CODI: Cornucopia of Disability Information

The Late Effects of Polio

The Late Effects of Polio:
From Taming a Mysterious Syndrome to Managing the Ravages of Time

Frederick Maynard, M.D.
Clinical Director, Department of Physical Medicine and Rehabilitation
Medical Director, MetroHealth Center for Rehabilitation
Cleveland, Ohio

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Good morning. It is a real pleasure to be here today and see so many old
friends, even a patient from Michigan. I am really thrilled to be here in
Southern California and participate in this Conference on Aging with a
Disability. I have been communicating with Dr. Campbell for a couple of
years now, sharing some of our different work, and becoming aware of this
study's goals. I am delighted to hear the results and learn what has been
found by comparing two major kinds of disability groups. I have also been
involved with conferences on spinal cord injury and aging. There was a large
one last spring in Denver. It is striking to note the number of similarities
between the health issues faced by aging people with any type of
long-standing disability from a motor impairment; i.e., quadriplegia,
paraplegia, polio with paraplegia or arm weakness, stroke, and hemiplegias.
As people live many years with these conditions, a number of similar new
problems often develop.

Dr. Campbell asked me to speak about some of the implications of recent
research for our thinking about the late effects of polio. First, however, I
should give some explanation for why I came up with the subtitle for my
talk: "From Taming a Mysterious Syndrome to Managing the Ravages of Time."
This title addresses a changing perspective over the last ten years on the
questions: What are the causes of the late effects of polio? How should we
view them? To what do we attribute them?  What can we do about them?

Before I address the question of causes for the late effects of polio, I
need to say a few words about "languaging." I have found that many of the
apparent disagreements between physicians, and sometimes between polio
survivors and their physicians, about the late effects of polio or what to
do about them relate to the labels that people use for what they are
experiencing. I would like to begin by sharing with you the labels that I
will use in this talk and their definitions.

New Health Problems Among Post-Polios

Table 1* shows several terms that have been used to describe the late
effects of polio. One way you can think about them is as new health problems
among people with a past history of polio. I have tried to adopt some of the
Institute of Medicine's new terminology, which includes the notion of
secondary conditions. Secondary conditions are any new health problems that
occur in people with another primary disabling condition. In this instance,
if you have had paralytic polio, then any other new medical condition that
may develop in your life can be correctly labeled a secondary condition,
since it comes afterward in time. This has often been confused in the
literature, which uses the term secondary complication.  Actually,
"secondary complication" is redundant because all complications are
secondary, since they follow the primary condition in time. A complication,
as we normally think about it, would fit into the second category in Table
1, a late effect of polio (the primary condition). Late effects of polio are
specific new health problems, or disabilities and rehabilitative problems,
which result from chronic polio-caused impairments (typically muscle
weaknesses). If you have a muscle weakness or a paralysis after your polio,
you have a polio-related muscle impairment, which may or may not result in
some loss of function in your life (a functional limitation). If the
functional limitation prevents you from performing an important life
activity or role, then you have a disability.

Post-polio syndrome is a term that has become very confusing, and sometimes
very frightening, which is why I used "mysterious syndrome" in the subtitle
of this talk. When people first started talking about post-polio syndrome it
was in this context: No one understands what is happening to polio
survivors; something has to be done about these new problems; why won't
anyone acknowledge that these problems are real? Dr. Lauro Halstead has
offered a definition of post-polio syndrome. It includes new muscle
weakness, fatigue, and pain, which are the most common new symptoms that
develop in a group of people with long-standing polio. I believe that the
new disability or handicap that occurs as a consequence of these new
disabling symptoms is the critical issue for defining who has post-polio
syndrome. If there are two, or even only one, of the three symptoms, I would
say a person has post-polio syndrome if he or she is having new functional
limitation or disability as a result of the symptoms.

I have often been asked the question, "If you have post-polio syndrome once,
can you recover from it and have it again?" The answer relates to how you
define the term post-polio syndrome.  I have the viewpoint that a person
could become newly impaired but then recover from the disability. Even if
the new symptoms do not totally disappear, if the person is rehabilitated
and newly accommodated to a degree of impairment, has figured out how to
cope with it, and is no longer disabled from it, then the person would have
recovered from the post-polio syndrome.  Of course, this means that later in
life a new problem could come along and again cause greater impairment and
disability.  So a person could have post-polio syndrome a second or third
time.

The other term that has been used in reference to new problems among polio
survivors is post-polio progressive muscular atrophy. This term is more of a
medical diagnosis which allows people to be classified in a lexicon of
neurological diseases.  It refers to the pathology of abnormal changes in
motor neurons which result in new muscle weakness. Atrophy, which is a
shrinkage of muscle, may or may not accompany the new weakness.  Slowly
progressive weakness and atrophy probably occur in all muscles that have
either clinical or subclinical signs of chronic partial denervation and
reinnervation from previous damage to motor nerve cells, such as the damage
from old polio.

The Need to Understand "Why"

The major question I want to address this morning is "why?"  Why are people
developing the late effects of polio? Do the symptoms really result from
some type of new muscle condition, such as post-polio muscular atrophy? Are
they a result of some yet unknown triggers in the body which affect the
nervous system? Or are the majority of the new problems being experienced by
polio survivors really due to the cumulative effects of aging? While I pose
this question as a dichotomy, my own opinion is that there is truth to both
positions.

You may ask: "Why is it worthwhile explaining to consumers, as well as
professionals, why people develop the late effects of polio?" I believe
there are good reasons for both professionals and consumers to understand
why. One reason is that from a professional perspective, how we treat a
condition, a disease, or a disability will relate to what we understand to
be causing it. Different causes for symptoms will necessitate different
treatment approaches, even if the severity of a symptom such as weakness is
exactly the same.  Understanding the cause of symptoms should guide
management strategies because it may give us different expectations for the
person's future. This relates to the expected life course of a person's
disease, including expected new functional limitations and disabilities, as
Dr. Campbell discussed so well.

From a lay person's perspective, the important reason for discussing "why"
is what some psychologists have called "the human need to understand." Any
time something happens to us, there is an inevitable response: Why did that
happen to me?  We always ask ourselves that question afterward. A number of
researchers are finding out that how you answer that question will have a
great deal to do with what happens afterward. How you respond and experience
something that happens to you -- for example, a disease or injury -- may be
independent of what the physical reality is.

But, as another famous philosopher said, "What is reality?" A study was done
with accident victims. It found that a person's outcomes did not relate to
whether most other people believed that an accident was the victim's fault
or another person's fault. What mattered was how the injured person himself
explained what happened to him. The people who did the best after a
disabling injury were not the ones who primarily blamed others or who blamed
themselves for what happened. They were the people who could accept some
responsibility for their own part in causing the accident, even if everyone
else in the world would have said, "It was all the other person's fault."  I
certainly enjoyed the remarks of the stroke survivor who wrote the book
titled Stroke: An Owner's Manual (see Josephs, 1992, under Plenary #3). This
title implies that you have to take ownership and responsibility for what
has happened to you, to take charge of the experience of post-stroke living
that you are going to have.

Recent Post-Polio Research

Now I want to share with you, briefly, some of the research about what is
causing the late effects of polio. The leading theory for the last ten years
is that most new weakness occurring in polio survivors is due to a
disintegration of the motor units. The words disintegration and/or
deterioration may not be the best words because they sound very negative.
Nevertheless, there is a shrinking in size of the motor unit: the nerve
cell, its attached nerve axons, and supplied muscle fibers. The leading
theories for why this disintegration is going on have included:
immunological factors, aging itself, chronic overuse from too much exercise
or abuse, environmental factors, and other metabolic or circulatory factors
affecting muscle and nerve.

In order to understand these theories, it is necessary to review nerve and
muscle physiology related to polio. Within the spinal cord are nerve cells
that connect through an axon, which is like a long wire that goes out
through the body, to eventually reach muscle. Once nerve fibers reach
muscle, they branch in various directions in smaller and smaller branches
until they finally reach an end plate. The end plate forms the connection
between nerve and muscle.

An electrical impulse starts in the nerve cell and runs down the axon like a
little electric current. When it reaches the end plate, it causes a small
release of chemical that makes the muscle fiber contract. Individual muscle
fibers interdigitate so a muscle is not really one long contracting band,
but many intertwining short fibers. Each muscle fiber is connected to its
nerve by one end plate. All of the muscle fibers that are connected to the
same nerve will contract at the same time. Normally, when an electrical
impulse comes down an axon, all the muscle fibers connected to it will
contract.

After polio, some nerve cells die from the viral infection. If all the
nerves that reach one muscle are lost, then the muscle will completely
atrophy and there will be no voluntary movement. However, more commonly,
after polio not all, but only some, of the nerves to a particular muscle
died. It could be 10%, 50%, or perhaps 75% of the cells that died. If even
10% of the nerves that normally reach a muscle survive, useful movement in
the muscle will remain. The muscle will be weak, but it will probably be
strong enough to be quite useful. This fact leads to some of the problems
that occur in polio survivors.

There are several mechanisms by which people recovered strength after acute
polio. One was that some cells temporarily didn't work and then recovered.
This often happened in what was called "nonparalytic polio." These people
had transient paralysis. Within several weeks, they were essentially fully
recovered in terms of their strength. In these instances, cells probably did
not die, but they temporarily didn't work. A second mechanism for regaining
strength after acute polio was muscle hypertrophy -- survivors worked hard
in therapy programs with exercise. What exercise does is make each little
muscle fiber a little fatter. It gets more protein in it. When all the
larger muscle fibers contract, you get more force. The person becomes
stronger.

The third mechanism for becoming stronger is more interesting and relates to
what we think accounts for the late effects of polio. It is called "nerve
sprouting." This is a compensation of the surviving nerve cells. New axon
branches grow out from axons of surviving nerve cells within the muscle, so
that the new axon sprouts reach some of the muscle fibers which had lost
their original nerve supply. Thus, in the post-polio muscles with mild or
moderate weakness, surviving motor units are much larger; that is, there are
more muscle fibers connected to the same nerve than is the normal case.
Research has shown this to be about two and one-half to three times as many
muscle fibers connected to an individual nerve cell as would occur normally.

Another issue is that newer research has shown that sprouting is not a
one-time event. Muscle with partial loss of nerve supply will constantly be
showing some muscle fiber breakdown and some new muscle fiber growth. Muscle
tissue is actually much more dynamic than most people think. Everyone is
aware that bone, for example, is constantly being broken down and built up
new in the body. This happens at a very fast rate when you are young and
your bones are growing and shaping.  When you get older, it is only gradual.
When you become very old, the dissolution becomes much faster than the
building up of new bone, and the bones become thinner, a condition known as
osteoporosis.

Muscle metabolism is similar.  There is a constant building up of new muscle
fiber and constant breaking down of some existing muscle fiber. If the
balance between the muscle build-up and the muscle breakdown shifts to
greater breakdown, then the person becomes weaker. A very strong stimulus to
muscle breakdown is disuse. Breakdown also accelerates with aging and with
many medical illnesses that result in decreased activity.

In post-polio syndrome, disintegration of motor units results from a
dying-off of the previous nerve sprouts. Whereas post-polio nerve cells
after full recovery and rehabilitation were much larger than normal nerve
cells and supplied two and one-half to three times as many muscle fibers, in
the later stages of post-polio these nerves shrink back to their original
size. Therefore, the post-polio person experiences his muscles becoming
weaker again, because he is losing the compensation mechanism, so effective
in his younger years, that immediately followed the original loss of nerve
cells from polio.

On a microscopic level, we know that this dying-back of giant motor nerves
is not an all-or-nothing phenomenon. There are many stages of degeneration
during which some of the nerve fiber branches are sick or in the process of
slowing down but are not yet unable to function. At this stage there is
often a defect in the release of acetylcholine, the chemical that connects
the nerve impulse to muscle contraction.  This fact probably explains why
sometimes replacing acetylcholine will help some polio survivors (see Trojan
& Cashman, 1989).

Another problem can be what is called "conduction blocking."  This occurs
when the electrical impulse comes down the nerve, reaches the branch point,
and goes only one way. Thus the impulse bypasses some of the nerve fiber
branches. This phenomenon is also thought to occur when you have slow
deterioration of the metabolism in some of the nerve fiber branches.

Immunological Studies

Now let us consider some of the recent research about what triggers nerve
and muscle deterioration in some post-polios.  Immunological theories about
the late effects of polio have been proposed because polio was a viral
infection, and viruses affect the immunological system. The immunological
system is our body's primary defense against infection. As the public knows
since the AIDS epidemic, viral infections can lead to later changes in the
immunologic system. There have been studies that have shown the antibody
abnormalities in symptomatic post-polios, particularly antibodies in the
cerebrospinal fluid.

Recently a great deal of interest was generated by a study published by
Sharief in 1991 in the New England Journal of Medicine. This study looked at
oligoclonal immunoglobulin bands in cerebrospinal fluid and found they were
predominant and elevated. Particularly the antipolio virus IG-M antibodies
were elevated in 56% of the post-polio survivors, but in none of the
asymptomatic post-polios or controls studied. This certainly suggests
something very specific to the post-polio condition.

Other research studies have contradicted this finding, and the jury is still
out as to whether there is a strong correlation between these abnormal
antibodies in the cerebrospinal fluid and the late effects of polio or
post-polio syndrome. To me, it is very intriguing that post-polio syndrome
may be associated with immunological abnormalities because the immune system
is greatly affected by general health, by your emotional health, and by life
style. These are issues that a person can control. Dr. Bernie Siegel has
written a great deal about what you can do as a cancer survivor to control
and influence your immunological system, and what this can do to cancer cell
growth. This issue should be remembered by post-polios.

Electrophysiological Studies

The next area of research is electrophysiologic studies, or EMG studies, of
nerve and muscle functioning in post-polios.  To summarize the work done by
a variety of people, weakened post-polio muscles with partially denervated
and reinnervated fibers have increased fiber density and increased jitter on
single fiber electromyographic studies. Additionally, increased motor unit
size has been found on macro-EMG, and its presence correlates with increased
jitter (Trojan, Gendron, & Cashman, 1991). What do these findings mean?
Essentially, they confirm the earlier theories that proposed these
abnormalities would result from a shrinking back in the size of enlarged
motor units that are typical of partially paralyzed post-polio muscles.

Animal Studies

A number of animal studies and some clinical studies have shown progressive
impairments of neuromuscular transmission with age and years since onset of
nerve loss. This confirms a problem with the release of acetylcholine at the
connection between nerve and muscle in post-polios. Dr. Cashman labels this
problem "a syndrome of delayed failure of reinnervation."  In other words,
rather than calling it a disintegration or a deterioration of the nerve
cells, he calls it a delayed failure of reinnervation, which emphasizes that
the growth of new nerve fibers doesn't keep pace with the rate of loss of
nerve fibers.

I want to share with you -- especially the professional group in the
audience -- one recent animal study by Dr. Pachter in 1991.  It is exciting
because it is the closest thing yet to an animal model for the post-polio
syndrome. He took a group of mice and cut one of the nerve roots at the
level of the spinal cord to one of the major leg muscles. What that means
is, he created a leg muscle that had lost half its normal nerve supply and
he had created a partially denervated muscle. He then tested the muscle for
twitch and tetanic tension. Twitch tension means that you give one
electrical shock to a nerve, and measure how much strength is produced by
the contracting muscle that responds to that electrical impulse. In tetanic
tension you give a long volley of repetitive electrical shocks to the muscle
so that all the muscle fibers eventually contract and contribute their
amount of strength to the force that is measured.

When these tests were done at one month after root section, as you would
expect after half the nerves to a muscle are lost, both the twitch and the
tetanic tensions or forces in the muscle were reduced. Three months later,
however, only the tetanic tension was reduced. This means that now one
twitch of the muscle was just as strong as it was before the muscle lost
half its nerve supply, or as in the control mice. However, if you did the
repetitive electrical shock, which would be more similar to an endurance
phenomenon of repetitive muscle use, the tetanic tension was still reduced.
At six months there was no difference between the control animals and the
ones with nerve damage.

Essentially, the remaining nerve roots to the muscles had completely
compensated and were successful in taking over, from the standpoint of
producing force or tension, both individual twitch tension and the tetanic
twitch tension.

Next, the researchers studied the mice after nine months. By then, both the
twitch and tetanic tensions were again reduced.  When they sacrificed the
mice and looked at their muscles under the microscope, changes of
chronically denervated and partially reinnervated muscles were found, and
these changes were very similar to what is typically seen in mice that are
considered old at 20 months of age. This kind of mouse normally has a life
span of 24 months. Therefore, the changes that are associated with normal
aging in mice were already seen at nine months in those muscles which had
been used actively after partial nerve loss. The mice had been able to run
around easily during the time when they had normal strength in the partially
denervated muscles.

I describe this study as a concurring piece of animal research evidence to
support the idea that the post-polio syndrome may result from a
deterioration of hyperfunctioning motor units, which may result from
metabolic failure of nerve cell bodies that have had to compensate for the
loss of nerve cells supplying the same muscle over a long time.

Hormonal Studies

Next, I would like to describe some new hormonal studies. They were done in
Milwaukee, and some of you may have read about them in the lay press. They
involve the role of growth hormone and aging. Growth hormone is secreted by
the pituitary gland.  After adolescence, a very low, but constant, level of
growth hormone is still produced.  Recently people have begun to measure
these very small amounts of growth hormone and look at the result in
relation to typical events associated with aging. Dr. Rudman tested growth
hormone levels in a group of polio survivors, both those with symptoms of
post-polio syndrome and those who were not complaining of any new difficulty
(Rudman & Shetty, 1991). He was measuring somatomedin C, the active part of
growth hormone, which stimulates nerve regeneration and sprouting and muscle
protein synthesis. It has been shown in animal studies that growth hormone
does play an essential role in allowing the reinnervation process to
continue on a constant level in muscle.

Recent studies have shown that by the age of 40, some people show an arrest
of growth hormone production and low levels of somatomedin C. If you first
look not at polio patients but at an aging population in general, gradually
rising percentages of people over age 40 will show an arrest of growth
hormone.  It is believed that this relates to what we think of as signs of
aging, such as baldness, muscles becoming smaller, arthritis, difficulty
walking.

When Dr. Rudman looked at post-polio syndrome patients, he found that nine
out of ten with new symptoms had low levels of somatomedin C, whereas all of
those who were stable post-polios still had normal levels. So he postulated
that in some polio survivors with post-polio syndrome, there is an arrest of
growth hormone. This provides another interesting piece of theoretical
knowledge about post-polio syndrome. It suggests that late effects of polio
may largely be a result of aging.

There are a number of changes in the body's function that researchers in
geriatrics have found to be associated with "normal" aging, as opposed to
being a result of new diseases that may occur as you become older. One is a
decline in motor nerve cell counts. It turns out that only a very small
percentage of motor nerve cells are lost until people are well over 60 or 70
years of age. We don't know if nerve cells that survive acute polio have
suffered a metabolic insult and may have a shortened life span. This has
still not been ruled out.  Decreasing cardiopulmonary capacity occurs
steadily with age.  As you become older, there is a steady decline of vital
capacity and breathing ability, as well as some changes in your heart
muscles' capacity. Collagen tissue (the connective tissue in your body that
holds your joints and muscles and bones together) becomes stiffer, again
pretty much in a straight-line relationship with age.

Another issue is that chronic diseases occur statistically at a greater
frequency as a population becomes older. These other conditions will have a
great deal of influence on who develops new post-polio syndrome problems.
Lastly, muscle disuse atrophy, as a result of general slowing down, often
occurs in older people. It probably isn't healthy, but many older people
simply lose interest in or ability to perform vigorous activity.

Exercise Studies

The next type of research I want to discuss concerns exercise studies. Dr.
Agre in Wisconsin has done a great deal of exercise work in post-polios and
has shown that post-polios who are weaker and show greater evidence for
initial polio involvement are the ones who most commonly develop new
symptoms (Agre & Rodriquez, 1991). Endurance time is the same in these
weaker post-polios, even though total work capacity is less. He found that
recovery of strength from exhaustion, however, was prolonged.

This finding adds support to the notion that interval training, or taking
frequent short rest periods, and pacing are indeed good ideas. Perceived
fatigue was the same in weak and strong post-polio subjects. This finding is
important because some people said, "Post-polio people are just complaining
more about getting tired easily." In fact, Dr.  Agre showed that there was
no research evidence to support this idea. He also did serial isometric
strength testing in post-polios. A fairly large number of post-polio
subjects, I think 30 or 40, were tested for maximum strength without
exercise intervention over a period of three years. Also a control group of
people without a history of polio were tested.

What is interesting to me is that the study was actually able to measure a
statistical decline in the neighborhood of about 1/2% per year in the total
maximum muscle force. It was a small decline, but the slope of the loss of
strength was exactly the same in the people who were weak from their
long-standing polio and in the group of people who never had polio. This
suggests that a very small loss of muscle strength is perhaps going on with
normal aging. However, this study was not able to show that the loss was
more accelerated in polio survivors.

The results of many exercise studies indicate that some polio muscles
certainly can increase in strength, some patients certainly can improve
their fitness, and interval training and pacing are critical to the success
of any exercise program. In other words, one could summarize the results of
exercise studies by saying that you cannot make broad generalizations.
Exercise is not always bad. Exercise can be helpful. Certainly stretching
exercises are commonly helpful. Conditioning training to improve
cardiopulmonary capacity is very helpful, if you can devise a way of doing
it. If you have extensive paralysis, it may be difficult to do enough work
to stimulate your heart to pump harder and therefore become more fit, or to
breathe harder. However, strengthening exercise in some muscles, in the
right patients, can be very helpful. In other patients, it is probably
futile and a waste of time to try strengthening exercises. That is why it
takes individual evaluation.

Stress

The next area of investigation about why some polio survivors become more
disabled is the role of stress. In a number of studies a high correlation is
shown between stress levels and symptoms of post-polio syndrome; that is,
complaints of weakness, pain, and fatigue. Dr. Richard Bruno has
hypothesized that polio survivors have a reduced capacity to secrete
cortisone in response to stress (Bruno, Frick, & Cohen, 1991). He has
suggested that this may relate to loss of cells in the area of the brain
controlling the body's response to stress. Autopsy studies of people who
died after acute polio do show reduced numbers of cells in the reticular
formation of the brainstem. Exactly what these changes mean and how much
they relate clinically to post-polio syndrome is not clear at this point.
Dr. Bruno's theory certainly adds some theoretical support to the common
wisdom that too much stress is not healthy, especially for polio survivors,
and that learning to control and reduce stress can be health enhancing.

I also need to remind everyone that experiencing progressive disability is
in fact stressful. You must be very much aware of this issue when you are
doing studies; for example, in the studies that Dr.  Campbell and her
colleagues have reported here. In order to make generalizable conclusions
about polio or stroke survivors, it is important to be sure that the group
of people you are studying in detail are not the atypical ones with many new
difficulties, because they are more likely to come into a clinic or a
support group, and may be more likely to volunteer for a study than
post-polios whose health is good and whose functional abilities are stable.
Post-polios coming to clinics are more likely to be distressed and looking
for answers; therefore their problems at the time of being studied may be
different.  Figure 1 illustrates how new health problems and functional
limitations in post-polios are related. Functional limitations can be
locomotor, such as how we walk around, or they can involve how we take care
of ourselves. Musculoskeletal pain problems may commonly be a result of
chronic muscle weakness and unusual ways of performing functional activity.
However, reduced cardiovascular fitness or general loss of health from heart
disease, diabetes, or cancer (conditions known as co-morbidities) probably
has nothing to do with the fact that you had polio. Nevertheless, if you are
a polio survivor with long-standing weakness and you develop these
conditions, you may well experience a great deal more new weakness or
fatigue than other people without a history of polio would experience.

An unfortunate truism for polio survivors that has been learned from a
number of studies about aging with a disability is that the functional
abilities that required the greatest effort during rehabilitation, that took
the longest, and that depended on the greatest personal determination to
ultimately achieve and accomplish are the very same abilities that will be
lost first as a person becomes older and weaker, whether from a condition
unrelated to the polio or from the late effects of polio.

Loss of functional abilities impacts greatly on people's life style,
including how they support themselves, what they do for themselves, and what
they may need other people to do for them. If a person has a new functional
loss, there are three generic choices for responding to it. First, you may
give up the activity; for example, you may have to quit skiing if your legs
become too weak. A lot of people do this when they get older. They give up
tennis, although they may keep golfing until they're well into their 80s.
Second, people can learn to do the lost functional activity differently.
They may need to develop new skills to be able to still do it independently
in a different way, or they may require new equipment to do it
independently. This choice for responding is the typical kind of thing done
through rehabilitation.

Third, but important, a person may choose to get help. This means getting
someone else to do what you cannot do for yourself, or what you cannot do
for yourself without risk of injury, or risk of wasting too much energy so
you can't do other things you would really like to do more. It may take some
patient explanation to family members or friends who are needed for
providing the help in order for this to be possible. Everyone in
rehabilitation believes that some governmental financial help should be made
available for people with severe disabilities who could live independently
from the standpoint of making decisions, if they could only have the extra
hands to help them.  

Epidemiologic Studies

The last area of research I would like to discuss is epidemiologic research.
Population-based studies of polio survivors in Minnesota have shown that 24%
to 40% are having new problems (Windebank, Litchy, Daube et al., 1991). My
colleagues and I also did a large study on the late effects of polio among
polio survivors in Michigan (Maynard et al., 1990). We found our sample also
had very high rates of symptoms of weakness, fatigue, and pain. They were
generally lower than what has been reported in the literature because most
other studies have sought out people volunteering to participate in
questionnaires. We used a more selected sample, although it still relied on
a statewide polio survivors' group. We particularly chose for study people
who were nonsymptomatic, in addition to those with symptoms, so that we
could look for correlations between subject characteristics and new
problems.

We used the concept of "period of physical best" in our interviews and
questions. The period of physical best is the time in a person's life after
acute polio and subsequent rehabilitation when they had the greatest
physical functioning, such as walking endurance or strength for strenuous
work. For people who acquired polio during childhood, this usually occurs in
early adulthood, when normal growth and development is complete. We used
this concept because it is very difficult retrospectively to know what is a
new symptom. For example, a loss of walking ability may have been present in
one person for 30 or 40 years, but it may be new in another person who never
had previous walking difficulty. If a researcher did not examine the person
30 years ago and then also today, it is hard to be certain about what is
new. Therefore, we let the post-polios define this time period for
themselves.

Table 2 shows what we found in our 120 people. Fifty-six percent reported
current difficulty with activities of daily living (ADL), up 25% from the
time of physical best.  Difficulty with intermediate ADL, such as getting
around in the community for shopping, etc., rose 25% from the time of
physical best, to a current total of 81% of our subjects.  Certainly, people
were becoming more disabled. As for the kinds of disabling conditions, hand
and wrist problems were probably the most common.  Our results support the
notion that overuse of the upper limbs is particularly common in people who
have long-standing weakness problems in their legs.  Greater use of the arms
and hands is an important compensation, but it does lead to shoulder and
hand arthritis, nerve compression syndromes, and other wearing-out problems
of the musculoskeletal system in the upper limbs.

If we looked for correlations as to which conditions were found on
examination of post-polio subjects who had the greatest losses in functional
independence, we again found upper limb problems common, as well as spinal
pain, lower limb weakness, and gait deviations. Many of these new problems
are related to the severity of the original polio, but the other strong
association was with having secondary conditions, or co-morbidities. Obesity
was strongly correlated with greater loss of functional abilities. Reduced
exercise capacity was also strongly correlated. People who were less fit
from a cardiopulmonary standpoint were in fact reporting greater functional
decline.  Elevated cholesterol ratios, interestingly, were also higher in
those losing function. I'm not sure that the average cholesterol level for
all of our subjects was higher than normal, but high levels were certainly
prevalent, particularly in men. There was a strong correlation between
decline and having any non-polio related condition, such as heart disease,
emphysema, stroke, etc. Prevalences for anemia and hypertension were
probably very close to what occurs in the non-polio population; perhaps they
were even lower than in an age-matched able-bodied population.

Implications for Management

About 35% of the 120 people had at least one other co-morbid condition.
Fifteen percent of the sample had elevated depression scores on the Brief
Symptom Inventory. These scores were unassociated with the severity of polio
weakness, but were associated with having other non-polio related medical
conditions. They were also associated with some personality factors,
including a pessimistic expectation for life in general and a resentful
style of anger coping; that is, a tendency to direct anger in on oneself.

To conclude my talk, I want to address what we can do about these new
problems. I like to emphasize the concept of re-rehabilitation, which is
going through rehabilitation efforts and evaluation the second or third time
when new problems develop. There is usually a great deal that can be done to
improve remediable or correctable conditions as well as figure out how to
best compensate for what may not be remediable. An important balance must be
found between "use it or lose it" on the one side (the motto known well to
polio survivors when they were young) and "conserve it to preserve it." The
body has to be much more gingerly taken care of when you are older than when
you are young and can better afford to abuse yourself because the body is
more adaptable. This can mean that you may need an electric cart at the same
time that you can still walk. I know a lot of people in this room who have
learned this.

People in a declining phase of physical capacity need to adopt energy-saving
techniques. They have to be flexible and creative, to invent and figure out
how to get around problems. This approach allows answers to be found. For
example, exercise can be helpful, as I mentioned before. However, there are
all types of exercises.  For example, aquatic exercises are particularly
helpful. Back care and joint protection flexibility exercises are often
crucial to prevent pain and preserve function.

There are many community resources for health promotion, including physical
therapy that can teach you how to do your own exercises; health clubs;
information on nutrition. Many of these health and wellness resources need
to be adapted specifically for people with long-standing motor disabilities.
Also, there is the whole issue of mental attitude and life style
enhancement. Support groups can be particularly helpful to address this in
one way or another. Attitudes and outlook on life can have major
consequences and can influence the immunological system.
  
Sunny Roller and I recently put a book together, which I have referenced
(Maynard & Roller, 1992). It presents a modular program that is designed to
establish an accessible and convenient community location for health
promotion efforts of exercise, nutrition, and life style enhancement. It is
designed to enable local people in your area to teach and facilitate
activities because people can't travel a long way to attend health promotion
activities. These are the goals of the program. It is crucial to find local
facilitators with professional expertise to lead these programs. The manual
basically provides a curriculum guide for them. The Stay Well manual is
dedicated to preventing the unnecessary progression of disability and
encouraging the participants to get well and stay well for years to come.

---------------------

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