Post-Polio Syndrome

Marge,

OMG! This is a very scary article.

I understand how the undamaged neurons grow sprouts that assist in improving muscle movement after polio (or after GBS/CIDP) and why these sprouts might cease to function after awhile, but I wonder why new sprout don’t grow to replace these…..

Thanks for informing us about these very important studies.

Suzanne

THANK you Marge!

Very interesting reading, and I also like to read these articles as a reminder that Im not mad 🙁 .

Marge,

Thank you for this article, I plan on showing it to my Dr. After suffering the ill affects of the Polio Vaccine back in the 1950’s and being paralyzed from the waist up for a few days, this article is making sense to me and the problems I have had for way to many years. All my parents were ever told was that I was having a reaction to the Polio vaccine and the doctors did nothing for me.It was a wait and see attitude. I can’t take any vaccines do to the fact that what they are intended to prevent always gives me a form of the disease.

Knowing what I know today about the horrors that vaccines can cause in some people, I’m leaning towards this article and it could be me with PPS.

The Drs blame everything on my Spinal Stenosis, but I wonder about that all
the time. I wonder if the Drs would be able to tell if I have PPS after all this time.

Dear Friends:

At one of our recent local GBS support group meetings, we had a physical therapist, I believe, who had some research about super-axons which have many branches after axonal damage due to GBS. Remeber that most everyone who has GBS has at least a small amount of axonal damage. The studies the physical therapist had seemed to suggest that the degradation of the super-axons happened most often with people who were extremely active after GBS. Extremely active is a relative term, but I took its meaning to people who jog a mile a day, hike two or three miles a day, or bicycle 10 miles a day on a regular basis. The super-axons tended to fail, decades after the initial onset of GBS, not a few years later. As I recall, the study was had a very small sample and it is difficult to draw conclusions and make projections based on just a very few case studies.

Lee

That is too scary of an article. Ugh.

m,

great info. thx. i wonder if any medically approved studies relate gbs to this &/or have done independent post gbs studies? as for me, i’m now prepared. even though the thought of it is being emotionally rejected by me at this moment. yee gads, it can’t be so. take care. be well.

gene gbs 8-99
in numbers there is strength

You are right, it is better to be informed. 🙂

Dear Marguerite:

I guess you are right about me being at risk more than some others. I see it as a risk versus benefit sort of thing. Exercising has some risk for people with GBS, but not taking exercise, in my opinion is a whole lot worse. A sedentary lifestyle will kill you. It is up to every individual to weigh the risks versus benefits, I can’t tell anyone what they ought to do. I just hope everyone makes their health and lifestyle decisions based on the best information they can get.

Lee

Hi,

Always use information to your advantage. I guess I see this as, using my condition as an example, something that goes along with age. From the days after onset, when treatment did it’s job, from that point forward, my body is now working with less. My arms didn’t go away, the nerves that operate them did, as an example and to keep it simple, so as we heal, we get more and more operating strength back. To what degree you get back, nobody knows until you get there. You can feel an operate like new agin, but there still could be a few degrees that really never happened. This is what I see not included in some way in the science. Or, as part of the reason. Adaption. I operate every day using more parts of my body then most, to preform a like function or task. Obviously because the nerves aren’t there. So asking the rest of my body to handle the chores while time goes by, definately puts strain, stress and operating strength into places that wern’t built to handle those kinds of loads. Take the chandalier over the dining room table, replace on of those delicate lights with a 1000 watt baby, and see what happens. The more active a person, replace another bulb agin, so to speak. I figured this out at year 2, after going berzerk on regular food(most should understand what I mean by that, ie hospital) and realizing that I can’t get any errobic excercising going, because the body wears out to fast to get any result. Couldn’t walk then yet either. Oh, oh. I can’t carry this weight around as I get older, should things not come around enough. So, first, stop the bleeding, then it’s been an ongoing battle ever since and still going. Only 25lbs to. Having such an active life before all this, who knows what will catch up to me down the road. As I’ve said many times, always plan for how you are in the present, and that applies to looking down stream too. Am I prepared for what may be years away, if nothing changes? What do I need to do, while I have the time to do it, to make it easier on me. Weight adds stress, so there’s my choice. One of my main considerations when I took excersise out of the day, or for me, therapy, because every day is therapy for me. A choice made on my capabilities that my body allows me to work with. As Lee pointed out, and there is no doubt about it, sedentary does kill. Do exercises, sit the rest of the day. Don’t, and sedentary isn’t so harmful and I can move, or be in motion most of the day. That’s my low impact way of trying to stay moving a lot, in hopes that 15 years from now, and not stuffing myself anymore, weight will peel off slowly, and sitting so much won’t shorten things up too bad. Working with what I got, to get results I may never see, but I’m not going to wait till I’m 70 and need an assistent to move then start a plan. Information helps with that, and I’m still learning about this post-gbs as likened to post-polio discussion, but I just look at it that with post-gbs, comes post-life too. With life, the body starts to deterioate as soon as it’s born, so to speak. Why we should all be born old, by the way. Either way, you end up in diapers. 🙂 What’s to be expected, as far as muscle weakness and strength, should be expected, to loose something in everyone over time, I’d assume. What name you put on it, I’m not sure. Stressing parts of a machine individually, will catch up to the whole every time. Your car says only rev enjine this high, gives you a warning when the needle sees red, but that same enjine can be run much higher revs at a steady rate, just won’t last as long. Women, confirmed in human nature studies, are in motion 35% more in a day, then males. Added stress right there, especially when the body isn’t up to full stength due to nerve loss. To me, this kind of stuff too, explains a lot of the science in those above posts. If post-anything is found through this research, then add another to deal with, so it has a value to us.

Marguerite. I saw your post with interest. I joined the US and UK boards in November 2004 with a post called “GBS relapse?” as I could not understand what was happening to me. I contracted GBS in 1990 the age of 51 , got back on my feet by 1994, and was walking 6 mi. by 2001. Pain and limited function have been my constant companions (as it has with many of us), but by 2004 I was beginning to notice that my function was apparently degrading at a faster rate than could be explained by the natural effects of anno domini. I saw two neurological consultants with inconclusive results, then had the good fortune to be examined by Professor Richard Hughes of Guy’s Hospital London, arguably the foremost UK expert on GBS and peripheral neuropathy. He is a man for whom I have the greatest respect. He diagnosed acute motor axonal neuropathy (AMAN), which has symptoms that are allied with PPS.
I agree with the comments already made on this post, the sad thing is that the possibility of these after effects were not communicated to many of us when we first contracted this illness, in my case 16 years ago. Possibly because the medics did not know: after all medical science has moved on a great deal in the last few years.
In my case I made a conscious decision at the outset that I would fight this illness every step of the way. It got me back on my feet again when the advice given to me at the time was to accept the permanent offer of an electric wheelchair, but in retrospect it seems that I may have put too great a strain on my body by my determination to get back to being as “normal” as possible again.
In the last couple of years I have seen a gradual decline in my muscular system, particularly in the back and shoulders. In other words, the “concrete overcoat” that I have been wearing post GBS is inexorably getting heavier, and the rate of deterioration appears to have increased this year.
This post is not a moan: I do not regret the decision I made in the slightest. I chose to fight and I would do the same again, but to those of you out there who are long-term GBS patients these words may give you some food for thought. Having said that, for all I know this degradation may have happened anyway even if I had not pushed my body to its limits. I shall probably never know, but at the age of 67 I care not. I shall keep fighting, because I know no other way to be true to myself.

It was a physical therapy doctor who conducted research on GBS survivors, studying the nerve damage and efficiency of the new nerve sprouts. She attended the GBS conference about four years ago in Marina Del Rey.

Thank you Marge for this input. I vividly recall visiting my neuro. a couple of years ago and gave him my list of problems and he stated I sounded like someone who had polio. Slowly but surely, the docs. have got to be learning more about this – but of course there are so, so many neuro. diseases…

I’ll chime in here Marge, I do remember that article.

[QUOTE=marguerite]Thank you very much. I’ll try to get a copy of her paper.

Regards,
Marge[/QUOTE]

Anyone have success finding a copy of this article? If so, I’d love to know where to read it.

Thanks

Was it DocDavid who posted the article on Roosevelt last week? (Before we lost the last two weeks?)

Yes it was, do you want it again? DocDavid

Doc,

I would like you to please, if its easy enough for you to do. I know it was sooo long. Thank you.

Did Guillain-Barre paralyse FDR ?
Have you had your flu vaccine? Did your doctor, or your nurse warn you of the possible side-effects? Did you know that it is possible to develop paralysis, pain, loss of feeling and even need for a ventilator as a result of flu vaccine? There is a rare condition called Guillain Barre Syndrome (GBS.) with all these features that can develop after flu vaccine, the chronic form of it is called Chronic Inflammatory Demyelinating Polyneuropathy (CIDP.). Most doctors have heard of GBS., very few have seen a patient, or treated it; even fewer have even heard of CIDP. GBS was first described in 1916, it develops rapidly with numbness and paralysis rising up from the feet, in some it paralyses breathing. CIDP develops slowly with vague pains, numbness and weakness defying diagnosis for some time; once developed the paralysis may persist for many years There are many people in this country contributing to the GBS/CIDP internet forum ‘[url]www.guillain-barre.com’[/url] who developed this paralysis two weeks after a flu vaccine, many of these would never have the vaccine again. Few doctors would have been aware of the paper on GBS, published five years previously, when FDR developed ascending paralysis in 1921,. Late this October the Washington Post carried the report from researchers at the University of Texas arguing that his disability was due, not to polio, as was previously thought, but to GBS, or even the chronic form C.I.D.P. Next time you are offered flu vaccine, think very carefully about having it. Do you want to be paralysed like FDR?

Today’s Washington Post carried a half-page story about a report by medical researchers at the University of Texas arguing that President Franklin D. Roosevelt’s famous disability was caused by GBS rather than by polio. According to the Post article, the medical researchers reached their conclusion by examining statistics regarding the likelihood of polio vs. the likelihood of GBS for someone Roosevelt’s age; the researchers’ numbers are 39% for polio vs. 51% for GBS. The researchers also examined statistics regarding the relative likelihood of each of 8 particular features of Roosevelt’s illness being caused by each illness (6 of the 8 features favor GBS). The article also notes counter-arguments put forth in response by two Roosevelt biographers contending that Roosevelt probably had polio rather than GBS.
Factors cited by one side or the other in the article include: Roosevelt was 39 when he became ill; GBS was more likely than polio to occur in adults; few doctors were aware of GBS in 1921; throughout the years until polio was largely eliminated through vaccination, many cases of GBS were misdiagnosed as polio; Roosevelt, as the son of a rich family, had relatively little contact with other children as he was growing up, might not have been exposed to the polio virus as a child, and hence it would not be surprising that he developed the disease at age 39; and Roosevelt visited a summer camp for poor NYC children 14 days before he developed symptoms (suggesting that he might have been exposed to the polio virus at the summer camp).

The article also describes Roosevelt’s activities on the day before his symptoms appeared. He was at a family summer home on an island in Canada’s Bay of Fundy. He felt tired and achy, but still took his wife and 2 sons sailing. They stopped at an island where they saw a small fire burning and spent an hour putting the fire out. After returning home, he took a group of children swimming at a pond. After the swimming, he raced the children over the two-mile distance from the pond to the house. When Roosevelt swung his legs out of bed the next morning, his left leg buckled. Within 3 days his legs were paralyzed and his arms and shoulders were week.
The article notes that vigorous exercise in the ealry stage of a polio infection is known to increase the risk of paralysis and suggests that, if Roosevelt had polio, his vigorous exercise the day before his symptoms appeared may have accounted for his paralysis.

After reading the article, I’m undecided. It seems unlikely that Roosevelt, even as the son of a rich family, would not have been exposed to the polio virus before age 39 (the article notes that only 1 out of 200 people who contact polio have even temporary paralysis, so it’s likely that a large percentage of the population were polio carriers back then). On the other hand, it also seems unlikely that a 39-year-old who suffered at most a moderately-severe case of GBS and who apparently did not suffer recurring attacks would not have had a fuller recovery. Of course, it’s possible that back in the 1920’s, doctors told polio victims that exercise would not aid their recovery and instead told polio victims to conserve their energy by avoiding physical activity whenever possible; if so, Roosevelt may have avoided doing the rehab exercises or even ordinary physical activity that would have furthered his recovery (if, in fact, he had GBS rather than polio).

However I do feel the cause of FDR’s disability whether Polio or GBS is a bit irrelevant now, what is relevant is how he acted as a role model and advocate for disabled people. It’s a pity there are not more like him today, I can count on one hand the number of people in the limelight, whether it be politics , business or showbiz, who have are role models for the disabled community worldwide.

Just a few weeks ago I wrote a letter to the Editor of my local newspaper about Influenza Vaccines (flu shots) and GBS: How the CDC has manipulated numbers to show an economic benefit for flu shots in the past, and that Congressional follow-up studies have shown their mandated Medicare funded project showed a disappointing 31-45% effectiveness “in preventing hospitalization from influenza or pneumonia.” In fact, some reports have shown Medicare payments were higer for those who had received the flu shot. The CDC is now saying that 40-50,000 lives are lost each year because of influenza. Just two years ago, this number was only 20-25,000. What is the really strange part of this doubled death rate? The three influenza viruses used this year are the same as the ones used last year – A/Moscow/10/99-like strain (H3N2); A/New Caledonia/20/99 strain (H1N1); B/Hong Kong/330/2001-like strain. If influenza deaths are doubling – Are we missing something from the CDC’s picture? And of course, I explained the rare possibility that flu shots cause a neurological illness called Guillain-Barre Syndrome. I included a web site, and suggested that they read the literature before getting the shot: [url]http://www.vaccineshoppe.com/US_PDF…e_2002.2003.pdf[/url]

Well would you Adam and Eve it!

On the Letters page in the national newspaper “Ireland on Sunday” in black and white (oh, alright I know! What colour did I think it would be!!!) a letter from a chap in Waterford about this very subject. And the page is headlined “Who says the vaccines we are given are safe?”

I’ve reprinted it below:

“Hardly anyone ever bothers to check up on the toxicity of the various drugs and vaccines that the medical profession usually prescribes for its patients, such as the flu vaccine.

Yet no vaccine has ever been proved totally effective and safe, and the flu vaccine is no exception. Ever since the flu vaccine was introduced, reports of its ineffectiveness and adverse reactions, including deaths, have been filling medical journals. Incidents include the 1976 swine-flu vaccination debacle in the United States with its hundreds of cases of Guillain-Barre paralaysis in vaccinees and numerous deaths. Some 4,000 law suits were lodged, costing over $3bn in compensatin.

Outbreaks of such deadly diseases as legionnaires’ disease also occur followng intensified flu vaccine campaigns.

The flu vaccine is cultured in chick embryos. It also includes the chemical preservative thiomersal, which is 50pc mercury and so can damage the brain, as the American government recently admitted. To inactivate (kill) the viruses harvested from chick embryos, the chemical formaldehyde is added. This is a known carcinogen, while there has been controversy since 1955 regarding its failure to inactivate the flu virus in the vaccine.”

Written by Patrick J Carroll, Waterford

Did anyone else see the piece on last night’s CBS Evening News about FDR? Here is a summary from US TODAY:

[B]Study raises doubts about FDR’s polio
30.10.03

By Anita Manning, USA TODAY
The disease that struck Franklin Delano Roosevelt in the prime of his life may not have been polio, as his doctors and history have believed. An analysis out Friday suggests that Roosevelt, whose work on behalf of polio patients gave rise to the March of Dimes, instead may have had Guillain-Barré Syndrome, a disease barely known by doctors of the day.

President Franklin Delano Roosevelt holds his dog Fala while talking to Ruthie Bie at his home in Hyde Park, N.Y.
By M.L. Suckley, FDR Library via AP

Researchers at the University of Texas Medical Branch in Galveston reviewed Roosevelt’s personal letters, medical reports and biographies that described the disease that FDR had in 1921 when he was 39. Armond Goldman, emeritus professor of pediatrics, and colleagues note that some of FDR’s symptoms were rare in polio, but fit a diagnosis of Guillain-Barré (GHEE-yan BAH-ray), an autoimmune disease that damages motor and sensory nerves.

Their diagnosis, in the Journal of Medical Biography, published by The Royal Society of Medicine in London, is based on an analysis that examined the frequency of paralytic polio and Guillain-Barré in adults of Roosevelt’s age at that time and the likelihood of his symptoms occurring in either of the two diseases.

The paralysis that crept up both sides of FDR’s body from legs to chest over a 10- to 13-day period is more typical of Guillain-Barré than polio, in which weakness or paralysis occur in a matter of three to five days and affect one side more than the other. The authors point out that at the time of FDR’s infection, polio was rampant, but it rarely struck anyone over age 30. FDR also suffered temporary facial paralysis, bladder and bowel problems and severe sensitivity to touch, none of which were common in polio.

All those symptoms are consistent with Guillain-Barré Syndrome, named for the scientists who described the illness in two French soldiers in 1916.

While he was president, Roosevelt’s paralysis was hidden from public view, but his struggle has become an inspiration to others with disabilities. In 1927, Roosevelt established a rehabilitation center in Warm Springs, Ga., to help other victims of polio, and helped launch the March of Dimes, which led to the development of polio vaccines.

FDR spent months at the center in Warm Springs, swimming in the soothing waters with other polio victims to try to restore their paralyzed limbs. The Roosevelt Warm Springs Institute for Rehabilitation still serves thousands of people each year. Institute spokesman Martin Harmon says people with Guillain-Barré are among those who come for therapy.

But Harmon isn’t buying the suggestion that Roosevelt didn’t have polio. He says Roosevelt was attended by several doctors and went through extensive therapy that would likely have resulted in some improvement if he had had Guillain-Barré. The suggestion that the diagnosis was in error is “extremely far-fetched,” he says. “It’s like rewriting history.”

But, says Goldman, Roosevelt’s physicians may not have known about Guillain-Barré, and if they did, the treatments available today were not known at that time. Goldman doubts that a diagnosis of Guillain-Barré would have made any difference to FDR.

The authors acknowledge the impossibility of a certain diagnosis more than 80 years after the fact, and they say Roosevelt’s doctors were among the top health experts of their day, so they can’t be faulted if they made a mistake.

“Making a diagnosis of the cause of FDR’s paralytic illness was far more difficult in 1921 than at the present time,” Goldman says. Even today, there are diseases and disorders whose causes are not known, but may be discovered by future generations. “In that respect, we are all prisoners of our times,” he says.[/B]

Guillain-Barré Syndrome
Introduction
This guide is written by neurologists and other specialists who have a particular interest in Guillain-Barré syndrome (GBS*). It is intended for patients who have been told that they have, or may have GBS, and for their relatives and friends. It is quite detailed and should be read after you have read the Quick Guide which gives you a rapid overview of the disease and should answer your immediate questions. It has to be honest and is meant to be reassuring. The information contained in this book is an accurate and up to date account of GBS. Situations may arise in which you receive apparently conflicting opinions and information from different doctors and health care workers about various aspects of GBS. Unfortunately this document cannot respond in words to the conflicts or concerns that this information may cause. Consequently if you do not understand or are worried by the information offered here, you must ask your medical specialist to explain. Don’t be scared to quote from these pages if you feel intimidated or neglected! Any good doctor should be willing to listen and to explain.
· Quick Guide >>
*Confusingly, ‘GBS’ is also an abbreviation for ‘group B streptococcus’.
· Group B Strep Support >>
What is GBS?
GBS is an uncommon illness causing weakness and loss of sensation that usually recovers completely after a few weeks or months. It is named after two French physicians, Guillain (pronounced Ghee-lan) and Barré (pronounced Bar-ray), who described it in 1916 in two soldiers who were affected by a paralysis but later recovered. It affects about one person in 40,000 each year, ie 1,500 persons altogether each year in the United Kingdom. It can occur at any age from infancy onwards but is slightly more common in the old; it is more common in men than in women; it is not hereditary; it is neither passed onto children nor is it infectious and it is not caught from or transmitted to anybody else. However, it does often develop a week or two after a throat or intestinal infection.
What are the symptoms?
The first symptoms are usually either tingling (pins and needles) or loss of feeling (numbness) beginning in the toes and fingers. Legs feel heavy and wooden, arms feel limp and hands cannot grip or turn things properly. These symptoms may remain mild and clear up within a week or two without need for hospital admission but most people need to be admitted to hospital. At the earliest stage, it may be difficult for the patient to persuade the doctor that there is anything physically wrong. Within a few days it is all too obvious that something has gone wrong: legs simply will not bear weight, arms become very weak and the doctor finds that the tendon reflexes have disappeared.

What happens next?
The worst degree of weakness is usually reached within four weeks and always within six weeks. Some patients deteriorate very rapidly to a state of severe paralysis over the course of a few days but this is uncommon. The patient then enters a plateau phase that usually lasts a few days or weeks during which the course of the disease seems stationary. Most people are so weak during this stage that they are confined to a hospital bed where rest is probably a good thing. However, it is very important to keep all the joints moving through a full range to stop them stiffening up. The physiotherapist is in charge of this physical therapy and will be pleased to advise relatives and friends on what they can do to help.
Symptoms
The severity of CIDP is extremely variable and the symptoms experienced vary considerably between patients. Initial symptoms may be vague and confusing to both the patient and the doctor. Subjective symptoms such as fatigue and sensory disturbance are difficult to communicate. In the early stages it may be difficult for the patient to persuade the doctor that there is anything physically wrong.
Early symptoms usually include either tingling (pins and needles) or loss of feeling (numbness) beginning in the toes and fingers, or weakness, so that legs feel heavy and wooden, arms feel limp and hands cannot grip or turn things properly. These symptoms may remain mild and result in only minor disruption the patient’s normal life. Alternatively they may become progressively and gradually worse over a period of several weeks, months or even years sometimes, but very rarely, to the extent that the patient is bed bound with profound weakness of the arms.
CIDP usually presents with both weakness and sensory symptoms, sometimes with weakness alone, and rarely with sensory symptoms alone. The arms and legs are usually affected together, the legs more than the arms. Prickling and tingling sensations in the extremities are common and may be painful. Aching pain in the muscles also occurs. Tendon reflexes are usually lost. As the disease becomes more severe, a tremor may develop, usually in the upper limbs. Very rarely patients may develop facial weakness.
Diagnosis
Health officials convinced the Chinese to rename the bulk of their polio to Guillaine Barre Syndrome (GBS). A study found that the new disorder (Chinese Paralytic syndrome) and the GBS was really polio (41). After mass vaccination in 1971, reports of polio went down but GBS increased about 10 fold.(Ref: Vaccination by Greg Beattie)
Tang XF, et al. Guillain-Barre syndrome or “new” Chinese paralytic syndrome in northern China? Electroencephalogr Clin Neurophysiol. 1996 Apr;101(2):105-9. PMID: 8647015; UI: 96245462.
A serial study of clinical and magnetic stimulation motor evoked potentials (MEP) was accomplished in 44 patients with the acute flaccid paralytic syndrome which occurred in Northern China in 1991. Control data were provided by 70 healthy subjects from the same area. The cases came from the same area where a so-called new “Chinese paralytic syndrome” had been reported. We found the clinical features of these 44 patients to be similar to those of classical Guillain-Barre. Prolongation of MEP latency at 2 sites or on 2 occasions was found in 36 patients of whom 26 showed obvious clinical and electrophysiological recovery within 4-8 weeks. Three cases showed reduced MEP amplitude with normal latency, but in 2 of them the amplitude recovered in 2-8 weeks. Only 2 cases had no response at all time. We think 41 patients (93.7%) had predominant nerve demyelination. The 3 other patients (6.8%) showed axonal degeneration which is within the range found in previous reports of classical Guillain-Barre. We conclude that the acute paralytic syndrome seen in the summer of 1991 in Northern China represents a classical Guillain-Barre syndrome with demyelination of motor and sensory fibers. There is no reason to consider any special nomenclature such as “Chinese paralytic syndrome” or “acute motor axonal neuropathy

Zhang X, et al. Guillain-Barre syndrome in six cities and provinces of northern China: is it a new entity? Chin Med J (Engl). 1995 Oct;108(10):734-8. Review. PMID: 8565657; UI: 96147668
Forty cases of Guillain-Barre Syndrome were reported, (GBS) which came from the regions where “Chinese Paralytic Syndrome” and “Acute Motor Axonal Neuropathy (AMAN)” were presented before. A study on their clinical, electrophysiological and pathological features was conducted, records on 3,733 GBS cases reported in northern China from 1978 to 1992 were reviewed and compared with cases of “acute moter axonal nouropathy”. The results showed that the clinical, electrophysiological and pathological features of GBS in north China are similar to those of typical GBS cases in western countries, though there seemed to be some special epidemiological features in age, seasonal and regional distribution. It was concluded that the GBS in northern China is demyelinating GBS dominantly, not a new entity.
Zhang Z, et al. [Risk factors for Guillain-Barre syndrome in northern China: a case-control study]. Chung Kuo I Hsueh Ko Hsueh Yuan Hsueh Pao. 1995 Aug;17(4):291-5. Chinese. PMID: 8575052; UI: 96147928.
We conducted a case-control study in northern China to estimate possible risk factors for Guillain-Barre Syndrome (GBS). Forty patients were consecutively seen at the PUMC hospital and the Second Hospital of Hebei Medical College between July and September 1991. The diagnosis was established following the NINCDS criteria for GBS. Among 36 patients with measurements of motor evoked potentials, 34 had evidences of demyelination. Eighty controls chosen from spouses or siblings, and neighbors or work/school mates, were matched by sex and age (+/- 3 years). Using the Mantel-Haenszel estimate of the odds ratio, cold rain, overloaded activities, a history of diarrhea, common cold, and exposure to organophosphorus one month before onset, significantly increased, at least six-fold, the risk for development of GBS. Cases and controls did not differ in the number of previous vaccinations. We suggest that a single antigent is less likely of etiological importance in GBS.
alth officials convinced the Chinese to rename the bulk of their polio to Guillaine Barre Syndrome (GBS). A study found that the new disorder (Chinese Paralytic syndrome) and the GBS was really polio (41). After mass vaccination in 1971, reports of polio went down but GBS increased about 10 fold.(Ref: Vaccination by Greg Beattie)

Tang XF, et al. Guillain-Barre syndrome or “new” Chinese paralytic syndrome in northern China? Electroencephalogr Clin Neurophysiol. 1996 Apr;101(2):105-9. PMID: 8647015; UI: 96245462.
A serial study of clinical and magnetic stimulation motor evoked potentials (MEP) was accomplished in 44 patients with the acute flaccid paralytic syndrome which occurred in Northern China in 1991. Control data were provided by 70 healthy subjects from the same area. The cases came from the same area where a so-called new “Chinese paralytic syndrome” had been reported. We found the clinical features of these 44 patients to be similar to those of classical Guillain-Barre. Prolongation of MEP latency at 2 sites or on 2 occasions was found in 36 patients of whom 26 showed obvious clinical and electrophysiological recovery within 4-8 weeks. Three cases showed reduced MEP amplitude with normal latency, but in 2 of them the amplitude recovered in 2-8 weeks. Only 2 cases had no response at all time. We think 41 patients (93.7%) had predominant nerve demyelination. The 3 other patients (6.8%) showed axonal degeneration which is within the range found in previous reports of classical Guillain-Barre. We conclude that the acute paralytic syndrome seen in the summer of 1991 in Northern China represents a classical Guillain-Barre syndrome with demyelination of motor and sensory fibers. There is no reason to consider any special nomenclature such as “Chinese paralytic syndrome” or “acute motor axonal neuropathy

Zhang X, et al. Guillain-Barre syndrome in six cities and provinces of northern China: is it a new entity? Chin Med J (Engl). 1995 Oct;108(10):734-8. Review. PMID: 8565657; UI: 96147668
Forty cases of Guillain-Barre Syndrome were reported, (GBS) which came from the regions where “Chinese Paralytic Syndrome” and “Acute Motor Axonal Neuropathy (AMAN)” were presented before. A study on their clinical, electrophysiological and pathological features was conducted, records on 3,733 GBS cases reported in northern China from 1978 to 1992 were reviewed and compared with cases of “acute moter axonal nouropathy”. The results showed that the clinical, electrophysiological and pathological features of GBS in north China are similar to those of typical GBS cases in western countries, though there seemed to be some special epidemiological features in age, seasonal and regional distribution. It was concluded that the GBS in northern China is demyelinating GBS dominantly, not a new entity.
Zhang Z, et al. [Risk factors for Guillain-Barre syndrome in northern China: a case-control study]. Chung Kuo I Hsueh Ko Hsueh Yuan Hsueh Pao. 1995 Aug;17(4):291-5. Chinese. PMID: 8575052; UI: 96147928.
We conducted a case-control study in northern China to estimate possible risk factors for Guillain-Barre Syndrome (GBS). Forty patients were consecutively seen at the PUMC hospital and the Second Hospital of Hebei Medical College between July and September 1991. The diagnosis was established following the NINCDS criteria for GBS. Among 36 patients with measurements of motor evoked potentials, 34 had evidences of demyelination. Eighty controls chosen from spouses or siblings, and neighbors or work/school mates, were matched by sex and age (+/- 3 years). Using the Mantel-Haenszel estimate of the odds ratio, cold rain, overloaded activities, a history of diarrhea, common cold, and exposure to organophosphorus one month before onset, significantly increased, at least six-fold, the risk for development of GBS. Cases and controls did not differ in the number of previous vaccinations. We suggest that a single antigent is less likely of etiological importance in GBS.

Doc David,

Thank you so much for that. I think I am correct in assuming you are copying and pasting this, and not typing it all out? Because if you were typing it all, I’m not sure I would know where to hang my head.:o