NeuroRehabilitation An InterdIIclplllllrr Journal

ELSEVIER

NeuroRehabilitation 8 (1997) 73-81

Post-polio syndrome: historical perspective, epidemiology and clinical presentation Anne C. Gawne*, Lauro S. Halstead The Post-Polio Program, National Rehabilitation Hospital, 102 Irving St. NW, Washington, D.C. 20010, USA

Abstract Paralytic poliomyelitis has plagued mankind for centuries. The incidence of acute paralytic poliomyelitis dramatically declined in 1955 only after the introduction of the inactivated polio vaccine. Post-Polio Syndrome (PPS) was described as early as the 1870s, but was not clearly recognized by the medical community until the early 1980s. This article reviews the history and epidemiology of acute paralytic poliomyelitis, as well as post-polio syndrome, from its early description by Charcot and others in 1875, to the modern roots of PPS research in 1954. Finally, we will describe the presenting features of PPS, in both clinical and population studies which represent two very different 'faces' of post-polio. © 1997 Elsevier Science Ireland Ltd. Keywords: Paralytic poliomyelitis; Post-polio syndrome; Epidemiology of polio and post-polio syndrome; Clinical features of post-polio syndrome

1. A short history of paralytic poliomyelitis

Poliomyelitis is an ancient disease with evidence for a case as early as 3700 B.C. An Egyptian stele, dating back from the period 1580-1350 B.C. depicts a young boy with a withered leg and a shortened deformed foot, characteristic of a polio affected limb [1]. Writings from the midBronze Age in Greece and from the 2nd to 6th

* Corresponding author. Spain Rehabilitation Center, University of Alabama at Birmingham, 1717 Sixth Avenue South Birmingham, AL 35233-7330, USA. Tel.: + 1 205-934-3490; Fax: + 1 202-975-4896.

centuries in Italy contain descriptions compatible with paralytic polio. Perhaps the earliest recorded first person account of polio is that of Sir Walter Robert Scott (born in 1771), who became ill at the age of 18 months, 'In the morning I was effected by the fever ... On the 4th, I lost the power of my right leg... The limb affected was much shrunk and contracted' [2]. The first clinical description dates back to 1789 by an English physician, Dr. Michael Underwood, who wrote, 'Where both lower limbs are paralytic, nothing seems to do any good but irons to the legs' [3]. In the United States, there were isolated reports of polio from as early as 1841. In 1894, it

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A.C. Gaune, L.S. Halstead / NeuroRehabilitation 8 (1997) 73-81

became a public health concern, with the first reported polio epidemic in Otter Creek Valley, Vermont, which affected 132 petsons [4]. Subsequently, there were 17 additional epidemics of varying intensity until 1907. By 1913, polio had affected over 25000 persons in every state of the US and every province of Canada. It was not until the epidemic of 1916, that polio truly became a national concern and provoked widespread public health interest. During this epidemic, 9000 cases were reported in New York City alone, resulting in 2343 deaths [5]. Almost all of the patients were children, most under the age of 5 years. Thus, polio became known as 'infantile paralysis'. The New York City Health Commissioner, Dr. Haven Emerson, felt helpless against combating the disease, stating in a New York Times report, ' ... fighting infantile paralysis consists largely in doing everything that seems effective in the hope that some of the measures taken will be effective' [6]. In addition to New York City, epidemics were reported in many states, including Ohio, Rhode Island, Kansas, Wisconsin and Illinois. Quarantines of 6-8 weeks became commonplace. Over the next 4 decades, polio epidemics became larger and more frightening, not because the absolute numbers of those affected was so large, but because the disease struck unpredictably and swiftly. The largest epidemic occurred in 1952 and affected more than 57879 people, 3145 of whom died. In 1953, more American children died of paralytic polio than of any other communicable disease. At all ages, polio took more male victims than female. All races contracted the disease in proportional numbers, although in the late epidemics, the death rate was higher among blacks who had less access to treatment, such as the iron lung, than whites. In early epidemics, in which no treatment existed, death rates among the races were similar. Epidemic poliomyelitis was found throughout the United States and Canada, in rural and urban settings alike. The highest concentrations of the disease were found in the growing suburbs of post-World War II America. Epidemics from year to year peaked and ebbed and could be explained in two ways: (1) by environmental conditions that either encouraged or

discouraged the spread of disease; and (2) by differences in the strength of the different strains of polio. There has been no definitive documentation explaining the occurrence of epidemics in any given year. During the early 1950s, efforts were ongoing to develop vaccine. Most notable were two Americans, Albert Sabin, who developed an attenuated live vaccine, and Jonas Salk, who introduced an inactivated virus vaccine. The preliminary discovery of the Salk vaccine was announced in public over the radio on April 4, 1954, by a syndicated newspaper columnist, Walter Winchell, who stated, 'Good Morning Mr. and Mrs. America, and all ships at sea... In a few minutes I will report on a new polio vaccine; it may be a killerL .. Attention all doctors and families: the National Foundation for Infantile Paralysis plans to inoculate one million children with a new vaccine this month' [7]. This was a blow to Salk and his colleagues, especially since he wasn't consulted before the alarm was sounded. Field trials on humans began soon after. On April 26, 1954, a 6-year-old boy, Randy Kerr, was the first child to be vaccinated [5]. He was followed by classmates in the New York public school system. The results of the trials were announced on April 12, 1955 in Ann Arbor, Michigan. The news of the success of the field trial was broadcast nationwide by NBC and changed the face of polio forever. Five years after the IPV became available, the Sabin attenuated live vaccine or oral polio vaccine (OPV) was introduced. Although the Sabin vaccine is felt by many to be superior to the Salk, it does have the great disadvantage of producing paralytic polio in an extremely small number of recipients. Nonetheless, by the mid-1960s, the live viral vaccine had become the choice both in the US and Britain, and endorsed by the American Medical Association. The impact this vaccine made on contributing to the decline in cases of acute poliomyelitis is shown in Fig. 1. [8]. By 1972, there were fewer than 0.01 cases per 100000 persons in the United States, and the death rate was immeasurably low. In 1979, the last case of indigenous wild virusassociated polio in the United States was reported. Worldwide, efforts to eradicate the virus

A.C. Gaune, L.S. Halstead / NeuroRehabilitation 8 (1997) 73-8/

75

- - case rate

100

---- death-rate 10

§

g :sc. CIl

ca

a:

0.1 0.01 0.001

+-----,-----r----,...-----....----r---1932

1942

1952

1962

1972

1982

Year Fig. 1. Reported rates per 100000 persons of poliomyelitis and death from poliomyelitis, United States, from 1932 to 1989. (Ipy = inactivated polio vaccine, opy = oral polio vaccine).

continue. In May 1988, The World Health Assembly declared that the World Health Organization (WHO) was committed to the global eradication of poliomyelitis by the year 2000 [9]. Even so, in 1993, WHO estimated an incidence of 110000 new cases worldwide, with a prevalence of over 10 million people with paralytic polio [10]. 2. Historical background of post-polio syndrome

For more than 100 years, it has been recognised that new muscle weakness occurs in polio survivors many years after their initial illness. The first descriptions appeared in 1875 in three separate case histories reported in the French literature [11-13]. All of these patients were young men who had paralytic polio in infancy. They developed new weakness not only in previously affected muscles, but also in muscles believed to be uninvolved. They all had physically demanding jobs and performed repetitive activities. In a commentary on one of the cases, Jean Martin Charcot suggested that a previous disease of the spinal cord may leave an individual more susceptible to a subsequent spinal disorder and that the new

weakness was secondary to overuse of the involved limbs [13]. Since these initial reports, there have been other sporadic reports of similar phenomenon. In 35 studies reporting almost 250 cases from 1900 to the early 1980s, investigators have described new problems, including weakness and fatigue occurring up to 71 years after the acute polio episode [14]. These changes were most commonly diagnosed as a form of progressive muscular atrophy, chronic anterior poliomyelitis, late motor denervation, and even forme fruste amyotrophic lateral sclerosis [15]. As awareness about these new problems grew, so did the number of hypotheses for their etiology. In 1954, at a staff meeting in Warm Springs, Dr. Clint Knowlton discussed neuromuscular fatigue and presented evidence to support his feeling that excessive exercise produced definitive damage to muscles that had been injured by polio. Dr. Robert Bennett acknowledged that this theory deserved much consideration [16]. They reported, however, that overwork weakness was not a new or original finding. Dr. Lovett, in a survey of his experience with the victims of the 1913 polio epidemic, re-

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A.C. Gaune, L.S. Halstead / NeuroRehabilitation 8 (1997) 73-81

portedly found that excessive activity caused deterioration rather than the expected and usual improvement in muscle strength [17]. On the other side of the Atlantic, in a presentation to the Royal Society of Medicine in 1962, Zilkha reviewed 11 patients with motor neuron disease who developed progressive weakness 20-40 years later [18]. He stated 'It could be suggested that the subsequent development of disease of the motor neuron in those patients with a previous history of poliomyelitis, usually 25 years before, is related to the occurrence of that earlier disease'. One of the early pioneers of the post-polio movement was a lay woman named Laurie. Although she did not have polio herself, four of her siblings were affected by the disease, and two subsequently died of respiratory complications. She was a volunteer in the use of the Kenny treatment of placing warm wool blankets on the limbs of polio victims [19]. In 1963, she recognized the growing needs of polio survivors, writing ' ... the most important need is immediate planning for their future, when, with the deaths of their parents who now care for them, they will be faced with the soul-killing prospect of vegetating in county homes with the senile'. Gini envisioned small, homelike, residence-care centers throughout the country that would provide a place where residents would ' ... have the opportunity to live-not merely to exist' [20]. The polio survivors communicated via the Toomey j. Gazette, a newsheet developed in one of the respiratory polio centers and named after John Toomey, a pioneer in the treatment of respiratory polio. Over the years, Toomey j. Gazette outgrew its parochial origins, changing its name to Rehabilitation Gazette, 'The International Journal for Independent Living by Disabled People'. It was based in St Louis and became, as Gini described ' ... the glue that holds the polios of the world together' [21]. In an article in the 1979 Rehabilitation Gazette, Larry Schneider, a polio survivor, drew attention to the deleterious effects of aging on polio survivors and to the lack of doctors who knew anything about the disease any more [22]. This article struck a responsive chord with many other individuals with a history of polio facing similar prob-

lems and prompted NBC to air a program on Prime Time Saturday on the subject. The producer

wanted to make the program 'as mild as possible' and not to overly alarm anyone, but the show had the opposite effect, frightening many polio survivors. Therefore, Gini introduced a special feature on post-polio aging problems in the Rehabilitation Gazette, with a questionnaire for readers to fill out, and details of a forthcoming conference in Chicago. One article written by a polio survivor pointed to the paradox confronting middle aged polio survivors with declining strength, 'It isn't their vices that are catching up to them, it's their virtues, good old-fashioned rehabilitative virtues: exercise, effort and physical achievement. In the 1940s and 1950s, hard work had made them strong. Now rehabilitation specialists were telling them to slow down, take it easy, perhaps all that exercising had not been such a good idea after all' [23]. In 1981, The International Year of Disabled People, Gini Laurie invited a number of specialists to an international symposium held in Chicago to discuss, 'What ever happened to the polio patient?'. This was the first of many post-polio conferences, and it attracted over 200 polio survivors, 70 in wheelchairs and 30 respirator users, to discuss the challenges these survivors faced [24]. This conference was the first to address not just the problem of functional deterioration, but also the increasing ignorance about polio and the neglect of polio survivors following the virtual elimination of the disease as a result of vaccines [25]. It prompted consumers to petition the National Institutes of Health to begin research and was the drive for the initiation of support groups throughout the country. This was the first of a number of conferences featuring scientists who subsequently studied these problems in depth. Among them was Lauro Halstead, a polio survivor himself, and David Weichers, a specialist in neuromuscular physiology and electrodiagnosis. The two of them agreed to collaborate in organizing a conference. Their original intention was 'to get together a bunch of elder statesman in our field and find out what they have to say'. But nothing happened [5]. At the second post-polio conference in St. Louis

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in 1983, Halstead summarized the frustrations attendees were feeling when he announced, 'Unless we look at this as a legitimate problem that needed to be studied in a scientific way, we're going to be here in a year or two from now all bitching and moaning and complaining, but no further ahead' [5]. The impetus to see the late effects of polio as a legitimate problem that needed to be studied in a scientific way led Halstead and Weichers to organize the first International Conference on post-polio syndrome the following year. The Warm Springs Rehabilitation Institute the Mecca for polio treatment for thousands of Americans, founded by Franklin Delano Roosevelt in Warm Springs, Georgia - was the setting for the 1984 conference. This conference brought together some of the world's experts on pathology, neurology, rehabilitation medicine, virus research and related fields [26]. This was the first medical conference devoted to clarifying the nature, pathogenesis and treatment of PPS. Among the topics discussed was the appropriate nomenclature. Should PPS be used? Is it really a syndrome? In addition, the possible etiology became a subject of debate. A second International Conference-also organized by Halstead and Weichers and held in the beautiful and historic setting of Warm Springs, Georgia - followed in 1986 [27]. Following these conferences, awareness of PPS grew both among physicians and survivors. Support groups and organizations such as the Polio Society (in Washington D.C.) were formed. 'They brought survivors of all degrees of disability together and revived their former togetherness and sharing of problems and information' [28]. The Gazette Rehabilitation organization became known as the Gazette International Networking Institute, chosen for its acronym GINI, after Gini Laurie [29]. The GINI meetings of both survivors and professionals continued on alternate years throughout the 1980s, and most recently in 1994. In 1994, the New York Academy of Science and the National Institutes of Health cosponsored another international meeting which cumulated in the publication of an issue of the Annals of the New York Academy of Sciences 'Post-polio syndrome, pathophysiology and treatment' [30]. The

77

occasion of this conference, which dealt with a number of new and exciting developments in this field, signaled that PPS had arrived as a legitimate and important area of scientific and clinical investigation. 3. Epidemiology Before 1913, over 25000 cases of acute polio were reported in the US and Canada. In the large polio epidemic of 1916, over 27000 cases occurred in the US, causing 6000 deaths [5]. Mter this epidemic, polio cases in the US subsided and did not begin to grow again in significant numbers until the early 1940s. As shown in Fig. 1, the number of poliomyelitis cases, both paralytic and non-paralytic, reported in the United States increased from 3820 in 1932 (3.1 cases /100000) to 57879 in 1952 (37.2 cases/100 000) [8]. Deaths from polio showed a similar pattern, going from 818 in 1932 to 3145 in 1952 [3D], During the big epidemics in North America in 1952-1954, the incidence of new cases was 15/100000, or about 40000 reported cases per year, with the majority occurring in children and young adults aged between 1 and 35. Mter the Salk Vaccine was introduced in 1955, the incidence dropped to 0.04/100000 by 1963 [8]. The last confirmed case of paralysis from domestic wild virus polio in the US occurred in 1979. Since then, paralytic polio only occurs as a rare complication of the oral vaccination. In the US between 1961 and 1964, there was an incidence of vaccine-related paralysis in 4.9/10 million doses compared to an incidence of 0.23/10 million in 1989, as Fig. 2 shows [8]. The greatest risk is from the initial immunization (1/700000) [31]. A survey by the National Center for Health Statistics in 1987 estimated there were more than 640000 survivors of paralytic polio [32]. Thus, despite the virtual elimination of new cases, paralytic polio remains one of the most prevalent neuromuscular diseases in this country. While PPS is more common in those who have experienced moderate to severe paralysis, the population based survey reported by researchers at the Mayo Clinic showed that as many as 64% of polio

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A.C. Gaune, L.S. Halstead / NeuroRehabilitation8 (1997) 73-81

25OOl\

en CI) en

I:J\

ctI

(.)

0

-

Total*

100

....

80

E :::::I Z

60

CI) ..Q

II Vaccine-associated

40

20 0 1960

1970

*excluding imported cases

year

1980

1989

Fig. 2. Reported cases of paralytic poliomyelitis (total and vaccine associated per 10 million doses of sabin vaccine) US, 1960-1989.

survivors develop new symptoms [33]. If this sample is representative of the larger population, then it is estimated that over 409000 people may be experiencing the late effects of polio. While some of this population has died since the original survey, there has also been an unknown and largely unexpected increase in the number of polio survivors in the US resulting from the influx of affected immigrants, refugees, and illegal aliens largely from Southeast Asia and Latin America. In 1991, the World Health Organization (WHO) estimated that 85% of children world-wide received three doses of the TOPV vaccine, a significant increase over the percentage in 1971(15%), due largely to the effort WHO put into their vaccination campaign [9]. While no cases of wild polio infection occurred in the Americas in 1993, WHO estimates that 110000 new cases occurred in the developing world; in particular Africa, Asia, and India, due to inadequate immunization [10]. Worldwide, the prevalence of paralytic polio is over 10 million and represents those at risk for developing PPS.

4. Clinical presentation of post-polio syndrome Post-polio syndrome is a cluster of .symptoms which occurs in individuals who had paralytic polio years earlier. Typically, these symptoms occur 30-50 years after the acute illness and include progressive weakness, fatigue, pain in muscles and joints and loss of function. Less common symptoms include breathing and swallowing difficulties and cold intolerance. Table 1 [34] lists the frequency distribution of the most common changes reported in several studies of post-polio populations [35-40]. Table 2 lists the most common functional changes that these people develop [34]. When examining this data, it is important to distinguish between 'the two faces of post-polio': the clinical studies and the population studies. The clinical studies, such as those done by Agre and Halstead examine the numerator data, or the symptoms seen in patients evaluated in post-polio clinics who came in because they were having new health problems [35,38,39]. In these studies, they found the most common symptoms were fatigue

A.C. Gaune, L.S. Halstead j NeuroRehabilitation 8 (1997) 73-81

79

Table 1 Comparison of most common new symptoms in subjects with a history of paralytic polio reported in six studies [34] Sympton

Codd N= 28 (%)

Halstead N=132(%)

Chetwynd N=694(%)

Agre N=79(%)

Ramlow N=474(%)

Halstead N=539(%)

Fatigue Joint pain Muscle pain New weakness Affected muscle Unaffected muscle Cold sensitivity

59 74" 48 71 66 15 46

89 71 71

48 60· 52 47

86 77 86 69 80 53

34 42" 38 38

87 a 80 79

NjA 69 50 29

NjA NjA NjA

NjA

NjA NjA

NjA

87 77

NjA

26

N = Number of subjects reported. "Most frequent symptom.

Table 2 Comparison of most common new functional problems in persons with a history of paralytic polio reported in four studies [34] Functional problem

Codd N=28(%)

Halstead N=132(%)

Agre N= 79(%)

Halstead N= 539(%)

Difficulty walking Difficulty climbing stairs Difficulty with ADLS

25

63 a 61 17

NjA 67" 16

85 a 82 62

NjA

14

= Number of subjects reported. "Most common new problem.

N

(59-89%), weakness in both previously affected and 'unaffected' muscles (42-87%), muscle and joint pain (48-100%). Less common symptoms included functional loss, difficulties with breathing and swallowing, and cold intolerance. On the other hand, the population studies such as those done by the Mayo Clinic and in Allegheny county [37,40], used both numerator and denominator data, with rather different findings, as one would expect since they were picked randomly for study because they had a history of polio, not because they were having symptoms. The Mayo Clinic study is an ongoing prospective study of all residents in Olmstead County, Minnesota with acute polio between 1935 and 1960 [37]. They found that 42% had new weakness, 60% had a combination of weakness, fatigue and pain, and only 10% had loss of function. In the Allegheny county population based study, which used validated

questionnaires, researchers found 29% of the respondents had new weakness, while 21% had diminished function [40]. The results of these population based studies strongly suggest that PPS is not as prevalent as earlier clinical studies had suggested. Patients most at risk for developing new problems are those who experience more severe acute paralytic polio, although some patients with typical PPS had a mild case of polio with good recovery. The onset of these problems is most commonly insidious, although many times it will be precipitated by an injury, a minor illness or surgery, weight gain or period of bed rest. Patients characteristically say that a similar event years earlier would not have caused the same decline in health and function. Likewise, new problems may begin when co-existing medical problems such as diabetes develop or worsen [41].

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As a result of these studies, specific diagnostic criteria have been developed to clinically define PPS. These include: • •







A prior episode of paralytic polio confirmed by history, physical exam and laboratory data. Standard electromyograph evaluation demonstrates changes consistent with prior anterior horn cell disease (AHCD): increased amplitude and duration of motor unit action potentials, an increased percentage of polyphasic potentials and, in weak muscles, a decrease in the number of motor units on maximum recruitment. Fibrillations and sharp waves may or may not be present. A period of neurologic recovery followed by an extended interval of neurological and functional stability preceding the onset of new problems. The interval of neurologic and functional stability usually lasts 20 or more years. The gradual or abrupt onset of new neurogenic, non-disuse weakness in previously affected and/or unaffected muscles. This may or may not be accompanied by other new health problems such as excessive fatigue, muscle pain, joint pain, decreased endurance, decreased function and atrophy. Exclusion of medical, orthopedic and other neurologic conditions that might cause the health problems listed above [42].

5. Conclusion The disorder of PPS is undoubtedly as old as paralytic polio itself. The term, however, and the recognition of the clinical entity are relatively recent. The late effects of polio began gaining widespread recognition in the early 1980s and the term PPS was coined at about the time of the first International Post-Polio Conference at Warm Springs, Georgia in 1984. In the intervening years, there has been a sharp and continuing interest given to the subject by clinicians and researchers, leading to a more precise possible definition of PPS, a better understanding of the possible etiologies and the development of and refinement of rational and effective strategies for its management. However, amidst this burgeoning interest, questions about PPS as a distinct clinical entity

remain: there is no pathognomonic test; the symptoms are subjective and fairly general. In addition, the pathogenesis remains elusive. Still, clinicians and researchers are faced with the ongoing challenge of recognizing and managing patients with PPS. The remainder of this issue of Neurorehabilitation will examine PPS in greater depth, giving guidance for the future. References [1]

[2] [3]

[4]

[5]

[6] [7] [8]

[9]

[10]

[11]

[12]

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[15]

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Bennett RL. Minutes of the Georgia Warm Springs Foundation staff meeting. Jan 1954. Bennett RL, Knowlton Gc. Overwork weakness in partially denervated skeletal muscle. Clin Orth 1967;12(4):22-29. Zilkha KJ. Discussion on motor neuron disease. Proc R Soc Med 1962;55:1028-1029. Laurie VW. Twenty years in the Gazette House. In: Rehabilitation Gazette 1978, vol 21. Laurie VW. Toomey j Gazette: horizontally and vertically yours. In: Randolph-Macon Woman's College Alumnae Bulletin, 1963. Dibernado G. Dear, dear editor. St Louis Weekly, May 1985. Schneider L. Those passing years. In: Rehabilitation Gazette 1980, vol 23. Mailot A. Age and the old polio. Do the virtous fade first? Rehabil Gaz 1981, vol 24. Raymond J, Laurie VW. The polio conference: a blueprint of creative cooperation for all who are disabled. Rehabil Gaz 1981, vol 23. Anderson AD. Loss of ambulatory ability in patients with old anterior poliomyelitis. Lancet 1972;18:1061. Halstead LS, Weichers DO eds. The Late Effects of Poliomyelitis. Symposium Foundation Miami, 1985. Halstead LS, Weichers DO eds. Research and Clinical Aspects of the Late Effects of Polio. March of Dimes Birth Defects Foundation, White Plains, NY, 1987. Laurie VW. The role of networking and support groups. In: Munstat TL, ed. Post-Polio Syndrome. London: Butterworth-Heinmann, 1991;112. Laurie VW. Rehabilitation Gazette 1982;25. Dalakas MC, Bartfeld, Kurland L, eds. The Post-Polio Syndrome: Advances in the pathogenesis and treatment. Annals New York Academy Sciences 1995, vol 753. Nkwone BM, Wassilak SG, Orenstein WA. Vaccine associated paralytic poliomyelitis. United States 1973-1984. JAMA 1987;257:1335-1340. Parsons PE. National center for health studies: letter to the editor. N Engl J Med 1991;325(15):1108.

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[33] Windebank AJ, Lichty WJ, Daube JR. Prospective cohort study of polio survivors in Olmstead County, Minnesota. In: Dalakas MC, Bartfeld H, Kurland LT, eds. The Post-Polio Syndrome: Advances in the Pathogenesis and Treatment. Annals New York Academy Sciences vol 753, 1995;81-86. [34] Gawne AC, Halstead LS. Pathophysiology and treatment of post-polio syndrome. CRC Critical Rev Phys Rehabil Med 1995;7(2):147-188. [35] Agre JC, Rodriquez AA, Sperling KB. Symptoms in a post-polio clinic. Arch Phys Med Rehab 1989;70:367 - 370. [36] Chetwynd J, Hogan D. Post-polio syndrome in New Zealand: a survey of survivors. N Z Med J 1993; 106:406-408. [37] Codd MP, Mulder DW, Kurland LT, Beard CM, O'Fallon WM. Poliomyelitis in Rochester Minnesota 1935-1955. Epidemiology and long term sequelae a preliminary report. In: Halstead LS, Weicher DO, eds. Late effects of Poliomyelitis. Symposium Foundation, Miami: FL, 1985;121-133. [38] Halstead LS, Rossi CD. New problems in old polio patients: results of a survey of 539 polio SUrviVorS. Orthopedics 1985;8:845-850. [39] Halstead LS, Rossi CD. Post-polio syndrome: clinical experience with 132 consecutive outpatients. In: Halstead LS, Weichers DO, eds. Research and Clinical Aspects of the Late Effects of Poliomyelitis. March of Dimes Birth Defects Foundation 23(4), White Plains NY 1987;13-26. [40] Ramlow J, Alexander M, Laporte R, Kaufman C, Kuller K. Epidemiology of the post-polio syndrome. A J Epidemiology 1992; 136(7):769-784. [41] Halstead LS. Late complications of Poliomyelitis. In: Goodgold J, ed. Rehabilitation Medici. St. Louis: C.V. Mosby 1988;328-342. [42] Halstead LS. Assessment and differential diagnosis for post-polio syndrome. Orthopedics 1991;14(11): 1211-1217.

Post-polio syndrome: historical perspective, epidemiology and clinical presentation.

Paralytic poliomyelitis has plagued mankind for centuries. The incidence of acute paralytic poliomyelitis dramatically declined in 1955 only after the...
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