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Bollenbach Polio Biology 6

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.

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

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 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.

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Bollenbach Polio Biology 5

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.

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

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

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Pain and Post-Polio

Pain And Post-Polio Syndrome

An Overview

PAUL E. PEACH, M.D.

Medical Director, Palmyra Post-Polio Clinic

Lincolnshire Post-Polio Library copy by kind permission of Dr. Peach

Polio survivors, not unlike the general population, will likely experience pain at some points in their lives due to a myriad of reasons. Unlike the general population, however, polio survivors are somewhat more likely to experience pain as a consequence of the residual paralysis or paresis of chronic polio. If a polio survivor is experiencing pain, this does not necessarily mean that the pain is a symptom of post-polio syndrome. Taking this yet one step further, even if a polio survivor has been appropriately diagnosed with post-polio syndrome and is experiencing pain, this does not necessarily mean that the pain is due to the symptoms of post-polio syndrome. If pain is being experienced, it is essential that an appropriate medical evaluation be made because the pain could be due to any number of factors ranging from very benign to quite serious.

The first step in assessing pain in a polio survivor is determining if a diagnosis of post-polio syndrome is appropriate and secondly if the pain symptoms are a part of the post-polio syndrome being experienced. Post-polio syndrome is diagnosed clinically and, unfortunately, no clinic test is specific to detect this syndrome. Therefore, a physician who has experience in managing and diagnosis post-polio syndrome should evaluate the person experiencing the pain. If the pain symptoms are due to the effects of post-polio syndrome, pain is most likely due to overuse of muscles, tendons, ligaments and/or joints. Other problems that can occur with post-polio syndrome are secondary nerve compression syndromes, commonly at the wrist and occasionally at the elbows.

Typical pain syndromes associated with post-polio late effects include muscle pain and cramping. The patients may describe fasciculation (a crawling sensation) which is exacerbated by pain, physical activities, stress and occasionally cold weather. Overuse of muscles and direct myogenic pain may be occurring and, again this is secondary to physical overuse. Typically, the myogenic pain and fasciculation will decrease or disappear entirely with rest. Occasionally heat, gentle stretching and light massage are useful adjunctive treatments as well. Strain injuries also are not uncommon. Areas affected include muscles, tendons, bursa and ligaments. These strain injuries may occur chronically or acutely. They may be posturally related or occurring as a result of overuse of arms, shoulders and lower extremities. Pain from the shoulders resulting from supraspinatus or occasional biceps tendinitis are not uncommon. Elbow pain and knee pain from progressive genu recurvatum is not uncommon. Genu recurvatum is a condition in which, because of weakness of the ligaments and muscles around the knee, there is progressive backward deformity of the knee, resulting in progressive pain, usually the back of the joint. Eliminating

chronic stressors, which may, in addition to symptomatic treatment, consist of protecting the joints through bracing, or decrease in crutch walking, can control these injuries and symptoms.

Another problem frequently seen is degenerative joint disease. Degenerative changes are potentiated if the patient has been walking on unprotected joints with chronic abnormal stresses. Typically, symptoms are improved by improving support with appropriate bracing, postural modification and improved seating support.

Nerve compression syndromes are much more prevalent in the polio population in those who are crutch or wheelchair ambulators. Carpal tunnel and ulnar nerve compression at the wrist is four times more prevalent in this group of polio survivors than in the general population. Chronic stressors, crutch walking and manual wheelchair propulsion are the primary aggravating factors. These are alleviated by reducing the stress on affected areas by use of power carts, thereby reducing crutch walking, and by the use of resting hand splints to provide better protection and positioning of the wrist. Radiculopathy may be a factor in some polio survivors, particularly those who have severe scoliosis or neck or low back hyperextension through weakness and chronically abnormal posture. If degenerative changes are present in the spine, this also is a factor. Decreasing abnormal postures may relieve this. If a body corset or body brace is not being worn, this may be an option in some cases. Improved seating positioning will also decrease symptoms sometimes in these cases. In other cases, traction may be indicated. Symptomatic treatment with medications and therapeutic modalities is also a benefit in many cases.

As can be surmised, polio survivors can experience pain as a result of a large number of factors. The first step in the treatment of pain should be in accurately diagnosing the cause of the pain. It is only at this point that an effective strategy for managing the pain can be developed.

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Dr Henry writes about Dorothea Lange

Dr. Henry writes about Dorothea Lange

Several months ago, I was watching a program on the History Channel. The program focused on the 1930s, the Great Depression years. Dorothea Lange was the subject of the documentary. Lange achieved some fame as a result of her many photos of individuals who were directly affected by the poverty and deprivations of the economic depression. When discussing Lange’s life, the narrator mentioned that Lange had polio as a child. She was left with a withered leg and a limp. With this information, I searched the Internet and discovered that there were several books about Dorothea Lange. I purchased one that included a biography of her life and many of her photos. Dorothea Lange, A Visual Life edited by Elizabeth Partridge, and published by the Smithsonian Press is filled with most of Lange’s most famous photographs.

Lange was born in Hoboken, New Jersey in 1895. She had one younger brother, six years her junior. At age seven, she fell ill to acute polio. The residual polio damage involved a withered right lower leg and a noticeable limp. Lange viewed her handicap as a determination factor in her life. She stated that her handicap shaped her very personality and was one from which she could never escape. In later years her limp might have been an asset in helping to disarm people on first encounters with her camera. She felt that her limp might have helped strangers be more accepting of her when she was photographing in the field.

When Lange was twelve years old, her father left the family and Lange, her brother, and her mother went to live with her maternal grandmother. This matriarchal family lived together until Lange left home at age twenty-three. Her mother was self-conscious about her daughter’s limp and encouraged her to attempt to walk more normally. As a result, Lange was even more self-conscious about her limp.

After the marital separation, Lange’s mother began commuting from New Jersey to Manhattan where she had a job at the New York Public Library. As a result, Lange was enrolled in a public school in the Lower East Side of Manhattan. She was the only Gentile among all Jewish children. She was essentially a loner

as a child. She went to an all girls’ high school in Upper Manhattan and this situation was slightly better. When questioned upon her graduation as to her plans for the future, she stated that she wanted to become a photographer. At this point in her life, she had never owned a camera. She did enter a teacher’s training

program, but also began working in a photographer’s studio. Her interest in photography grew and she left the teacher’s training program. She was mostly a self-taught photographer.

At the age of twenty-three, she left New Jersey with a friend to travel the world and utilize her photographic skills. She ended up in San Francisco and opened a photographic studio where she specialized in portraits. Her business was successful. She did marry and had two sons. When the bread lines appeared during the depression years, she began photographing the pathos of the people affected severely by the Great Depression. These photographs are a realistic and artistic witness to the human drama of this time in our country’s history.

Perhaps Lange’s most famous photograph is “Migrant Mother,” taken in 1936. This photo is of a tired and worn female migrant worker. She is holding a small child and there are two other children leaning on her shoulders. The photograph needs no explanation. The majority of Lange’s photographs are expressive and

gripping with human emotion. During World War II, Lange photographed the plight of some of California’s Japanese Americans who were displaced to camps.

Lange was diagnosed with inoperable esophageal cancer in August 1964. Despite this death sentence, Lange completed two major projects during the last year of her life. The first was the completion of her collection of photographs of The American Country Woman. This collection demonstrated Lange’s great respect for the traditional woman. Her other project during that last year was preparing a review of her work for the Museum of Modern Art. Lange died on October 11, 1965.

Lange was likely a sentimentalist. She once said, “Sentiment and sentimentality, they are difficult concepts to manage.” Many of Lange’s photographs include the subject’s feet. Was her inclusion of feet in her photographs an expression of her own sensitivity about her own polio damaged right foot? What did Lange say about her own handicap? She said, “I was physically disabled, and no one who hasn’t lived the life of a semi-cripple knows how much that means. I think it perhaps was the most important thing that happened to me, and formed me, guided me, instructed me, helped me, and humiliated me.”

I think that many of us with residual damage from polio can identify with these words. How much did polio impact on your life? Was it the most important thing that happened to you? Has the event of polio in your life formed, guided, instructed, helped, and humiliated you?

It was certainly an event that changed my life. Because of my experience with polio, I am sure that it guided me to seek a medical education and profession. At a young age, polio instructed me in the hard reality that good innocent persons could suffer unexplained adversity. Many times the self-consciousness of my handicap caused me to feel the shame and humiliation of being crippled. Did polio “help” me? Perhaps my experience with polio helped me to have some insight about putting others at ease. These are all hard questions. Probe your own feelings in answering these questions for yourself.

I think that Dorothea Lange was like many of us. She was marked by a distinct limp from childhood polio. She was a lonely and self-conscious child. She set a goal for herself and she accomplished that goal. She had an intuitive understanding and could identify with the sadness and pain of others. Her photographs reflect the genius of her sensitivity. Viewing her photographs is a lesson for us all.

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

July 1999

Originally published in the Central Va PPS Support Group (PPSG)‘s newsletter, The Deja View, in 1999. Reference:

Dorothea Lange A Visual Life edited by Elizabeth Partridge, Smithsonian Institution Press, Washington and London, 1994.

At the time of writing the book was only listed at Amazon. For more Hardback information on Online Bookstores see our Book Store List.

Paperback

All quotations of Dorothy Lange are taken from interviews recorded in this reference book. Exact page

numbers are available upon request.

Masters of Photography – Lange – Articles and Photographs

http://masters-of-photography.com/L/lange/lange.html

Migrant Mother photograph at the above site

http://masters-of-photography.com/L/lange/lange_migrant_mother.html

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

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

Created: 1st August 1999.

Last modification: 22nd January 2010.

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Neuromuscular Diseases

Disease

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Neuromuscular Diseases

Muscle Diseases (Myopathy)

Dermatomyositis (DM): DM is an auto immune muscle disease which occurs in children and adults. The cardinal sign of this disorder is the presence of a rash commonly over the upper chest and back or shoulders. Occasionally, a purplish (heliotrope) discoloration is present over the eyelids. Along with the rash, muscle weakness in the hips and shoulders is noted. The disease develops over weeks to months. The cause is unknown but involves inflammation of the blood vessels in the skin and muscle. Diagnosis is clinical with supportive evidence from blood levels of muscle enzymes (CK or creatine kinase), and EMG findings. Many people undergo muscle biopsy for a definitive diagnosis. The disease responds well to oral steroids but

is sometimes resistant and may require treatment with azathioprine or IVIG.

Polymyositis (PM): PM is similar to DM but doesn’t have the rash. Symptoms develop over weeks to months in most cases. The cause is usually unknown but occasionally, PM and DM are associated with cancer or rheumatoid conditions. Treatment is similar to that of DM.

Drug–induced myositis: Several medications may lead to muscle damage. These include certain cholesterol lowering agents, colchicine, and ipecac.

Inclusion Body Myositis (IBM): IBM develops more slowly than either PM or DM. Typically, a diagnosis is not reached for several years. Weakness is more asymmetric and there is no rash. The cause is unknown but may represent a degenerative condition with secondary inflammation as opposed to PM where inflammation is primary. Perhaps because of this, IBM responds less well to steroids and other immune suppressing therapies.

Muscular Dystrophy

Duchenne‘s muscular dystrophy (DMD): DMD is a progressive hereditary disease that presents in boys during infancy or early childhood. Affected children will be slow to walk and may fail to master certain motor activities by the appropriate age. Initially, patients have weakness in shoulder and hip girdle muscles initially but, over years, become weak in hand and foot muscles as well as respiratory and cardiac muscles. The disease progresses to death often by the age of 20 due to heart failure or respiratory compromise. A severe deficiency or absence of the protein dystrophin underlies this disease but the exact mechanism is unknown. Diagnosis is clinical with supportive evidence from EMG and CK elevation. Definite diagnosis is now possible

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by muscle biopsy or by genetic testing of blood. The disease partially responds to high doses of oral steroids but there is no cure. A milder form of DMD is known as Becker dystrophy and results from a partial loss of dystrophin. In some cases, women who carry the abnormal gene have some mild symptoms of muscle disease (cramps, slight weakness, mildly elevated CK) and are known as manifesting carriers.

Limb–girdle dystrophy(LGD): LGD may be a severe muscle disease beginning in infancy or becoming noticeable only during adulthood depending on the variety. In some cases there is an abnormality of a muscle membrane protein related to dystrophin (see DMD). Weakness is predominately located in the shoulder and hip girdle muscles In affected adults the disease progresses slowly and is usually not life-threatening. This disease is inherited in some cases and there is no known treatment.

Myotonic dystrophy (DM): Unlike most muscular dystrophies, DM usually shows severe distal weakness prior to the development of proximal weakness. It is inherited in a dominant fashion (meaning an affected person has a 50% chance of passing the disease to each of his or her children). Symptoms can be evident at birth or not be noticeable until adulthood. Drooping of the eyelids (ptosis), swallowing muscles and cataracts are other frequent features of the disease. No cure or effective treatment is available.

Diseases of the Neuromuscular Junction

Myasthenia gravis (MG): Auto immune disease where the target of inflammation are the acetylcholine receptors on the muscle membrane. MG may occur at any age and common early symptoms are double vision, droopy eyelids, difficulty swallowing, or generalized weakness. The onset may be gradual over months or develop rapidly over several days or weeks. Diagnosis is clinical with supportive evidence including presence of acetylcholine receptor antibodies, positive tensilon test, or abnormal electrodiagnostic testing. A number or therapeutic agents are available and include steroids, IVIG, plasmapheresis, azathioprine, pyridostigmine and surgical removal of the thymus gland.

Acquired Nerve Diseases (Polyneuropathies)

Axonal Polyneuropathies

Diabetic polyneuropathy occurs in many patients with either insulin-dependent or non-insulin dependent diabetes mellitus. It’s severity can be correlated to some degree with the severity and duration of hyperglycemia. The disease has a predilection for small unmyelinated nerve fibers which carry information on temperature and pain so that the early symptoms are reduced pain awareness and the inability to detect temperature. Paradoxically, the symptoms tend to be associated with burning of the toes or bottom of the foot. The symptoms develop symmetrically and often spare the hands. Significant weakness is unusual although it can be quite painful. Diagnosis is clinical and may be confirmed with NCS. Other causes may need to be ruled out. There are many medicines that ameliorate the pain (amitriptyline, nortriptyline, gabapentin, carbamazepine, capsaicin) but these do not treat the underlying neuropathy. A human

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protein called Nerve Growth Factor (NGF) may help treat the underlying neuropathy and reduce the symptoms. NGF is being studied in a clinical research trial at BGSM and other centers around the country. Click here for information on this study.

Vitamin B12 deficiency may lead to a number of serious conditions including peripheral neuropathy. This may occur in persons who are strict vegetarians, people who are malnourished, and may also happen to otherwise healthy people on normal diets who develop pernicious anemia. In this auto immune disease, the body makes antibodies against its own cells in the gut lining which leads to an underproduction of intrinsic factor, the protein which is responsible for binding B 12 in the intestine and getting the vitamin into the bloodstream. Absence of the vitamin leads to anemia which is resistant to iron therapy and may cause neuropathy and a more serious condition of degeneration in the spinal cord called subacute combined degeneration. This may occur in addition to neuropathy and causes weakness, sensory loss and incoordination. The peripheral neuropathy of vitamin B12 is not unusual and presents with tingling/numbness in the feet sometimes associated with more painful altered sensations (dysesthesias). Weakness is uncommon except in cases where there is concomitant subacute combined degeneration. The diagnosis is confirmed by NCS and by testing the blood vitamin B12 level. One important point that is overlooked is that many patients with neuropathy from B12 deficiency do not have the anemia or changes in the white blood cells that frequently seen in this disorder. Treatment is with vitamin B12 injections or oral therapy depending on the severity of the deficiency and the underlying cause. Treatment may not be successful in completely restoring the nerves to pre-deficiency function.

Neuropathies associated with paraproteins: Paraproteins are abnormal proteins in the blood which are sometimes markers for malignancy but maybe of benign origin. Sometimes these are associated with nerve disease and cause a wide range of symptoms from severe sensory involvement to primarily weakness. These neuropathies are much more common in the older age groups (>60 yrs) and are often of mild severity. The neuropathy is slowly progressive but occasionally progresses more rapidly. The symptoms can be treated with medicines that ameliorate the pain (amitriptyline, nortriptyline, gabapentin, carbamazepine, capsaicin) but this doesn’t affect the underlying neuropathy. When the disease is severe, treatment of the nerve disease can be attempted with steroids and other immunosuppressants.

Neuropathies associated with thyroid disease: There is an association between hypothyroidism and polyneuropathy. When it does occur the symptoms are typical of all neuropathies: tingling/burning and sharp, sudden, lancinating pain in the feet and hands. More commonly, carpal tunnel syndrome is a presentation of hypothyroidism.

Toxic neuropathies: Many drugs are known to cause neuropathy. The most common are the chemotherapeutic agents vincristine, cisplatinum, taxol. Some others include cyclosporine, metronidazole, dapsone, and amiodarone. Pesticide exposure can cause neuropathy. Rarely, heavy metal intoxication (lead, arsenic, mercury) can cause neuropathy.

Alcoholic neuropathy: Heavy alcohol use may cause a neuropathy which is mostly sensory. Burning and tingling in the feet is first noted and the involved area may ascend over months to years. Abstention from alcohol use may alleviate the symptoms and will

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prevent further nerve deterioration.

Cancer–associated: Neuropathies of all types may be associated with cancer and are known as paraneoplastic neuropathy. One special condition should be mentioned. A rapidly progressive symmetric or asymmetric purely sensory neuropathy may be the first indication of certain tumors usually small cell lung tumors. NCS can make the diagnosis of pure sensory neuronopathy but further testing would need to be performed to determine if the cause was a malignancy. Treatment of the malignancy may improve the neuropathy.

HIV (AIDS) associated neuropathy: Many types of neuropathy are associated with HIV infection. The most common is a painful, symmetrical neuropathy affecting the feet. Patients usually complain of burning, tingling and altered sensation. Treatment is difficult and includes nortriptyline, carbamazepine, and gabapentin.

Demyelinating Polyneuropathies

Acute Inflammatory Demyelinating Polyneuropathy (Guillain–Barre Syndrome): AIDP starts with tingling in the legs and arms, sometimes mild weakness or difficulty walking, and is associated with back pain in roughly half of the cases. Over hours to several days the neuropathy progresses to cause numbness and weakness throughout the body. The nerves that control breathing, heart rate, and eye movements can be involved necessitating hospital admission. The cause of the condition is unknown but is believed by many doctors to be an auto immune disease triggered by the body’s response to an infection. Most commonly, there is inflammation of the myelin, the nerve coating, but preservation of the nerve fiber is such that even in severe

cases the long term prognosis for significant improvement is quite good. Diagnosis is clinical but is supported by NCS and spinal tap findings. The course of the disease is shortened by treatment with IVIG or plasmapheresis. Steroids do not appear to be of value in this disease. This disease has a distinct, rapid presentation and is a life-threatening condition. If you think you have this YOU SHOULD NOT BE WASTING YOUR TIME SURFING THE WEB.

Chronic Inflammatory Demyelinating Polyneuropathy (CIDP): Like AIDP, there is inflammation of the myelin in this disease but the course of the illness is usually much slower. Symmetrical or asymmetrical numbness and tingling in the feet with or without weakness are often the first symptoms. The disease may be slowly progressive or can wax and wane. The cause is unknown. Most cases are idiopathic but the disorder is sometimes associated with paraproteins, HIV, and cancer. Diagnosis is

rmed by NCS. First-line treatment is with steroids or IVIG. Plasmapheresis may be used in more severe cases. Other treatment includes azathioprine or cyclosporine.

Hereditary Peripheral Neuropathies

Hereditary Motor and Sensory Neuropathy: (Charcot-Marie-Tooth disease) This is the most common type of inherited neuropathy. There are 2 main types: demyelinating (type 1) and axonal (type 2) although it usually not possible to differentiate them without nerve conduction studies (NCS) or genetic testing. The

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inheritance is dominant meaning a person with CMT has a 50% chance of passing it down to each of his or her children. Typically, CMT patients have unusually high arches noted from early in life but are normal into the teenage years. CMT children frequently turn their ankle and may be “clumsy” as they trip over their toes frequently. Sometimes the disease isn’t recognized until patients are much older (40-60 yrs) Commonly, CMT patients complain of weakness more than numbness/tingling/burning despite profound involvement of their sensory nerves. The disease is slowly progressive and, although many patients need to wear a brace to help keep their feet from dragging, most patients are not disabled or wheelchair bound and have a normal life expectancy. Research has shown that the most common form of CMT (Type 1A) is caused by an overexpression of a myelin gene, PMP-22. The exact function of this protein is currently unclear and there is no current treatment for the underlying disease.

Hereditary Neuropathy with Liability to Pressure Palsies (HNPP): This disease is probably widely under diagnosed. Like CMT Type 1 A, it is a demyelinating neuropathy and may be the result of an under dosage of a myelin protein (PMP-22) which is overproduced in CMT 1A. This disease should be considered in patients with multiple entrapment neuropathies as these are common in HNPP. Symmetrical burning/numbness/tingling in the feet may also be present. As in CMT, the exact cause is unknown and there is no treatment other than pain medicines and avoidance of entrapment neuropathies.

Entrapment (Compression) Neuropathies

Carpal Tunnel Syndrome (CTS): CTS is the most common entrapment neuropathy. Persons with CTS complain of tingling or numbness in their fingers especially the thumb, index and middle fingers. Occasionally, the tingling is irritating and awakens people from sleep or bothers them when they read the newspaper, Weakness is unusual but people often complain of dropping things if they aren’t looking at them. CTS is caused by irritation of the median nerve as it passes from the middle of the wrist into the palm through a tunnel created by ligaments and bones called the carpal tunnel. CTS can be easily diagnosed by NCS and is treated with splinting the wrist at night in mild cases or surgical release of the ligaments which form the roof of the tunnel in more severe cases.

Ulnar Neuropathy at the Elbow: Another common entrapment neuropathy, this disorders typically begins with elbow pain with tingling (“hit your funny bone” sensation) in the ring finger and little finger. If the condition is left untreated, grip strength becomes reduced and the muscles of the hand may atrophy causing the tendons and bones to appear more prominent. Here, the ulnar nerve is irritated as it passes between two bones along the inside of the elbow (ulnar groove). This is also diagnosed with NCS EMG and can be treated with splinting and padding the elbow, or with surgery. The surgery is more involved than in CTS as the nerve is typically moved out from the bones and is placed in the forearm.

Tarsal Tunnel Syndrome: This neuropathy is less common than the others and is more difficult to treat and diagnose. Tingling or pain along the toes and bottom of one

foot is the most common presentation. Weakness of foot muscles is rare and it is unusual for the symptoms to be in both feet. Ankle injuries may predispose people to have such symptoms. The tibial nerve is irritated as it passes between the Achilles

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tendon and the prominent bone at the inside of the ankle. NCS is occasionally useful in making the diagnosis but specialized testing may be necessary. In severe cases, surgeons can decompress the tibial nerve at the ankle by cutting the overlying ligaments. Surgery is less successful than in CTS.

Peroneal neuropathy at the knee: This usually occurs in people who cross their legs or squat for prolonged periods of time like gardeners. All of these maneuvers compress or stretch the peroneal nerve as it crosses over a bone (fibula) along the outside of the knee. Trauma is another common reason to develop this problem. People may become unable to flex their ankle upward (foot drop). Occasionally, there is also numbness along the outer portion of the calf or top of the foot. The weakness usually goes away by itself if the leg-crossing and squatting is discontinued. Surgery is rarely necessary.

Sciatic neuropathy: The sciatic nerve forms from after nerve roots from the lower lumbar and sacral spine participate in the plexus. The nerve has 2 divisions (peroneal and tibial) which divide behind the knee. Sciatic neuropathy would be an uncommon cause of “sciatica” and is most often seen in the setting of hip fractures or hip surgeries. Severe motor vehicle accidents and penetrating trauma also cause sciatic neuropathies. On occasion, these occur following improper placement of an intramuscular injection into the buttock. The so-called “wallet-neuropathy” produces mild sciatic symptoms after prolonged sitting on a hard surface. In this setting, generally male patients may complain of tingling/numbness on their feet or calves and with a mild foot drop. Wallet neuropathy resolves spontaneously after switching the wallet to the other pocket.

Nerve Plexus Diseases

Brachial plexopathy: The brachial plexus is a complicated network of nerves in the shoulder. These are commonly damaged in several settings including birth trauma, severe motor vehicle accidents and penetrating trauma (bullet and stab wounds), and due to lung and breast malignancies. Sometimes these occur without clear reason (idiopathic) and are called idiopathic brachial plexopathy. There are a variety of names for this disorder including neuralgic amyotrophy, Parsonage-Turner syndrome or brachial plexitis. The cause is unknown but may be auto immune or post-viral as this disorder often follows surgery or viral infections. Severe shoulder pain heralds the disease and may last for days to weeks. Following this, people may notice weakness, numbness, or atrophy of their muscles. Usually, there is spontaneous improvement without specific treatment. Some experts recommend a short course of oral steroids if the process is caught early while there is still pain.

Lumbosacral plexopathy: The lumbosacral plexus is a complicated network of intertwining nerves located in the pelvis. These nerves may be damaged following severe trauma or occur in relation to hip/pelvic surgeries. Occasionally, a hematoma from a catheterization procedure causes a plexopathy. Idiopathic lumbosacral plexopathies are much less common than idiopathic brachial plexopathies but may occur. One special type of lumbosacral plexopathy should be mentioned is diabetic amyotrophy.

Diabetic amyotrophy: This disorder is often seen in recently diagnosed diabetics

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and may be the first sign of the disease. Typically, there is the development over hours to days of severe pain in the groin and upper thigh followed by weakness of bending the hip and/or straightening the knee. The muscles of the upper leg may become atrophied. The disease may progress for some weeks then commonly improves spontaneously over months. Occasionally, amyotrophy occurs bilaterally. The cause is unknown but may be vascular in nature. To date there has been no treatment for this disease, although there are reports of IVIG and oral steroids being effective.

Nerve Root Diseases (Radiculopathy)

Cervical radiculopathy: Impingement of bone or disk material on a cervical nerve root can cause neck pain which radiates into the arm, weakness of arm and shoulder muscles, and numbness. The most common cervical radiculopathy is C6-7 which may cause neck/arm pain, weakness of the triceps, and numbness in the middle fingers. The C5-6 root tends to cause numbness in the thumb and index finger in association with deltoid and biceps weakness. The C7-8 root may cause numbness in the ring and little fingers in association with decreased grip strength or fine coordination of the fingers. If the symptoms are mild, no diagnostic testing may be necessary. If severe, an MRI scan of the neck and/or an EMG are helpful in confirming the diagnosis. Conservative therapy consists of warm compresses, cervical collar, physical therapy and occasionally traction. Surgery may be performed to decompress the nerve root by a neurosurgeon or orthopedic surgeon.

Lumbosacral radiculopathy: This is sometimes known as sciatica. Impingement of bone or disk material on a nerve root in the low back can cause pain which radiates into the hip, buttock, and leg. Numbness and weakness may also occur. The most common roots to be affected are the L4-5 and L5-S1 roots. L4-5 radiculopathies present with back pain, numbness on the outside of the calf and sometimes weakness of flexing the ankle upwards or foot drop. S1 root disease often causes numbness on the back of the calf and bottom of the foot associated with weakness on pointing the toe. If the symptoms are mild, no diagnostic testing may be necessary. Most low back pain resolves spontaneously within 2 weeks and current recommendations are to continue with your normal activities as much as can be tolerated. Prolonged bed rest should be avoided. Low back pain associated with weakness is more serious and an MRI scan of the lower back and/or and EMG are helpful in confirming the diagnosis. Conservative herapy consists of non-steroidal medications (such as ibuprofen), heating pads and physical therapy. A neurosurgeon or orthopedic surgeon can decompress the nerve root in the operating room.

Degenerative Disk Disease: As people age, the intervertebral disks become less pliable and more calcified like bone. Years of stress on the vertebrae cause constant breakdown followed by build up of new bone at the point where the vertebrae touch each other. The condition can mimic cervical or lumbosacral radiculopathies. Bony overgrowth may narrow the openings for the nerve roots (foramina) and will diminish the size of the spinal canal. This condition is called cervical stenosis in the neck and lumbosacral stenosis in the low back. The process can be accelerated through trauma, arthritis, obesity, and years of physical labor.

Cervical stenosis often presents with neck pain with or without radiation into the arms and with difficulty walking due to poor balance or leg stiffness/weakness. The

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diagnosis is clinical with supporting evidence from a cervical MRI scan or myelogram. If symptoms are mild, it can be treated with non-steroidal medications or sometimes with epidural injection of steroids. More severe symptoms can be treated with decompressive surgery.

…..

Lumbosacral stenosis often presents with low back pain sometimes with radiation into the buttock or leg(s) but weakness is uncommon. Some patients with this disorder will have cramps (neurogenic claudication) in their calves or thighs. Sometimes symptoms can be relieved by bending over and flexing the spine forward. Back pain due to stenosis may also improve on walking as opposed to back pain from lumbosacral radiculopathy which may worsen with movement. The diagnosis is clinical with supporting evidence from an MRI scan or myelogram. If symptoms are mild, it can be treated with non-steroidal medication or sometimes with epidural injection of steroids. More severe symptoms can be treated with decompressive surgery

Motor Neuron Disease

Motor Neuron Diseases are a group of diseases which are unified by their selective involvement of upper and or lower motor neurons. There are likely to causes for these diseases even within the groupings listed below. Some points in common are that MNDs tend to relatively spare eye movements and bladder/bowel function.

Amyotrophic Lateral sclerosis (ALS) or Lou Gehrig‘s Disease: This disease affects both upper (UMN) and lower (LMN) motor neurons (see principles of neuroanatomy) producing progressive spasticity, weakness, and atrophy of the limb muscles. Typically, the disease begins with painless weakness and wasting of the muscles of one hand or one foot. Sensory complaints should not be present but muscle twitching or fasiculations may be noted. Another common presentation of this disease is the gradual onset of difficulty speaking (dysarthria) or swallowing (dysphagia). This is due to involvement of the bulbar muscles. The disease is progressive at a variable rate but is often marked by plateaus and extremely rare reports of spontaneous regression. Depending on the age of onset and the type of presentation, the average life expectancy is around 3 years. Some people live much longer with approximately 10% surviving longer than 10 years. The cause of this disease is unknown. Diagnosis is clinical with supportive evidence from NCS/EMG. Frequently, MRI scans of the brain or spine are necessary to rule out tumors or degenerative spine disease. Riluzole is the first drug to receive FDA approval for the treatment of ALS. The drug has been shown to extend the life expectancy of patients by several months.

There are several clinical syndromes that may be related to ALS but can also be caused by other disorders. They are named according to the type of motor neurons which degenerate. Progressive Muscular Atrophy (PMA) involves only LMNs, Pseudobulbar Palsy affects the UMNs of the face and throat muscles, Progressive Bulbar Palsy involves LMNs of the face and throat muscles.

BGSM is actively involved with ALS and, frequently, the physicians at BGSM are involved with clinical trials of experimental agents. Click here for an update on current research protocols offered at BGSM, Basic scientists at BGSM are also actively

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involved with the study of motor neuron development and survival.

Multifocal motor neuropathy with conduction block: This recently described disease may mimic ALS. Usually, there is a very slow development of weakness and wasting in one hand or arm with minimal sensory changes. UMNs do not degenerate in this disease. NCS may show conduction block, an electrophysiologic finding that suggests focal axon dysfunction or demyelination. This disease can respond dramatically to IVIG.

Polio: Unlike all the other motor neuron diseases considered here, polio has an abrupt onset, is self limited and improves spontaneously. Polio is caused by infection with the polio virus which begins with fever and lethargy and progresses to paralysis of all or some of the muscles. The majority of cases occur in infants and can occur following administration of the oral polio vaccine (OPV). The risk of contracting polio from the vaccine is 1 in 2.5 million. Recovery may be full or partial depending on the degree of LMN degeneration. Adults who suffered polio as a child frequently have scoliosis of the spine and atrophy of one or more limbs. These patients may develop a variety of symptoms (weakness, fatigue, pain) years after their infection known as the post-polio syndrome.

Spinal Muscular Atrophy (SMA): There are a variety of SMA disorders which affect infants and adults. These disorders affect only LMNs and in adults are very slowly progressive. One of the SMAs that can mimic ALS is Kennedy’s disease or X-linked Spinobulbar Muscular Atrophy. As the disorder is linked to a gene on the X-chromosome and is recessive, only males will get the disease and females are carriers. Kennedy’s Disease is marked by proximal weakness in the limbs and by weakness of facial muscles. Other features include a sensory neuropathy, decreased fertility, and enlarged breasts. This disease does not shorten life expectancy but may result in mild to moderate disability. [go to featured topics].

Monomelic an

y: This rare form of MND usually affects one arm with weakness and wasting and occurs mostly in males in their teenage or early adult years. The disease may progress rapidly for 1-2 years then very slowly progress or halt with minimal recovery. This should not be confused with ALS. (ref Donofrio’s article]

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Neuromuscular Diseases Read More »

Breathing and Sleep Problems in Polio Survivors

Breathing and Sleep Problems in Polio Survivors Prepared by International Ventilator Users Network (IVUN) WWW.ventusers.org Reviewed by Nicholas S. Hill, MD, Tufts-New England Medical Center, Boston, Massachusetts

It is critically important that polio survivors, especially those diagnosed with post-polio syndrome, obtain proper testing, diagnosis, and management of breathing and sleep problems. The problems may result from weak breathing muscles in the chest and abdomen (diaphragm and intercostals). Pulmonary function tests (mostly noninvasive) can measure the strength of respiratory muscles and usually include a test for forced vital capacity (FVC) – the maximum amount of air that can be exhaled. This test is typically administered when a person is sitting in the upright position, but also should be administered when a person is lying down (supine position). People who may not experience breathing problems sitting up may find themselves struggling to breathe when lying down. This problem is known as orthopnea, and a marked decrease in FVC while lying down indicates that the diaphragm is weak. The late E.A. Oppenheimer, MD, a pulmonologist with years of experience treating polio survivors, described it, “As one ages with the late effects of polio, respiratory muscle strength may decrease. This may be particularly evident when you lie down, because in this position, the diaphragm has to work harder both to pull air in and also to push the intestines and other abdominal organs which are out of the way when one is upright due to gravity,” Polio survivors also may have obstructive sleep apnea (OSA), central sleep apnea (CSA), a combination of OSA and CSA, and/or hypoventilation (an imbalance in the gas exchange in the lungs due to too little breathing – carbon dioxide builds up and oxygen drops). In obstructive sleep apnea, the upper airway collapses and blocks the flow of air so the person stops breathing periodically. These cessations of breathing are known as apneas and hypopneas. An overnight sleep study may be helpful to confirm the presence of OSA if it is suspected, based on snoring and daytime sleepiness.

Most sleep laboratories are set up to detect obstructive sleep apnea, for which the appropriate treatment is continuous positive airway pressure or CPAP, but not to measure carbon dioxide levels directly, which would be the best way to detect hypoventilation, for which the appropriate treatment is bilevel or positive pressure ventilation. The test for a high carbon dioxide level would be to measure arterial blood gases (requiring blood to be drawn via needle from an artery – usually in the wrist) or to monitor end-tidal or transcutaneous CO2, which is usually not done. However, sleep labs look for sustained drops in oxygen saturation during sleep that would be indicative of hypoventilation and then can proceed to additional testing to confirm hypoventilation, if needed. When a bilevel device, a form of positive pressure ventilation, is prescribed, it will provide two levels of pressure; inspiratory (IPAP) to help blow air into the lungs, and expiratory (EPAP) to help keep the airways open and to blow off CO2. These pressures can be set and adjusted separately. IPAP settings are higher than EPAP settings, with a span of at least 8 to 10 advised for adequate breathing assistance, e,g. IPAP of 14, EPAP of 4. Bilevel units with a backup rate are recommended for people who may not be able to initiate a breath on their own, particularly at night. The bilevel device can provide timed backup breaths.

It is important for individuals to understand that polio survivors do not forget to breathe” when they become overly fatigued. What happens is that the muscles become too weak to

move sufficient air, especially during sleep. Post-polio syndrome can also sometimes cause central sleep apnea which causes the brain to temporarily “forget” to signal breathing muscles to take a breath. This is evident during a sleep study when there is no chest wall movement for at least 10 seconds, indicating that the individual is not breathing and is apneic. Bilevel ventilation administered using a nasal or face mask can help with either problem.

Although a polio survivor may not have breathing or sleep problems when initially diagnosed with post-polio syndrome, periodic testing is important because such problems may develop over time or a change of breathing machine and/or settings may be warranted.

Breathing and Sleep Problems in Polio Survivors Read More »

Bollenbach Polio Biology 4

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.

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.

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

Created: 20th May 1999

Last modification: 21st January 2010.

Bollenbach Polio Biology 4 Read More »

The Polio Vaccine and Simian Virus 40

http://www.chronicillnet.org/online/bensweet.html

After Thirty Years, Prominent Polio Vaccine Researcher Confirms Suspicions About Monkey-Virus Contamination

By T.J. Moriarty

Over the past fifteen or more years, the immune system has been increasingly more challenged. Indefensible disorders such as AIDS and HIV as well as conditions like Chronic Fatigue Syndrome (CFS) and Persian Gulf War-Related Illnesses are the new epidemics of the Silicon Age. By comparison, the days of polio and small pox epidemics seem crudely forgiving when we consider that today’s viral mutants repeatedly outsmart gains made in vaccine development.

However, it seems the days of polio are still with us – not in the form of acute viral outbreaks of fever and paralysis – but in the “uncharted” data on the long-term effects from the simian (monkey) viral contaminated polio vaccines given to countless children and adults three decades ago. Even more, what other “undetectable” monkey viruses have been transmitted in the vaccine batches of late? These unanswered questions continue to resurface in today’s research and still riddle retired scientist Ben Sweet. “No one really knows if there are any dangers, but no scientist can definitively say there aren’t any, that is what’s scary,” says Sweet.

As a senior research scientist for a major pharmaceutical company from 1959 to 1964, Dr. Sweet was one of those responsible for the research, development and field testing of the killed respiratory virus vaccine.

Contaminated Polio Vaccines

Scientific literature states that some polio vaccines given between 1955 and 1961 may have contained low-levels of live monkey viruses. As many as 26 of the simian contaminants were readily detected but still other viruses, like SV40 slipped past rigorous quality control testing procedures available at that time. The simian viruses were inadvertently introduced into the vaccine pool because the polio virus was grown in monkey (Rhesus, Patas, or Cynomolgus) kidney cells.

In his 1960 paper, “The Vacuolating Virus : SV40” Sweet and co-author MR. Hilleman write, “This new virus represents the detection for the first time of a hitherto “non-detectable” simian virus of monkey renal cultures and raises the important question of the existence of other such viruses. All three types of Sabin’s live polio virus vaccine were contaminated.”

Dr. Sweet told Chronic Illnet about the alarm that circulated around the discovery of the SV40 virus in 1960, “It was a frightening discovery because, back then, it was not possible to detect the virus with the testing procedures we had. It only showed up in the cells of the African Green monkeys — the species being used exclusively by our company. We had no idea of what this virus would do thirty years ago.”

Sweet says there were two things that the research team had determined: “First, we knew that SV40 had oncogenic properties (cancer-causing) in hamsters which was bad news. Secondly, we found out that it hybridized with certain DNA viruses – like adeno virus – such that the adeno virus would then have SV40 genes attached to it. We couldn’t clean up the adeno virus vaccine seed stocks grown in monkey kidney cells only”. The seed stocks apparently were always contaminated but the vaccines were still administered.

: Confusion Surrounding the “Killed” Vaccine

Possibly the most unsettling part of his research that he carries with him thirty years later, is knowing that an untold number of people (possibly in the 10’s of millions) were exposed with this virus whether they were given the “live” or “killed” polio vaccine.

“Even the people who received a killed polio virus vaccine could have been infected. Those papers we wrote were incorrect at the time, stating that formalin killed vaccines were free of simian SV40 virus. But the new information regarding the killed ones was never published,” he added. By then it was too late. These findings came after the mass inoculations with the polio vaccine.

The distinction between “live” and “killed” vaccines is a critical one. The scientific community and the American public was told that “killed” vaccines were undoubtedly safe because formalin was used to destroy any contaminating simian virus. The thirty-nine or so simian viruses prior to SV40, were probably inactivated with formalin, but not SV40. The virus eluded the virus-killing behavior of formalin, This now meant even the “killed” vaccines unintentionally contained small amounts of active virus, “So it’s a likely possibility that a some of those individuals injected with supposedly inactivated adeno virus vaccines that had the SV40 contaminant or SV40/adeno hybrid could also be producing antibodies to it.”

Due to the molecular “kinetics” of virus inactivation, Sweet and other researchers believe other viruses — similar to SV40 — could also have been present in the vaccines if they too could circumvent formalin inactivation

There were specific laboratory difficulties associated with adeno virus — now carrying an attached form of SV40. Sweet describes, “When we started growing the vaccines, we just couldn’t get rid of the SV40-contaminated virus. We tried to neutralize it, but couldn’t. Either adeno or SV40 would come out down the line.”

Chronic Illnet: What were you thinking at the time when you realized people were being exposed to SV40 about the long-term effects, considering we’re still in the dark?

Sweet: “We really didn’t think about it until we found out it was oncogenic and now, with the theoretical links to HIV and cancer, it just blows my mind.”

Chronic Illnet: Was there any temptation to just scrap the whole project, make an announcement and move on?”

Sweet: “Sabin and, more specifically, Salk vaccines were already widely in use by then. We were, of course, always worried about possible vaccine contaminants present because we didn’t know what these monkey cell cultures were carrying. We were always worried about encountering a new, undescribed virus. Always. When we found out there were viruses present in the Rhesus -cynom systems, and the possibility that each monkey assay system was different from another, the temptation was there to transfer the studies to another system. But it was too late to switch gears and start using raccoon or chicken systems, because then you could be dealing with another whole set of viruses.’

Chronic Illnet: What was the political climate?

Sweet: “You had to be careful, very careful. When the virus appeared oncogenic in hamsters, we wanted to do tests to determine if it caused malignant transformation of normal cells in culture. In reality, we did not although an outside agency confirmed the findings.”

Sweet also described another inherent problem in vaccine development — the controversy and

killed) and Sabin (live) formulas. Despite common knowledge, both Salk and Sabin were definitely contaminated. The Salk vaccine had already garnered prestigious appeal as a “safe vaccine”.

Long-term Studies Encouraged Three Decades Ago

In his 1960 paper, Sweet, et al, stressed the need for studies on the long-term effects on humans to determine the pathogenicity of these agents for man. “When the ‘contaminated’ vaccines were released, we really felt confident patients needed a substantially higher level of infectious SV40 and/or they had to receive multiple shots to elevate the body’s viral count high enough to cause the harm.” To some, the term “contaminated” carries with it an intent of malice, but Dr. Sweet says this is clearly not the case. Sweet noted that persons fed live SV40 contaminated polio virus vaccine orally, or inactivated Salk-type vaccine intramuscularly, showed strong evidence of antibody production to polio viruses. In additon, the vaccine recipients were not showing significant harmful effects or antibody production, in the short term, to SV40 – which was encouraging. “Less concerning long-terms effects could be noted,” he says.

At the time of the discovery of the human exposure to SV40, there was no evidence that the virus was present or active in vaccine recipients. In recent years, however, SV40 has been isolated in human tissue, two from the brains of patients with PML (progressive multifocal leukoencephalopathy) and another from a metastatic melanoma patient. Results of this study appeared in the paper “Human Exposure to SV40 : Review and Comment” by Shah and Nathanson in the Journal of Epidemiology in January of 1976. Important from that report is the only definitive origin of where human exposure came from, “With the exception of viral vaccines, no pharmaceutical product intended for human use requires the use of simian cultures.” Based on their interpretations, the authors estimate somewhere between 10-30 million people of the 98 million injected were exposed to at least SV40.

Today’s Polio Vaccine Research – Long-Term Effects

To date, the polio vaccine has been administered to an estimated ninety-seven percent of children in the United States.

Although there are no “proven” scientific facts about the possible perils of contaminated or even “purified” polio vaccines, there are a handful of credible researchers with theories too intriguing and carefully outlined to disregard. Their theories, if proven, may offer a new link in conquering the immunodeficiency diseases of this century.

Microbiologist Howard Urnovitz is one member of a team who believes many of today’s “new”

syndromes like Chronic Fatigue Syndrome, Gulf War-Related Illnesses and even HIV have, “some association with the possible contaminants in the vaccine.” He says we may be paying the price for “prevention” years later, as the uncertainty about the effects on our immune system from the vaccine continues to unfold.

Was SIV Also Present? Is There an Evolution of HIV from the Vaccines ?

There is also a concern whether another virus of primate origin — Simian Immunodeficiency Virus (SIV) — could also have been present in the original vaccines. That possibility cannot be ruled out. But only testing of the original polio vaccine samples and seed stocks would give a reliable or closely definitive answer, Sweet stressed the need for studies on the original simian isolates and the antisera prepared against them and their possible relationship to SIV. At this point, future studies may be lost due to the impossibility of retrieving such samples.

At the 8th Annual Houston Conference on AIDS, Urnovitz suggests that HIV-1 may have also originated from the contaminated polio vaccines through the recombination with normal human genes. “It is very likely that HIV-1 may have been a result, and that it may in fact be a monkey-human hybrid. His theory states that the contaminating viruses have “archived” themselves in the body’s nerve tissue. These virus fragments then resurface at a later date when the immune system becomes challenged. An opportunistic infection or exposure to toxins could be the “trigger” that stimulates the reappearance of these virus fragments.

“This virus ‘archiving’ could be igniting the symptoms of central nervous system disorders, chronic fatigue and joint pain that have been linked to more than a dozen unexplained epidemics,” he added.

Dr. R. Stricker’s paper entitled “The Polio Vaccine and the Origin of AIDS” that appeared in the January 1994 edition of Medical Hypothesis is yet another theory highlighting a potential link. Stricker states, “The transfer of monkey viruses to man via vaccines is particularly relevant to AIDS since the causative agent HIV, is thought to be derived from a simian precursor virus.” He says the evolution of HIV remains to be proven but is nonetheless startling, “Is it only a coincidence that HIV infection manifested itself at the same time as the introduction of vaccines that are now known to have been contaminated with simian viruses?”

The collection of theories on the origins, pathways and the sheer number of potential “victims” from the contaminated vaccines is certainly unsettling. Although each theory has its own individual elements, a cohesion exists: The cross-species cultivation of vaccines is clearly laden with risks — risks that may be irreversible, carrying consequences too great to endure. But to what extent, if any, irreparable damage has been inflicted upon humanity is still blurry. For consumer activist Barbara Loe Fisher, co-Founder & president of the National Vaccine Information Web Site, the fact that the original vaccines were contaminated and current polio vaccines are still grown on African Green monkey tissues, is just one more indication that government vaccine officials have created dangerous public health policies without making sure they have the solid science to back them up.

“Who is minding the public health when the FDA allows drug companies to produce vaccines grown on animal tissue cultures and they don’t even know if this practice is facilitating cross species transfer of animal viruses into man?” says Fisher.

Highlighting the fact that American parents are legally required to vaccinate their babies with 10 different viral and bacterial vaccines, Fisher warns, “No one really knows the latent, long term effects on the human immune and neurological systems. With 200 vaccines in the research pipeline, more than 100 scores on the brink of being licensed, vaccine research had better get back to the basic science before another AIDS epidemic is created in a vaccine lab.”

For more information on this topic, refer to the highlighted phrases for hyperlinked information and additional sources. Chroniclllnet is pleased to provide online the well researched book entitled “America’s Biggest Cover-Up”:50 More Things Everyone Should Know About The Chronic Fatigue Syndrome Epidemic and Its Link To AIDS,” by Neenyah Ostrom. This book offers important information about the history of The Chronic Fatigue Syndrome (CFS) Epidemic-both failures and successes. The opinions and perspectives offered by Ms. Ostrom are her own and do not necessarily reflect those of the Chroniclllnet editorial staff. We feel much of the material offers important insight on the direction of research on CFS and AIDS and strongly recommend its reading. More related material can be found on TST Audio-on-demand and Amazon books. You can also order these books at 800-278-2252.

The Polio Vaccine and Simian Virus 40 Read More »

Dr Henry writes about Michaels Tune

Dr. Henry writes about Michael’s Tune

I have commented in previous articles how the event of polio in history has entered my life when I least expected it. Last October 30 (1998) , the Rochester Cathedral Choir from Rochester England performed a concert at my church. An information sheet was provided regarding the various pieces performed and the composers. I scanned this information and noticed under the biographical sketch for Herbert Howells the following: “He was deeply affected by two events: hearing (with his friend, the composer Ivor Gurney) the first performance of Vaughan Williams’ “Fantasia on a Theme of Thomas Talis” in Gloucester Cathedral; and the death from polio, at the age of nine, of his son, Michael (after whom he named his tune for the hymn “All My Hope On God Is Founded”).” The death of his son from polio jumped off the page at me. I began a little research into this event in the life of Herbert Howells (1892-1983).

English composer Herbert Howells was born in 1892 in Lydney in Gloucestershire, England. He was the youngest of eight children in a family that struggled to maintain a livelihood. His older sister taught him piano and in his youth he assisted his father at the organ at a local Baptist chapel. At age eleven, he joined the choir of the local Anglican Church. His musical talent was recognized and his career took off with great promise. In 1915 at the age of twenty-three, he developed a severe case of hyperthyroidism or Graves Disease. He had a resting pulse of 130. He was unable to walk and talk at the same time. He was given six months to live. With this death sentence, he agreed to try an untried new experiment with radium. He was given radium treatments twice a week for two years. The treatments proved to be effective as Howells lived to age ninety. During World War I, he felt some guilt that he was unable to serve in the British army as many of his musical peers did. In 1920, he married Dorothy Dawe, a young singer. In 1923, a daughter, Ursula, was born, and on April 12, 1926, a son, Michael, was born. Nine years later on September 3, 1935, Michael contracted polio. Howells kept a diary throughout most of his life. His entries for the onset of Michael’s illness are as follows:

Wednesday 4 (September): Mick’s coming to our room in early morning. Temperature. Bad Back. Dr. Nanda sent for. Herbert arrived with coat he thought Mick had lost. Dr. N at 2:30 (PM), Chill? To St. B (riavels) for medicine. At 9 o’clock in Taylor’s car.

Thursday 5: Mick worse. Dr. N at 11:15. Orders for London. Ambulance and Cheltenham Flier – London – Dr. Dowling, Nursing Home, Dr. Hunt, Fearful anxiety.

Friday 6: Nursing Home at 8:45 (AM) – Dr. H at 9 AM. With M most of the morning – lunch with Scotts. M again at 2:30 (PM). Grave change. Mrs. Fisher came – Mick worse always. Dr. H 7 PM. Hope, then despair. Dr. Brunton. Dr. Fisher,,, Mick died at 10:10 PM +

These brief diary entries provide witness to the potential rapid nature of the polio virus’s ability to invade the central nervous system resulting in death. On Tuesday, September 3, 1935, nine year old Michael had been busy mowing lawns. He began to feel unwell that evening and was sent to bed early. The next day he was clearly ill with fever, chills, and a “bad back.” The next day his illness was grave and Dr. Nanda, his

first doctor, ordered that Michael be transferred to London. He was taken by ambulance to the Gloucester railway station and rode the Cheltenham flier train to London. Michael arrived in London about twenty four hours prior to his death. He was to be seen by four additional doctors during those twenty-four hours in London. Twelve year old sister Ursula recalled Michael’s appearance as they drove him to the Gloucester railway station. She stated that he was turning ‘bluey-black’ as his lungs began to fail. This early observation would indicate that Michael had contracted a severe case of bulbar polio. In the mid 1930s available iron lungs were small in number. There was one iron lung in London, but it was on the other side of town. Sister Ursula stated in an interview years later: “It would have been possible to get it (the iron lung) to him, but the doctors felt that it might be kinder to let him die given that he would anyway be totally paralyzed for the rest of what would have been a much shortened life. So they had this awful decision to make, but fortunately he died while they were deliberating.”

Had an iron lung been available to Michael, there is the possibility that he would have recovered to a significant extent as many survivors of iron lung bulbar polio were able to do. However, Michael’s polio was in 1935 and not ten years later when the iron lung was more readily available. As survivors, we may tend to forget that many children and some adults succumbed to acute polio during the epidemic years. During the great polio epidemic in New York City in 1916, 2500 children died of acute polio. This occurred before the invention of the iron lung. Following the invention of the iron lung, there is no doubt that the negative pressure iron lung cylinder tank with bellows saved thousands of lives around the world. Today, positive pressure ventilators (the descendants of the iron lung) save lives on a daily basis as one has done for me since 1971.

Michael was buried on September 11 at Twigworth where his parents had been married. Sister Ursula remembers the time period following Michael’s death. “Herbert (Michael’s father) was an extremely emotional person. I don’t know what he was like religiously before Michael’s death, but afterwards, every weekend we went to Gloucester (from London to Twigworth). We used to live in church. But that was an emotional thing as Michael was buried there. As far as religion goes I think he adored the music and the buildings – he adored cathedrals. Emotionally, he had a sort of spiritual sense. I know he said to me, about a year before he died when we sitting one day in the dining room: ‘I don’t believe there’s anything’. I was very surprised that he said it as definitely as that. That was the only surprise I had. Not that he didn’t believe. It was the fact that he said it, and came out with it.”

Shortly after Michael’s death, it was twelve year old Ursula, who having observed her inconsolable and ever grieving father, suggested that he should write about Michael in music. Thus, Hymnus Paradisi, an English Mass, made its first stumbling steps toward the great achievement which a Gloucester audience witnessed for the first time fifteen years later. Also in memory of Michael, Howells wrote the music for the hymn “All My Hope On God Is Founded.” For many years thereafter, Howells wrote church music. His biographer, Paul Spicer, wrote that Howell’s music “marked him out as the greatest contributor to the

music of the Anglican Church in this century.”

Despite Howell’s doubt about a merciful God, perhaps his son’s death allowed the love of God to be expressed through his music. I have had the opportunity of hearing “All My Hope On God is Founded” as performed by the Chancel Choir of River Road Church, Baptist during a Communion Service. The words and music of this hymn are inspiring to anyone who has suffered a personal loss or is in despair. The hymn consists of five verses. The first three verses were written by Jaachim Neander (1650-1680). The last two verses were apparently written by Robert Seymore Bridges (1844-1930). In memory of his son, Michael Howells, Howells set the five verses of this hymn to a new tune called “Michael.” If you have never had the opportunity of singing or hearing this hymn, I hope you might have the opportunity some day.

All My Hope On God Is Founded

All my hope on God is founded;

He doth still my trust renew.

Me through change and chance He guideth,

Only Good and only True,

God unknown,

He alone

Calls my heart to be His own.

Pride of man and earthly glory

Sword and crown betray his trust;

What with care and toil he buildeth

Tower and temple, fall to dust,

But God’s power

Hour by hour,

Is my temple and my tower.

God’s great goodness aye endureth,

Deep His wisdom passing thought:

Splendour, light and life attend Him,

Beauty springeth out of nought.

Evermore,

From His store

New-born worlds rise and adore.

Daily doth the Almighty Giver

Bounteous gifts on us bestow;

His desire our soul delighteth,

Pleasure leads us where we go.

Love doth stand

At His hand,

Joy doth wait on His command.

Still from man to God eternal

Sacrifice of praise be done,

High above all praises praising

For the gift of Christ His Son.

Christ doth call

One and all:

Ye who follow shall not fall.

References:

Spicer, Paul, Herbert Howells, Poetry Wales Press Ltd, Bridgend, Wales. 1998. Information Bulletin, Rochester Cathedral Special Choir, Rochester, England, 1998.

Musical Information provided by Carl Freeman, Minister of Music of River Road Church, Baptist, Richmond, Virginia.

Additional information provided by Lynn Singleton of East Sussex, England and Hilary Hallam of Lincoln, England.

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

May 1999

Originally published in the Central Va PPS Support Group (PPSG)‘s newsletter, The Deja View, in 1999.

Rochester Cathedral

http://www.net-west.co.uk/webs/rochester-cathedral/

The above document no longer available.

The Choirs of Rochester Cathedral

http://www.cathmus.ndirect.co.uk/rocheste.html

The above document no longer available.

A resource page devoted to 20th century British composer Herbert Howells

http://www.gprep.pvt.k12.md.us/~gldaum/howells/howells1.html

The above document no longer available.

The Music of Herbert Howells (Brent Millar)

http://members.aol.com/umethodist/mypage/phowells.html

The above document no longer available.

The Pillar of Fire – An introduction to the music of Herbert Howells (1892-

1983)

http://www.stpetersnottingham.org/music/pillar.htm

Includes link to RealAudio file of St. Peter’s Church Choir, Nottingham,

performing Herbert Howells Psalm 47 v5-9 chant.

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

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.

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

Created: 31st May 1999.

Last modification: 24th January 2010.

Dr Henry writes about Michaels Tune Read More »

Bollenbach Polio Biology 3

Polio Biology III

What About If We Need The Virus Later?

Eddie Bollenbach

A Lincolnshire Post-Polio Library Publication

23rd April 1999

Viruses are tricky creatures. We don’t understand everything about them. Until recently we didn’t even know how polio got inside the cells it infects. But we are learning new things all the time. Polio virus is one of the most cultured (grown) viruses for laboratory study. And yet, there are aspects of its life cycle which remain puzzling. For example, how are the virus’s protein subunits assembled after they are produced, inside cells, during infection? Or, what is the effect of a mutation (change) in one of the protein subunits that assemble to produce the case inside which the genes of the virus reside? One thing we do know is that polio virus mutates a lot during infection. Its small component of genes is simply too little to contain the “Proof Reading” enzymes found in larger cells with larger genomes. When polio is eradicated from this earth, which may happen soon, should we keep this virus to continue studying it or should we discard it and allow it to crumble inside the steel of autoclaves throughout the world? This is not a question that will come without controversy.

The World Health Organization recommended in 1996 that the World’s known stocks of Smallpox Virus, held by the U.S. Centers for Disease Control and Prevention and the Russian State Research Center of Virology and Biotechnology, be destroyed. The last known outbreak of Smallpox was in Somalia in 1977. So the destruction of laboratory stocks seems like a fitting end to this historical scourge. But what if we learn about a new disease in the future which involves smallpox infection. Suppose smallpox is now dormant inside some people? What if the virus is being held by rogue states that plan to use it as an agent of biological warfare? Or what if we simply want to study it to learn more about viral diseases? These considerations have resulted in President Clinton balking on WHO’s directive to destroy smallpox stocks by June 1999. The US will keep its laboratory stocks of Smallpox.

Despite the fact that wild polio infection has not been seen in the Western Hemisphere for quite a few years, we are continuing to learn more about how polio may be harming those it infected 40 years ago. The Pasteur Institute is involved in studies centering on the molecular aspects of a polio infection and

have discovered that inside the spines of those of us with PPS polio virus genes (and likely proteins) persist. As we gather more evidence it will become important to find out the mechanism of this persistence. The protein case that surrounds the virus will be a target of much of this research. The polio virus is so small that a big chunk of its genetic material is devoted to the protein case. If a virus loses a gene to make the properly shaped protein for the case it would be impossible for the virus to assemble itself and spread. This could be what allows polio virus to persist. This aspect of virus biology could help explain the Post-Polio Syndrome. At this moment the two main contenders for explaining PPS are the

“Wear out Theory” and the “Viral Persistence Theory”. One doesn’t need a live virus to explain our woes; the other does.

So, I guess I would side with President Clinton’s ideas on maintaining Smallpox stocks. The world is safe from smallpox and we can only learn more by studying the virus. We just don’t know enough about them even though we seem to have eliminated the future threat of new epidemics.

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

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

Created: 23rd April 1999

Last modification: 21st January 2010.

Bollenbach Polio Biology 3 Read More »