Myalgic Encephalomyelitis, Chronic Fatigue Syndrome and Post-Polio Syndrome

Polio By Any Other Name?

Knowing that there have been comparatively mild poliovirus outbreaks that damaged the brain and sometimes the spinal cord without causing paralysis or even weakness may dispose of some long-standing Polio Fictions, explain new findings about post-polio syndrome, and solve a mystery that’s nearly sixty years old.

One Polio Fiction has already been banished: We know that “non-paralytic” polio is a misnomer. David Bodian showed in 1949, and Alan McComas confirmed in 1997, that paralytic and “non-paralytic” polio are not separate conditions but a single disease whose obvious symptoms are determined by the location and number of neurons killed by the poliovirus.

Bodian even found that more brain stem neurons can be damaged, and damaged more extensively, in “non-paralytic” than in paralytic polio. As a matter of fact, the location of damaged brain neurons Bodian found in “non-paralytic” polio was the same as in monkeys injected with body fluids from Sabin’s Summer Grippe patients. What’s more, some people with “non-paralytic” polio have damage only in the brain stem and not in the spinal cord.

The finding that damage to the brain-activating system may be the only damage after poliovirus infection could explain why fatigue is reported more frequently than muscle weakness in both paralytic and “non-paralytic” polio survivors, as well as our Surveys’ finding of no relationship between the severity of post-polio fatigue and the number of limbs originally paralyzed or the severity of the polio attack, as indicated by whether polio survivors had been hospitalized or the length of their hospital stay.

What’s more, a mystery dating from 1934 may finally be solved by understanding the brain-altering effects of even a “mild” poliovirus.

In 1934 an illness resembling Iceland disease struck 150 doctors and nurses who were caring for polio patients at the Los Angeles General Hospital. Since 1934 there have been more than three dozen outbreaks of a similar illness that was at first diagnosed as “poliomyelitis,” then as “abortive” or “atypical poliomyelitis,” and finally named “myalgic encephalomyelitis (also known as enteroviral encephalomyelitis),” meaning muscle pain with inflammation of the brain and spinal cord.

Myalgic encephalomyelitis (also known as enteroviral encephalomyelitis), or M.E., was coined by British infectious disease specialist Melvin Ramsay when three hundred staff members of London’s Royal Free Hospital became ill in 1955 with symptoms identical to those seen in Los Angeles twenty-one years earlier.

As with polio, the initial M.E. (also known as enteroviral encephalomyelitis) symptoms included headache, neck pain, low-grade fever, and muscle pain, often followed by weakness. M.E. (also known as enteroviral encephalomyelitis) patients were irritable and anxious, overwhelmingly sleepy, and had brain wave slowing and “conspicuous changes in their levels of concentration” that persisted for months after the acute illness, signs and symptoms common among children who had recovered from polio.

But unlike polio, paralysis was very rare, there were frequent reports of numbness or tingling, and there were hardly any breathing problems - and almost invariably no deaths. Also unlike polio, some of the acute symptoms of M.E. (also known as enteroviral encephalomyelitis) remained for years.

Many patients continued to have “exhaustion and fatigability” that were “always made worse by exercise and emotional stress,” and had persistent poor concentration, word-finding difficulty, and “an inordinate desire to sleep.”

Some M.E. (also known as enteroviral encephalomyelitis) patients reported exhaustion, that they were “not as quick or incisive in thought” as before their illness, “a decreased ability to learn, and a decline in their short-term memory” that lasted for decades.

Some patients from the 1934 Los Angeles outbreak never recovered.

Despite the differences between polio and M.E. (also known as enteroviral encephalomyelitis), an association with the poliovirus was suggested by the fact that of more than a dozen M.E. (also known as enteroviral encephalomyelitis) outbreaks before the introduction of the polio vaccine in 1954, nine occurred during or immediately after outbreaks of polio, and several involved hospital staff who cared for polio patients.

MORE UNRECOGNIZED EPIDEMICS

Could it be that, as in Cincinnati and in Iceland, a “mild” “non-paralytic” poliovirus was responsible for M.E. (also known as enteroviral encephalomyelitis) outbreaks? Perhaps. But we’ll never know.

The few times it was looked for, poliovirus was not found in M.E. (also known as enteroviral encephalomyelitis) patients. And once the polio vaccine had been distributed, none of the polioviruses could have caused M.E. (also known as enteroviral encephalomyelitis) in anyone who had been vaccinated.

But something unexpected, frightening, and totally unrecognized happened after the polio vaccine was distributed: The number of M.E. (also known as enteroviral encephalomyelitis) cases went through the roof.

In 1972 Ramsay was joined by another British infectious disease specialist, Elizabeth Dowsett, who inherited all of Ramsay’s patients and their records upon his death in 1990.

In 1998 Dowsett, founder of the CFS Diagnostic and Management Service in Essex, England, reviewed the twenty-five hundred M.E. (also known as enteroviral encephalomyelitis) patients she or Ramsay had seen since 1919, and plotted the cases of M.E. (also known as enteroviral encephalomyelitis) against reported cases of polio.

When the Salk and then Sabin vaccines brought the yearly number of British polio cases below twenty-five in the early 1960s, the number of M.E. (also known as enteroviral encephalomyelitis) patients took off.

In Ramsay’s and Dowsett’s practice alone, between 1960 and 1980 the number of M.E. (also known as enteroviral encephalomyelitis) patients increased fiftyfold.

Between 1980 and 1990, the number of patients with M.E. (also known as enteroviral encephalomyelitis) increased yet again by a factor of fifty!

Throughout the world, thirty-two M.E. (also known as enteroviral encephalomyelitis) outbreaks were recorded after the polio vaccine was distributed.

Something other than the poliovirus was causing M.E. (also known as enteroviral encephalomyelitis).

Post-Polio Syndrome, Chronic Fatigue Syndrome and Myalgic Encephalomyelitis Parallels

But while British M.E. (also known as enteroviral encephalomyelitis) cases skyrocketed unnoticed during the 1980s, a “new” disease discovered in the United States got lots of attention. Residents of Nevada reported strange symptoms - fatigue, difficulty concentrating, and aching muscles - that were called “Chronic Fatigue Syndrome.”

At first CFS (also known as enteroviral encephalitis) was dismissively nicknamed “yuppie flu.” CFS (also known as enteroviral encephalitis) was said to be a psychosomatic disorder, a form of emotional exhaustion or depression, that was thought to give overworked, affluent, upwardly mobile twentysomethings an acceptable way out of their superstressed work lives.

But research since 1984 has compiled more and more evidence that CFS (also known as enteroviral encephalitis) and M.E. (also known as enteroviral encephalomyelitis) are physical, not emotional, illnesses.

What’s more, our studies and Surveys, combined with those of other researchers, have found remarkable similarities between the signs and symptoms of post-polio brain fatigue, CFS (also known as enteroviral encephalitis), and M.E. (also known as enteroviral encephalomyelitis):

• Polio survivors and CFS (also known as enteroviral encephalitis) and M.E. (also known as enteroviral encephalomyelitis) patients report disabling fatigue that is triggered or made worse by physical exertion and emotional stress.

• Polio survivors and CFS (also known as enteroviral encephalitis) patients both have “overactive” lifestyles. As with polio survivors, CFS (also known as enteroviral encephalitis) patients are worriers who have very stressful, overextended, overcommitted lives that leave them straining for achievement, perfection, and constantly feeling pressured for time. Also like polio survivors, CFS (also known as enteroviral encephalitis) patients feel they “have to do everything” and try to make other people happy—to the point of neglecting or even harming themselves—and have great difficulty disappointing people by saying no.

• Nearly half of polio survivors and CFS (also known as enteroviral encephalitis) patients have sleep apnea or hypopneas.

• Polio survivors and CFS (also known as enteroviral encephalitis) patients have belly problems, including decreased contraction of the intestines.

• In polio survivors and CFS (also known as enteroviral encephalitis) patients there is a relationship between fainting and fatigue. In both groups purple feet indicate that blood pools in the leg veins, and there is evidence of damage to the nerves that control skin blood vessels.

• Polio survivors with fatigue and CFS (also known as enteroviral encephalitis) and M.E. (also known as enteroviral encephalomyelitis) patients report difficulty with attention, word finding, thinking quickly, and memory. On neuropsychologic testing, attention and word finding are abnormal and thinking ability is slowed in fatigued polio survivors and CFS (also known as enteroviral encephalitis) patients. Despite these difficulties, both groups of patients have high-normal or above-normal IQs and have no impairments of memory or thinking. Both groups have been found to have more years of education and are more likely to be professionals than the general population.

• Up to 85 percent of patients with CFS (also known as enteroviral encephalitis) have brain wave slowing similar to that seen immediately after polio and which we have found in fatigued polio survivors.

• White spots were found on MRI in the brain’s myelinated neurons in fatigued polio survivors and in CFS (also known as enteroviral encephalitis) patients. These white spots are similar to but smaller than those in the brains of multiple sclerosis patients, who also can have severe fatigue and difficulty focusing attention.

• White spots were found on MRIs in the gray neurons of the brain-activating system in polio survivors with fatigue and in one study of CFS (also known as enteroviral encephalitis) patients. The SPECT scanner, a newer brain-imaging device that has not yet been used to study polio survivors, has found decreased activity of brain stem neurons in two studies of CFS (also known as enteroviral encephalitis) patients.

• Fatigued polio survivors and CFS (also known as enteroviral encephalitis) patients release less of the brain-activating hormone ACTH.

• More prolactin is released in fatigued polio survivors and CFS (also known as enteroviral encephalitis) patients, suggesting that less of the brain-activating neurochemical dopamine is being produced in both groups. U.S. veterans diagnosed with Gulf War syndrome, who report symptoms similar to those in polio survivors with brain fatigue and CFS (also known as enteroviral encephalitis) patients, were found to have less brain dopamine in the basal ganglia and abnormalities of brain stem neurons that are part of the brain-activating system.

• Growth hormone is lower in polio survivors with new muscle weakness and in CFS (also known as enteroviral encephalitis) patients. Since growth hormone release is stimulated by dopamine, it’s possible that damage to brain dopamine neurons causes lower growth hormone levels in polio survivors and CFS (also known as enteroviral encephalitis) patients. Since there was no improvement when growth hormone was given to polio survivors or CFS (also known as enteroviral encephalitis) patients, lower growth hormone levels are most likely the result of damage to the brain and not the direct cause of fatigue or muscle weakness.

DOES THE POLIOVIRUS CAUSE "CHRONIC FATIGUE SYNDROME" (ALSO KNOWN AS ENTEROVIRAL ENCEPHALITIS)?

The striking parallels between the signs, symptoms, and studies of post-polio fatigue, M.E. (also known as enteroviral encephalomyelitis), and CFS (also known as enteroviral encephalitis) caused us to propose the Brain Fatigue Generator model of post-viral fatigue syndromes.

The Brain Fatigue Generator model says that it’s normal for neurons in the brain stem and basal ganglia to become “tired” during the course of the day. This tiredness decreases brain activation and produces typical feelings of fatigue: difficulty paying attention, not wanting to get out of a chair, and the overwhelming desire to just slip between the sheets and go to sleep.

After a good night’s sleep in those who don’t have post-polio syndrome or CFS (also known as enteroviral encephalitis) and M.E. (also known as enteroviral encephalomyelitis), brain-activating system neurons are refreshed, and fatigue disappears. However, in post-polio syndrome, M.E. (also known as enteroviral encephalomyelitis) and CFS (also known as enteroviral encephalitis) patients, fatigue is not relieved by sleep, because brain-activating neurons were damaged and are never refreshed.

The symptoms of fatigue - in both polio survivors and CFS (also known as enteroviral encephalitis) and M.E. (also known as enteroviral encephalomyelitis) patients - result from a virus damaging brain-activating neurons.

The CFS (also known as enteroviral encephalitis) research community was excited by the Brain Fatigue Generator model because it explained post-polio fatigue for which there is a complete chain of evidence: We know which virus damaged brain-activating neurons, and we have MRI, EEG, hormonal - even autopsy evidence - of that damage, which is related to the signs and symptoms of fatigue.

In 1995 we were asked to present the BFG model at the First World Congress on Chronic Fatigue Syndrome in Brussels, on which CFS (also known as enteroviral encephalitis) specialist David Bell commented in The CFIDS Chronicle:

What seems extraordinary is the similarity of theresidual deficits caused by poliovirus and the clinical symptoms present in chronic fatigue syndrome. The similarities are tantalizing. For years we have been looking for an anatomic model of chronic fatigue, particularly post-infectious fatigue. It is possible that the post-polio syndrome is an example of CFS (also known as enteroviral encephalitis) caused by a specific infectious agent? The work by Dr. Bruno and co-workers may become immensely important not only to the many persons who suffered polio but to those with CFS (also known as enteroviral encephalitis) as well.

Given the “tantalizing” similarities, could CFS (also known as enteroviral encephalitis) and M.E. (also known as enteroviral encephalomyelitis) be caused today by a “mild” poliovirus infection? Absolutely not.

As we discussed, anyone vaccinated against polio would be immune to all polioviruses, including those that caused the Summer Grippe, Iceland disease, and that might have been responsible for M.E. (also known as enteroviral encephalomyelitis) in the years before the vaccine.

But there may very well be a link between polio, the skyrocketing of M.E. (also known as enteroviral encephalomyelitis) cases in Britain, and the appearance of CFS (also known as enteroviral encephalitis) in the United States. It may be that the vaccine that eliminated polio had an unintended consequence.

The elimination of poliovirus left a vacuum that had to be filled. It was the blue jays versus the robins again. But this time the blue jays were all three polioviruses and the robins were other members of the enterovirus family to which polioviruses belong.

Apparently all three polioviruses had been blue jays, dominant over the other enteroviruses in their ability to multiply in the intestines. With poliovirus disappearing in vaccinated countries, other enteroviruses took over the polioviruses’ intestinal breeding ground and filled the vacuum.

With polioviruses gone, other enteroviruses were able to multiply, spill into the bloodstream, and enter the brain.

In 1990 Elizabeth Dowsett looked for antibodies to nonpolio enteroviruses in her M.E. (also known as enteroviral encephalomyelitis) patients. Fifty percent had antibodies to the first nonpolio enterovirus ever discovered, the Coxsackie B virus, named for Coxsackie, New York, the town where it was found to have paralyzed children in 1948.

Yes, paralyzed. It isn’t just the polioviruses that enter and kill neurons in the spinal cord and brain-activating system. Neuron damage, weakness, paralysis, and symptoms of brain fatigue caused by enteroviruses can be so similar to that caused by polioviruses as to be indistinguishable.

One Coxsackie virus, named A7, produces paralytic symptoms so similar to polio that it has been named poliovirus Type IV.

Other nonpolio enteroviruses that cause damage and symptoms similar to the polioviruses include all the other Coxsackie viruses, the ECHO viruses (which in 1956 were the first viruses associated with an M.E. (also known as enteroviral encephalomyelitis) outbreak), enterovirus 71, and viruses that cause illnesses that evoke some faraway places with strange-sounding names: central European encephalomyelitis, Australian X, Japanese B, and St. Louis encephalitis.

The only direct evidence linking an enterovirus, damage to the brain-activating system, and CFS (also known as enteroviral encephalitis) came in 1994.

A thirty-two-year-old woman who had had CFS (also known as enteroviral encephalitis) for five years took her own life. 

Her autopsy revealed Coxsackie B virus - the same virus for which Dowsett found antibodies in her patients - in both the hypothalamus and brainstem, the very heart of the brain-activating system.

Remembrance of Children Past

On the way back from the 1995 CFS (also known as enteroviral encephalitis) conference in Brussels, we stopped in London and met Elizabeth Dowsett for the first time. She described her experience with M.E. (also known as enteroviral encephalomyelitis), not only in adults but also in children.

Despite my knowing about the Summer Grippe and Iceland disease, it had never occurred to me that children were getting M.E. (also known as enteroviral encephalomyelitis) today.

Dowsett’s experience with children echoed a familiar and disturbing past.

In 1988 Dowsett studied an outbreak of what she calls “Summer Flu” in British grade school students in East Anglia. A quarter of the children in the school district had the flu that summer, and about 10 percent remained ill when school began in the fall.

The children reported “profound fatigue and difficulty with memory, attention and were falling asleep during the day” - symptoms that had not improved when children were contacted two years later.

Because of this outbreak of what she thought was M.E. (also known as enteroviral encephalomyelitis), Dowsett decided to study a much larger group of schoolchildren to see just how common chronic fatigue was in children after they’d had what appeared to be the flu.

In 1995 she sent questionnaires to nearly three thousand British schools and surveyed 330,000 children. She found that nearly 10 percent had had an illness that looked like M.E. (also known as enteroviral encephalomyelitis).

Half were unable to go to school and had to be tutored at home; the rest required modified class schedules because of difficulty with focusing attention, thinking clearly, word finding, and staying awake during the day.

These symptoms reminded us of the students with Iceland disease and Edith Meyer’s description of kids who returned to school after having had polio, whom she found to have “fatigability and fleeting attention.”

The parallels between Elizabeth Dowsett’s findings in children with chronic fatigue, young people with Iceland disease, and polio survivors were too great to be ignored.

When we returned to the United States, I applied to the CFIDS Association of America and received a grant to perform the first study of brain functioning in young people with CFS (also known as enteroviral encephalitis).

We studied a baker’s dozen subjects who met the 1994 Centers for Disease Control criteria for CFS (also known as enteroviral encephalitis), were on average sixteen years old, and had no psychological diagnoses. We compared these CFS (also known as enteroviral encephalitis) kids to ten nonfatigued young people.

We found that the more fatigue CFS (also known as enteroviral encephalitis) kids reported, the more difficulty they had staying awake during the day, concentrating, and focusing attention.

We administered all the tests of attention, concentration, thinking, and memory that we have used since 1992 to study fatigue in polio survivors.

As we have found in adult polio survivors with fatigue, as others have found in adults with CFS (also known as enteroviral encephalitis), and as Edith Meyer found in young people who had polio, attention test scores were either abnormal or significantly lower in the fatigued kids than in those without CFS (also known as enteroviral encephalitis).

With this study the circle had been completed.

Individuals with chronic fatigue - be they adults or young people, polio survivors, those with CFS (also known as enteroviral encephalitis) or M.E. (also known as enteroviral encephalomyelitis) - share an inability to stay awake during the day, to concentrate, and to focus attention.

We think the simplest explanation for these findings is the Brain Fatigue Generator model: that various viruses damage the brain-activating system, damage that causes the signs and symptoms of chronic fatigue.

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Post-Polio-Like Syndrome Following Non-Polio Enteroviral Neurological Disease

Delayed Neurological Deterioration and Recurrence of Earlier Symptoms Following:

Myalgic Encephalomyelitis (M.E.) • Enteroviral Rhombencephalitis • Enteroviral Encephalomyelitis / Meningoencephalomyelitis • Enteroviral Poliomyelitis-Like Syndrome

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A post-polio-like neurological syndrome may occur years or decades after previous non-polio enteroviral motor neurone injury, with recurrence or progression of earlier neurological symptoms. This possibility has been described in case literature, although it is less well established than classical post-polio syndrome.

Dr Betty Dowsett (2001) also described late neurological deterioration in patients she diagnosed with M.E., including individuals who had remained clinically stable for 40 years or more. She identified striking clinical similarities with post-polio syndrome.

Neurological, Neuromuscular, Bulbar, Respiratory, Autonomic and Musculoskeletal Symptoms

1. Recurrent muscle weakness: Recurrence or progression of previously experienced muscle weakness.

2. Abnormal muscle fatigability: Rapid muscular exhaustion and reduced endurance.

3. Asymmetric weakness and muscle atrophy: Unequal limb weakness, muscle wasting and loss of motor function.

4. Muscle pain, cramps and fasciculations: Myalgia, painful spasms and involuntary muscle twitching.

5. Delayed neurological deterioration: New or worsening symptoms after years or decades of relative stability.

6. Reduced or absent reflexes: Hyporeflexia or areflexia associated with lower motor neurone damage.

7. Joint pain and stiffness: Painful joints, reduced mobility and restricted range of movement.

8. Joint instability: Weakness of supporting muscles, potentially causing joint subluxation or dislocation.

9. Joint contractures: Progressive tightening of muscles, tendons and surrounding tissues, restricting joint movement.

10. Degenerative joint complications: Osteoarthritis and accelerated joint wear resulting from altered biomechanics and abnormal loading.

11. Abnormal gait and posture: Walking difficulties, compensatory movements and overuse of less-affected muscles.

12. Spinal and skeletal complications: Scoliosis, postural abnormalities, limb-length discrepancies and chronic back pain.

13. Bulbar dysfunction: Dysphagia, dysarthria, dysphonia, facial weakness and tongue weakness.

14. Respiratory muscle weakness: Reduced respiratory muscle strength, impaired coughing, nocturnal hypoventilation and breathing difficulties.

15. Fatigue and exercise intolerance: Reduced physical capacity and difficulty sustaining activities.

Additional Symptoms and Complications Reported in the Literature

16. Overwhelming physical and mental fatigue: Profound physical exhaustion and mental fatigability, including disproportionate exhaustion following relatively minor activities. Described by Dowsett.

17. Cognitive disturbances: Difficulties with short-term memory, concentration, attention, mental processing and other cognitive functions. Reported by Dowsett and recognised in classical post-polio syndrome.

18. Temperature dysregulation and hypothermia: Episodes of abnormally low body temperature or difficulty maintaining normal temperature regulation. Reported by Dowsett.

19. Cold intolerance: Increased sensitivity to cold temperatures, particularly affecting weakened muscles and limbs. Recognised in classical post-polio syndrome.

20. Low blood pressure and autonomic dysfunction: Episodes of hypotension or abnormal blood pressure regulation. Reported by Dowsett, with autonomic instability also documented during severe enteroviral neurological disease.

21. Sleep disturbances: Disrupted sleep, insomnia, excessive daytime sleepiness and sleep-related breathing problems. Documented in classical post-polio syndrome.

22. Nocturnal breathlessness: Sudden episodes of breathlessness during sleep, potentially associated with respiratory muscle weakness, nocturnal hypoventilation or sleep-disordered breathing. Specifically described by Dowsett.

23. Progressive swallowing difficulties: Worsening dysphagia, choking, difficulty handling food or liquids and increased aspiration risk where bulbar weakness is present.

24. Speech and voice deterioration: Recurrent or worsening dysarthria, reduced vocal strength, altered voice production and difficulties speaking for prolonged periods. Voice-production problems were described by Dowsett.

25. Cranial nerve dysfunction: Facial or eyelid weakness, abnormal eye movements and other cranial motor deficits. These are documented following non-polio enteroviral neurological disease, although delayed recurrence is less well established.

26. Neuropathic pain: Burning, shooting or otherwise neuropathic pain involving affected limbs or other body regions. Chronic neuropathic pain has been reported following acute flaccid myelitis.

27. Bowel and bladder dysfunction: Constipation, altered bowel function, urinary retention or other neurogenic bladder symptoms where the original neurological injury involved relevant pathways. These are documented in acute or persistent neurological disease, but are not established defining features of delayed post-polio-like syndrome.

28. Declining functional mobility and independence: Increasing difficulty walking, climbing stairs, dressing, transferring, lifting objects and undertaking repetitive physical activities. Dowsett described deterioration after long periods of apparently stable functioning.

29. Secondary skeletal and mobility complications: Muscle imbalance, joint deformity, reduced bone loading, osteoporosis or fracture risk, and an increasing need for orthoses, mobility aids or other supportive equipment.

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Important Clinical Distinction

Classical Post-Polio Syndrome (PPS) occurs following poliovirus infection.

Post-Polio-Like Syndrome describes a similar neurological presentation that has been reported following non-polio enteroviral motor neurone injury.

Both may involve overlapping neuromuscular, bulbar, respiratory and musculoskeletal complications, particularly when the original infection affected spinal anterior horn cells or brainstem motor neurones.

Dr Betty Dowsett's Clinical Observations (2001)

In The Late Effects of ME — Can They Be Distinguished from the Post-Polio Syndrome?, Dowsett described patients with late neurological deterioration following decades of clinical stability.

She reported:

• Physical and mental fatigue.
• Cognitive disturbances.
• Muscular and joint pain.
• Muscle weakness and wasting.
• Respiratory difficulties, including nocturnal breathlessness.
• Hypothermia and temperature dysregulation.
• Low blood pressure.
• Swallowing difficulties.
• Voice-production problems.
• Progressive walking difficulties and reduced mobility.

Dowsett considered these findings clinically similar to late post-polio complications and proposed that previous non-polio enteroviral neurological disease could produce comparable late effects.

Her observations are historically significant, but the original infections and the mechanisms of delayed deterioration were not systematically confirmed in all patients.

Evidence From Non-Polio Enterovirus Infections

A 2017 case report by Suzuki and colleagues documented a post-polio-like syndrome developing approximately 35 years after enterovirus 70-associated neurological disease.

The patient experienced renewed progressive limb weakness following a long period of relative neurological stability, with muscle atrophy, reduced reflexes and electrophysiological abnormalities consistent with previous motor neurone injury.

Modern studies of EV-A71 rhombencephalomyelitis and non-polio enterovirus-associated acute flaccid myelitis also document:

• Lasting spinal anterior horn cell and motor neurone injury.
• Persistent asymmetric limb weakness and muscle atrophy.
• Brainstem and cranial nerve dysfunction.
• Bulbar impairment, including dysphagia and facial weakness.
• Respiratory muscle dysfunction.
• Joint instability, contractures and other musculoskeletal complications.
• Long-term neurological disability and reduced functional independence.

However, the delayed syndrome following non-polio enteroviral encephalomyelitis remains insufficiently characterised.

The listed symptoms are recognised across poliomyelitis, post-polio syndrome, Dowsett's clinical observations and non-polio enteroviral neurological disease.

They are not all established features of a distinct delayed non-polio post-polio-like syndrome.

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Recurrence of Earlier Neurological Symptoms

A patient with previous non-polio enteroviral encephalomyelitis may experience renewed or progressive neurological difficulties years after the original infection.

This may resemble classical post-polio syndrome, particularly where the original infection caused damage to spinal anterior horn cells, brainstem motor neurones or associated neuromuscular pathways.

Possible explanations include:

• Delayed deterioration of previously injured motor units.
• Progressive failure of compensatory collateral reinnervation.
• Secondary musculoskeletal complications associated with longstanding muscle weakness.
• Persistent neurological deficits becoming more apparent with ageing.
• Development of another neurological or medical condition.

Following acute motor neurone injury, surviving neurones may compensate by developing additional branches to reinnervate previously denervated muscle fibres.

Although this process can restore a degree of muscular function, these enlarged motor units may become increasingly vulnerable to further deterioration over time.

This mechanism is recognised in classical post-polio syndrome and is biologically plausible following non-polio enteroviral anterior horn cell injury, although it has not been conclusively established as the cause of delayed deterioration in these patients.

Recurrence of earlier symptoms does not necessarily indicate persistent enterovirus, renewed viral replication or reactivation of the original infection.

New or progressive weakness, bulbar impairment, breathing difficulties, cognitive changes or autonomic symptoms require appropriate neurological investigation to establish their cause.

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Relevant Research and Historical Clinical Literature

1. Dowsett, E. G. (2001)

The Late Effects of ME — Can They Be Distinguished from the Post-Polio Syndrome?

Presentation to the All-Party Parliamentary Group, House of Commons, 31 January 2001.

Historical clinical observations describing late neurological deterioration and similarities between M.E. and post-polio syndrome.

2. Suzuki, S., et al. (2017)

Post-Polio-Like Syndrome.

The American Journal of Medicine.

Clinical case report documenting delayed neurological deterioration following non-polio enterovirus 70-associated disease.

3. Jubelt, B., and Drucker, J. (1993)

Post-Polio Syndrome: An Update.

Seminars in Neurology.

Review discussing the neurological mechanisms and clinical presentation of classical post-polio syndrome.

4. Chang et al. (2019)

Enterovirus A71 Neurologic Complications and Long-Term Sequelae.

Journal of Biomedical Science.

Review of EV-A71 neurological disease, including brainstem encephalitis, poliomyelitis-like paralysis, muscle atrophy and long-term complications.

5. Lee et al. (2012)

Extracorporeal Life Support for Critical Enterovirus 71 Rhombencephalomyelitis: Long-Term Neurologic Follow-Up.

Pediatric Neurology.

Long-term follow-up describing persistent neurological, bulbar and respiratory complications after severe EV-A71 rhombencephalomyelitis.

6. Andersen et al. (2017)

Acute Flaccid Myelitis in Childhood: A Retrospective Cohort Study.

European Journal of Neurology.

Study documenting motor neurone injury, spinal grey-matter abnormalities, cranial nerve involvement and persistent weakness following acute flaccid myelitis.

7. Helfferich et al. (2020/2021)

Acute Flaccid Myelitis: Cause, Diagnosis, and Management.

The Lancet.

Review of acute flaccid myelitis and its associated neurological, motor and rehabilitation complications.

8. UK Health Security Agency (2025)

Clinical Management of Acute Flaccid Paralysis or Acute Flaccid Myelitis.

Guidance addressing non-polio enteroviral acute flaccid paralysis, neurological investigation and clinical management.

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Conclusion

A post-polio-like neurological presentation following non-polio enteroviral motor neurone injury is medically plausible and has been described in published case literature.

The recurrence or progression of earlier neurological symptoms may resemble classical post-polio syndrome, particularly when the original illness involved the spinal anterior horn cells, brainstem motor neurones or related neuromuscular structures.

This may include recurrent muscle weakness, abnormal muscle fatigability, muscular atrophy, pain, bulbar impairment, respiratory dysfunction and secondary musculoskeletal complications.

Dr Betty Dowsett's historical observations also highlighted late neurological deterioration after prolonged periods of clinical stability.

However, long-term neurological sequelae are much better established than a distinct syndrome emerging decades after recovery from non-polio enteroviral encephalomyelitis.

Further longitudinal research is required to establish the frequency, clinical characteristics and underlying mechanisms of delayed post-polio-like neurological deterioration following non-polio enteroviral disease.