Firth Part of the Article  By: Lauro S. Halstead, MD
 Published in: Scientific American
  LAURO S. HALSTEAD is director of the spinal-cord injury and the post-polio programs

By: Lauro S. Halstead, MD
Published in: Scientific American Journal
 LAURO S. HALSTEAD is director of the spinal-cord injury and the post-polio programs at the National Rehabilitation Hospital in Washington, D.C., and clinical professor of medicine at the Georgetown School of Medicine. He received his M.D. from the University of Rochester in 1963 and a master of public health degree from Harvard University in 1970. Halstead taught rehabilitation medicine and epidemiology at Rochester and Baylor College of Medicine for more than 20 years. His research interests include the late effects of polio, metabolic and endocrine changes in persons with spinal-cord injury, enhancing fertility in men with spinal-cord injuries and developing outcome measures for rehabilitation patients.
In the first half of the 20th century, the scourge of paralytic poliomyelitis seemed unstoppable. A major polio epidemic hit the New York area in 1916, and in the following decades the epidemics grew in size and became more deadly. The epidemic of 1952, for instance, affected more than 50,000 Americans and had a mortality rate of about 12 percent. It is difficult to realize today the extent of the fear and panic that gripped the public. Polio haunted everyone: families stayed at home; swimming pools were closed; public events were canceled.
Children in particular were at risk. With the introduction of Jonas E. Salk's injected killed-virus polio vaccine in 1955 and Albert B. Sabin's oral live-virus vaccine six years later, the epidemics were brought to an end. By the mid-1960s the number of new polio cases dropped to an average of 20 a year. Polio had been vanquished. Or so it seemed.
For the average American, polio no longer meant a disease but a vaccine. Medically, polio came to be regarded as a static, nonprogressive neurological disorder. It was believed that after rehabilitation and reeducation most survivors could reach a plateau of neurological and functional stability that would last more or less indefinitely -- and that is where our understanding of polio as a chronic disease remained until fairly recently.
Then, in the late 1970s, reports began to surface that people who had recovered from paralytic polio decades earlier were developing unexpected health problems such as excessive fatigue, pain in muscles and joints and, most alarming of all, new muscle weakness. Because there was little in modern medical literature about delayed neurological changes in polio survivors, the initial response by many physicians was that the problems were not real. For a time they were dealing with a cluster of symptoms that had no name -- and without a name there was, in essence, no disease. Having a name -- even if imprecise and misleading as to causation--at least confers an element of credibility.
By sheer weight of numbers, persons experiencing the late effects of polio finally started attracting the attention of the medical community, and in the early 1980s the term post-polio syndrome was coined. Today the syndrome is defined as a neurological disorder that produces a cluster of symptoms in individuals who had recovered from paralytic polio many years earlier. These symptoms typically appear from 30 to 40 years after the acute illness. The major problems are progressive muscle weakness, debilitating fatigue, loss of function and pain, especially in muscles and joints. Less common are muscle atrophy, breathing problems, swallowing difficulties and cold intolerance. Of all these health problems, however, the critical symptom of post-polio syndrome is new progressive weakness.
Patients most at risk for post-polio syndrome are those who had suffered a severe attack of paralytic polio, although some patients who seemingly had a mild attack have also developed the syndrome. The onset of these new problems often is insidious, but in many cases they appear to be precipitated by specific events such as a minor accident, a fall, a period of bed rest or surgery. Patients characteristically say that a similar event several years earlier would not have caused such a large decline in health and function.
My own experience seems to be typical of both recovery from paralytic polio and the new development of post-polio syndrome. I contracted polio during the epidemic of 1954 while traveling in Europe after my freshman year in college. I was 18 years old. My six-month journey of recovery took me from iron lung to wheelchair to foot brace and then to no assistive device at all. At times, improvement in strength seemed to happen overnight. Although my right arm remained paralyzed, the rest of my body regained most of the strength and endurance I had before my illness. As a result, I thought of myself as cured. I returned to college, learned to write with my left hand and even played intramural squash. On the morning of the third anniversary of the onset of my polio, I reached the summit of Mount Fuji in Japan after a climb of over 12,000 feet. As I watched the sun rise, I thought, "Polio is behind me. I have finally conquered it."
With the conquest of Mount Fuji fresh in my mind, I began to look for other mountains to climb. After college, I entered medical school. Internship and residency initiated yet another cycle of physically demanding years. In short, I got on with my life while polio receded ever further in my memory. Several years ago I began developing new weakness in my legs. As the weakness progressed over a period of months, I went from being a full-time walker who jogged up six flights of stairs for exercise to having to use a motorized scooter full-time at work.
Historical Background
Post-polio syndrome, it turns out, is not a new disorder after all. It was described in the French medical literature in 1875, and then, as often happens in medicine, it was forgotten. Over the next 100 years, approximately 35 reports on post-polio weakness were published in the medical literature. By 1984 a growing awareness of the delayed effects of polio prompted me and other researchers to organize an international conference at the Warm Springs Institute for Rehabilitation -- the great polio treatment mecca in southern Georgia established by Franklin Delano Roosevelt, who was paralyzed by polio in 1921 at the age of 39. Roosevelt felt that swimming in the warm waters of a natural spring at a health resort strengthened his muscles, and in 1926 he purchased a hotel there and turned it into a nonprofit foundation.
A second international meeting on post-polio syndrome was held at the Warm Springs Institute in 1986, and in the following years there was a dramatic increase in basic and clinical research into the long-term effects of polio. In 1994 the New York Academy of Sciences and the National Institutes of Health cosponsored another international meeting that culminated in the publication of a special issue of the Annals of the New York Academy of Sciences: "The Post-Polio Syndrome: Advances in the Pathogenesis and Treatment." That conference signaled the acceptance of post-polio syndrome as a legitimate clinical entity.
Surprisingly, accurate figures about the number of Americans who have had paralytic polio are not available and probably never will be. There is no national registry of persons who were diagnosed with the disease, and there is no way, after all these years, to compile accurate figures from state and local health departments. The best estimate is based on information from the federal government's National Center for Health Statistics, which collects data on health and disability issues every year from a random sample of U.S. households. Based on data from the 1987 survey, the National Center for Health Statistics calculated there were more than 640,000 survivors of paralytic polio, which would mean there are more survivors of paralytic polio than there are persons with multiple sclerosis, amyotrophic lateral sclerosis or even spinalcord injury.
Since 1987 an unknown number of polio survivors have died, but immigrants, refugees and illegal aliens have added an unknown number to the U.S. population of polio survivors. No one knows how many survivors of paralytic polio have post-polio syndrome. Some studies indicate the figure could be as high as 40 percent. If this estimate is accurate, then the total number of persons in this country currently suffering from post-polio syndrome could reach 250,000.
Knowledge of how the poliovirus infects the body can be helpful in understanding the possible causes of post-polio syndrome. It is a small RNA virus that can enter the body when contaminated water or food are ingested, and even when contaminated hands touch the mouth. The vast majority of persons who become infected either have no symptoms or experience a self-limited illness characterized by fever and gastrointestinal upset for several days. The poliovirus, which replicates in the lymphoid tissue of the throat and small intestine, either passes harmlessly from the gut or travels in the blood to all parts of the body. In a small minority of infected persons--usually 1 to 2 percent--the virus invades the central nervous system and produces an unpredictable amount of paralysis. Soon,  Second Part of the article.

The Polio Crusade

THE POLIO CRUSADE IN AMERICAN EXPERIENCE A GOOD VIDEO THE STORY OF THE POLIO CRUSADE pays tribute to a time when Americans banded together to conquer a terrible disease. The medical breakthrough saved countless lives and had a pervasive impact on American philanthropy that ... Continue reading..http://www.pbs.org/wgbh/americanexperience/polio/

Erradicación de La poliomielitis

Polio Tricisilla Adaptada

March Of Dimes Polio History

Dr. Bruno




A 41-year-old man developed an acute illness at the age of 9 months during which, following a viral illness with headache, he developed severe weakness and wasting of the limbs of the left side. After several months he began to recover, such that he was able to walk at the age of 2 years and later was able to run, although he was never very good at sports. He had stable function until the age of 18 when he began to notice greater than usual difficulty lifting heavy objects. By the age of 25 he was noticing progressive difficulty walking due to weakness of both legs, and he noticed that the right calf had become larger. The symptoms became more noticeable over the course of the next 10 years and ultimately both upper as well as both lower limbs had become noticeably weaker.

On examination there was wasting of the muscles of upper and lower limbs on the left, and massively hypertrophied gastrocnemius, soleus and tensor fascia late on the right. The calf circumference on the right exceeded that on the left by 10 cm (figure1). The right shoulder girdle, triceps, thenar eminence and small muscles of the hand were wasted and there was winging of both scapulae. The right quadriceps was also wasted. The wasted muscles were also weak but the hypertrophied right ankle plantar flexors had normal power. The tendon reflexes were absent in the lower limbs and present in the upper limbs, although the right triceps was reduced. The remainder of the examination was normal.

Figure 1

The patient's legs, showing massive enlargement of the right calf and wasting on the left


What is that nature of the acute illness in infancy?
What is the nature of the subsequent deterioration?
What investigations should be performed?
What is the differential diagnosis of the cause of the progressive calf hypertrophy?



An acute paralytic illness which follows symptoms of a viral infection with or without signs of meningitis is typical of poliomyelitis. Usually caused by one of the three polio viruses, it may also occur following vaccination and following infections with other enteroviruses.1 Other disorders which would cause a similar syndrome but with upper motor neurone signs would include acute vascular lesions, meningoencephalitis and acute disseminated encephalomyelitis.


A progressive functional deterioration many years after paralytic poliomyelitis is well known, although its pathogenesis is not fully understood.2 It is a diagnosis of exclusion; a careful search for alternative causes, for example, orthopaedic deformities such as osteoarthritis or worsening scoliosis, superimposed neurological disorders such as entrapment neuropathies or coincidental muscle disease or neuropathy, and general medical causes such as respiratory complications and endocrinopathies.3


Investigations revealed normal blood count and erythrocyte sedimentation rate and normal biochemistry apart from a raised creatine kinase at 330 IU/l (normal range 60–120 IU/l), which is commonly seen in cases of ongoing denervation. Electromyography showed evidence of denervation in the right APB and FDI with polyphasic motor units and complex repetitive discharges, no spontaneous activity in the left calf and large polyphasic units in the right calf consistent with chronic partial denervation. Motor and sensory conduction velocities were normal. A lumbar myelogram was normal. Magnetic resonance imaging (MRI) scan of the calves is shown in figure2.

Figure 2

Axial T1 weighted MRI scan (TR 588 ms, TE 15 ms) of the calves, showing gross muscle atrophy and replacement by adipose tissue on the left, and hypertrophy of the muscles on the right, with only minor adipose tissue deposition


The differential diagnosis of the progressive calf hypertrophy is given in the box.

Causes of calf muscle hypertrophy

Chronic partial denervation

  • radiculopathy

  • peripheral neuropathy

  • hereditary motor and sensory neuropathy

  • spinal muscular atrophy

  • following paralytic poliomyelitis

    Neuromyotonia and myokymia

  • Isaac's syndrome

  • generalised myokymia

  • neurotonia

  • continuous muscle fibre activity due to: chronic inflammatory demyelinating polyradiculopathy, Guillain Barre syndrome, myasthenia gravis, thymoma, thyrotoxicosis, thyroiditis

    Muscular dystrophies



  • tumours

  • amyloidosis

  • cysticercosis

    Link here