Post-Polio Newsletter 49a

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POST - POLIO NETWORK (NSW) INC.

N E W S L E T T E R #49a

Editor: Gillian Thomas        PO Box 888 Kensington
Email: gillian@post-polionetwork.org.au        NSW AUSTRALIA 1465
Website: www.post-polionetwork.org.au        Phone No: (02) 9663 2402

President's Corner        Gillian Thomas

This Newsletter has a been long time coming as our volunteer resources have been stretched to the limit this year. For your patience, you have been rewarded with a bumper issue which should keep you in reading material for some time to come!

Another result of our over-stretched resources is that the Annual General Meeting (AGM) which was to be held on 22 September has been deferred until December. A Seminar is still being held on 22 September though – full details appear on page 2.

The AGM will now be held on Saturday 15 December, from 3:00 to 4:00 pm, in conjunction with a Support Group Conveners' Workshop. Holding the AGM at this time will also mean that many country Conveners who are usually unable to attend will be able to participate. We have been very fortunate to secure funding of $2,727 (excluding GST) from the Department of Family and Community Services' International Year of Volunteers grants. The funding will contribute towards Conveners' transport and accommodation costs to attend the Workshop, and the Mini-Conference to follow on Sunday 16 December. Support Group Co-ordinator Neil von Schill will shortly be in touch with Conveners about arrangements for the Workshop.

Plans are progressing for the visit by Dr Halstead and his wife Dr Jessica Scheer in December. The Management Committee has set the registration fees for the Seminar series in Canberra, Sydney and Newcastle as follows: members $40, carers/family $20, non-members $80. The cost will include a Conference program and light refreshments. Bookings will be essential and Registration Forms including venue details, dates and times will be sent out at the end of September. Raffle tickets will also be sent out at that time to those members who have indicated their willingness to buy or sell tickets to help fund Dr Halstead's visit.

A successful funding submission was made to Randwick City Council under its Small Grants program. Funding of $475 (excluding GST) was granted to help establish a Post-Polio Support Group in Sydney's Eastern Suburbs. The funding will enable a public meeting to be held, and will go towards venue hire, advertising, printing and postage, and light refreshments. Members in the region will be invited, as well as polio survivors living in the area who have previously not been aware of the Network. Attendees at the meeting will learn about the Network's support group structure, and how participating in a local support group can help polio survivors and their families better understand and manage the late effects of polio. While the major outcome sought from the meeting is the establishment of a Network Support Group, it is hoped that a model for the development of support groups in other areas of NSW not yet serviced will be another outcome.

Happy reading, and the Committee hopes to catch up with existing and new members alike at the 22 September Seminar.

Unless otherwise stated, the articles in this Newsletter may be reprinted provided that they are reproduced in full (including any references) and the author, the source and the Post-Polio Network (NSW) Inc are acknowledged in full. Articles may not be edited or summarised without the prior written approval of the Network. The views expressed in this publication are not necessarily those of the Network, and any products, services or treatments described are not necessarily endorsed or recommended by the Network.

2002 Seminar Update

Dr Elizabeth Ellis has accepted our invitation to present the results of her research into sleep-disordered breathing in polio survivors. She will speak at a Seminar to be held on Saturday 2 March 2002. She reports that over 50% of the questionnaires sent to members were completed and returned to the research team – a very pleasing response rate. The data is currently being analysed.

We are also pleased to announce that the Seminar to be given by Canadian virologist and non-paralytic polio survivor, Dr Marcia Falconer, which was deferred this year, has now been re-scheduled to Saturday 18 May 2002. We are planning to hold a day-long Mini-Conference and expect that Marcia will present topics including Non-Paralytic Polio and Post-Polio Syndrome, and The PolioVirus - Getting to Know Your Old Enemy.

Further details of both these Seminars, including venues, will be advised in upcoming Newsletters, but please note the dates in your diaries now.

The Late Effects of ME
Can They Be Distinguished From The Post-Polio Syndrome?
Dr EG Dowsett MBChB, Dip Bact
Dr Dowsett is Honorary Consultant Microbiologist to the Basildon and Thurrock Hospitals NHS Trust and a Member of the [UK Government] Chief Medical Officer's Working Party on ME/CFS. This article was originally a presentation to the All Party Group of MPs on ME/PPS on 31 January 2001. The article is © Lincolnshire Post-Polio Network, was published in their Library in February 2001 and is reprinted here with permission.

Introduction

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]

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.

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.

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 with 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 he remembered that ME is a life-long disability where relapse is always possible.

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.

What are the Late Effects of ME?
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, is striking and requires further explanation.

Which Group of ME Sufferers are Chiefly at Risk of the Late Effects? [4]
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 polio viruses among some 69 enteroviruses currently in circulation is deemed to have solved all problems!

What Is The Post-Polio Syndrome? [5,6,7]
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). Ninety-five percent 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. Modern 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.

Suggested New Criteria for the Diagnosis and Assessment of the Post-Polio Syndrome [7]

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.
A period of recovery.
A period of stable functioning for 10-50 years.
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].

Is it Possible that Many Patients Diagnosed as Having ME are Sufferers from
an Illness Clinically Identical to “Non-Paralytic” Polio? [6,8]

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:

Patients whose nervous system damage was not clinically obvious at the time of diagnosis.
Those who had minimal paralysis for a short period and were misdiagnosed as non-paralytic polio.
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.
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 (eg, Motor Neurone Disease), and especially those which are treatable.

Is it Necessary to Differentiate Between the Late Effects of ME and the
Post-Polio Syndrome? [8,9,10]

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.

What is the Evidence that the Late Effects of ME and the Post-Polio Syndrome Can Be Caused by Enteroviruses Other Than Polio Viruses 1-3?

[11] 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.
[12] From the late 1940s, studies in the USA indicated that outbreaks of major or minor enteroviral illness (e.g. 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 [Table 1], Ohio (1947) Delaware and Connecticut (1949).
[13] In the UK, an outbreak of poliomyelitis affecting an Edinburgh housing estate from August 1961 to 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.
TABLE 1. 1947 OUTBREAK OF SUMMER 'FLU, CINCINNATI, USA [12]

DIAGNOSIS	CASE No	CSF CELL COUNT	VIRULENCE OF POLIO VIRUS	3 LABORATORY TESTS FOR COXSACKIE VIRUS (NON-POLIO ENTEROVIRUS)			SUMMARY OF LABORATORY FINDINGS
Summer Flu	1	0	Polio HV	-	-	-	High virulence polio virus only
	2	40*	Non paralytic polio LV	-	-	-	Low virulence polio virus & infection of CSF
	3	3	"	+	+	+	Low virulence polio virus & coxsackie virus
	4	150*	"	+	+	+	Infection of CSF & low virulence polio virus & Coxsackie virus
Non Paralytic Polio	5	734*	Polio HV	-	-	-	Only high virulence polio virus & infection of CSF
	6	27	Polio HV	-	-	-	Only high virulence polo virus
	7	70*	-	-	-	-	Only Coxsackie virus & infection of CSF
Paralytic Polio	8	107*	Polio HV	-	-	-	Only high virulence polio 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

How May Symptoms of the Late Effects of ME and Polio Be Explained? [9,10]

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.

Muscle Weakness and Wasting [14]

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.
Comment [15]

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 of 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.

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 per 100,000 to 500 per 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 per 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 3 times 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].

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]

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]

References

RICHARDSON J. Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Enteroviral - Mediated Organ Pathology. The Haworth Press Inc. New York, London Oxford. ISBN 0-7890-1127-1 (in press).
DOWSETT 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.
Echo Viruses and Meningitis. Scottish Centre for Infection and Environmental Health, Weekly Report, 7.11.2000.
RAMSAY AM, DOWSETT EG. Then and Now. An epidemiological introduction (in the Clinical and Scientific Basis of Myalgic encephalomyelitis/Chronic Fatigue Syndrome. HYDE BM, GOLDSTEIN J, LEVINE P. Eds). The Nightingale Research Foundation, Ottawa, Ontario, Canada, 1992 Chapter 7 : 81-84.
DALAKAS MC. Post-polio Syndrome 12 years later (in the Post-polio Syndrome - advances in the pathogenesis and treatment. DALAKAS MC, BARTFIELD H, KURLAND LT. Eds). Annals of the New York Academy of Sciences. 1995; 753 : 11-18.
FALCONER M, BOLLENBACH E. Late Functional Loss in Nonparalytic Polio. American Journal of Physical Medicine and Rehabilitation. 2000; 79 (1) 19-23.
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.
JOHNSON EW: A Clarification of “nonparalytic” polio: 3
RL : Paralytic vs “Nonparalytic” Polio. Distinction Without a Difference?: 4-12.
HALSTEAD LS, SILVER JK: Nonparalytic Polio and Postpolio Syndrome: 13-18.
opus cit. reference 6)
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, BARTFIELD H, KURLAND LT. Eds.) Annals of the New York Academy of Sciences. 1995; 753 : 257-275.
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.
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.
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.
SELWYN S, HOWITT LF. A Mosaic of Enteroviruses. Polio, Coxsackie and Echo infection in a group of families. The Lancet. 1962. 2 : 548-551.
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.
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.
HALLAM H. Polio Survivors need holistic multidisciplinary assessment because the standard physical assessment is not adequate. LincPin Newsletter, 19 June 1999, Lincolnshire Post-Polio Network.
ROTBART HA, MCCRACKEN GH, WHITELY RJ et al. Clinical significance of enteroviruses in serious summer febrile illnesses of children. Paediatric infectious diseases. 1999. 18 : 869-74.
ROTBART HA, O'CONNELL JF, McKINLAY MA. Treatment of Human Enterovirus Infection. Antiviral Research. 1998. 38 : 1-14.
DOWSETT 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) : 29-42.
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.

I Didn't Have Polio - Did I ?
Marcia Falconer, PhD

Dr Dowsett and other researchers suggest that fibromyalgia, also known as myalgic encephalomyelitis (ME), is virtually identical to post polio syndrome. The acute illness caused by a group of closely related viruses, including polio strain 1, polio strain 2, polio strain 3, Coxsackie and Echo viruses, can be quite similar. Survivors of all these viruses have the possibility of developing virtually identical symptoms years after the initial infection. People who were diagnosed with polio call this group of symptoms, post polio syndrome or PPS. People who had Coxsackie or Echo viruses, or who had undiagnosed polio, call it fibromyalgia or ME. Those of us who had diagnosed polio can be assured that the problems we are experiencing have a physical cause and that there are some things we can do to help alleviate the symptoms; things such as pacing, using aids, and perhaps investigating some medical and alternative medical procedures. However imagine the problems encountered by people who had undiagnosed polio, or a related enterovirus, and now have PPS-like symptoms. Here is the true story of one such person.

Three weeks after the end of first grade, Ellen felt sick. She had a moderately high temperature and an upset stomach. World War II had ended four years previously and the family didn't have a car so her mother took her to the doctor by streetcar. Years later Ellen recalled the trip, especially the piercing headache made worse when the conductor rang a bell as he approached each cross street.

The doctor told Ellen to put her chin on her chest. Ellen remembered this because she did it even though it hurt. After taking her temperature, testing her reflexes and looking at her throat, the doctor told them to go home by taxi. Almost 50 years later, Ellen could still remember how good it felt to finally lay down on the cool sheets of her bed. After this, she recalled only snatches of events; a horrible backache, being carried from her bed to the bathroom, being unable to stand any light from the window. After an unremembered amount of time, she began to feel better.

Boredom. Ellen, still in bed, remembered the boredom and trying to cut out paper dolls, but her right hand and arm were clumsy and she kept cutting off “important” parts of dresses or the feet of the dolls themselves. In fury, she threw the scissors and heard it clunk against a hated piece of furniture. Her father had brought her old baby potty chair up to her bedroom. By grasping the arms of potty chair, Ellen could move from the bed to the potty and use it but the humiliation of doing this at the grand age of six, remained for a long time.

The rest of the summer she spent in bed or on the sofa. Her friends weren't allowed to visit though she remembered them waving at the window as they went off to do something interesting. Finally Ellen returned to second grade. At first she wasn't allowed to run during recess, but eventually she had no restrictions except those imposed on her by her body, and these she thought of as quite normal. For the rest of her school years Ellen was terrible at sports and hated them. Quite often she was tired. Dead tired, when everyone else thought she should feel fine and be helping the family to unload the car or some such thing. But the summer illness of her childhood was forgotten.

Fast-forward to 37 years later. Ellen now works as a secretary and does much typing. She's a two-handed touch typist but her right hand, arm and shoulder are starting to give her problems. The muscles twitch oddly after she does any repetitive work. But she ignores this.
Skip another 5 years. Ellen is a medical secretary and notices that she often “trips” while walking down the smooth hallway floors. And sometimes she is so unbearably tired that she can't think straight, much less function as a secretary. While taking a report to another floor, she trips and falls upstairs, badly bruising herself.

Ellen knows something is wrong and fears the worst. Her right arm and leg muscles are obviously getting weaker. There is almost continuous pain in her arm, leg and lower back. At night the muscles seem to have a life of their own, twitching so it's hard to fall asleep. Driven by desperation and fear, Ellen finally sees her doctor. After a general examination, the doctor pronounces Ellen to be fine. There is no obvious physical cause for her pain and the weakness she is experiencing in her muscles just means she needs to exercise more! And lose some weight.

Ellen takes on a program of aerobic exercise and muscle strengthening. She loses weight, but the pain and fatigue she feels from the exercise classes soon outweigh any benefits. She tells her doctor that exercise makes things worse, but the doctor either isn't listening or doesn't believe her. In frustration, Ellen leaves the doctor's office. It is getting hard to go up and down stairs and to open heavy doors, but since outwardly she looks fine, nobody believes her. At some point Ellen also begins to believe that it may be “all in her head”.

Then at a chance meeting in a shoe store, Ellen meets Susan. Brought together by the difficulties of buying shoes when one foot is almost a whole size different than the other foot, they feel like kindred souls. Three hours later the two women are still talking and are amazed at their similarities. Sue's more understanding doctor has diagnosed her virtually identical symptoms as fibromyalgia, also called myalgic encephalomyelitis (ME), and suggested Sue join a support group. Ellen accompanies Sue to the next support group meeting and is vastly relieved to find that not only is there another person with similar problems, but there is a whole group of people who can relate to her problems.

If we were able to go back and diagnose both Ellen and Sue during their childhood illness, we would find that Ellen had polio, strain 2 virus, while Sue had a related virus, Coxsackie A7. The symptoms during their acute illnesses were virtually identical and the problems they are encountering some 35 or more years later also are virtually identical. One had polio, the other had a very similar disease that is just not called “polio”.

Ellen does not know that she had polio as a child. The doctor never diagnosed poliomyelitis and she was never hospitalised. She only remembers bits and pieces of being sick the summer she was six years old. Unless she undergoes a series of tests, she will never know that her increasing muscle weakness and pain are due to previous polio. Rather than being able to learn what is useful and helpful to polio survivors who are experiencing post polio syndrome, Ellen will be counselled to do what is in vogue to treat fibromyalgia. Right now the suggestion is to “exercise away” the pain, something which may very well worsen her muscle condition.

People who were diagnosed with paralytic polio and have obviously affected limbs still have trouble convincing some doctors that post polio syndrome (PPS) is “real” and not in their heads or simply the result of using crutches for too long. People with a history of non-paralytic polio have even greater difficulty convincing the medical establishment that their fatigue, muscle weakness and pain are related to childhood polio. These people have a history of polio, either documented by hospital stays or by family stories but there are many people who had polio and don't even know it.
The statistics of polio look something like this: in 100 cases of polio (both diagnosed and undiagnosed cases), only 1 person will have paralytic polio. Ten people will have non-paralytic polio and all will have some nervous system damage which means they may develop PPS later in life. The remaining 89 people do not even know they had polio. The majority will have had no symptoms at all. Some had a fleeting stomach upset and felt a bit ill but none of these will have had nerve damage. However somewhere between 10 and 20 people will have had undiagnosed polio, possibly even paralytic polio as was the case with Ellen. These people are all at risk of developing post polio syndrome but will not realize that they had polio and hence will never even think of this as a possible reason for their symptoms!

Finally, nobody knows the infection rate for the viruses closely related to polio. But the number of cases is likely to be high with many undiagnosed. The symptoms produced by these viral infections are numerous, but include muscle weakness and/or paralysis in some cases. Because they do not cause visible epidemics of childhood paralysis, as the 3 strains of polio virus did before immunisation began, doctors and researchers do not considered them to be a problem. Perhaps, for 90 percent of the people who contract these viruses, there is no problem. But the remaining 10 percent - still a large number of people - may go on to develop fibromyalgia or other symptoms similar to those of post polio syndrome.

It is unlikely that people will devote sufficient money to developing a test to differentiate between people who had polio virus strains 1, 2 or 3 and people who had a closely related virus. Therefore, perhaps the best thing to do would be for doctors and people experiencing fibromyalgia, to initiate contact with people who deal with PPS. Perhaps, indeed, it is one large group of people who suffer from the same basic group of symptoms and who, together, can help each other deal with these problems in their lives.

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