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Dr Henry writes about Debilitating Fatigue

Dr. Henry writes about Debilitating Fatigue

As you may recall, several months ago, I wrote about the problems that many polios face with fatigue. Many experience peripheral muscle fatigue which may manifest itself with muscle weakness and/or pain, and others may experience central fatigue which may be experienced with mental fatigue, increased sleep requirement, difficulty maintaining wakefulness, difficulty with word finding, and emotional factors such as difficulty with anxiety and depression. I mention all this because I feel that central fatigue has been my most difficult problem, and yet this type of fatigue is probably the least understood.

Beginning near the end of May 1996, I began to experience an immense degree of fatigue. I had first felt this type of fatigue in 1990. In 1991, I had numerous medical tests that did not uncover any particular new problem. Later in 1991, I acquired an electric scooter and also began attending our support group. There was more understandable medical information available with the support group than I had found from any medical source. I can state this with honesty as I am a physician myself. As a result, I improved and resumed my practice for the next five years in my usual workaholic, Type A way. As many polios, change is very difficult, and recently I have made the decision that many of you have made. I have recently given up the practice of psychiatry, and am trying to accept a totally disabled status. As you can imagine and perhaps know, this is no fun. In the process of making this decision, I had numerous medical tests again, and as before, no other meaningful medical problem was discovered.

All of this has increased my interest in the existence and explanation of the etiology of central fatigue. We have a very technically written book in our library entitled, The Post Polio Syndrome, Advances in the Pathogenesis and Treatment published by the New York Academy of Sciences in early 1996. There is a chapter in this book about the “Pathophysiology of a Central Cause of Post-Polio Fatigue” written by four authors including Richard L. Bruno. The text reports that postmortem histopathology performed on deceased polio victims fifty years ago revealed the consistent presence of polio virus lesions in specific brain areas, particularly the reticular activating system. One medical researcher during that time reported that 34% of 258 patients with acute spinal, spinal/bulbar, and nonparalytic polio demonstrated brain functioning difficulties along with motor difficulties. Thus, it is almost probable that current problems with central fatigue may be related to the original viral infection in a similar manner as current problems with motor fatigue are related to the original damage to motor units and the wearing out of the surviving motor units. Those of us who have been overachievers, workaholic, driven Type A personalities may be particular vulnerable to the onset of central fatigue of a debilitating degree. Bruno mentions that in one survey that 91% of polios with PPS reported new or increased fatigue, 41% reported that fatigue was significantly interfering with performing or completing work, and 25% reported fatigue interfering with self-care activities. Some post polios have reported more significant problem with central type fatigue than new motor weakness or pain. Hopefully, continued research will provide more scientific understanding of central fatigue without the necessity of post-mortem exams.

As with the original polio viral infection, none of us are experiencing the identical types or severity of

symptoms with PPS. It does seem that the more damaging and extensive original infections resulted in a greater potential for the onset of PPS, particularly if the original infection occurred in childhood. The effect of aging seems to have some impact if one had polio in childhood. However, if one had a good motor recovery from the original infection, there may be greater risk for overworking and wearing out motor units resulting in more difficulty with new motor weakness. Of course, most of what I am reporting is theoretical, and I welcome spoken or written discussion.

Henry Holland, Richmond., Virginia, USA. Henry4FDR@aol.com

23rd April 1998

Originally published in the Central Va PPS Support Group (PPSG)‘s newsletter, The Deja View, in 1996.

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© Copyright Henry Holland 1998 1999 2000.

Copyright is retained by The Lincolnshire Post-Polio Network and/or original author(s). Permission is granted to print copies of individual articles for personal use provided they are printed in their entirety. Links from other Internet WWW sites are welcome and encouraged. We only ask that you let us know so that we can in future notify you of critical changes. Reproduction and redistribution of any articles via any media, with the exception of the aforementioned, requires permission from The Lincolnshire Post-Polio Network and where applicable, the original author(s).

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Created: 26th April 1998

Last modification: 22nd January 2010.

Dr Henry writes about Debilitating Fatigue Read More »

Post-Polio Syndrome

 

Post-Polio Syndrome

Lauro S. Halstead

Scientific American April 1998 Vol 278 Number 4:36-41

Lincolnshire Post-Polio Library copy by kind permission of Dr. Halstead and Scientific American

Reprinted with permission. Copyright © 1998

by Scientific American, Inc. All Rights Reserved.

 

http://www.sciam.com/

The copyrights of artwork on pages 36, 37, 38, and photographs on pages 40 and 41 of the original Scientific American Journal article are not owned by Scientific American Inc. and were therefore excluded from the permission to reproduce granted to us by the publisher.

Decades after recovering much of their muscular strength, survivors of paralytic polio are reporting unexpected fatigue, pain and weakness. The cause appears to be degeneration of motor neurons.

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.

Mechanism of Infection

A distinctive characteristic of acute polio infection is the predilection of the poliovirus for the nerve cells that control muscles. These nerve cells, or motor neurons, consist of a cell body located in the anterior horn of the spinal cord and a long tentacle, or axon, that extends to the muscles. Near the end of each axon, tiny sprouts branch out to individual muscle cells. At the nerve-muscle interface, or synapse, the sprouts from the axon release acetylcholine, a neurotransmitter that causes the muscle fibers to contract. A motor neuron and the group of muscle cells that it activates are called a motor unit.

With uncanny precision, the poliovirus invades the motor neurons, leaving intact adjacent nerve cells that control the functions of sensation, bowel, bladder and sex. How this exquisitely targeted behavior occurs was a mystery until recently, when researchers identified poliovirus receptors at the nerve-muscle interface. These receptors apparently allow the poliovirus to enter an axon and then to migrate to the nerve cell body in the anterior horn of the spinal cord. The poliovirus typically infects more than 95 percent of the motor neurons in the spinal cord and many other cells in the brain. The infected cells either overcome the virus or die.

The extent of paralysis is unpredictable. Motor neurons that survive develop new terminal axon sprouts in response to an unknown stimulus. These new sprouts reinnervate, or reconnect, with the muscle fibers left orphaned by the death of their original motor neurons. In a sense, the growth of additional axon sprouts is the body’s effort to keep as many orphaned muscle cells as possible alive and working. A single motor

neuron that initially stimulated 1,000 muscle cells might eventually innervate 5,000 to 10,000 cells, creating a giant motor unit. These vastly enlarged motor units make it possible for fewer motor neurons to do the work of many.

Another adaptation that leads to increased strength is the enlargement of muscle cells when they are regularly exercised. These two compensatory adaptations–increase in muscle size and axon sprouting–are so effective that up to 50 percent of the original number of motor neurons can be lost without the muscle losing clinically normal strength. These adaptations are neither static nor permanent, however. To the contrary, after recovery from acute polio there is an ongoing process of remodeling of the motor units that consists of both denervation (losing old sprouts) and reinnervation (gaining new ones). It is this process of remodeling or constant repair that allows the motor units to achieve a steady state of muscle strength. When this steady state is disrupted, new muscle weakness occurs.

There is a growing consensus among researchers that post-polio syndrome involves a slow degeneration of the terminal axon sprouts that innervate the muscle cells. David O. Wiechers and Susan L. Hubbell, then affiliated with Ohio State University, proposed this explanation in the early 1980s after diagnostic tests indicated that the functioning of motor neurons in polio survivors progressively worsens as the number of years from their recovery increases. More recently, Daria A. Trojan and Neil R. Cashman of the Montreal Neurological Institute and Hospital, after examining the results of muscle biopsy and electromyographic (EMG) studies in their laboratory and by researchers elsewhere, postulated that there are two types of disintegration of the motor neurons: a progressive lesion and a fluctuating one.

The progressive lesion, in their view, occurs when the normal regeneration of the sprouts from the axon to the muscles is interrupted and malfunctioning sprouts are not replaced. This interruption of the repair process produces irreversible, progressive muscle weakness. The fluctuating lesion, on the other hand, is thought to be caused by defective synthesis or release of the neurotransmitter acetylcholine. Cashman, Trojan and others have demonstrated that muscle weakness and fatigue can be reversed in some patients with post-polio syndrome by the drug pyridostigmine, which enhances the effectiveness of acetylcholine

in triggering muscle contractions. Other researchers are testing another class of agents known as nerve growth factors, which stimulate both nerve and muscle cell growth.

Possible Causes

Degeneration of the axon sprouts can explain the new muscle weakness and fatigue, but what causes the degeneration in the first place remains a mystery. The most plausible hypothesis proposes that the muscle weakness is simply the result of overuse of individual motor neurons over time. This explanation assumes that after recovery from polio the surviving giant motor neurons must labor more than normal neurons just to maintain daily activities. After many years of continued overuse, these enlarged motor neurons eventually suffer from a kind of metabolic exhaustion that leads to an inability to regenerate new axon sprouts to replace degenerating ones. There is no direct way to measure metabolic fatigue in motor neurons, but evidence to support this hypothesis can be inferred from abnormalities on muscle biopsies, electrodiagnostic tests and clinical response to exercise.

In addition, some researchers report that some motor neurons in the anterior horn of the spinal cord of polio survivors appear to be smaller than normal. It is believed that these smaller motor nerve cells were somehow damaged at the time of the acute polio infection and that they are vulnerable to premature failure. Normally, significant attrition of motor neurons does not occur until a person reaches the age of 60 years or more. Because polio survivors have a greatly reduced number of motor neurons, the loss of even a few functioning motor units could result in a disproportionate loss of muscle function.

Attrition of motor neurons because of aging alone, however, may not be a significant factor in post-polio syndrome. Several studies have failed to find a positive relation between the onset of new weakness and chronological age. To the contrary, these studies suggest it is the length of the interval between onset of polio and the appearance of new symptoms that is a determining variable.

Persistence of the poliovirus in the body–or, more precisely, viral particles that have lain dormant for many years and then are reactivated by some unknown mechanism–may also play a role. Researchers at a number of centers have reported poliovirus-like RNA fragments in the spinal fluid and spinalcord tissue of some patients with postpolio syndrome but not in polio survivors who do not have the syndrome. These small RNA fragments, however, do not appear to have any infectious potential. Whether these findings are simply incidental or indicate a possible viral role is not known.

Other causes of post-polio syndrome, such as an immune-mediated response, hormone deficiencies and environmental toxins, have also been proposed. Although some of these hypotheses, and others, seem plausible–and none has been completely excluded–at the present time there is not enough evidence to justify strong support for them.

No definitive tests exist for post-polio syndrome. Diagnostic tests of the blood, muscle biopsies and EMG recordings of muscle activity often show essentially the same abnormalities in polio survivors with post polio syndrome as in those without it. Therefore, diagnosis relies primarily on systematically ruling out other causes of a patient’s symptoms.

Diagnosis and Treatment

A set of criteria for diagnosing post-polio syndrome has been developed by the Post-Polio Task Force, a group of researchers, clinicians and polio survivors. The onset of new muscular weakness after many years of stable functioning is perhaps the most characteristic symptom. Yet many of the symptoms of post-polio syndrome are so general that ruling out all possible causes is often impractical. For instance, new weakness may result simply from the lack of use of the muscles. Muscle weakness from disuse can mimic post-polio syndrome and complicate it. Regardless of the underlying cause, once the weakness begins it may initiate a cascade of other complaints that makes the original symptom impossible to identify.

As with many other chronic conditions, the

essence of good medical care is to relieve

symptoms, improve muscular function and

enhance the patient’s sense of well-being. This

management strategy is frequently referred to

as bracing and pacing. Effective intervention

can be as simple as prescribing a cane or a

wheelchair or as complicated as putting

someone in an iron lung or providing some

other form of assisted ventilation. For both

physical and psychological reasons, patients

are encouraged to remain as active as

possible. The new lifestyle, however, should

incorporate regular rest breaks. An exercise

 

MOST COMMON new health problems reported by post-polio patients in several clinical studies are fatigue, muscle pain, joint pain and weakness. Functional problems include walking and stair climbing.

vigorous and even include aerobic workouts.

program is desirable for virtually all patients. For some, this may be nothing more strenuous than gentle stretching or various types of yoga. For others, it may be considerably more

 

With certain types of exercise in carefully monitored settings, some patients have been able to regain and maintain muscle strength. Although there are no magic bullets, medications can occasionally be helpful: for example, low doses of a tricyclic antidepressant may relieve muscle pain in some patients, and pyridostigmine may reduce fatigue and improve muscle strength.

As a general rule, the progression of symptoms is fairly slow and the overall prognosis is good, unless there are severe breathing or swallowing difficulties. Yet when reserves of strength and stamina are low, a minor change in the stability of the motor neurons can result in a disproportionately large loss of muscular function, which often is psychologically devastating.

Personal Legacies of Polio

Most polio survivors tell a story of struggle and triumph: the sudden, random onset of paralysis, the gradual restoration of strength seemingly as a result of individual willpower and, finally, for many, resumption of an active, productive life, which leads them to believe they have put polio behind them.

The story, for most, is made possible by denying their disability and the reality of what was lost and the life that might have been. Perhaps the most famous example of disability denial is provided by our 32nd president, Franklin D. Roosevelt. Although he regained normal use of his arms fairly quickly after his polio illness, he spent many years in a heroic, but largely unsuccessful, effort to relearn to walk. Even after he became president, Roosevelt went to extraordinary lengths to disguise the extent of his disability. In the waning months of his life, he experienced increasing muscular weakness that appears to be compatible with post-polio syndrome.

Virtually every polio survivor I have met has displayed self-deception or denial. Until recently, most of us tended to avoid other polio survivors and polio help groups. We knew we weren’t physically normal, but if we thought about it at all, we considered ourselves as inconvenienced, not disabled. By retraining the muscles that remained, we felt we could do just about anything, even become president, like Roosevelt.

Later in life, when polio survivors begin to experience the new weakness of post-polio syndrome, the denial usually is still intact, which makes understanding and accepting the new changes all the more difficult. As they begin to accept the fact that they are disabled, they may be overcome by feelings of anger, bitterness and despair. Fortunately, a post-polio support movement has sprung up, and there are now more than 300 support groups throughout the country. In my own case, it took me several years after developing post-polio syndrome before I joined a support group and began talking with other polio survivors about my new weakness and pain. Only then did I start to grieve for the body I lost 35 years earlier.

Many post-polio survivors exhibit an extraordinary commitment to exercise, a legacy from their recovery from polio. When a physical therapist prescribed 10 repetitions twice a day to strengthen a certain muscle, patients typically would do 20 or more repetitions three times a day. For many, exercise became a daily obsession, for others, almost a religious devotion. Thus, survivors of polio developed a special relation to their bodies unknown to able-bodied persons. They experienced a new mastery over their muscles and movements, an element of control that had not existed before polio. It was a visceral lesson that carried over into other aspects of their lives and probably accounts for why so many polio survivors have excelled at school and at work.

Individuals who have recovered from paralytic polio have, on average, more years of formal education than the general population, and they take on marriage and family responsibilities at approximately the same rate as persons who are not disabled. Also, the rate of employment of polio survivors is reported to be about four times the rate of other disabled persons.

Over the past few decades much of the leadership for the disability movement has come from polio survivors. Their efforts have led to the founding of the Independent Living movement and to the passage of legislation such as the Architectural Barriers Act and the Americans with Disabilities Act.

What is not widely known is that many of these leaders were among the most disabled: walking with braces and crutches, riding motorized wheelchairs and attached to portable ventilators. In his novel about the plague, Albert Camus wrote, “It helps men to rise above themselves.” He could have been describing polio.

Social Legacies

Polio has had a far-reaching effect on medicine. The successful development of a safe vaccine after years of effort was a triumph of enormous propertions. It involved the eager participation of millions of ordinary Americans, initially through door-to-door fund-raising and later in volunteering their children to participate in the 1954 field test of the Salk vaccine. The massive research effort to develop a polio vaccine led to many discoveries that have since revolutionized the fields of virology and immunology.

The polio epidemics accelerated the development of rehabilitation medicine. In contrast to traditional medicine with its focus on the curing and repairing of diseased organs, rehabilitation medicine emphasizes the rebuilding of body functions and the teaching of the skills necessary for independent living. The principles developed to treat polio patients decades ago are essentially the ones used today to rehabilitate persons with head and spinal injuries, strokes and degenerative disorders.

The intensive care unit that is now an integral part of every modern hospital is another legacy from the era of polio epidemics. When large numbers of polio patients requiring iron-lung ventilators started to overwhelm the staff in rehabilitation centers, the iron lungs were clustered together so they could be readily monitored by only a handful of nurses. In addition, regional respiratory centers were created to treat the most severely affected polio patients. Some of these centers have survived and continue to provide care for persons with spinal-cord injuries.

The money that originally funded these respiratory centers was raised by the National Foundation for Infantile Paralysis, which later became known as the March of Dimes. It was Eddie Canter, the famous singer and entertainer, who suggested that Americans could be asked to mail dimes to support the fight against polio. For a while, the fight against polio brought out many of the best qualities of American society: neighbors carried food to families quarantined at home, teen clubs raised money to help hospitalized classmates, and women’s groups adopted local polio wards for the year.

Then the vaccines were developed, and not only did polio disappear in America but the war against polio seemed to be forgotten–along with the survivors. Once held up as examples of heroic human fortitude, thousands of polio survivors who continued to need medical and financial help were largely ignored by the public. As veterans of other wars would continue to discover, the public does not like to be reminded of the wounded and the dead after the war is over. Also, as with other conflicts, the polio war left more wounded and uncounted survivors than are generally recognized.

Even the miracle vaccines have their problems. Most scientists agree that the Sabin oral vaccine is superior to Salk’s injected one; however; the oral polio vaccine is not free of risk. In fact, it causes the very disease it is designed to prevent in 10 to 15 people every year because of either a mutation in the virus or an immune deficiency in the recipient that allows the weakened virus to take hold and produce paralysis. The federal government has changed its vaccination policy and is now recommending two initial immunizations with the injected killed-virus vaccine followed some time later by two doses of oral live-virus vaccine. In theory, this combination provides the advantages of both vaccines and, we hope, will end forever this nation’s rendezvous with polio.

The Author

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.

Further Reading

POST-POLIO SYNDROME. Edited by Lauro S. Halstead and Gunnar Grimby. Hanley & Belfus, Philadelphia, 1995.

A SUMMER PLAGUE: POLIO AND ITS SURVIVORS. Tony Gould. Yale University Press, 1995.

CURRENT TRENDS IN POST-POLIOMYELITIS SYNDROME. Daria A. Trojan and Neil R. Cashman. Milestone Medical Communications, New York, 1996.

IN THE SHADOW OF POLIO: A PERSONAL AND SOCIAL HISTORY. Kathryn Black. Addison Wesley, 1996.

POST-POLIO SYNDROME: A NEW CHALLENGE FOR THE SURVIVORS OF POLIO. A CD-ROM published by Bioscience Communications, New York, 1997.

MANAGING POST-POLIO: A GUIDE TO LIVING WELL WITH POST-POLIO SYNDROME. Edited by Lauro S. Halstead. NRH Press and ABI Professional Publications, Falls Church, Va., 1998.

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Post-Polio Syndrome Read More »

Differentiating PPS from Aging

Differentiating PPS From Aging

DR STEVEN DINSMORE

Dr Dinsmore is assistant professor of Clinical Medicine at the Center for Aging, University of Medicine and Dentistry of New Jersey, School of Osteopathic Medicine. This article is reprinted from Polio Network News, Vol. 12, No.2 with permission of Gazette International Networking Institute, St. Louis, MO.

Post-polio Syndrome demonstrates the difficulty of separating disease from normal aging. When individuals first presented with symptoms of post-polio syndrome, many were told they were just getting older Some are still given this explanation. To a certain extent this is true, but experience and thoughtful observation reveal a process above and beyond normal aging. There is a slow multi-system decline in aging that interacts with the injury sustained during acute poliomyelitis. In the life of post-polio survivors, a degree of disability emerges that places them on a different trajectory from the slow accumulation of disability experienced in normal aging.

ETIOLOGY OF AGING

The overall cause of aging itself is not known. There are probably several mechanisms operating simultaneously that produce age-related decline in organ and tissue function. In some cells, reproduction is limited to a certain number of generations, distant organ failure may change the systemic milieu in a way that negatively alters cell function. Subtle conformational changes in critical proteins of cell

i may damage some cell types. In neurons, the accumulation of byproducts of cellular metabolism during the lifetime of the cell may be injurious.

CHANGES OF NORIAAL AGING

In normal aging there is a slow multi-system decline. The onset of decline and rate of change vary from organ to organ. The heart is fairly resistant to aging. The size of the heart is similar, however the thickness of the heart wall is slightly increased. Early diastolic filling is reduced. There is age-related decrease in maximum heart rate but a compensatory increase in volume per beat. Maximum oxygen consumption is reduced with age but it is uncertain if this is due to decreased cardiac output or decreased peripheral uptake of oxygen.

The forced vital capacity of the lungs decreases after age 27 by approximately 25ml/year The surface area of the air sacs in the lungs decreases by 4% per decade after age 30. These changes resemble those in emphysema.

Renal (kidney) blood flow is decreased from 1200mi/min in youth to 600 ml/mm at age 80.

How well the kidney removes waste products from Mood is stable until the middle of the fourth decade then declines.

Immune system changes also occur with aging:

  • the involution of thymus gland;

antibody response to vaccination decreases;

  • autoantibodies (antibodies to self structures) increases;

T-cell function diminishes;

  • T suppressor cell function increases.

Infectious diseases such as pneumonia and influenza rise exponentially after the age of 25 along with an increased incidence of cancer and autoimmune disease.

Changes in the brain with normal aging include:

  • A decrease in weight;
  • A decrease in cortex nerve cell size;
  • A decrease in the speed of central processing;
  • A significant decline in long-term memory (delayed recall) by age 50;
  • A loss of substantia nigra neurons (400k @ birth, 200k @ age 80). These are the cells of

paramount importance in Parkinson’s disease. When the count drops to between 200k and

  • 100k, individuals become asymptomatic with Parkinson’s disease;
  • Aging of an important population of brain motor neurons (basil ganglia).

Large samples of the population studied in the course of standardization of the Wechsler Adult Intelligence Scale (1955) indicated that there is a steady decline in cognitive function, starting at 30 years of age and progressing into the senium. All forms of cognitive function demonstrated decline although, certain elements of the verbal scale (vocabulary, fund of information, and comprehension) withstood the effect of aging better than those of the performance scale (block design, reversal of digits, picture arrangement, object assembly, and the digit symbol task).

The aging neuromuscular system is of most interest in the post-polio syndrome. Tomlinson and Irving have provided evidence that the motor neuron pool is stable until approximately age 60. Thereafter the motor neuron population diminishes. In some cases motor neuron numbers may decrease to 50% of the middle life count. There is also reduced terminal sprouting. In individuals over 65 it is not uncommon to

see fiber type grouping (unpublished observations, which supports the observation of motor neuron dropout.

In addition to the alterations in the motor neuron there is change in muscle. It is observed that there is loss of muscle mass with aging. This loss will cause increased use of the remaining muscle for activities of daily living and, subsequently, may further stress those motor units already at the threshold of maintaining performance.

THE MOTOR UNIT IN POST-POLIO SYNDROME

In people who had acute paralytic poliomyelitis there is electrophysiologic evidence that the motor unit is unstable. Fibrillation potentials, positive sharp waves, and fasciculations are observed in musc post-polio individuals who have no new complaints. These findings imply that the motor neuron is not performing normally This instability can be demonstrated throughout the life of the polio survivor and worsens as the individual ages. These findings represent a continuous remodeling of the motor unit occurring at the level of the terminal nerve. As some terminal nerve/muscle connections are lost, the orphaned muscle may be reconnected to a terminal nerve from another motor neuron. A time comes when the disconnection rate overtakes the reconnection rate. Subsequently muscle fibers are lost and new weakness begins. This critical threshold is more related to the time since the acute poliomyelitis rather than absolute chronological age. New weakness that is noted at age 45 is a significant divergence from normal aging on two counts. First as noted, age-related motor neuron and terminal nerve loss are deferred until age 60. Second, in normal aging the weakness that accrues is subclinical.

It is the change in the motor unit which is at the heart of the post-polio syndrome and, in light of the observed electrophysiologic alterations in the motor unit, it is evident that the post-polio motor unit is not behaving as a normal aging motor unit. There are three possible causes for this altered performance.

  1. The motor unit is expanded. Many motor neurons are carrying a greatly increased load of muscle fibers to compensate for those motor neurons that were lost during the acute poliomyelitis. It is uncertain if the cellular metabolic machinery can carry this increased load for a lifetime. Those motor neurons that escaped from acute poliomyelitis uninjured may be injured later by this chronic increased load.
  2. Not all surviving motor neurons escaped uninjured. Many neurons showed evidence of injury but subsequently recovered. These motor neurons may have an unpredictable lifetime performance and especially be unable to support an expanded motor unit.
  3. Motor units are stressed by an increased demand for firing. It has been demonstrated that the select muscle groups are greatly overused. The motor neurons controlling the motor units within these muscle groups are also overtiring. This may have a long-term damaging effect.

AGING AND POST-POLIO SYNDROME

I do not wish to imply that aging is not a factor in post-polio problems. Certainly the length of time a motor neuron carries an increased burden is critical. But it is the aging process itself that underlines the tendency of cell function to be less effective over time. There is something inherent in the youth of the neuron, or something lost with cell aging, that allows a young motor neuron, injured or uninjured, to be capable of handling an expanded muscle fiber population.

Immunologic findings in post-polio syndrome may or may not be related to aging. These findings may include: an increased CD4/CD8 (helper/suppressor) ratio, an immune activation where unexpected, a MHC class I expression in muscle, and an infiltration of muscle with lymphocytes and macrophages. Spinal cords of survivors who had poliomyelitis examined years after the original injury revealed mild perivascular and intraparenchymal inflammation. Some have also revealed oligoclonal bands in the cerebral-spinal fluid. These observations are consistent with an upregulation of immunologic function, possibly an autoimmune action., If an autoimmune process is present, this is in keeping with the observation of increased autoimmunity with aging. There is a slow multisystem decline in aging which becomes a factor but is not the cause of post-polio syndrome. For example, increased cardiopulmonary demands that have always been present due to a sub optimal gait or body mechanics become more critical as age encroaches on cardiac and pulmonary reserve. Decreased pulmonary reserve due to scoliosis crosses the threshold and becomes functionally limiting due to loss of lung elasticity and diminished ventilatory capacity of aging. These changes of aging would have been silent in a similar aged individual who never had paralytic poliomyelitis.

In summary the physiology of normal aging is a slow multisystem decline. Post-polio syndrome is a more rapid oligosystem decline (neuromuscular). The divergence in performance of the post-polio

individual from the course of normal aging represents a distinct pathophysiology However, the pathology of aging likely plays a role in the emergence of the post-polio syndrome.

In normal aging there is loss of muscle mass, some may be to disuse. The loss of strength does not usually become functionally meaningful in the healthy elderly. Most osteoarthritis produces only minor disability The cause of greatest decline in performance is due to change in central motor control. The average individual also complains of some loss of productivity and decreased stamina. In disease-free aging, there is a gradual, almost imperceptible decline in function due to the combined effects of declining cardiopulmonary capacity, muscle strength, central motor control, and accumulating osteoarthritis.

The post-polio person also experiences these changes, which may be noted at a much earlier age (45 vs. 60). Change is also much more dramatic than seen in normal aging. The osteoarthritis seen in the hips and knees of an individual with abnormal gait may also be profound.

In practice, the post-polio person stands out from the average geriatric center individual on several counts. Polio survivors are more constrained to new weakness and fatigue indicating an oligosystem (1 or 2 system) failure vs. multisystem failure. A typical geriatric patient has one or more medical problems. For example, a prior pneumonia and cardiac disease is a common combination. A modest fatigue is sometime present, but is accounted for by a clear medical pr uncommon. A complaint of specific focal new weakness is even more uncommon. Thus the post-polio survivor with their defining features usually stands out on this basis alone.

PPS vs. Aging: Interventions

Interventions to promote neuromuscular and cardiovascular fitness are different in the post-polio and general population. Increasing muscle strength may be accomplished by conventional techniques of muscle training constrained only by the cardiac and orthopedic status of the individual. An otherwise healthy elderly individual may enter graduated weight training. As their training progresses they are able to increase their limit to produce a modest degree of soreness and fatigue. This approach would be deleterious to a post-polio survivor. In short, the training principles for the geriatric population are parallel to those of the younger adult population with allowances made for baseline cardiovascular and joint condition. In the post-polio individual there must be no residual pain and minimal fatigue after training. Some post-polio people are unable to pursue cardiovascular or strength training due to extensive motor neuron and attendent muscle loss.

Differentiating PPS from Aging Read More »

Take a Look at Estrogen

Take a Look at Estrogen

by Tom Walter

Tom Walter is a Polio Survivor. Up until a few years ago, 30 years or so on from recovering from Polio, he walked unaided with only a slight limp, working and living a normal life. He didn’t even know any other people with Polio. He now has difficulty swallowing and breathing and spends most of his days in a wheelchair or propped up in bed. With his laptop computer he collects and dispenses advice and information on post-polio syndrome. Tom, or TominCal as he is known by his email name, is highly regarded and respected as a source of reliable information by the online post-polio community worldwide. In 1997 he was interviewed by Susan Kelleher of the Orange County Register for an article “Polio strikes back.”

LincsPPN Web Administration.

HORMONE THERAPY MAY BE RIGHT FOR WOMEN WITH PPS

Recently I read that nearly half of all post-menopausal women in the United States who are candidates for taking the hormone Estrogen are not doing so. That could be a mistake with long-term consequences for them, and in particular for women with PPS who don’t produce Estrogen at all because they’ve had both ovaries removed or who have a lowered production of Estrogen during and after menopause.

Then a short time later I saw an article in the local “Orange County Register“¹ newspaper about a study published in the “Annals of Internal Medicine” reporting that only 47 percent of U.S. women doctors surveyed who are post-menopause take Estrogen supplements. Their reasons for taking it were to control hot flashes and other symptoms of menopause, as well as to reduce their risk of heart disease and Alzheimers.

The study went on to say that as more and more doctors themselves take Estrogen they are more and more likely to prescribe the hormone for patients.

Some women fail to take Estrogen alone, or along with other hormones, because of perceived or experienced side effects such as increased vaginal bleeding or dryness, bloating or hot flashes. But these symptoms can often be overcome by adjusting the dose or combination of the many different varieties of hormone replacement therapy now available. Others may feel they are at increased risk for endometrial or breast cancer.

These concerns should certainly be discussed with a personal physician who must be consulted anyway if the decision is made to take the hormones that are available by prescription. But it seems that much of the fear of Estrogen and failure to pursue the therapy can be traced to misinformation, flawed or incomplete clinical studies of the past and “wives tales.”

While I don’t know of any studies that have been done of Estrogen specifically in PPS women, I think certain inferences can be drawn from information that is available. There are several anecdotal reports from females with PPS that the addition of Estrogen to their regimen has led to decreased pain, an increased feeling of well-being and even improved breathing.

I recall a study from Germany about 10 years ago showing that Estrogen in post-menopausal women greatly reduced the symptoms of carpal tunnel syndrome. (That was of interest to me at the time since I was working with women machine operators and assemblers in manufacturing who were prone to that condition.)

OSTEOPOROSIS

Both men and women who have had residual muscle atrophy or weakness from polio are at increased risk for osteoporosis (thinning of the bones) because of the inability to exercise those muscles and the resultant lack of muscle tension on the bones. And, or course, this risk is increased with the onset of PPS. At advanced stages, osteoporosis can be an extremely painful condition and is often the cause of bones that are easily broken in older women and those with PPS.

In her article of 1994 on the subject, Dr. Daria Trojan, co-head of the PPS clinic at Montreal Neurological Institute stated,

“Currently the most effective treatment for this is Estrogen replacement therapy at menopause. Estrogen therapy is most effective when started early after menopause. Estrogen therapy can prevent early post-menopausal bone loss, can increase bone mass in the spine by 5 percent in women with osteoporosis, and can reduce fractures by 50 percent.”

MEMORY AND BRAIN CELLS

Earlier studies have shown that Estrogen Replacement Therapy (ERT) in post- menopausal women may reduce the risk for Alzheimer’s disease and help slow the loss of verbal memory.

A new study from the National Institute on Aging (NIA) in the December, 1997, issue of the journal “Neurology” is the first to document the effects of Estrogen on age-related changes in memory over a long period of time and is one of the first documenting an effect on visual memory.

By looking at Estrogen use in 288 women enrolled in the NIA’s Baltimore Longitudinal Study of Aging (BLSA) between 1978 and 1994, researchers were able to examine the relationship between Estrogen therapy and short-term visual memory.

The investigators collected information on Estrogen use during visits to the NIA for memory testing as part of the BLSA, one of the largest and longest ongoing studies of aging in existence, and were able to show that women who were on Estrogen during the memory testing period performed better than women who had never received treatment.

Furthermore, some participants who began Estrogen therapy between their regular visits to the NIA were able to maintain stable memory performance whereas women who never took Estrogen showed predicted age-associated decreases in memory over a six-year period, on average.

“Animal studies show that Estrogen can directly influence structural characteristics of neurons in the brain, particularly in regions that are important for new learning,” said Susan Resnick, Ph.D, principal

investigator of the study. “These regions are also most vulnerable to neuron loss seen in Alzheimer’s disease. Thus, lessening the effects of these changes with ERT holds promise as a drug intervention.”

CHOLESTEROL AND HEART ATTACK

Researchers from the National Institutes of Health reported in the March, 1997, issue of the “New England Journal of Medicine” that postmenopausal women who took Estrogen for as little as a month were found to have a 50 percent reduction in a substance in the blood called plasminogen-activator inhibitor type 1, or PAI-1.

Levels of PAI-1 go up in postmenopausal women, increasing the blood’s tendency to clot. This, in turn, raises the risk of coronary artery obstructions. Because Estrogen reverses this trend, it lessens the tendency to clot and, like taking aspirin, reduces heart disease risk, the authors suggest.

Previous studies have shown that when women take Estrogen pills, it raises HDL (the ‘good’ cholesterol) and lowers LDL (the ‘bad’ cholesterol) in their blood.

OSTEOARTHRITIS

” . . . new research indicates that Estrogen may play a role in the prevention of osteoarthritis, the most common form of arthritis,” said Michael C. Nevitt, PhD. His research results were published in the October 14, 1997, issue of “Archives of Internal Medicine.”

Nevitt and colleagues studied hip x-rays for signs of osteoarthritis in 4,366 postmenopausal women age 65 or older and through interviews identified participants who took Estrogen prior to when their x-rays were obtained.

Researchers found that the women who were currently taking Estrogen had nearly a 40 percent lower risk of having any osteoarthritis in the hip compared to women who had never used Estrogen. Their risk of developing moderate to severe disease was even lower, Nevitt said.

In addition, researchers found that current users who had taken Estrogen for 10 years or longer had a greater reduction in the risk of any hip osteoarthritis (43 percent lower risk) compared to users for less than 10 years (25 percent lower risk).

Osteoarthritis is a degenerative joint disease that is characterized by the breakdown of the joint’s cartilage — the part of the joint that cushions bones where they join together. Cartilage breakdown causes bone to rub against bone, resulting in pain and loss of movement. It most commonly affects the elderly in the hands and weight-bearing joints such as the knees, hips, feet and back.

Tom Walter

16th March 1998

Take a Look at Estrogen Read More »

Dr Henry writes more on Post-Polio Brain Fatigue

Dr. Henry writes more on Post Polio Brain Fatigue

I have written in the past about post-polio brain fatigue. This symptom complex that many of us experience involves a feeling of total body fatigue, difficulty remaining alert, word finding problems, concentration difficulties, and occasional forgetfulness. These problems are usually absent when we are well rested. In the November/December issue of the newsletter of the Florida East Coast Post-Polio Support Group, there is an article written by Donald Peck Leslie, MD, of the Shepherd Center, Inc. of Atlanta, Georgia entitled “POST- POLIO FATIGUE: WHAT IS IT? WHAT CAN WE DO ABOUT IT.” It is a lengthy article that summarizes the development of PPS and many of the theories regarding the causes of PPS. I was particular interested in some of the information relating to PPS brain fatigue and will attempt to relate it to you.

Quoting from Dr. Leslie’s article,

Fatigue is the most commonly reported and the most debilitating of the post-polio sequelae which affects the nearly two million North American polio survivors and the least studied. Among polio survivors in my practice, over 90% report new or increased fatigue. Of these, approximately one half report fatigue which is significantly interfering with performing or

completing their work. As many as one fourth of them have fatigue which interferes with their self-care activities. Other literature supports these percentages and is very similar. Fatigue has reported to be triggered or increased by physical exertion in again greater than 90% and by some emotional stress in over 60%. It is important that polio survivors distinguish between physical tiredness and the decreased endurance they associate with new muscle weakness, and what is called “Brain Fatigue.” This is characterized by problems with attention and thinking. Between 70% and 95% of polio survivors reporting fatigue complained of problems with concentration, memory, attention, word finding, maintaining wakefulness, and thinking clearly.

Dr. Leslie’s article continues,

Problems with attention, memory and thinking suggest that the symptoms of post-polio fatigue cannot be explained merely by the polio virus damaging the anterior horn cells of motor neurons in the spinal cord. Autopsies which were performed 50 years ago on people who died after having polio, whether they were paralyzed or not, showed that the polio virus almost always damaged specific areas in the brain as well as in the spinal cord. There were severe lesions in the reticular formation, vestibular nuclei, cerebella roof nuclei, and periaqueductal gray. Moderate lesions were seen in the paraventricular hypothalamic nucleus, posterior hypothalamic nuclei, and substantia nigra. Mild lesions were found in the globus pallidus and putamen, locus ceruleus, medium raphe nuclei, preoptic hypothalamic nuclei, and thalamic nuclei.

As you can ascertain, the polio virus involved more of the brain than most of us would have ever known. These damaged areas include the brain’s activating system that helps us remain awake and to focus our attention. The virus also damaged nerve cells that produced neurotransmitters such as the endorphins (our own source of morphine), serotonin, dopamine, and ACTH (adrenocorticotrophic hormone). Dr. Leslie mentions that reports during the great polio epidemics indicated that many patients did experience drowsiness, lethargy, and even coma. About one third of patients with spinal, bulbar, and even non paralytic polio had disorientation, apathy, and prolonged sleep.

Dr. Leslie writes:

I heard data presented by Dr. Richard Bruno when he reported to the New York Academy of Sciences, and also was published in the Archives of Physical Medicine and Rehabilitation in 1993, an article entitled, “Neuropsychology of Post-Polio Fatigue.” These findings indicate fatigue in chronic fatigue syndrome as well as polio survivors is associated with impairment of attention and information processing speed but not of memory or thinking ability. Given the findings of frequent and severe polio virus lesions in the brain’s activating system, it was hypothesized that damage to the brain’s activating system is probably responsible for both fatigue and impaired attention in polio survivors.

In trying to find evidence for this hypothesis, MRI (magnetic resonance imaging) was done on some polio survivors with brain fatigue symptoms. In a study reported in the Archives of Physical Medicine and Rehabilitation in 1994 entitled “The Neuroanatomy of Post-Polio Fatigue,” white spots were seen in the brain’s activating system in a majority of PPS patients with brain fatigue and were not seen in any of the PPS patients without fatigue.

I realize that much of this article is technical in nature, but the information does indicate that research is being conducted to help explain what is happening to many of us, and hopefully, better treatment will eventually result.

I will continue with Dr. Leslie’s remarks and his discussion about the white spots and the possible effect of ACTH in post polio brain fatigue. He writes,

Finding these spots on MRI supports the theory that fatigue and problems with attention in polio survivors may be related to damage the polio virus did to the brain’s activating system. The association of these spots and the brain’s activating system with the symptoms of post polio fatigue suggested that the effects of polio virus on other brain areas might also be evident in polio survivors. Polio virus lesions were often seen on autopsy in the

hypothalamus, in the brain area that automatically controls the body’s internal environment and its response to stress. To test the function of the hypothalamus, researchers measured polio survivors blood concentration of ACTH, one of the body’s stress hormones whose release is triggered by the hypothalamus. ACTH was measured following an overnight fast, which is a mild stress known to cause the release of ACTH in normal individuals. ACTH was increased outside of the normal range as it should be following stress in polio survivors who reported no or mild fatigue. However, there was no ACTH increase in subjects reporting severe daily fatigue. Further, the higher the ACTH, the lower the subjects reported fatigue and the less difficulty with memory, muscle weakness, and staying awake during the day. Obviously these findings indicate that the hypothalamus had not been activated in the subjects with post-polio fatigue and ACTH production is reduced in these individuals. This is an interesting conclusion because ACTH has been found in humans to promote alertness, increase attention, and decrease fatigue by directly stimulating the brain’s activating system.

Thus, a decrease in ACTH production may prevent brain activation and contribute to the symptoms of post-polio fatigue.

Dr. Leslie also mentions that the reduction in the body’s own morphine (decrease of enkephalins and beta endorphins) in post-polio brain fatigued patients helps to explain why polio survivors have a nearly double sensitivity to pain.

In summary, Dr. Leslie writes:

Taken together, these findings may suggest a model for the cause of post-polio fatigue:

  1. Polio virus damaged the brain activating system;
  2. MRI and hormonal findings suggest the damage to the brain activating system is present today in polio survivors;
  3. Neuropsychological test showing impaired attention in patients with post-polio fatigue.

Therefore, the polio virus damage to the brain activating system may cause decreased brain activation, impair attention, and generate the symptoms of post-polio syndrome.

The article continues for another three double column pages to explain the involvement of dopamine in post-polio brain fatigue. I found this medical article to be most interesting and to lend some medical rationale to what many of us are experiencing with trying to understand and live with post-polio brain fatigue. I should emphasize that all of this information is theoretical, but to me, a lot of its makes sense. We just never had any idea the degree of havoc that the polio virus accomplished once it invaded our central nervous systems. We all thought that the initial brain attack was over and we just had to deal with the residual loss to our motor systems forty or more years ago. This remarkable virus is more of a “deja vu” than we realized.

Henry Holland, Richmond., Virginia, USA. Henry4FDR@aol.com

15th February 1998

Originally published in the Central Va PPS Support Group (PPSG)‘s newsletter, The Deja View, in 1998.

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Dr Henry writes more on Post-Polio Brain Fatigue Read More »

A Pound of Prevention is Worth a Ton of Therapy

A Pound of Prevention Is Worth a Ton of Therapy

Richard L Bruno, Ph.D., Director of the Post-Polio Rehabilitation and Research Service, Kessler Institute for Rehabilitation, East Orange

Dear Tabby: Forty years ago I caught a virus that killed half of the nerves in my spinal cord and brain stem. The nerves that survived were damaged by the virus but have been doing double the work to make up for the nerves that were killed. Even though my leg has been paralyzed for forty years, I have always been very hard-driving and am constantly busy: I work two jobs, have ten kids, take care of my 90-year-old mother and mother-in-law who live with me, volunteer at a hospital and a homeless shelter, and raise money to “Save the Whales” in my spare time. Other people who caught this virus are and are having severe problems with fatigue, new muscle weakness, and pain. However, I feel line right now-except for daily headaches. Should I change my lifestyle to try to prevent new problems? – “Symptomless in Seattle”

There has never been a longitudinal study that looks at the emergence of post-polio sequelae (PPS) in polio survivors who have no symptoms. However, each time someone surveys polio survivors, the percentage of individuals reporting PPS goes up. When Mary Codd did the first population-based study at the Mayo Clinic in 1983, she found that 22.4% of paralytic polio survivors had PPS. The 1987 National Health Interview Survey estimated that of America’s 1,63 million polio survivors, 66% who had paralytic polio and 24% who had non-paralytic polio had PPS. In England, where they don’t even believe in PPS, 78% of the 1940’s-era graduates of one polio hospital are reporting “new symptoms.” Something must be going on that causes more and more polio survivors to report PPS as the years go by. But what? In 1985, Laura Halstead reported (Halstead and Rossi, 1985) that PPSdeveloped in those who were at least 10 years old when they had had polio and in those who had had a more severe infection, i.e. those who had been hospitalized at polio onset and had had more limbs paralyzed. In 1988, Klingman and colleagues found that it wasn’t just the severity of the polio but how much you recovered in the succeeding years that predicted new symptoms. That is, the more damage the polio virus did and the more your central nervous system recovered the more axonal sprouts you created and the bigger your motor units became), the more you had to lose and the more likely you were to have PPS. Then, in the 1985 and 1990 National Post-Polio Surveys, Nancy Frick and I (Bruno and Frick, 1987: 1991) found that both physical overexertion and emotional stress are reported by polio survivors to trigger PPS. Further, we reported that polio survivors who were “Type A” (hard-driving, time-conscious, and overachieving) were more likely to develop PPS. It appears that both physical and emotional stress on a polio-damaged and overworked central nervous system led to the development of PPS. This conclusion is supported by the 1991 findings of Paul Peach at Warm Springs. He found that in individuals who already have PPS, the symptoms of fatigue, weakness, and pain just get worse if patients don’t follow their therapists’ recommendations to decrease physical and emotional stress. So what do polio survivors like “Symptomless in Seattle” do if they don’t currently have symptoms? Well, it doesn’t take “Dear Tabby” or even a post-polio specialist to figure out that people with a smaller number of polio-damaged and severely overworked neurons are at risk for developing symptoms that result from chronic physical and emotional stress. Will all polio survivors eventually develop PPS? Will ALL polio survivors develop ALL post-polio sequelae -from fatigue through swallowing problems? Certainly not. But just as people who’ve had a heart attack are advised to reduce stress and their fat intake, shouldn’t polio survivors without PPS try to protect their damaged and overworked nerves? We advise all polio survivors to follow the Post-Polio Golden Rule: IF SOMETHING YOU DO CAUSES FATIGUE, WEAKNESS, OR PAIN, YOU SHOULDN’T BE DOING IT. Why shouldn’t polio survivors try to protect their quality of life by decreasing physical and emotional stress through the moderation and pacing of activities, the use of appropriate assistive devices (especially those that were readily discarded so many years ago), and reducing hard-driving, Type A behavior (see Agree and Rodriguez, 1991: Bruno and Frick, 1991: Young, 1991)? Will these self-care activities prevent the onset of PPS? No one knows. But self-care is the foundation of therapy for PPS and both our patients’ reports and the research literature clearly show that the progression of PPS is at least halted and symptoms reduced when patients start to take care of themselves. So it’s hard to imagine that self-care won’t have some preventative effect with regard to PPS And if prevention is possible, it would certainly be a lot less difficult and expensive than the physical, occupational and psychological therapy that are necessary to treat post-polio syndrome. What if self-care merely holds PPS off for a while, or if it reduces the severity of symptoms when they do occur? Or what if self-care has no long-term effect on PPS? Why should polio survivors spend their lives beating up their bodies and their spirits taking care of everyone around them, to the point where they don’t even spend a moment of the day thinking about, let alone caring for, themselves? Why should anyone live like that? As you know, polio survivors say, “Self-care is selfish! I feel too guilty to take care of myself.” Self-care, moderation, and reduced stress have been recommended as the foundation for a peaceful and even happy life for nearly 2,500 years, since the time of the Buddha. Taking care of yourself isn’t selfish, say the Buddhists. They say that since compassion for everyone is the basic principle that leads to peace and happiness, people cannot be peaceful or happy if they spend their days exhibiting compassion for the whole world with the exception of just one person: themselves. Dear “Symptomless”: I don’t know anything about viruses. But I do think it makes sense for you to start taking better care of yourself. Why is it so hard for us to take care of ourselves? Why should you be doing for everyone else and ignoring and abusing yourself? Don’t you at least deserve not to have your head hurt all the time? Why don’t you start by doing one thing for yourself for each thing you do for someone else? Maybe you won’t prevent new physical problems. But the worst that could happen is that other people will still be helped and you’ll feel better. Why should you “Save the Whales” and not save yourself – Tabby Source: Newsletter of the New Jersey Polio Network

This site is now maintained by Chris Salter, of the Lincolnshire Post-Polio Network Original Document Preparation: Tom Dempsey. Last modification: 10th January 1998

A Pound of Prevention is Worth a Ton of Therapy Read More »

The Post Polio Syndrome and re-rehabilitation

The following information has been made available with the permission of the Easter Seal Society of Washington. The opinions expressed are those of the individual writer(s) and do not necessarily constitute an endorsement or approval by the Easter Seal Society or Polio Outreach Advisory Council. Although it does not imply endorsement, it is provided as a service for those seeking such information. Always consult your doctor before trying anything recommended in this information or any other publication. For additional information concerning post-polio please contact your local Easter Seal Society, post-polio support groups, or other such services in your area.

THE POST-POLIO SYNDROME AND RE-REHABILITATION

Frederick M. Maynard, M.D.

There appear to be many causes for the late effects of polio and the Post-Polio Syndrome. Many problems result from aging of the previously damaged muscles and limbs. If a polio survivor becomes ill from medical problems unrelated to their polio history, general debilitation may cause progression of their post-polio weakness and lead to new symptoms. Additionally, occasionally polio survivors develop unexplained new muscle atrophy and weakness. This condition is known as Progressive Post-Polio Muscular Atrophy.

During the past five years, a Post-Polio Research and Training Program has been established at the University of Michigan Hospital in Ann Arbor, Michigan. A Post-Polio Clinic is held weekly to investigate causes for new symptoms among polio survivors and to develop re-rehabilitation programs for them. Using modern rehabilitation methods and techniques, these polio survivors are able to be helped and can usually be restored to their customary levels of functioning. Many of them, however, need to return to or begin using braces, crutches, canes, wheelchairs, and a variety of adaptive equipment in order to compensate for the newly developed weakness and loss of functional abilities. Research continues to be done in order to discover what factors may predispose some polio survivors to progression of their weakness and development of new disabling medical problems. By sharing some of formation with medical professionals and consumers, it is hoped that rehabilitation outcomes can be improved. The goal of this presentation is to explain what we have learned about the late effects of polio and how to manage their disabling effects. Acute poliomyelitis is a viral infection which invades the body through the gastrointestinal tract. The central nervous system is the only place where permanent damage to the body results from the infection. Within the central nervous system, polio virus can destroy motor nerve cells located in the spinal cord. Some nerve cells are permanently destroyed, whereas others are only temporarily damaged. After a son has recovered from the acute poliomyelitis infection, the body attempts to repair the damage Polio survivors usually can regain some strength during the first two years following the polio infection, if proper exercise and therapy are performed. There are three ways in which this recovery occurs. First of all, some nerve cells are only temporarily damaged and as they recover, strength improves. Second, muscle fibers innervated by surviving nerve cells can increase their size and become stronger through traditional strengthening exercises. The third mechanism for improvement is due to sprouting of new nerve twigs from the undamaged nerve supply. These new nerve sprouts grow to reach muscle fibers which have lost their nerve supply. Surviving nerve cells thus are connected to more muscle fibers and there is an increased number of muscle fibers per nerve cell. This means that surviving nerve cells do two to three times as much work on an individual basis during muscle contraction. The resultant increased metabolic work may predispose these nerve cells to overfatigue and early degeneration later in life. After 25 or 30 years of high intensity muscle work, many of the new nerve sprouts begin to wear out and degenerate. Motor units begin to shrink back to their original number of muscle fibers per nerve cell. For the polio survivor this means a shrinking of muscle size and decreasing strength. This process has been shown to occur very slowly at an estimated rate of about 1% of muscle strength per year. Epidemiological studies suggest that as many as 25% of polio survivors will experience loss of strength or other post-polio symptoms. Progressive post-polio muscular atrophy occurs most commonly in polio survivors who have consistently used their residual muscles at high intensity for many years. It is believed to result from chronic overuse damage of the partially re-innervated muscles. Other factors which contribute to late muscle deterioration in polio survivors include: normal age related loss of motor nerve cells; age related decrease in circulation which can cause slow decrease in the size of muscle fibers, and the effect of environmental toxins which can hasten nerve degeneration. Additionally, as people become older they often become less active and this leads to further disuse atrophy. If a person becomes severely ill from other health problems, such as a heart condition, pneumonia, arthritis or a fracture, they also may become weaker from disuse atrophy. Because polio survivors have decreased muscle and nerve reserve capacity, disuse atrophy can become more significant in terms of degree of weakness-related loss of functional ability. Most new pain problems that are seen in polio survivors result from repetitive strain injuries to the weakened muscle fibers and muscular tissues. When musculoskeletal pain develops, a person normally must rest the part in order to resolve the pain and inflammation. However, rest leads to further weakness and atrophy. Thus a vicious cycle of increasing weakness, increasing pain, and increasing disability can result. Management of the late effects of polio attempts to control those factors contributing to loss of functional abilities in three ways. First, pain and inflammation of muscles, joints and supportive tissues must be reduced though traditional therapy techniques. This includes the use of anti-inflammatory medications, heat, stretching, and other methods of physical therapy. Second, any activity which is the pain must be changed. Frequently an increased amount of weakness in leg muscles demands a return to the use of canes, crutches, braces, or wheelchairs in order to avoid continued strain. It is understandable that polio survivors often do not wish to return to the use of these assistive devices but they may be necessary to reduce the pain resulting from strain and to stop the vicious cycle. Third, polio survivors should exercise on a regular basis. There are three types of exercises that are normally recommended. Flexibility exercises are most important. They must be done to keep the spine flexible and mobile, as well as to prevent tightness of muscles and joints. Conditioning exercises should be done to promote cardiopulmonary fitness. It can often be challenging to design conditioning exercises for polio survivors because of limited strength in extremities for doing sustained exercise. Swimming is an excellent type of activity for achieving some cardiovascular conditioning without overly straining limb muscles. Carefully designed strengthening exercises can also be utilized. Patients must be careful to not exercise too vigorously and produce new injury and symptoms. Often it is the muscles which were not severely involved with polio that can benefit the most from resuming mild strengthening exercises. If an attempt at strengthening exercises is carried out and new muscle pain and weakness develop, then it is clear that the weakened muscle is susceptible to overuse injury and further exercise of that muscle should be discontinued. Some of the most common new problems among polio survivors are pain syndromes in the upper limbs. Degenerative arthritis of the shoulder is particularly common among polio survivors who have used crutches and canes for walking over many years. Additionally, arthritis of the wrist and hand, and carpal tunnel syndrome from thickening of the ligaments in the wrist, are very common among cane and crutch users. In order to help reduce the occurrence of these problems, it is recommended that the lightest possible leg braces be used and that polio survivors avoid becoming overweight. Additionally, wide grips on canes and crutches can lessen strain on wrists and hands. Many of the most severely affected polio survivors, who can only ambulate with great effort using crutches and braces, should be encouraged to use wheelchairs or electric carts when traveling the longer distances that are needed to be active in their communities. Of course, this requires that their communities develop accessible public buildings and promote removal of architectural barriers to people who have mobility limitations, Another common medical problem among older polio survivors is arthritis in the back and the joints of the lower extremities. Arthritis of the knee is particularly frequent among people who have walked for many years without bracing of the knee and have severe quadriceps muscle weakness. Pain and arthritis of the lower back can develop because of abnormal walking with severe limps and because of scoliosis in the spine. It is important to attempt to correct leg length discrepancies and reduce gait deviations through the use of corrective shoes, canes, crutches and appropriate lower extremity bracing in order to prevent these biomechanically-induced problems. Psychological stress from the development of new impairments and disabilities is another important and real problem for polio survivors who experience the late effects of polio. Our experience has shown that associations of polio survivors who join together for supporting each other can be very helpful. Polio survivors can learn from each other more quickly than learning from health care professionals. They can share methods for re-adapting their lifestyles and altering their customary ways of doing life activities. They can also effectively work with community and government organizations for improving accommodations and facilities for people with physical disabilities and handicaps. In order to avoid depression and to reduce stress from loss of income and enjoyable leisure time activities, patients must be encouraged to creatively find new adaptations for their physical problems in order to remain productive in their lives and active in leisure time activities. Our experience with polio survivors in Michigan has been that pain can be eliminated or managed in virtually all cases. Rehabilitation techniques can sometimes restore losses of muscle strength and can usually improve fatigue through more efficient ways of using residual strength and energy. Lifestyle adaptations and the use of new assistive devices can promote continued productive and satisfying activity, New handicaps from the late effects of polio can be prevented through re-rehabilitation, This site is now maintained by Chris Salter, of the Lincolnshire Post-Polio Network Original Document Preparation: Tom Dempsey. Last modification: 4th January 1998

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Therapeutic Electrical Stimulation TES

Therapeutic Electrical Stimulation (TES)

Ruth Wyler

Therapeutic electrical stimulation (TES) is an old technique with a new application: treatment of muscles weakened by the Post-Polio Syndrome. To inform its readers, the newsletter staff sent its rolling reporter to learn about this technique and to interview some of the people who are using it. Low-level electrical stimulation, such as TES, has been used for years to help heal broken bones and skin wounds not responding to conventional treatment and treat selected cases of chronic pain. More recently it has been used to treat patients with chronic neuromuscular disorders, such as cerebral palsy, spina bifida, incomplete spinal cord injuries and stroke. Dr. Karen Pape, Director of the Magee Clinic in Toronto is a pioneer in this use of TES. Using TES, she has produced improvement in conditions previously considered untreatable. Since its establishment in the mid-80s, over 2000 such patients now visit the Magee Clinic each year. They learn how to use its TES program, to redevelop and strengthen their wasted muscles and to improve their overall strength, coordination and well-being. The use of TES to treat post-polio syndrome began in 1989 when a young Canadian woman, Catherine Bell, was referred to Magee Clinic for treatment of her muscle weakness. The improvement in her symptoms with TES therapy was so marked that word spread. Dr. Pape said in her letter to this reporter that approximately 120 polio survivors have come through the clinic to date, and just under 100 of these are currently on the program. She emphasized that this technique does not treat the basic (initial) loss due to polio. It is for the progressive muscle weakness seen years later and the muscle atrophy from disuse due to injury or illness. All referrals to the Clinic are made by a physician, and prospective clients are prescreened by the Clinic before they come to Toronto. Approximately 50% of those referred are turned down. Overweight is the most common reason for refusal. In addition to making movement more stressful, excess body fat decreases the amount of electrical current reaching the muscles during TES and can make the treatment less effective.

WHILE CLIENT SLEEPS

TES treatment involves placing electrodes at prescribed places on the surface of the skin over muscle, and then stimulating the muscle with a small electrical current for 5 to 8 hours a night while the client sleeps. Clients can control the amount of stimulation. The electrical charge is painless and is felt, if at all, as a slight “tickle.” The stimulator is a battery-operated device run on one 9-volt or three AA batteries, which need to be replaced from every few days to two weeks, acccording to the amount of power needed by the individual.

TES is not used alone. It is a special technique added to an overall rehabilitation program such as is used in most centers treating post-polio syndrome. As at other centers, the Magee Clinic treatment program is individually designed for each client. In addition to non-fatiguing exercise to increase endurance and function, Dr. Magee stresses the importance of proper nutrition to preserve muscle mass and control weight. The program is designed essentially to be carried out at home. As with all rehabilitation programs, it requires a long-term commitment and self-discipline.

SOME REACTIONS

How do some of its users feel about it? After 2 years, Catherine Bell was able to walk down a flight of steps again without fear of her leg collapsing. She could take long walks with her husband and work again, although she changed to a job less physically demanding. She feels she has regained at least 75% of the strength and stability she had before she had developed post-polio syndrome 4 years ago.

Anne Heaney of Manhattan, and Herbert Laster of Hastings-on Hudson, have had similar experiences with 2 and 1 years’ use, respectively. Both have improved mobility but not to the level before the post-polio syndrome struck. However, Ms. Heaney feels continuing leg and arm improvement, even after 2 years of TES. Mr. Laster fears that while he is stimulating several muscle groups, others continue to weaken.

DRS. HALSTEAD AND DRAKE TRYING TES

Two physicians have just recently begun using the TES program for their own post-polio weakness. Dr. W.P. Drake, an internist in Oracle, Arizona, has seen a slight improvement. Dr. Lauro Halstead, Director of the Post-Polio Program at the National Rehabilitation Hospital in Washington, DC, has seen no change in 7 months of TES. However, he is not certain that he is a suitable candidate for this type of therapy.

TES RESULTS WITH MAGNETIC RESONANCE IMAGING SCANS

Although there is no agreement as to how TES achieves its effect, many believe it acts by improving circulation to the muscle. Magnetic Resonance Imaging (MRI) scans have shown actual growth of musculature with the TES program. MRI is a technique that produces life-like imaging of muscle involvement in the post-polio syndrome and enables doctors to measure the effects of various therapies.

In terms of muscle function, Dr. Pape says the Magee program can usually raise muscle strength 1 to 1.5 grades (on a scale of 0 to 5) over the course of 1-1/2 to 2 years of treatment. Changes are usually noticed in 3 to 6 months. She states they have not found an effect on the overwhelming fatigue experienced by some people with post-polio syndrome.

The Magee Clinic has been treating clients with post-polio syndrome for just 4 years. Results of the program are available for only a few individuals, those for the whole treatment group are still being gathered. Each of the three doctors interviewed, as well as Dr. Pape, expressed the need for studies to answer questions such as: Who is most likely to benefit from the TES program? What is the best treatment regimen with TES? How long will the benefits persist?

Magee Clinic methods are being watched by rehabilitation centers throughout the world. Few centers in the United States currently are offering TES for treatment of post-polio syndrome. Additional information may be obtained from:

The Magee Clinic 5160 Yonge St., Suite 505 North York, Ontario, Canada. M2N 6L9 (416) 733-1783 Fax (416) 733-1721

This site is now maintained by Chris Salter of the Lincolnshire Post-Polio Network, Original Document Preparation: Tom Dempsey. Last modification: 10th January 1998

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Polio More than Once

POLIO MORE THAN ONCE

Read from Marti Whiting’s nursing book – Brown, Amy F., Medical and Surgical Nursing II, W.B. Saunders Company 1959. “Incidence: Some authorities state that as high as 80 per cent of the population in this country has had poliomyelitis at some time, which was not recognized and which left no residual paralysis. …… It is thought that probably one case in about a hundred cases becomes paralyzed.” Under symptoms it describes the difference between minor illness and major illness. “Minor Illness: These brief illnesses are commonly seen during epidemics of poliomyelitis, usually last only 24 hours, and are more frequent in children than in adults. Clinical manifestations include fever, headache, vomiting, listlessness, and sore throat. The minor illness may be followed by signs of paralytic or nonparalytic poliomyelitis or may represent the entire case of the disease.” “Major Illness: This term relates to both paralytic and nonparalytic poliomyelitis. Lesions have developed within the central nervous system to an extent sufficient to cause neurologic symptoms. If there is a sudden onset, fever, vomiting, and a severe headache commonly occur. These symptoms may be accompanied by pain in the extremities. Soreness and stiffness of the neck, back, and hamstring muscles become prominent early. About half the patients with major illness have paralytic poliomyelitis.” “Spinal Paralytic Poliomyelitis: This is the classic form of poliomyelitis. The clinical diagnosis becomes definite with the presence of flaccid paralysis. In the order of frequency, the muscles most commonly paralyzed are those of the legs (by far the most frequent), arms, back, thorax, face, intercostal region, and diaphragm.” “Bulbar Poliomyelitis: This, the most serious form of poliomyelitis, occurs in 10 to 20 per cent of paralytic patients in an epidemic. These are the cases in which cranial nerve nuclei are involved. Weakness of the pharynx and vocal cords results in an inability to swallow or to talk clearly, and sometimes in regurgitation of fluids through the nose. Some patients have symptoms and signs indicating involvement of the automatic centers of the medulla, particularly the respiratory center. Respiratory failure may progress rapidly.” “In 1949, three different poliomyelitis viruses were identified: Type I, Brunhilde; Type 2, Lansing, and Type 3, Leon. A typeing program, completed in 1951, revealed that all the numerous “strains” of poliovirus belonged in one or another of these three types. The diseases they cause can not be distinguished by symptoms, and all are called poliomyelitis. Infection by one virus type, however, confers immunity only against itself. It is, therefore, possible to have paralytic poliomyelitis twice, or even three times, from infection by the different virus types.” This site is now maintained by Chris Salter of the Lincolnshire Post-Polio Network Original Document Preparation: Tom Dempsey. Last modification: 14th December 1997

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