Parallels Between CFS / CFIDS / M.E and Post-Polio / Post-Viral Fatigue Syndrome

While a retroviral agent makes a great deal of sense as the primary trigger for CFS / CFIDS / M.E., there are other possibilities–and because diagnostic criteria have been so muddled, even when the cause is pinned down, many people with this diagnosis might really have been stricken by something else.

Some researchers have long believed a hit-and-run virus might cause CFS/M.E. At first glance, it is hard to see how a virus that is only briefly in your body can have lasting effects for years or even for the rest of your life. Yet there is precedent! It is simply not a precedent familiar to anyone who has grown up with effective vaccines against polio.

Polio has been thoroughly studied, so it provides a foundation for understanding how a hit-and-run virus can produce symptoms along the lines of those in CFS/M.E. It also provides guidance about what can and cannot be done for such patients. In particular, the graded exercise regimen favored by some clinicians is exactly the opposite of the right course for post-polio patients, and for patients with post-viral fatigue syndrome (PVFS) due to a different infection that caused similar physical damage.

Note: Polio is not the only pathogen that can cause the damage discussed in this lens. It is simply the most widely recognized.

Aside: Not long ago, debate was hot about whether or not XMRV (a novel retrovirus) is the long-sought cause of CFS / CFIDS / M.E. Links to information about XMRV are included toward the end of this lens. As with every other pathogen that has at some point appeared to be the cause of this illness, XMRV turned out not to solve the puzzle. Retroviruses are still high on the research list, partly because the diagnostic criteria make sure any hit-and-run viral involvement is long past detection before tests are run. Take a look a polio to see why a hit-and-run pathogen could be involved in a current medical mystery.

Basis of This Article

This write-up is primarily based on the article “Parallels Between Post-Polio Fatigue and Chronic Fatigue Syndrome: A Common Pathophysiology?” by Richard L. Bruno, Ph.D.1 , Susan J. Creange, Ph.D., and Nancy M. Frick, Lh.D.

I cannot make the article itself available due to copyright considerations. For the article, see American Journal of Medicine, 1998, 105 (3A): 66-73. The article examines parallels between post-polio sequelae and CFS/M.E. in much greater detail than this write-up. Searching online or in libraries for that article or for articles that mention both CFS and polio yields much more information than it used to, but what you find will often be intensely technical, like the primary source for this web page.

This write-up contains medical terms. It also translates a lot of medical jargon into simpler language to give you some grasp of the post-viral fatigue hypothesis, even if you cannot understand all the specifics.

Why It Matters (Hit and Run versus Persistent Virus)

You may be wondering why it matters whether CFS / CFIDS / M.E. is caused by a hit and run virus like polio, or a persistent pathogen such as a retrovirus or a virus in the herpes class.

  • If it’s a hit and run virus, it is only in your body for a limited period of time. After that, you cannot pass it along to someone else. It also isn’t still able to do more harm to you. It only gets one shot at you, and from that point on you are dealing with the aftermath.
  • If it’s a persistent virus, it can attack repeatedly and you could pass it along to someone else. You wouldn’t necessarily pass it along continuously–perhaps only during flareups, like people with better-known persistent viruses such as herpes simplex.

In either case, the virus probably is not able to cause sickness in everyone who catches it. We would all need to know more about the infectious agent before we could know how easily people can give it to each other. Some viruses can spread through as little as kisses or shared drinks–think of mononucleosis (glandular fever) or chicken pox. Others need blood exposure–think of HIV. Those examples are persistent viruses that stay in the body for the rest of the patient’s life even though the patient may no longer be ill.

The USA Centers for Disease Control declared years ago that CFS patients must not donate blood or organs to other people. The CDC diverted to other purposes money earmarked by Congress for CFS research and attacked researchers who published studies that pointed to an infectious agent, but nobody wants to repeat the mistake made when HIV got into the blood supply.

Since XMRV findings were published, in 2010 the UK NHS began to recommend that M.E. patients should not donate blood. It’s only a recommendation, and the announcement said this is out of concern that the blood donation might make the M.E. patient sicker. But if you have been diagnosed with CFS / CFIDS or M.E., it’s probably safest not to donate blood and not to register as an organ donor.

If it turns out that CFS / M.E. / CFIDS does not involve a persistent virus, these recommendations will have erred on the side of caution. There is no need to panic–everybody would be sick if the culprit were highly contagious and caused illness in everyone who caught it.


Before polio vaccines came along, research focused mostly on damage polio causes to spinal motor neurons. These are central nervous system cells that operate muscles.

However, postmortem investigations over half a century ago consistently found additional polio lesions in specific areas of the brain. Even mild cases damaged the brain stem and heavily laced the midbrain with lesions. Other areas damaged or destroyed included:

  • basal ganglia
  • hypothalamus
  • thalamus and caudate nuclei
  • putamen
  • globus pallidus
  • periaquiductal gray matter
  • locus ceruleus
  • median raphe nuclei and especially the substantia nigra

To translate that into somewhat less technical language, polio damages portions of the brain responsible for cortical activation, the reticular activating system (RAS), and various functions managed by the hypothalmic-pituitary-adrenal (HPA) axis.

  • RAS is important for regulating wakefulness and sleep. Acute damage to RAS in polio patients causes drowsiness, lethargy, prolonged somnolence, rousable stupor, and even coma.
  • The HPA axis is involved in managing the immune system, memory and emotion, among other things. It’s a pivotal control center.
  • Basal ganglia help maintain cortical activation. They are believed to be the gateway for sensory input to the thalamus. Lesions in the basal ganglia interfere with the ability to maintain targeted attention (the ability to concentrate).
  • Lesions in the putamen cause insensitivity to visual stimuli (even when it is major) and difficulty transferring attention from one focus to another.

Unsurprisingly, “mental changes” were noticed in polio patients with such damage. One researcher found that in a high proportion of children who recovered from polio in terms of motor disability, for months after the acute motor effects eased up, mental difficulties such as fatigue and “fleeting attention” remained. Another researcher found disorientation, apathy, sleep disorders, irritability and other such changes in about one third of a group of polio patients, some of whom had non-paralytic forms of polio.

At an extremely detailed level, there are notable differences between the symptoms of CFS/M.E. and polio. At a broad level, though, the symptoms overlap remarkably.

“Summer Flu” Was Really Polio

Polio loves to go from one person to another by way of water. Without air conditioning, a dip in the community swimming pool was a great way to cool off in the summer… and a great way for a water-borne disease to spread. Paralytic polio is not the only illness people can get that way.

If you were born before polio vaccines, you might remember “summer flu.” If you are young enough not to personally know anyone who came down with it, you may have heard parents or grandparents talk about it.

About a decade before he invented the polio vaccine that is named for him, Albert Sabin became intrigued by an outbreak of “Summer Grippe” in Cincinnati. Similar outbreaks were called “summer flu” in Los Angeles, “Iceland Disease” in that country, and so on.

Over about twenty years starting in 1934, more than a dozen outbreaks were documented. Nine occurred immediately after polio outbreaks, and some involved hospital staff who tended polio patients. This was a flu-like illness that swept through entire cities or regions as an epidemic in summer, which is low season for flu but high season for polio. Symptoms included headache, low grade fever, stomach pain, nausea, sore throat, generalized aching… and occasionally stiff neck, a hallmark of polio.

Before polio vaccines, a flu-like illness with stiff neck required immediate hospitalization and a workup to determine whether it was paralytic polio. Patients afflicted with “summer flu” had numbness or paresthesia (a sense of prickling, tingling, or something crawling on the skin even though there is no objective reason for the feeling), but seldom respiratory involvement or paralysis or muscle atrophy. Cerebrospinal fluid (CSF) protein was usually normal. Polio virus was not found. There were hardly any fatalities.

Unlike patients recovering from paralytic polio, these patients took anywhere from months to years for recovery from the acute illness. They had profound fatigue that was aggravated by exercise or emotional stress. They also had difficulty concentrating, a tremendous need for sleep, decreased ability to learn, problems with short term memory, and other signs of cognitive impairment. They showed slowing of the electroencephalogram (EEG) with emergence of theta activity, like polio patients.

When “summer flu” outbreaks were first noticed, doctors misdiagnosed many polio cases as summer flu because they did not realize polio could present with anything milder than at least partial paralysis. Eventually, after years of epidemics of polio and summer flu, someone noticed that regions which had an epidemic of summer flu were almost untouched when an epidemic of paralytic polio later ravaged the areas around them. It became clear that the summer flu epidemics were being caused by a different form of polio virus.

The vast majority of people who acquire the polio virus get no symptoms or serious aftereffects. A small percentage (on the order of 5%) get sick. The illness can range from so-called summer flu to non-paralytic polio (also called aseptic meningitis) to paralytic polio. This pattern is important to remember when looking for the involvement of infectious agents in other disorders such as CFS/M.E. An agent that causes devastating consequences for some people can have little or no effect on the vast majority of people.

Three Types of Polio Virus

There are three types of polio virus. One is inclined to cause paralytic cases. Another is much easier to catch, causes “summer flu” symptoms at a much milder level than paralytic polio, and leaves the patient immune to the paralytic type. The third type is between those extremes and not often mentioned.

When vaccines began to be made, the type that causes summer flu turned out to make itself dominant in the vaccines. David Bodian, a Johns Hopkins pathologist, is credited with discovering that damage to neurons in the brain stem and the anterior (front) horn of the spinal cord is the calling card for polio viruses. He also found that to get distinct paralytic polio symptoms, the proportion of motor neurons that have to die is stunningly high. As many as 60% of spinal cord motor neurons must be killed by polio for muscle weakness to occur, and even more for paralysis, on the order of 70%.

In other words, the human body can continue living, breathing and even moving after astounding amounts of injury in those critical areas.

That does not mean people can take major injury there and still function with complete normalcy. Non-paralytic polio is not harmless. Like the more dramatic Type I that causes paralytic cases, polio Types II and III leave permanent damage in the same portions of the central nervous system (CNS). Non-paralytic polio simply does not leave as much damage as paralytic polio.

Any form of polio leaves a patient with fewer “spare parts” in the CNS. As time goes on, some neurons that survived the initial viral assault fail or die, either due to aging or as a delayed result of the damage inflicted during active infection. The neurons that remain have to do more work than neurons in the same area for an unafflicted person because there are fewer neurons to share the load. One researcher’s studies indicated the load on a post-polio patient’s remaining neurons in the most heavily damaged areas can be as much as sixteen times greater than the load on comparable neurons in a healthy person.

Some neurons that survive the initial illness rebound temporarily, then die under this abnormally heavy stress. Regardless of which polio virus a person caught, every post-polio patient no longer has as much of a safety margin for neuron loss as a person who never had any such disease. Each additional neuron lost has more impact because it is a larger portion of what the person has available. Each patient’s exact symptoms and severity depend upon how many neurons have been lost, and exactly where. As with other diseases that damage the CNS, such as multiple sclerosis, the exact mix of symptoms and the severity are highly individual and tend to vary for each patient across a personal range. However, there is often a general pattern:

  • Steeply downhill, perhaps devastatingly so, with the initial illness.
  • Gradual recovery to a greatly improved functional level which may, in some cases, appear to be fully normal. The patient then tends to plunge into activities that were curtailed during the initial illness.
  • As weakened neurons succumb under strenuous usage, the patient goes downhill again. This frequently does not go as far as the depths of the initial illness, but subsequent rebounds are not to the height of the earlier recovery.
  • From this point on, short to medium term ups and downs occur, but the long term overall trend is gradual loss of functionality.

Some doctors express the rule for these patients as “use it to lose it.” The more a patient pushes to do as much physical activity as possible, the sooner additional neurons will be overstressed and die, and the more additional function will be permanently lost.

Doctors accustomed to treating post-polio patients know this, but the advent of widespread vaccination has made those doctors a vanishing breed.

In the USA, the National Institutes of Health and the U.S. Public Health Service found that new symptoms (fatigue, muscle weakness and pain) occur in 25% to 40% of non-paralytic polio survivors, compared to 66% of paralytic polio survivors. Patients with post-polio sequelae (PPS) emphatically distinguish between increased muscle weakness, which gets the most attention from scientists, and what they call “brain fatigue” which includes greater difficulty with cognition and concentration. Motor control problems tend to draw more attention when anyone says the word “polio,” but “brain fog” is a significant issue too.

Hit and Run Viruses Other Than Polio

A high level resemblance between CFS/M.E. and post-polio sequelae is obvious. The comparison leads some researchers to believe that CFS/M.E. may be the long term consequence of a relatively brief infection by an unknown virus that causes CNS damage similar to that inflicted by non-paralytic polio.

The culprit need not be polio itself, a disease now rare in developed countries due to widespread vaccination. (Coxsackie is implicated in at least some cases of M.E. by scientists in the UK.) Polio is far from the only virus with a fondness for damaging its favorite portions of the central nervous system. Encephalitide viruses known to be able to cause lesions in the reticular formation, putamen, thalamus, hypothalamus and white matter include:

  • Australian X
  • Coxsackie B1-6
  • Equine
  • Enterovirus 71
  • Japanese B
  • St. Louis encephalitis

Symptoms of the above viruses include significantly impaired cortical activation and fatigue. Some viruses capable of causing damage similar to polio can be clinically indistinguishable from (non-paralytic) polio. These include:

  • Central European
  • Encephalomyelitis
  • Coxsackie A9
  • Coxsackie B1-6
  • Echoviruses
  • Enteroviruses 70 and 71

Even worse, Coxsackie A7 virus can produce a paralytic syndrome so much like paralytic polio that this virus is often called Type IV polio. There could be others that have not yet been pegged as capable of similar effects. For example, there are many varieties of Coxsackie and echo viruses, not just the varieties specifically noted.

As with polio, a virus can be capable of causing such severe illness, yet only cause it in some people it infects, not everyone it infects–vulnerability can vary from person to person. Also as with polio, the virus has to be looked for while it is still in the body, if tests are available to detect it. Waiting too long before checking for the virus guarantees failure to find it.

Current diagnostic guidelines for CFS/M.E. involve waiting to see whether symptoms persist for at least six months. That is at least twice as long as the window of opportunity for detecting many of these hit-and-run viruses. The viruses are long gone by the time anyone looks for them.

The treatment commonly cited for post-viral syndromes is reducing physical and emotional stress, using assistive devices, conserving energy, getting adequate rest and pacing activities. If CFS/M.E. is a post-viral syndrome, the ultimate answer to it is likely to be prevention, which implies identification of the responsible virus and development of a vaccine or effective treatment against it.

Final Remarks

Polio has been thoroughly studied for more than half a century. Considerable medical knowledge about it has been available for a long time.

Live virus vaccine is administered orally. Killed virus vaccine is administered via injection. The live virus vaccine is well known to cause polio, albeit usually non-paralytic, in a small fraction of the patients who receive the vaccine. The proportion of vaccine recipients who develop polio varies by batch of the vaccine. Recipients of live vaccine also shed live polio virus into their environment for a while after receiving the vaccine.

Because it is cheaper and easier to administer, live virus vaccine continued to be widely used in developing nations after killed vaccine became available. It is sometimes impractical to store and administer killed virus vaccine properly in locations with poor infrastructure.

As far as I have been able to determine, the UK is the only First World nation that continued to use live virus vaccine for decades after killed vaccine became available. The pattern of illness in young (teens to early twenties) British M.E. patients is often very much like the pattern for non-paralytic polio, and practically the opposite of the pattern of illness in American CFS patients of the same age.

The UK was awarded Polio Free status by the World Health Organization a few years ago while still administering live vaccine. Shortly after WHO announced it was considering a worldwide polio eradication program, NHS announced it would switch to killed vaccine.


I am not a medical professional. Years ago I was a volunteer sysop in an online forum for people with chronic illnesses. The forum was so highly regarded that some doctors sent patients to it to learn how to live with their illnesses. I did a fair amount of translating from medical jargon into something more understandable for the benefit of the forum’s members.

Several additional articles have been published since the one I used for the core of the information in this lens. Because polio has been so well studied for such a long time, the basic concepts in this lens have not changed. If you need a detailed understanding of this topic, please consult the original medical literature. I’m no substitute for that!

References Cited by Main Article

The article I used as the basis for this web page cites a long list of references. Click here to see the references on a separate page.

Books for Post-Polio Patients

The Polio Paradox: What You Need to Know
You may have heard the phrase use it or lose it to inspire people to exercise. For post-polio patients, it's more accurate to say use it to lose it. The goal is not to push yourself to do more than yesterday. Instead it's better to find out what works for you and what doesn't.

Post-Polio Syndrome: A Guide for Polio Survivors and Their Families
Life after polio is a balancing act, doing only as much as the body can handle so you can enjoy whatever you do. Some other chronic illnesses have a similar effect on day to day life.

Living with Polio: The Epidemic and Its Survivors
No medical text can match the voices of people who have dealt with a disease themselves. Doctors and scientists can tell you what's happening in clinical terms. Patients can tell you about living with it. That’s what this book is–it draws from the personal stories of more than a hundred patients.

In the Shadow of Polio: A Personal and Social History
You might think being one step removed from a first person patient account must be less powerful, but in this case it is so potent you might not be able to put the book down. Polio vaccine came along in time for me not to remember the terror wrought by the disease. Kathryn Black writes about her mother's polio and interweaves that with what was happening in research and medicine. It's a compelling read.