured, specimens from 2 children with clinical poliomyelitis, yielded a non-          polio enterovirus, (eponymously called Coxsackie after the neighbourhood in which they lived). This finding opened a Pandora's box of some 70 previously undiscovered enteroviruses of which 14 strains were later found to have neurogenic potential equal to that of polio viruses.

b.(12)From the late 1940s, studies in the USA indicated that outbreaks of major or minor enteroviral illness (eg. Paralytic or non paralytic and non specific summer 'flu") could be caused by varying proportions of virulent and non virulent polio viruses combined with other neurogenic enteroviruses, for example in Akron and Cincinnati, Ohio (1947) Delaware and Connecticut (1949).

c.(13)In the UK, an outbreak of poliomyelitis affecting an Edinburgh housing estate from August 1961- February 1962 (a period when polio immunisation with the Salk (injectable) vaccine had recently been introduced) provided evidence that a "mosaic" of enteroviruses, including Polio type 3, Coxsackie viruses B2 and B4, Echo viruses 5 and 15 could act in combination to enhance virulence in individual patients, to block the spread of polio virus type 3 and to interfere with vaccine efficiency. Each virus type appeared sequentially until the arrival of Echo virus 5 in November which ended the outbreak by the following February (as indicated by serial sampling of the local school sewer). It has to be remembered that a sudden change in the virulence and spread of enteroviruses in the 20th century has been due to alterations in human hygienic behaviour rather than to viral mutations.







Summer Flu 




Polio HV

       -                -                  -

High virulence polio virus only



Non paralytic polio LV 

       -                -                  -

 Low virulence polio virus &   infection of CSF




          +                    +                        +

 Low virulence polio virus & Coxsackie virus




          +                    +                        + 

Infection of CSF &  low virulence polio virus & Coxsackievirus


Non Paralytic 




Polio HV

          -                     -                        -

Only high virulence polio virus & infection of CSF



Polio HV

          -                     -                        - Only high virulence polio virus




        +                    +                       + 

Only Coxsackie virus &  infection of CSF

Paralytic Polio



Polio HV

        -               -                  -

 Only high virulencepolio virus and infection of CSF


KEY * Raised cell count in cerebro-spinal fluid indicates infection in the central nervous system

Polio HV - Polio type one virulent.

Polio LV - Possibly polio type two, low virulence (non paralytic)

Coxsackie Is a neurovirulent, non polio enterovirus


It has to be accepted that some degree of encephalitis has occurred in all these cases and that the areas chiefly affected include the upper spinal motor and sensory nerve roots and the spinal nerve networks traversing the adjacent brain stem a (nerve centre controlling all vital bodily functions which is always damaged). The most troublesome symptoms of both conditions are progressive muscle weakness fatigue and pain, and the commonest cause of relapse over use of repaired nerve networks and an inappropriate response to physical or mental stress in combination with the increasing effect of normal ageing.

FATIGUE: This is almost always central and due to damage affecting the Reticular activating system (which keeps the brain awake and alert as well as maintaining some control over muscular activity). Fatigue is characteristically intermittent, but profound and incapacitating and related even to minor activity.

(14) MUSCLE WEAKNESS AND WASTING: This may have a central cause (as above) or a local origin due to loss of motor units controlling individual muscles (including the breakdown of repair to these over time). Metabolic, immune or ongoing viral injury to muscle fibres, are other possibilities where infection persists.

PAIN: This is a severe symptom which is difficult to treat and is usually due to dysfunction of the thalamus, an important sensory relay station in the brain stem Failure to produce natural painkillers (e.g. endorphins and encephalins), may be an additional factor.

INAPPROPRIATE REACTION TO PHYSICAL OR MENTAL STRESS: This also arises from injury to the brain stem which normally controls the production of cortisol (a steroid required for stress control) via the hypothalamus, pituitary and adrenal glands . In the absence of an efficient response, even minor stress can cause catastrophic collapse in these patients. NB. Because of the many and varied symptoms arising from encephalitic damage to the brain, all symptoms reported, however bizarre they may seem, must be taken as possible evidence of organic disease.

MANAGEMENT: Despite promising reports from the USA of anti-enteroviral agents(18) and of Dopamine receptor agonists(9) (to correct some deficiencies in neurotransmission) no specific medical treatment is yet available in the UK and the main principles of management rely upon conservation of energy. reduction of stress. and simplification of manual tasks at home or at work. These objectives cannot possibly be achieved without financial and social support, aids to mobility, house conversions and suitable rehabilitation facilities. In the USA it is claimed that (with counselling, if necessary, for those who find such adjustments to life style difficult) 91% of patients will stabilise in view of the fact that, at this stage, the disability is only slowly progressive. Patients have to be cautious about drugs, especially those acting on the central nervous system including psycho-active preparations and alcohol. In general, these patients need less anaesthetic but higher doses of pain killers than usual and more time to convalesce from surgery. There are now many new options for muscle problems including modern orthoses and corrective surgery


a. There has been little government interest or support for patients suffering from the late effects of ME or from the post-polio syndrome.    It is generally expected that survivors of polio will gradually disappear because of successful immunisation or the UK population 40 years ago. However the fact that "Post-polio", by any other name, can arise from currently circulating enteroviruses has not been taken into account. The Chief Medical Officer's Working Party on ME (set up in 1999 and funded privately by the Linbury Trust) has made it clear that its remit is only with management, and that all discussion about the cause, epidemiology and social benefit requirements of these patients is ruled out. It seems that it will be difficult to advise on rational management in the absence of such vital information.

b. The potential size and cost of the problem. This is impossible to assess in the UK because no official epidemiological surveys have been made. However, increasing numbers of patient support groups and individual research workers have been making their own calculations. In the case of ME, prevalence appears to range from 300/100,000 to 500/100,000 in occupations at high risk of infection(2), but no information is yet available about the number likely to suffer late effects (except that it may have trebled in the last 10 years)(4).

The number likely to be affected by the post-polio syndrome has been calculated as between 200-270/100,000 currently(7), but no account has been taken of survivors from non-paralytic polio which could easily double that figure. Possible costing for ME support has been based on 3x the cost of maintenance for multiple sclerosis on the supposition that ME is 3 times as common(4). The only costs that we can be sure of are those derived from the failure of appropriate management, and of inappropriate assessments which waste vast sums of money and medical time while allowing patients to deteriorate unnecessarily(16).

c. Some Immediate Steps that Could Be Taken (7,17,18,19,20)   These patients could be referred to NHS rehabilitation clinics and welfare facilities as for any other chronic neurological disease, but physiotherapy must include exercise suitable for patients with some damaged muscle fibres which have been overused while others are normal and liable to deconditioning(7). Separate "ME" and "Post-polio Clinics" are more expensive and often inaccessible. We should be educating doctors and paramedics now about the very common and seriously disabling effects of neglect(7).  Rapid diagnostic tests for enteroviruses, anti-­enteroviral drugs and possible vaccines are already in preparation here, or in use (in the USA) to deal with the tremendous burden of circulating enteroviral infections, (for example, leading to febrile respiratory infections, viral meningitis and myocarditis let alone unnecessary admissions to hospital and inappropriate prescription of antibiotics in children)(17,18). These methods could well be employed for the benefit of young people in the UK and to prevent the rising tide of ME in schools - the commonest cause of long term absence and subsequent educational deficit!(19,20)

d.    Research workers must be encouraged and appropriately funded to work in this field. However they should first be directed to papers published before 1988, the time at which all specialised experience about poliomyelitis and associated infections seem to have vanished mysteriously!(11,12,13)

E.G. Dowsett MBChB, Dip Bact.

Honorary Consultant Microbiologist

Basildon and Thurrock Hospitals NHS Trust Address for correspondence:

January 2001

(1)RICHARDSON J. Myalgic Encepalomyelitis/Chronic Fatigue Syndrome and Enteroviral - Mediated Organ Pathology. The Haworth Press Inc. New York, London Oxford. ISBN 0-7890-1127-1 (in press)

(2)DOWSETF EG, RICHARDSON J. The Epidemiology of Myalgic Encephalomyelitis (ME) in the UK - 1919-1999. Evidence submitted to the All Party Parliamentary Group of MPs on ME 23.11.99

(3) Echo Viruses and Meningitis. Scottish Centre for Infection and Environmental Health, Weekly Report, 7.11.2000

(4) RAMSAY AM, DOWSE'UI' EG. - Then and Now. An epidemiological introduction (in the Clinical and Scientific Basis of Myalgic encephalomyelitis/Chronic Fatigue Syndrome. HYDE BM, GOLDSTEIN 3, LEVINE P. Eds): The Nightingale Research Foundation, Ottawa, Ontario, Canada, 19q~; Chapter 7 81-84

(5)     DALAKAS MC. Post-polio Syndrome 12 years later (in the Post-polio Syndrome - advances in the pathogenisis and treatment. DALAKAS MC, BARTFIELD H, KURLAND LT. Eds) Annals of the New York Academy of Sciences: 1995; 753:11-18

(6) FALCONER M, BOLLENBACH E. Late Functional Loss in Nonparalytic Polio. American Journal of Physical Medicine and Rehabilitation. 2000; 79(1):19-23

(7) Basic information leaflet for health professionals on Post-polio syndrome/late effects of polio. Lincolnshire Post-polio network, 69 Woodvale Avenue, Lincoln, LN6 3RD, UK. October 2000

(8) JOHNSON EW: A Clarification of "nonparalytic" polio: 3

BRUNO RL : Paralytic vs. "Nonparalytic" Polio. Distinction Without a Difference?: 4-1 ~ HALSTEAD LS, SILVER JK: Nonparalytic Polio and Postpolio Syndrome: 13-18 (see opus cit. reference 6)

(9) BRUNO RL, SAPOLSKI R, ZIMMERMAN JR, FRICK NM. Pathophysiology of a Central Cause of Post-polio Fatigue. (in the Post-polio syndrome - advances in pathogenesis and treatment. DALAKAS MC, BARTHELD, H KURLAND LT: eds.) Annals of the New York Academy of Sciences. 1995; 753 : 257-275.

(10) BRUNO RL, FRICK NM, CREANGE MA, ZIMMERMAN JR, LEWIS T. Polio Encephalitis and the Brain Generator Model of Post-Viral Fatigue syndromes. Journal of Chronic Fatigue Syndrome. 1996; 2(2,3): 5-27

(11)DALLDORF G, SICKLES GM, PLAGER H, GIFFORD R. A virus recovered from the faeces of "poliomyelitis" patients. Pathogenic for suckling mice. Journal of Experimental Medicine. 1949; 89: 567-582

(12) MELNICK JL. LEDINKO N, KAPLAN A, KRAFT E. Ohio Strains of a Virus Pathogenic for Infant Mice (Coxsackie Group). Simultaneous occurrence with poliomyelitis virus in patients with "summer grippe”. Journal of Experimental Medicine. 1950 : 91:185-195

(13) SELWYN S, HOWITI' LF. A Mosaic of Enteroviruses. Polio, Coxsackie and Echo infection in a group of families. The Lancet. 1962; 2: 548-551

(14) LANE RJM, BARRETT MC, WOODROW D.  Muscle Fibre Characteristics and Lactate Responses to Exercise in CFS. Journal of Neurology Neurosurgery and Psychiatry. 1998; 64: 362-367

(15) Letter from Parliamentary Under Secretary of State, Department of Health Yvette Cooper) to Matthew Taylor MP 20.6.2000 re Post-polio Syndrome in UK.

(16) HALLAM H. Polio Survivors need holistic multidisciplinary assessment because the standard physical assessment is not adequate. Lincpin Newsletter June 19,1999.

(17) ROTBART H, MCCRACKEN GH, WHITELY RJ. et al. Clinical significance of enteroviruses in serious summer febrile illnesses of children. Paediatric infectious diseases. 1999; 18: 869-74

(18) ROTBART HA, O'CONNELL JF, McKINLAY MA. Treatment of Human Enterovirus Infection, Antiviral Research. 1998; 38:1-14.

(19) DOWSETI' EG, COLBY J. Long Term Sickness Absence due to ME/CSF in UK Schools - an epidemiological study with medical and educational implications. Journal of Chronic Fatigue Syndrome 1997; 3 (2): 2942

(20) RANGEL L, GARALDA ME, LEVIN M, LEVIN M, ROBERTS H. The course of severe chronic fatigue in childhood. Journal of the Royal Society of Medicine. 2000: 93:129-134