Bollenbach

Variant of Covid Virus

– Kindly shared with us by Eddie Bollenbach M.A. biology

You have probably heard of the new variant of COVID

virus in the United Kingdom and also another mutant

strain in South Africa with similar mutations to the UK

variant. Let’s constrain ourselves to the UK mutant.

The reproductive number or Ro of the wild strain is

1.1 which means 10 infected people will typically

infect 11 others. It is believed that the reproductive

number Ro of the mutant strain is 1.5, which by division you can find that the new  virus seems 70% more infectious. 10 people will most commonly infect 15 people.

The difference in infectivity is not enough to mean we cannot control the virus by  mask-wearing, social distancing, and hand washing. It can be handled.

Now, since the genetic code of the new variant differs in 6 places in the spike  protein, but USA Today says 8 places, the result is that two amino acids in the  spike protein are different from the wild type. A protein is a long chain of amino  acids linearly bonded to one another. Then this long line of amino acids folds a  couple of times to give us the shape of the protein. A change of 2 amino acids in  the spike protein will result in a slightly different shape for the spike protein. In  this new variant, there are a whopping 17 new mutations altogether.

Since the shape of the spike protein matters because it is the target of antibodies  induced by vaccination the concern arises regarding the antibody shape combining  with the new spike protein shape.

The good news is vaccinologists believe the vaccines will still be effective and  work. Continuing research is going on now in Britain to measure this.

This variant will soon be all over the world if its Ro is higher than that of the wild  strain. The US hasn’t closed its border to people from the UK because the strain is  probably here already and it will be treated the same way as our original wild-type  strain.

In the foreseeable future we will learn more about this variant so stay tuned.

Polio Biology XII

Genetics of the Post-Polio Syndrome

Eddie Bollenbach

A Lincolnshire Post-Polio Library Publication

24th January 2006

It has been a while since the last Polio Biology column and much has happened in the field of neurodegeneration since the last installment. It’s too bad we don’t have as much focused medical research that specifically targets the Post-Polio Syndrome, nevertheless we can learn much about ourselves from work occurring in the general field of neurodegeneration. Actually, in a very real sense, Post-Polio Syndrome is the result of neurodegeneration, or the loss of vitality, synaptic connections, and resilience of our motor neurons.

One of the facts about PPS that has always bothered me is the generally accepted cause of the syndrome as deriving from overuse. Two mental roadblocks for me in accepting this idea are:

1. Only 40% (the most frequently seen number) to 20% of people who have had polio develop the syndrome with its new weakness, fatigue, pain, and variety of complications. It is logical to infer that if one had paralytic polio which resulted in residual weakness, one should develop PPS because we all overuse weak muscles innervated by too few neurons. In a survey by Marcia Falconer and me, soon to be published here at Lincolnshire, we found no difference in incidence of PPS, or severity of PPS, between polio survivor couch potatoes, or those who have worked hard physical jobs throughout their lives or participated in regular vigorous physical activity[1]. There have been other survey reports that have since supported this since our finding two years ago[2].
2. Sometimes, it seems, people with severe initial damage escape PPS while others with less severe damage, even some who have had what was thought of as non-paralytic polio, succumb to PPS[3]. Since those with severe damage are weaker throughout life, overuse would be greater for their severely damaged neuromusculature.

In any event, late neurodegeneration must involve several steps. It is obvious that a prerequisite is a susceptibility to late spinal neurodegeneration. There is a very interesting study about late neurodegeneration, after physical damage to the spinal cord, published in 2003 entitled: “Discrete Gene Loci Regulate Neurodegeneration, Lymphocyte Infiltration, and Major Histocompatibility Complex Class II Expression in the CNS”. The title is a mouthful. The rest of this installment will explain the significance of this article to our problems with PPS and to it’s possible treatment.

The above study involved the experimental destruction of motor neuron axons (referred to as avulsion of the ventral roots of the spinal cord) in two genetically different strains of rats. The authors also crossed the

two mating strains of rats and avulsed the offspring of these two mating types. Some rats developed a late neurodegeneration (as we with PPS) and some did not. The ones that did not had different genes in several areas of their chromosomal makeup which controlled immune responses in the spinal cord. The ones who did experience late degeneration had different genes in these locations.

RESULTS:

Four points (genes) on rat chromosomes labeled VRA1, VRA2, VRA3, and VRA4 acted to determine susceptibility to late neurodegeneration. Three of these loci determined whether or not immune cells (white blood cells or MHC II cells would present in the damaged areas after the original lesions healed). The corresponding (Synectic) locations on human chromosomes controlling a late immune reaction in the spinal cord after recovery are 8q12, 8q22.1, and 1p35.2-36.11, and 16p13. To explain the chromosomal notation there are 22 pairs of chromosomes along with a pair of sex chromosomes in the human. The first number, e.g., 8 above, indicates the gene is on chromosome number 8. The q designates that the location is on the long arm of the chromosome. Each chromosome has a narrow area called a centromere which separates a long arm from a short arm. The chromosomes are observed after they are stained and the second number, 12, designates the staining band when counted out from the centromere. The location 1p means the first chromosome’s short arm (p) and the numbers following indicates that the gene is within the bands 35.2-36.11.

Figure 1 Diagram of one human gene with its loci and designation criteria

(US Library of Medicine)

SIGNIFICANCE:

In the past three years researchers at the Karolinska Institute in Sweden have demonstrated the presence of immune activity in the spinal cords of people suffering the Post-Polio Syndrome but not in patients who had polio with no late neurodegeneration. This immune activity was detected by the presence of immune chemicals derived from the same immune cells discussed earlier. Physicians at Karolinska have treated patients with intravenous immunoglobulin, which cleared the intrathecal space and spinal fluid of these immune chemokines and cytokines which directly attack motor neurons. Several patients treated with IVIg reported an increased vitality and quality of life, less pain and fatigue, and a general decrease in symptoms. [4, 5, 6, 7]. The work, which indicated a genetic basis for late neurodegeneration, strongly implies that late neurodegeneration is the result of T lymphocyte infiltration and macrophage type II instigation controlled by specific genes (which control the production of cytokines and chemokines, immune chemicals resulting from immune activation within the spine). I believe these two lines of inquiry outlined above fit nicely together to give us a picture of what may be happening inside the spinal cord ventral roots in Post-Polio Syndrome. If so, some unresolved questions about PPS are closer to resolution:

1. Why does PPS only happen to some of us? (Because we are genetically different from one another.) 2. Why does it occur with different degrees of severity? (There are several genes at work that may differ.)
2. And finally, can it ever be treated? It seems we can improve our lot by decreasing the immune activity in the spinal cord. Possibly through the use of drugs to diminish the cytokines found in PPS, or possibly by infusion of IvIg or a smaller defined antibody immunoglobulin as yet uncovered. Plainly, we can interrupt PPS by finding ways to turn off the effects of immune chemicals inside our spinal cords. If these ideas pan out PPS should be manageable in the near future.

References.

1. Falconer, M. and Bollenbach, E. Survey results in process. Lincolnshire, 2006. 2. Rekand T; Kõrv J; Farbu E.; Roose M.; Gilhus N.E.; Langeland N.; Aarli J.A, “Lifestyle and late effects after poliomyelitis. A risk factor study of two populations” Acta Neurologica Scandinavica, Volume 109, Number 2, February 2004, pp. 120-125(6).[PubMed Abstract]
2. Falconer, M. and Bollenbach, E. “Late Functional Loss in Non-Paralytic Polio”, Am J Phys Med Rehabil. 2000 Jan-Feb; 79(1):19-23.[PubMed Abstract]
3. Gonzalez, H. et al “Prior poliomyelitis – evidence of cytokine production in the central nervous system” J. Neurol Sci. 2002 Dec 15; 205(1); 9-13.[PubMed Abstract]
4. Gonzalez, H. et al “Prior Poliomyelitis – IvIg treatment reduces proinflammatory cytokine production” J. Neuroimmunol. 2004 May; 150(1-2): 139-44.[PubMed Abstract]
5. Kaponides, G. et al “The effect of intravenous immunoglobulin in patients with post-polio syndrome – an uncontrolled pilot study. Submitted at the Karolinska Institute 2005. 7. Gonzalez, H. et al. “Intravenous immunoglobulin for the post-polio syndrome’; a randomized controlled trial. Submitted as PhD Thesis at the Karolinska Institute 2005

The Lincolnshire Post-Polio Network

Registered Charity No. 1064177

An Information Service for Polio Survivors and Medical Professionals

All enquiries, book requests, medical article requests, membership fees, items for newsletters and donations to

The Secretary, Lincolnshire Post-Polio Network

PO Box 954, Lincoln, Lincolnshire, LN5 5ER United Kingdom

Telephone: +44 (0)1522 888601

Facsimile: +44 (0)870 1600840

Email: info@lincolnshirepostpolio.org.uk

Web Site: www.lincolnshirepostpolio.org.uk

The Lincolnshire Post-Polio Network takes great care in the transcription of all information that appears at this site. However, we do not accept liability for any damage resulting directly or otherwise from any errors introduced in the transcription. Neither do we accept liability for any damage resulting directly or otherwise from the information available at this site. The opinions expressed in the documents available at this site are those of the individual authors and do not necessarily constitute endorsement or approval by the Lincolnshire Post-Polio Network.

© Copyright Eddie Bollenbach 2006

© Copyright The Lincolnshire Post-Polio Network 2006 – 2010.

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).

Document preparation: Chris Salter, Original Think-tank, Cornwall, United Kingdom.

Created: 25th January 2006.

Last modification: 21st January 2010.

Last information content change: 26th January 2006.

Polio Biology XI

The Biology of Fatigue

Eddie Bollenbach

A Lincolnshire Post-Polio Library Publication

6th August 2000

William Shakespeare, Sonnet XXVII: ‘Weary with toil, I haste me to my bed.’

Everyone has experienced fatigue, even Shakespeare. It is a reaction the body has evolved to maintain a healthy steady-state. It is a countermeasure to overuse and acts to avoid damage to muscles and nerves. If our bodies, sculpted through millions of years of evolution, had no way to tell us that it is time to shut down, we wouldn’t have gotten this far. So my first point in this essay is to emphasize that fatigue is not just the province of people living with post-polio syndrome. Everyone in the human family has experienced fatigue.

One area of the biomedical literature which has examined fatigue, and its components, is the discipline of sports medicine. The 2000 Sydney Olympics is on the docket and you can be sure that trainers and sport’s physicians are studying every aspect of fatigue that can effect their athletes. Why? Fatigue degrades performance. An understanding of all of its manifestations allows athletes to take steps to avoid and minimize the likelihood of a poor performance.

Of course we with post-polio syndrome live with fatigue. It is a much more common state for us and does not abate easily and normally as it does for an athlete. We have to be especially careful about it and also knowledgeable about it if we are to improve our lives.

Elite athletes know about fatigue to win medals, we must know about fatigue to improve our lives. Who knows more about the biology of fatigue, the elite athlete or the post-polio survivor? I hope this essay can help improve our general knowledge, from the biological perspective, and allow us to intelligently use this information to improve our lives.

Biology of Fatigue.

Throughout this series we have mentioned the motor unit. This is the nerve/voluntary muscle unit of contraction. The nerve depolarizes (that means the charge on the outside of the cell membrane (+) rushes inside (-) resulting in the charge on either side canceling). This depolarization moves along the nerve away from the Central Nervous System eventually to a voluntary muscle. When an activity requiring muscle contraction begins (running is a good example) the rate of depolarization and re-polarization (which requires energy) is rapid in the motor unit. The nerve cell depolarization triggers depolarization in the muscle cell membrane. The muscle cell depolarizes and the muscle fiber contracts (shortens) due to

the activity of proteins inside the muscle fiber. The muscle and nerve quickly recover and re-polarize. This uses nutrient energy. Then they fire again. If this rapid firing is not interrupted, either by other motor units taking over (which we lack- see Polio Biology X), or because of maximum intensity exercise over a long period, the nerve, nerve/muscle junction, and/or the muscle fiber itself will fatigue.

Inside the nerve the energy used to re-polarize the membrane is derived from specialized molecules, nutrients, and enzymes. As they become depleted waste products accumulate. If the waste products interfere with normal energy production and utilization we have metabolic fatigue inside the cell. The same can happen in the muscle fiber where chemicals like lactic acid, ammonia, and creatine build up faster than they can be excreted. All of this biochemistry, which may manifest as a feeling of burning inside a muscle, cramping, weakness, pain, or creepy crawly feelings are the result of fatigue, specifically localized fatigue. Any fatigue in the nerve, muscle fiber, or entire motor unit (muscle and nerve) constitutes localized fatigue.

If fatigue occurs in any nerves above the motor unit it is called Central Fatigue. It too is a common protective mechanism for the muscles and nerves below it and athletes experience it mostly as a consequence of over training. I get the sense that many polio survivors think that Central Fatigue is reserved for them and is a unique and disturbing symptom not known to others. This is not so.

There is a way to measure the magnitude of subtypes of Central fatigue. If you use a small electric shock to stimulate a muscle and measure the maximum force of contraction you can use this as a baseline of strength of contraction. If you then prompt a person to contract the same muscle as vigorously as possible you can measure the difference between tetanic contraction (of the unit with the electric pulse) and the maximum voluntary force possible. This is one measure of one subtype of Central Fatigue. We don’t know a lot about Central Fatigue at the molecular level but it manifests itself, often, as a loss of drive or motivation to perform. Again, one can appreciate the role of Central Fatigue in protecting the nerves and muscles by inhibiting their over work at the level of the Central Nervous System.

There is a part of the human brain you may have heard about: The Reticular Formation. Nerve cell firing there keeps us awake. Some say, or have said, that polio damage has affected the reticular formation and that this is why some of us sleep so much and cannot easily rouse. I think this would be a very difficult idea to prove because of the complexity of the arousal system and the role of Central Fatigue in overwork, blood gases, and other factors. If you experience a blow to the head the neurons of the Reticular Formation can all depolarize and you will be rendered unconscious. If re-polarization occurs (hopefully in a short while) you will awaken. Anyway, this depolarization and re-polarization is how all neurons work.

Let’s get back to Central Fatigue. Any negative effect on muscular performance, which is generated above the motor unit, is Central Fatigue. This includes inhibitory processes arising in the brain. We know less about this but we do know that it occurs in athletes as well as in polio survivors. The Central Nervous System is involved to a large extent in the regulation of muscular activity. (Bompa 1990)[1]. Elements within the Central Nervous System result in a number of psychological factors, and emotions, which can degrade muscle performance and result in a loss of drive due to Central Fatigue. (McComas 1996)[3].

During prolonged exercise in an athlete, or during any activity which exceeds the fatigue point for a polio survivor, the blood chemistry changes. Amino acids, which make up proteins, change with respect to their relative abundances. Those amino acids with branched chains decrease and fatty acids increase. Examples of branched chain amino acids are leucine, isoleucine, and valine. Tryptophan is an amino acid but is not a

branched chain amino acid. The ratio or Tryptophan/BCAA rises during fatigue, which results in a biochemical alteration of tryptophan to 5-hydroxytryptamine (5-HT) in the brain. You may know (5-HT) by its more commonly used name of serotonin.

To make a very complicated story short serotonin can act on serotonin receptors in the brain to cause sleep and also increase the mental effort (motivation) needed to maintain muscular activity. It’s all rather complicated chemically, and this is but one theoretical biochemical pathway of many that helps explain Central Fatigue.

We’ve also heard of dysfunction of the hypothalamus and pituitary to explain Central Fatigue in post-polio syndrome. As is to be expected, these areas are implicated in Central Fatigue for elite athletes too. Possible indicators of Central Fatigue, cited by Lehman et.al. (1993)[2] include an impaired neurotransmitter metabolism, with increased cerebral 5-hydroxyrtyptamine (5-HT) concentration, partial hypothalamic and pituitary dysfunction, with resultant dysfunction of the neuro-endocrine axes.

It has been observed that over-training in athletes (which happens often for our normal activities) results in faulty prolactin metabolism as well as adrenocortical insufficiency. Well, enough of the biochemistry.

Suffice it to say that fatigue is a complicated phenomenon which involves motor units and the CNS and regulates the body by preventing overuse on many levels. There is not much difference in the CNS aspects of fatigue comparing elite athletes and polio survivors in my opinion. We just must do more with less and get to fatigue sooner.

I’ve never heard of anyone trying Branched Chain Amino Acids to help with Central Fatigue but I believe they are available at health food stores. To do any good (and they may not) you probably need 10 to 20 grams. Ask a physician before you try this. The fatigue is there for a purpose. If you reduce it without addressing the root of it you could hurt yourself.

References.

1. Bompa TO (1990): Theory and methodology of training: The key to athletic performance. (2nd ed.) Dubuque: Kendall/Hunt Publishing Company.
2. Lehmann, M., C. Foster, and J. Keul. Overtraining in Endurance Athletes: A Brief Review. Medicine and Science in Sports and Exercise. 25(7):854-862, 1993.
3. McComas AJ, Stuart DG, Thomas CK and Pierce PA (Eds) (1996): Fatigue: Neural and muscular mechanisms. New York: Plenum Press, pp. 457-469.

The Lincolnshire Post-Polio Network

Registered Charity No. 1064177

An Information Service for Polio Survivors and Medical Professionals

All enquiries, book requests, medical article requests, membership fees, items for newsletters and donations to

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Telephone: +44 (0)1522 888601

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Email: info@lincolnshirepostpolio.org.uk

Web Site: www.lincolnshirepostpolio.org.uk

The Lincolnshire Post-Polio Network takes great care in the transcription of all information that appears at this site. However, we do not accept liability for any damage resulting directly or otherwise from any errors introduced in the transcription. Neither do we accept liability for any damage resulting directly or otherwise from the information available at this site. The opinions expressed in the documents available at this site are those of the individual authors and do not necessarily constitute endorsement or approval by the Lincolnshire Post-Polio Network.

© Copyright Eddie Bollenbach 2000

© Copyright The Lincolnshire Post-Polio Network 2000 – 2010.

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).

Document preparation: Chris Salter, Original Think-tank, Cornwall, United Kingdom.

Created: 6th August 2000

Last modification: 21st January 2010.

Last information content change: 7th August 2000

Polio Biology X

In PPS Manual Muscle Testing Problems Arise From Judgement and Biology

Eddie Bollenbach

A Lincolnshire Post-Polio Library Publication

18th March 2000

When acute polio struck it was essential to measure the extent of paralysis quickly. One of the techniques used was manual muscle testing. There isn’t too much to it really. The physician holds a hand against a patient’s limb and coaches the patient to push as hard as possible. Depending on the judgement of the tester the patient’s muscle strength is graded from 1, (Trace Strength), to 5, (Normal Strength). This assessment was very valuable because it provided a clinician with enough resolution in measurement to quickly evaluate the extent of neuromuscular paralysis from acute polio in one session.

From the standpoint of muscle biology these tests made sense too. During acute polio, motor nerves, and all their branches to muscle fibers, die. The muscle fibers are then unable to receive motor stimuli from the brain and spinal cord to induce voluntary movement. A manual muscle test would quickly show that many or all muscle fibers were orphaned and had no ability to do work. Appropriate therapy could then be initiated.

The biology of Post-Polio Syndrome is distinct from that of acute polio. In PPS end fibers of motor nerves begin to lose function. This is a slow process which involves fatigue more often than muscle incompetence. Let me explain. If a normal person is standing it is possible that 30% of the muscle fibers in his leg are contracted to maintain his upright position and posture. When those 30% get tired they automatically rest (switch off) — isn’t the human body an ingenious creation? — and another different 30% of fibers contract to allow the first group to recoup. This can go on for hours. Someone with PPS may have only 40% of his original muscle fibers. When he or she stands they have only 10% in reserve, so in a short while there are no substitutes to take the load off. The result is fatigue of contracting muscles.

In the case described above what would show on manual muscle testing? On contraction against a clinician’s hand strength may show normal (5). But this is instant strength, which is what manual muscle testing measures. Many people with PPS are not down in the (1) trace range, especially if they recovered well from their acute polio. They are in the 5,4,3, and 2 ranges.

Dr. Sharrard in 1953[1] found that in order to identify any weakness, by this kind of testing, more than half the anterior horn cells had to have been destroyed during the original polio infection. Other clinicians have also demonstrated the problems with manual muscle testing in grading PPS involvement.[2,3]

The biology of PPS explains the problem. What we should be looking for is fatigue in previously involved muscles, or less frequently in uninvolved muscles. Manual muscle testing just doesn’t do that. The PPS health professional should be clear about what is being measured by manual muscle testing. It may be, for many, that what is being measured is the original weakness and not the new loss.

References.

1. Sharrard, W. J. W.: Correlations between the changes in the spinal cord and muscular paralysis in poliomyelitis. Proc. R. Soc. Lond. 40:346, 1953.
2. Perry, J.; Barnes, G.; and Gronley, J. K.: The postpolio syndrome. An overuse phenomenon. Clin. Orthop., 233: 145-162, 1988. [Lincolnshire Library Full Text]
3. Grading For Manual Muscle Testing (attributed to Dr. Perry – Rancho Polio Clinic). [Polio Survivors’ Page] <URL:http://www.eskimo.com/~dempt/grading.htm>

The Lincolnshire Post-Polio Network

Registered Charity No. 1064177

An Information Service for Polio Survivors and Medical Professionals

All enquiries, book requests, medical article requests, membership fees, items for newsletters and donations to

The Secretary, Lincolnshire Post-Polio Network

PO Box 954, Lincoln, Lincolnshire, LN5 5ER United Kingdom

Telephone: +44 (0)1522 888601

Facsimile: +44 (0)870 1600840

Email: info@lincolnshirepostpolio.org.uk

Web Site: www.lincolnshirepostpolio.org.uk

The Lincolnshire Post-Polio Network takes great care in the transcription of all information that appears at this site. However, we do not accept liability for any damage resulting directly or otherwise from any errors introduced in the transcription. Neither do we accept liability for any damage resulting directly or otherwise from the information available at this site. The opinions expressed in the documents available at this site are those of the individual authors and do not necessarily constitute endorsement or approval by the Lincolnshire Post-Polio Network.

© Copyright Eddie Bollenbach 2000

© Copyright The Lincolnshire Post-Polio Network

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).

Document preparation: Chris Salter, Original Think-tank, Cornwall, United Kingdom.

Created: 25th January 2000

Last modification: 21st January 2010.

Polio Biology IX

Peering at Post-Polio Syndrome under the Microscope

Eddie Bollenbach

A Lincolnshire Post-Polio Library Publication

25th January 2000

The Microscope is an instrument that revolutionized the study of biology. Before it existed everyone believed the human body was only composed of amorphous flesh. After Galileo and Janssen, the simultaneous inventors of the earliest microscopes at the beginning of the 17th Century, we knew that we were composed of tiny structures called cells. The human body contains about 10 trillion cells, small circumscribed entities with an organized internal anatomy and a complicated biochemistry. These parts together are the essence of life.

In human beings there are cells of many different types. For our purposes we will concern ourselves with just two of the types of cells that are affected, both acutely and persistently by polio: motor nerve cells and, secondarily, striated muscle cells.

A fairly accurate mental picture of a motor nerve cell can be conjured up by imagining a tree uprooted and cleaned of soil from its roots. The roots of our cell are called dendrites and they would be located inside the spinal cord. Each rootlet would be connected to the branches of another nerve cell above it. Our motor neuron has a branch coming extremely close to a muscle fiber (a long thin cell that can contract (shorten) and elongate).

Picture one nerve cell with 1000 branches, each branch of the cell innervates a single striated muscle fiber. If you can do this you are imagining a “giant motor unit” which is often alluded to in the polio literature. Giant motor units result after acute polio when muscle fibers lose their connection to a branch because the whole tree (nerve cell) dies. Surviving neurons grow extra branches and connect in the process of recovery from polio damage. This giant motor unit consists of a motor nerve connected by end fibers (branches) to 1000 muscle fibers.

When an EMG is performed the technician can tell if muscle fibers are all part of the same motor unit (if there are giant motor units). When the nerve fires, all the muscle fibers connected to it by its end fibers (branches) also fire synchronously. This will show a characteristic pattern recognizable in the EMG.

Striated muscle fibers are encased in bundles. I’ve tried to draw a representation of a group of striated muscle fibers below, although they are not as uniform in shape as my diagram implies. Some are round, some oval, some angular and so on. Anyway, I thought I could make a couple of interesting points about how polio, and post polio syndrome, affect the muscle fibers using these diagrams.

Figure 1.

On the left we have a cross section of a bundle of normal

muscle fibers. For the sake of understanding polio we’ll

suppose that all of them are innervated by healthy nerve cells

and are part of the same motor unit. In an individual with

Amyotrophic Lateral Sclerosis the entire bundle dies sparing

no fibers because the entire nerve cell dies with all of its

branches (the entire motor unit.)

Figure 2.

To the left we have a diagram of a muscle bundle but notice

that individual fibers (dark centers) are dropping out. It is

significant that the entire bundle, with all fibers, is not dying

but only a few scattered fibers. This is characteristic of post

polio syndrome under the microscope. It suggests the nerve cell

is not dying but rather end fibers are degenerating. It is possible

that the fibers dying here could be picked up and reinnervated

by another nerve, creating an even bigger giant motor unit.

This process is ongoing in patients who have had polio with

giant motor units getting bigger and bigger. When a real big

one reaches the threshold of cellular exhaustion an entire

muscle bundle may die.

At times, under the microscope, muscle biopsies of PPS patients show the loss of entire groups of fibers as happens in ALS. However, in ALS this is the rule while in PPS it is rare. I should add here that the warning against overuse is to spare the muscles and not the neurons. In polio biopsies muscle fibers sometimes appear abnormal with internal nuclei and a ragged shape. These microscopic muscle fiber features are probably due to fewer fibers, because of loss of nerve branches, working harder to maintain function.

Obviously the loss of muscle fibers is the result of stress on the motor nerve (our tree mentioned by analogy earlier). There is the obvious stress of age changes limiting new sprouting and shifting the dynamic compensation mechanism where denervation and reinnervation continue with the advantage tipping toward loss of nerve branches. And we now know that there is a lot of inflammation in the spinal cords of people who had polio. There are infiltrates of lymphocytes (white blood cells which mediate cellular immunity) and also anti-polio antibodies. Poliovirus RNA has even been found in PPS spinal cords. Obviously all of this is stressing the giant motor units we were left with after recovery from polio. These recent microscopic and ultra-microscopically derived facts still leave us with a mystery: is it one cause or many causes which result in our plight. I believe many.

The Lincolnshire Post-Polio Network

Registered Charity No. 1064177

An Information Service for Polio Survivors and Medical Professionals

All enquiries, book requests, medical article requests, membership fees, items for newsletters and donations to

The Secretary, Lincolnshire Post-Polio Network

PO Box 954, Lincoln, Lincolnshire, LN5 5ER United Kingdom

Telephone: +44 (0)1522 888601

Facsimile: +44 (0)870 1600840

Email: info@lincolnshirepostpolio.org.uk

Web Site: www.lincolnshirepostpolio.org.uk

The Lincolnshire Post-Polio Network takes great care in the transcription of all information that appears at this site. However, we do not accept liability for any damage resulting directly or otherwise from any errors introduced in the transcription. Neither do we accept liability for any damage resulting directly or otherwise from the information available at this site. The opinions expressed in the documents available at this site are those of the individual authors and do not necessarily constitute endorsement or approval by the Lincolnshire Post-Polio Network.

© Copyright Eddie Bollenbach 2000

© Copyright The Lincolnshire Post-Polio Network 2000 – 2010.

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).

Document preparation: Chris Salter, Original Think-tank, Cornwall, United Kingdom.

Created: 25th January 2000

Last modification: 21st January 2010.

Polio Biology VIII

Post-Polio Pathogenesis

Eddie Bollenbach

A Lincolnshire Post-Polio Library Publication

27th November 1999

There are words we use to describe aspects of pathology, which means the study of disease. Often, when we look for a clue to unlock a mystery like Post-Polio Syndrome we neglect the words invented by epidemiologists and get confused about what we are truly seeking. Let me give you an example of what I’m getting at. Everyone with the debilitating and uncomfortable fatigue of Post-Polio Syndrome eventually asks the question: “what is causing this?” When they find out they have PPS they may obsess about the cause. When you talk to people they will tell you PPS is caused by the overwork of already over-burdened muscles. Or some may say it is caused by aging of a damaged neuromuscular system (this really doesn’t tell us much — muscles or nerves? — how is the aging manifesting itself to cause [that word again] damage)? Some are beginning to say that PPS is caused by latent viral particles inside cells of the central nervous system.

Ever since the writings of Copernicus we, in the Western Hemisphere, have used reductionism in our thinking to the extent that we think problems must always have a single cause. So we say this, not that. And we seek until we find a single simple explanation. Nothing but a single understandable cause, it seems, will relieve the nagging uncertainty about what is going on inside our bodies. I don’t think things are this simple, especially inside the nervous system.

Let’s get back to the words that epidemiologists use to clarify aspects of disease. First, there is the etiology of a disease. Etiology means cause. When we are asking what is the cause we are really asking for the etiology. The etiology could be very simple: “People who overuse muscles enervated by giant motor units (one nerve cell with multiple fibers) will over tax those nerves and the nerves will die”. This is the most common idea for an etiology of PPS right now. Another epidemiologist’s word, which is a bit more complex in its meaning, is pathogenesis. The pathogenesis of a disease is the mechanism, or steps which occur in the disease manifesting itself. This can be very complicated.

We have found, recently, that motor nerve cells infected with polio virus do not die the way we thought they did. We thought that if a neuron was infected with polio virus the virus multiplied inside the cell and lysed it. The infected cells were always killed in this lytic model. This is one reason why many medical doctors think that once an individual recovers from acute polio it is clear sailing for life. Now we know differently. Many infected cells did die because the cell itself, not the virus, proceeded through a series of programmed steps toward its own death and disintegration. This programmed cell death occurs after certain cell structures have been damaged and appears to be an evolutionary adaptation that removes cells

which have no chance of normal function. The process is called apoptosis. Many polio infected cells underwent apoptosis and not lysis. The significance of this is that many cells that were infected did not apoptose and consequently trapped viral particles inside. Pathogenic organisms that live inside cells have a neat adaptation. They evade the immune system by being safely tucked away where immune processes cannot remediate. Add to this the blood brain barrier and you have an ideally insulated hideaway. The blood brain barrier consists of extremely tight junctions between capillary cells nourishing the brain and spinal cord. Because of it many drugs can’t even get into the brain and this has been a problem in medical intervention for tumors and other disorders of the central nervous system. But I digress.

There are other pathogens which elude immune attack by living inside cells. The tubercule bacillus is one of them. Now also, with polio, we have detected unquestionable signatures of the virus in a little more than half of those studied who have PPS but we find no virus in people who have had paralytic polio without late effects.[1] What are the role of these polio viruses in PPS? Are they etiological or are they a part of the pathogenesis of this disease? I think right now there is a consensus building that they may be a part of the pathogenesis of Post-Polio Syndrome.

What results in their release? It is likely that cells are suddenly undergoing apoptosis many years after acute polio. Why? Overuse? Immune attack? Age? Each answer leads to a new question. And it seems we’ve arrived where we started, looking for causes. One thing is for sure: we will find many steps in the pathogenesis of PPS along the way toward understanding an etiology.

References.

1. J Neurol 1999 Jun;246(6):472-6, Postpolio syndrome: poliovirus persistence is involved in the pathogenesis., Julien J, Leparc-Goffart I, Lina B, Fuchs F, Foray S, Janatova I, Aymard M, Kopecka H. [PubMed Abstract]

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The Lincolnshire Post-Polio Network takes great care in the transcription of all information that appears at this site. However, we do not accept liability for any damage resulting directly or otherwise from any errors introduced in the transcription. Neither do we accept liability for any damage resulting directly or otherwise from the information available at this site. The opinions expressed in the documents available at

this site are those of the individual authors and do not necessarily constitute endorsement or approval by the Lincolnshire Post-Polio Network.

© Copyright Eddie Bollenbach 1999 2000

© Copyright The Lincolnshire Post-Polio Network 1999 2010.

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).

Document preparation: Chris Salter, Original Think-tank, Cornwall, United Kingdom.

Created: 27th November 1999

Last modification: 21st January 2010.

Polio Biology VII

Holistic Polio

Eddie Bollenbach

A Lincolnshire Post-Polio Library Publication

17th October 1999

On reflection, it is quite obvious that everything in the body works together. Put another way: nothing can happen inside the body without an effect on all parts of the system. After reading some recent articles on nerve and muscle function I started thinking about Post-Polio Syndrome and how closely a skeletal muscle fiber and attached nerve work together. The relationship is so close that it is quite impossible, at times, to tell what the primary cause of neuromuscular weakness is. This is particularly true when we are focusing on the synapse, the gap between nerve and muscle through which stimulant chemicals like acetyl-choline act. Without a nerve connection a muscle is an orphan and incompetent. Without a muscle a motor-nerve is useless. It is commonly understood that in Post-Polio Syndrome the end fibers of an axon (long fiber which is part of a nerve cell) break down leaving a small but effectively insulated moat between muscle and nerve. Since each nerve end fiber innervates only one muscle fiber the muscle cell is then cut from stimulation. Without stimulation we know that the receptors of stimulation on the surface of the muscle fiber are forever lost.[1]

I think most of us assume that the loss of end fibers in PPS is due to overuse. And we have a tendency to extrapolate to say that if this could only be remedied we would defeat our foe. However, during the increased neuromuscular load of exercise the earliest response of the neuromuscular system is to allow for increased efficiency of nerve stimulation. A later response is the production of muscle protein and the consequent hypertrophic growth of muscle fibers. Also, even in normal neuromuscular systems there is only one end fiber per muscle fiber. During synaptogenesis several fibers may innervate one muscle but eventually all lose touch but one. This evolutionary competition for muscle fibers by nerves is believed to result in efficient and varied innervation of muscle because different kinds of fibers have different effects on the contraction of muscle.[2] In normals there would be a tendency toward a diversity of muscle tension strength along the length of a muscle which would be produced by the natural competition of early nerve type synapses. Polio obviously alters this process by killing neurons. This allows for secondary synaptogenetic events.

What happened to skeletal muscle fiber receptors while they were left without stimulation for months during acute polio? We know now that they break down. People hoping for cures to spinal injury must exercise their muscles with electrical stimulation to keep muscle cell receptors alive. The old maxim “Use em or lose em” applies here. We with polio are in a position of slow loss of both end fibers and muscle receptors. How can we say that polio is a nerve disease when it is also, obviously, a muscle disease? And, by the way, I’m not convinced that the “cause” of PPS is overuse. There could be a host of other reasons

why these end fibers of nerves, and/or muscle receptors, lose function. When analyzed there may be more than one cause. With some of the advances appearing now in measuring and differentiating antibodies, along with similar advances in DNA and RNA cloning techniques, which have been used to identify polio virus fragments in PPS, it may not be long until we have more definitive answers. Until then we should understand that we are a system and that whatever proximately caused our PPS, reversing secondary and tertiary problems will likely prove very difficult, because we are whole.

References.

1. Akaaboune, M., Culican, S.M., Turney, S.G. et al. 1999. Rapid and reversible effects of activity on acetylcholine receptor density at the neuromuscular junction in vivo. Science 286(5439):503-507.) [PubMed Abstract]
2. Introduction To Muscle Physiology and Design, University of California at San Diego, 1999. http://muscle.ucsd.edu/musintro/jump.shtml

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The Lincolnshire Post-Polio Network takes great care in the transcription of all information that appears at this site. However, we do not accept liability for any damage resulting directly or otherwise from any errors introduced in the transcription. Neither do we accept liability for any damage resulting directly or otherwise from the information available at this site. The opinions expressed in the documents available at this site are those of the individual authors and do not necessarily constitute endorsement or approval by the Lincolnshire Post-Polio Network.

© Copyright Eddie Bollenbach 1999 2000.

© Copyright The Lincolnshire Post-Polio Network 1999 – 2010.

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).

Document preparation: Chris Salter, Original Think-tank, Cornwall, United Kingdom. Created: 17th October 1999.

Last modification: 21st January 2010.

Polio Biology VI

The Polio War and Vaccine Strategy

Eddie Bollenbach

A Lincolnshire Post-Polio Library Publication

6th August 1999

The beginning of the end for polio arrived in 1955 when the Salk vaccine was released for general use. The Salk vaccine is a concoction comprised of killed polio virus yet it still retains the capacity to stimulate the immune system to produce humoral immunity to live polio virus. Humoral immunity means that the immunity is restricted to the blood. A person with humoral immunity is protected from live polio virus migrating from the intestine, where it begins multiplying, to the Central Nervous System, where it does lasting damage. The Salk vaccine is produced by subjecting live virus to formaldehyde until it is damaged enough to prevent it from causing a polio infection but not damaged enough to prevent it from stimulating an antibody response in the blood. It is delivered by injection intramuscularly. During those early years of Salk, from 1955-1961, there were many cases of polio, a significant number of which occurred in individuals who had already been vaccinated with the Salk vaccine. Like all vaccines, it wasn’t 100% effective, and in the midst of an epidemic it slowed the rate of infection somewhat but didn’t eliminate new cases of polio as quickly as we would have liked.

The only other way to produce immunity in 1955 was to become infected with polio and recover from it. This produces a stronger and longer lasting “active” immunity. The body responds with a potent immune response if it is infected with a live polio virus. But even if you became infected naturally and recovered, you would have strong immunity to only one of the three strains of polio, the strain you were infected

with. The Salk vaccine would give you a weaker but effective “active” immunity and it would work against all three polio strains because the vaccine is trivalent (which means it contains all three strains).

The use of vaccines like the polio Salk vaccine to immunize an “individual” against a polio infection is only one of the considerations of an epidemiologist trying to eliminate the disease from a “population”. The Salk vaccine produces humoral immunity so it protects the inoculated individual, but how well does it protect the “population”? How well and how fast can it diminish the prevalence of polio? During an epidemic the virus is entering and exiting hosts. Some individuals have “silent” infections and never show symptoms. Some have mild symptoms that abort and resolve quickly while others have muscular symptoms without paralysis.

Of course, in an epidemic, many develop lasting symptoms of paralysis. The common thread that runs through all of these categories of polio is that in each type the virus enters the body orally, grows in the small intestine, and exits in fecal material. In order to stop an epidemic you must concentrate on interrupting this virus life cycle. You must stop the virus from multiplying and exiting the body. This

reproductive process is the mindless engine of a polio epidemic. This is also what epidemiologists think about when they want to stop an epidemic. It is interesting to note that the epidemiologist is thinking about prevalence in populations while most of us are thinking about infected individuals.

In 1961 Albert Sabin’s live polio vaccine was introduced in the United States. This vaccine is different than the Salk vaccine in that the polio virus is alive, can infect individuals, but is attenuated (weakened) so that the virus becomes impotent to harming the Central Nervous System, except in extremely rare cases. There is a low, but finite chance of contracting paralytic polio from Sabin live virus vaccine. The chance of infection is in the vicinity of 1 in a million or so vaccinations. This past year the Centers for Disease Control in Atlanta recommended that all new vaccinations in the United States be done with the Salk vaccine since there have been no cases of natural polio in the Western Hemisphere in years. The CDC recognized that Sabin vaccine associated cases of polio were the only cases that had occurred. It made more sense to avoid vaccine related cases and to use the dead virus Salk vaccine which produces good blood (humoral) immunity to protect individuals. The epidemics of the past were gone.

Source:”Summary of Notifyable Diseases–United States, 1992″ in Morbidity and Mortality

Weekly Report,41(55):46, September 1993, CDC, Atlanta, Georgia.

What is the advantage of the Sabin live vaccine then? Should we get rid of it all? Can it offer any advantage in the war on polio that cannot be had with Salk vaccine? The Sabin vaccine is the epidemic killer. It is the vaccine that can go beyond protecting an individual. It interrupts the life cycle of polio virus. Sabin is given orally and infects the small intestine. Once this begins the body responds with a cascade of biochemical events triggered by this gut infection. The end result is high cellular and antibody mediated durable immunity inside the intestine. So, if wild polio happens to be ingested it is killed in the gut. It cannot multiply and be eliminated in fecal material. The life cycle of the virus is stopped. The Salk vaccine does not do this. One can be immune from paralytic polio due to the Salk vaccine and yet still take in wild virulent polio, have it multiply in the gut, and eliminate millions more live wild polio virus particles into the environment to infect others. Epidemiologists have speculated that we might still have epidemic conditions in the Western Hemisphere now if it were not for the Sabin vaccine. It can put out the fire of an epidemic affecting a population, producing gut as well as humoral immunity, and even be passed on to others who may develop some immunity even though they have not been vaccinated. Of course the price of all this is the rare yet tragic cases of vaccine related polio. But in the face of an epidemic, as we now have in Angola, Sabin will work there as it did in the United States and continues to in those regions of the world where the polio virus can still spread rapidly through an unprotected population. Soon there

will be a glorious day when we will have eliminated polio. I hope that when this comes to pass we all understand that the most potent weapon we had in our arsenal against polio virus proliferation and spread, was the epidemic killing Sabin vaccine.

1. Lincolnshire Post-Polio Directory – Polio Virus, Vaccine and Eradication

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The Lincolnshire Post-Polio Network takes great care in the transcription of all information that appears at this site. However, we do not accept liability for any damage resulting directly or otherwise from any errors introduced in the transcription. Neither do we accept liability for any damage resulting directly or otherwise from the information available at this site. The opinions expressed in the documents available at this site are those of the individual authors and do not necessarily constitute endorsement or approval by the Lincolnshire Post-Polio Network.

© Copyright Eddie Bollenbach 1999 2000

© Copyright The Lincolnshire Post-Polio Network 1999 – 2010.

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).

Document preparation: Chris Salter, Original Think-tank, Cornwall, United Kingdom.

Document Reference: <URL:http://www.zynet.co.uk/ott/polio/lincolnshire/library/bollenbach/biology6.html> Created: 6th August 1999

Last modification: 21st January 2010.

Polio Biology V

How To Avoid Limiting Variables While Exercising

Eddie Bollenbach

A Lincolnshire Post-Polio Library Publication

4th August 1999

It seems that we with PPS are in an awful fix. We have aches and pains and weakness which others can often counter with exercise. But we are told not to exercise. Rest is the prescription for us but often this, although necessary, results in disuse problems. These can mimic the same symptoms of overuse: aches and pains, atrophy, and an increasing intolerance for movement. If we are able we should stretch and use any unaffected muscles regularly. But we want to pick an activity that confers maximum benefit and doesn’t make things worse.

During the past polio epidemics many physicians encouraged patients to swim. Swimming has many ideal aspects for polio patients who are not too disabled to participate. One plus is that swimming is not “muscle specific”. This means that you use a lot of muscles and can even rest some while you are using others. No “Limiting Variable” problems to this activity as far as one single muscle group goes. You can simply switch to another muscle group. There is no minimum (or maximum) intensity of exercise in swimming either. You can float around luxuriating in a weightless environment, completely supported, while getting range of motion exercise by moving limbs, or you can simply rest. On the other hand you can swim rapid laps if you can tolerate it and if your doctor suggests it. If you are lucky enough to be able to do the laps your unaffected muscles will improve tolerance for the exercise and all of your body will get more oxygen. Done properly this could help a great deal. Done improperly it will hurt. But, if you are doing something wrong you can be confident that your body will tell you. You simply will not be able to continue.

To give you an example of the lack of specificity which avoids limiting variables in this form of activity let me provide some pool scenarios for someone with post-polio syndrome. You can tread water while remaining upright. While you tread water you can kick or not kick your feet. You can move arms from side to side while treading or you can push down. This can be stationary or you can move forward. If you move forward you can do it with a sidestroke with or without a kick, or you can dog paddle with or without a kick. You can do a crawl swim with or without a kick or a backstroke, using opposing muscles to the crawl, with or without a kick. When you do a sidestroke emphasize your strong muscle side. You can do all of this with or without assistive floatation devices. There is such a range of possibilities that by varying conditions one can avoid limiting variables altogether thereby avoiding strain and overuse of a particular muscle group.

I have always felt that stopping all movement worsened PPS and introduces confusion regarding disuse

and overuse weakness and fatigue. We are so tired from the effect of overused muscles that we sometimes stop everything without the understanding of the limiting variable principle. It is one or a group of muscles that is often being overused that cause smothering body fatigue. When we react by stopping everything we become deconditioned and can actually exacerbate the problem. It is very important to undergo a complete evaluation by a specialist and, with the specialist’s blessing, begin some kind of a movement program. I recommend pool exercise because they eliminate the gravity that has taken its toll over our lives. There is hope and conditioning after PPS. Finding the way without straining limitations is one path toward feeling better.

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The Lincolnshire Post-Polio Network takes great care in the transcription of all information that appears at this site. However, we do not accept liability for any damage resulting directly or otherwise from any errors introduced in the transcription. Neither do we accept liability for any damage resulting directly or otherwise from the information available at this site. The opinions expressed in the documents available at this site are those of the individual authors and do not necessarily constitute endorsement or approval by the Lincolnshire Post-Polio Network.

© Copyright Eddie Bollenbach 1999 2000

© Copyright The Lincolnshire Post-Polio Network 1999 – 2010.

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).

Document preparation: Chris Salter, Original Think-tank, Cornwall, United Kingdom.

Polio Biology IV

Polio And Limiting Variables

Eddie Bollenbach

A Lincolnshire Post-Polio Library Publication

20th May 1999

In the natural sciences the topic of “limiting reagents” presents a challenge to undergraduate college students. A typical problem involving “limiting reagents” goes something like this: suppose you want to produce the chemical silver iodide. You make the following two elements react: silver and iodine. If you mix 1 gram of silver and 1 gram of iodine together, and they react, which one will run out first? To find this answer calculations must be made by a student with some knowledge of introductory college chemistry. One of the two ingredients will be used up. This will stop the reaction. Some excess amount of the other will remain after the reaction has stopped. The reagent (silver or iodine) that is used up first limits the extent of the reaction because it is gone. Without it there can be no more silver iodide produced.

The aforementioned example can be applied to biological and medical problems too. For example, if a marathon runner runs faster than his ability to provide oxygen to the fuel within his muscles he will exhaust himself. He needs oxygen and fuel (food) but his limiting factor here is oxygen. On the other hand if he doesn’t eat for a day or two before his race he may become exhausted and perform poorly not because of a limit of oxygen but because of a limit of fuel. In both cases we can understand poor performance due to the limiting effect of one essential component of muscular performance.

Polio imposes a change to an individual’s limiting variables. During the fatigue, exhaustion, and pain of post-polio syndrome something has run out. Because of the damage and remodeling of our neuromuscular system’s anatomy and physiology, post-polio fatigue/pain states are caused by different limiting variables than those which stopped our able bodied athlete above in his tracks. I’ve been thinking about this for a while, particularly when someone barks about performance enhancers like creatine, various amino acids, magnesium supplements, herbs, mestinon, and a host of other products. These could really help a lot if they were limiting factors for the polio survivor. For example, if high energy compounds were in short supply inside our muscle fibers creatine could supply the missing energy and restore normal muscle kinetics. But if there are too few muscle fibers with normal energy within them creatine shouldn’t help much. So, are any of these limiting? If the answer is no then what is the limiting variable in post-polio syndrome?

A hallmark of human anatomy and physiology is complexity. A good example of this is the fact that pain and fatigue can be often be relieved by small doses of antidepressants. This works for reasons completely outside of the limiting variable analysis. For example, normal muscle tension may exhaust post-polio muscles but if a drug can drop the muscle tension below that which is normal for an individual he will feel

better. There are a number of other examples and some of the chemicals PPS patients use that make them feel better should be used, even though they do not represent limiting variables.

To improve endurance, strength, muscle power, and muscle recovery after exercise for those with PPS we must examine limiting variables. Every credible study done to date implicates the neuromuscular system. That is, the nerve muscle unit that results in muscle contraction. Whether the trouble in PPS starts deep in

the nerve cell bodies inside the spinal cord or at the nerve muscle junction, peripherally, the problem is still the motor nerve and its muscle. There are not enough motor units functioning normally in a person with PPS. The normal fibers are then driven over the threshold of normal function and so they act up. The “acting up” is the pain/fatigue and other symptoms associated with the disability. I believe the limiting variable in PPS is the number of normally functioning striated muscles enervated by motor nerves. To treat this situation properly we must conserve the overworked motor neurons. Then this leads to other problems because of the complexity of human anatomy and physiology I mentioned above.

Some of us feel so bad when we experience the affects of PPS that we get into bed, sit around, and rest too much. Then we don’t feel better because we, paradoxically, are on a downward functional spiral. I want to write this again. I believe the limiting variable in PPS is overuse of muscles with too few skeletal fibers normally attached to motor nerves. But what about the muscles which aren’t affected to the point where their limiting variable is too few fibers? By over resting them can we impose on them another limiting variable and make ourselves worse? When we rest good muscles day after day they become deconditioned. They then lose essential proteins for normal function, the ability to process oxygen and utilize energy, and even lose the ability to properly burn fuel. They all get exhausted but not for the same reason our polio affected muscles do. How can we prevent this?

What can we do while conserving our affected muscles? Can we address the limiting factors that contribute to post-polio derived morbidity while restoring what become limiting factors in other muscles due to a lack of conditioning? I believe so and in doing so we can maximize our health while minimizing our symptoms. In the next installment of this column I will share some of my ideas about how this can be accomplished.

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The Lincolnshire Post-Polio Network takes great care in the transcription of all information that appears at

this site. However, we do not accept liability for any damage resulting directly or otherwise from any errors introduced in the transcription. Neither do we accept liability for any damage resulting directly or otherwise from the information available at this site. The opinions expressed in the documents available at this site are those of the individual authors and do not necessarily constitute endorsement or approval by the Lincolnshire Post-Polio Network.

© Copyright Eddie Bollenbach 1999 2000

© Copyright The Lincolnshire Post-Polio Network 1999 – 2010.

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).

Document preparation: Chris Salter, Original Think-tank, Cornwall, United Kingdom.

Created: 20th May 1999

Last modification: 21st January 2010.