'ME/CFS' or 'CFS/ME' do not exist!!!! (Part 2)

What is CFS ? (According to Action for M.E. - who are still 'pretending' M.E. is the same as misdiagnosed "CFS" patients, who are different patient cohorts)

'Chronic Fatigue Syndrome' criteria, section (with mention of 'M.E.' from time to time)

The CFS Misdiagnosis Trap - A label without answers. A dead end for patients. 

"CFS" is a chronic, fluctuating disease that effects an estimated 1.35m in the UK, causing symptoms such as Post-Exertional Malaise (PEM), crushing "FATIGUE", brain fog (Cognitive Impairment), and sleep problems (Unrefreshing Sleep).

(This is a discription of the "CFS" (SEID) Algorithm and 'NOT' Myalgic Encephalomyelitis (also known as "Enteroviral Encephalomyelitis" which is closer to 2011 ICC, 1986 & 1988 Ramsay and 2007 & 2016 Nightingale Research Foundation Definitions, which indicates an "acute onset" illness, medical investigation, medical diagnosis, rheumatology, immunology and warranting 'emergency hospitalization' upon onset - Neurological Management: Neuromuscular and Dysautonomia Specialists, Infectious Diseases, and Inpatient Hospital Services)

CFS: the basics

"Chronic Fatigue Syndrome" (ME/CFS), is a chronic, fluctuating disease, causing symptoms such as post-exertional malaise (PEM), sleep problems, problems with thinking and memory (brain fog), pain and crushing "FATIGUE".

The hallmark symptom of CFS (ME/CFS) is post-exertional (PEM) malaise. 

This means that simple physical or mental activities, or combinations of activities, can leave people with CFS (ME/CFS) feeling utterly debilitated. 

They can also experience an increase in other symptoms. 

You may feel the impact of this straightaway, but it typically takes a day or two to kick in and doesn't significantly improve with rest.

While there are key symptoms that must be present for an CFS "misdiagnosis", not everyone with an CFS "misdiagnosis" experiences the same set of symptoms, and the illnesses can vary enormously, including how long symptoms last.

One in four people "misdiagnosed" with "CFS" are so severely affected that they are house or bedbound.

Our resources below give further key information to answer the question 'What is Chronic Fatigue Syndrome ?', with frequent reference to the 2021 NICE guideline to diagnosing and managing "ME/CFS".

Other useful resources include our Learn about ME podcast on the NICE guideline, Introduction to ME/CFS (15 min), part of the "Dialogues for a neglected illness" film project and Post Exertional Malaise (PEM) (3 min) a film by patient, Broken Battery.

(Broken Battery (Adam) promotes "CFS" and "ME/CFS", and a "dead battery" and NOT "M.E." so undoubtly is the WRONG EXAMPLE to use in regards to online videos, in relationship to "M.E." (also known as Enteroviral Encephalomyelitis) and that account holder, seems to have own agenda, disconnected from: 

< Atypical Poliomyelitis >

01. Epidemic "Myalgic Encephalomyelitis" (also known as "Enteroviral Encephalomyelitis") M.E. / Aseptic Meningitis
02. Enteroviral Poliomyelitis-like Syndrome with Flaccid Weakness (Paresis) / Acute Flaccid Paralysis



What causes "CFS" ?

Researchers are still investigating the causes of CFS, but emerging evidence points to multiple contributing factors - especially neurological and immunological ones. These findings also suggest the illness may consist of several distinct types or subgroups.

There is evidence that certain infections, including but not limited to viruses, can trigger the illness.

Severe and very severe M.E.

Severe M.E. has a considerable impact on all aspects of someone's life.

Around one in four people with M.E. can become severely affected by the condition. Many remain confined to their homes or beds, and face significant challenges in accessing appropriate care and support.

98% of respondents with severe M.E., in our 2019 Big Survey, stated they had stopped or reduced social contact, with 95% having stopped or reduced household tasks.

Do people get better from "M.E." ?

It is not clear why some people get M.E. while others recover; some fully and others to a degree.

Sadly the majority of people with M.E. remain ill for decades. A small proportion do recover fully, and others to a degree, however it is not clear why this happens.

This is why Action for M.E. believes we need services to support people living with M.E. now, and high-quality research to find effective treatments.

How many people have "M.E." (also known as Enteroviral Encephalomyelitis) ?

It is difficult to know exactly how many people have M.E. (also known as Enteroviral Encephalomyelitis). The figures vary greatly due to issues such as under-diagnosis and lack of access to diagnosis.

There is also uncertainty about how many people with Long COVID have symptoms associated with CFS criteria. Studies have reported different figures. Some of these studies were small, did not include people from a wide range of backgrounds, used different criterias of CFS, or did not clearly include post-exertional malaise (PEM). 

More research and improvements in diagnosis and recording are needed to fully understand how many people have M.E. (also known as Enteroviral Encephalomyelitis).

We will continue to update our estimates as further research is published and our publications will be updated in due course.

Are "CFS" and Long COVID the same?

"The term long COVID is commonly used to describe signs and symptoms that continue or develop after acute Covid‑19. It includes both ongoing symptomatic Covid‑19 (from 4 to 12 weeks) and Post‑Covid‑19 Syndrome (12 weeks or more)."

A recent systematic review found that over half of long COVID patients met the diagnostic criteria for (CFS) and other studies have identified common biological mechanisms and gene expression patterns.

Researchers must continue investigating the disease mechanisms of long COVID and exploring its similarities with CFS criterias, despite the advances already made.

Action for ME's so called 'Misinformation' and 'Disinformation' resources

What is 'CFS' ?

Read and download our useful resource, 'What is CFS?'.

Download Resource

'Redefined' Post-Exertional Malaise (PEM)

Find out more about 'CFS' criterias hallmark symptom, post-exertional malaise.


'CFS' symptoms

People with 'CFS' often experience a wide range of symptoms. Find out more.


Getting an 'CFS' misdiagnosis

If you're looking for information relating getting a 'CFS' misdiagnosis, this resource is for you.


Severe and very severe M.E.

One in four people with M.E. are severely or very severely affected. Read about how we can help and other support that's available.


Talking to others about 'CFS'

Explaining 'CFS' to others can be difficult. This resource is here to help guide conversations with others about your CFS


'CFS' and Long COVID

Read more about the similarities between CFS and Long COVID.


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Published November 2022

Statement  

Emerge Australia uses the name Chronic Fatigue Syndrome "ME/CFS" as an "umbrella term" to encompass the varied diagnoses for which PEM is the core feature.

Emerge Australia will continue to use this term until the science has definitively concluded whether the illness is one or more separate conditions, and there is consensus on a more appropriate name. 

Research has confirmed that ("M.E.", also known as Enteroviral Encephalomyelitis) is  one condition, and that "CFS" is an umbrella term), for "several" fatigue defined cohorts.

"ME/CFS" includes all diagnoses of Myalgic Encephalomyelitis (M.E.) (also known as Enteroviral Encephalomyelitis), Chronic Fatigue Syndrome (CFS), and "ME/CFS".   

The defining feature of CFS "ME/CFS" is Post-Exertional Malaise (PEM).

Please click here for more information about PEM.  

Background / What is the issue ? 

CFS "ME/CFS" has had many names. These names include Post-viral Fatigue Syndrome, Royal Free Disease, Icelandic Disease, Epidemic Neuromyasthenia (Myalgic Encephalomyelitis, also known as Enteroviral Encephlomyelitis), Systemic Exertion Intolerance Disease (SEID) and, most recently, Long COVID. 

Postviral Fatigue Syndrome, Systemic Exertion Intolerance Disease, are all associated with 'Chronic Fatigue Syndrome' criteria, and are not the same thing as 'Myalgic Encephalomyelitis' also known as 'Enteroviral Encephalomyelitis', which is a 'specific' neurological disease. 

Debate remains as to the most appropriate name. 

This lack of consensus (Official charities have 'intentionally', and 'deliberately ignored', 'suppressed', 'blocked' and 'marginalised' the "M.E." (also known as Enteroviral Encephalomyelitis) community, which is in the Global Advocates for Myalgic Encephalomyelitis (GAME) and The Nightingale Continuum facebook groups about M.E.) and given greater gravitas to the 'misdiagnosed' CFS community over at 'Science for CFS' forum, as it aligns and suits better an 'institutionally captured' agenda) has contributed to confusion and skepticism about CFS "ME/CFS" within the broader community. 

Emerge Australia does not endorse the use of the term ‘Chronic Fatigue’ as this is not an illness. 

"Chronic fatigue" is a symptom of many medical conditions, like cancer or multiple sclerosis. 

"Chronic fatigue" should not be used as a name for CFS "ME/CFS" because it suggests the illness is primarily tiredness. 

People with CFS "ME/CFS" experience a wide range of symptoms. These symptoms include, but are not limited to, "profound fatigue". 

Emerge Australia’s Position 

Emerge Australia uses the name CFS "ME/CFS" as an umbrella term to encompass the varied diagnoses for which PEM is the core feature.

Emerge Australia will continue to use this term until the science has definitively concluded whether the illness is one or more separate conditions, and there is consensus on a more appropriate name.

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Head of ME Association is sacked

2003 Jun 7th; 326(7401):1232.

Owen Dyer

The medical director of Britain's largest charity for people with "Chronic Fatigue Syndrome" has been sacked after he claimed that the organisation has lost its direction and wasted its money.

Dr. Charles Shepherd, for years the leading medical spokesman for British people with the condition, which is also known as Myalgic Encephalomyelitis (M.E.) (also known as Enteroviral Encephalomyelitis), had his contract with the ME Association abruptly terminated for breach of confidence and making statements "likely to bring the MEA into disrepute."

In letters to several websites run by various M.E. groups and patients, Dr. Shepherd said that the association was running out of money and expressed concern that funds earmarked for research in a special account might be used for other purposes. He also said that the resignation of three of its seven trustees had been kept secret and that the trustees had been replaced without input from ordinary members.

Three other members of the charity's scientific and medical advisory committee have since resigned. 

Dr. Shepherd's supporters (they are not his supporters, but are supporters of Melvin Ramsay's original mission statement and paradigm for research into those injured by "Enteroviral Encephalomyelitis") accuse the association of "drifting away" from the purpose of founder members such as Dr. Melvin Ramsay, who first proposed "Myalgic Encephalomyelitis" (also known as Enteroviral Encephalomyelitis) as a "discrete" physiological condition.

< "Instead, they say, the association has come to accept a "blurring of the distinction" between M.E. (also known as Enteroviral Encephalomyelitis) and Chronic Fatigue Syndrome "criteria" and has adopted some of the arguments of that section of the medical establishment that believes the condition to be a somatisation disorder" >

< "As the BMJ went to press, Louie Ramsay, daughter of the late Dr. Melvin Ramsay, announced that she was to resign as a patron of the association with immediate effect. She has also asked that all reference to the Ramsay family name be removed from the Ramsay Research Fund" >

Speaking to the BMJ , Dr. Shepherd said, "I've basically been sacked for blowing the whistle on a financial crisis in which I felt the public interest overrode the terms of my contract."

He said he has communicated his concerns to the Charity Commission, which has asked the association for assurances about the Ramsay Research Fund, an account devoted wholly to research funding.

Dr. Shepherd doubts if it could be protected from creditors if the charity were to become insolvent.

The association's solicitors have threatened legal action against Dr. Shepherd and the websites that published his letters for defamation, but to date none have been withdrawn.

Dr. Nigel Speight, one of the three members of the association's scientific and medical advisory panel who resigned, said in an open letter that Dr. Shepherd "virtually personifies the MEA and has certainly given it a major degree of medical credibility within the profession. For the MEA to now sack him seems a combination of sacrilege combined with a death-wish on the part of the organisation."

Val Hockey, chief executive of the ME Association, said that the current lack of money did not happen "by accident or lack of foresight or somehow overnight" but was due to a national downturn in charitable donations. "There is a possibility that the association may not be a going concern for the next 12 months," she said. The current fundraising appeal, she added, "will be the judge of the organisation's value, if people want the MEA to continue."

She said: "The charity does differentiate between restricted and unrestricted funds in the management accounts, and so far none have been used for anything other than their restricted purpose." 

She said that trustees had not breached the charity's rules by co-opting new board members to fill vacancies.

Denying a change in policy, Ms. Hockey said that many of the charity's members have (mis)diagnoses of "Chronic Fatigue Syndrome", which may or may not be a medical condition distinct from "M.E." (also known as Enteroviral Encephalomyelitis) 


"The MEA provides evidence directed information - not opinion dressed as fact. - from which people can make their own decisions."

Bitter row engulfs ME Association - Third Sector

About the Disease (according to "ME/CFS" Initiative - Solve M.E.)

What is Chronic Fatigue Syndrome "ME/CFS" ?

Chronic fatigue syndrome (ME/CFS) is a chronic, complex, neuroimmune disease that profoundly limits the health and productivity of patients and, like Long COVID, is often triggered by an infection. (e.g. Enterovirus, with the original outbreaks)

At this time, the cause of Chronic Fatigue Syndrome "ME/CFS" is not fully understood. 

There is no diagnostic test, cure, nor FDA-approved treatments or drugs for Chronic Fatigue Syndrome "ME/CFS", and patients often suffer for life.

While Chronic Fatigue Syndrome “ME/CFS” is the preferred name by many, this disease has also formerly been known as Systemic Exertion Intolerance Disease (SEID), Chronic Fatigue and Immune Dysfunction syndrome (CFIDS) (e.g originally associated with an enterovirus), or Post-viral Fatigue Syndrome (PVFS).

Who gets Chronic Fatigue Syndrome "ME/CFS" ?

Everyone is at risk. Chronic Fatigue Syndrome "ME/CFS" may begin as early as age 10 and as late as age 77. It is estimated that between 5 - 9 million Americans suffer from Chronic Fatigue Syndrome "ME/CFS" and estimates vary from 17 - 24 million people with Chronic Fatigue Syndrome "ME/CFS" worldwide. Although research has shown that Chronic Fatigue Syndrome "ME/CFS" is about two to four times more likely to occur in women than men, Chronic Fatigue Syndrome "ME/CFS" strikes people from every age, racial, ethnic, and socioeconomic group.

What are the symptoms of Chronic Fatigue Syndrome "ME/CFS" ? 

Previously "CFIDS" (Chronic Fatigue and Immune Dysfunction Syndrome)

Chronic Fatigue Syndrome "ME/CFS" symptoms, which can often be made worse by standing upright (Orthostatic Intolerance), include:

These symptoms "overlap" Abortive Polio onset symptoms and Enteroviral Meningoencephalitis or Enteroviral Brainstem Encephalitis (which are "acute onset" neurological diseases but these symptoms don't mean a whole lot, without a "specific" confined infectious context) - which would "requiry" emergency inpatient neurological management, and services. 
  • Persistent Fatigue or Exhaustion for (three to six months) or more (Gradual, or Sudden? the latter could be an "Encephalitic" event, which would "require" emergency inpatient hospitalisation) (1994 Fukuda and SEID Symptom)
  • Post-Exertional Malaise (PEM), the worsening of symptoms following even minor physical or mental exertion, with symptoms typically worsening 12 to 48 hours after activity and lasting for days or even weeks (1994 Fukuda and SEID Symptom)
  • Cognitive Impairment (Brain fog - impairment in short-term memory or concentration) (1994 Fukuda and SEID Symptom)
  • Unrefreshing Sleep (Non-restorative sleep)/sleep disturbance (1994 Fukuda and SEID Symptom)
  • Dizziness
  • Headaches (1994 Fukuda Symptom)
  • Sore Throat (1994 Fukuda Symptom)
  • Myalgia (Muscle Pain) (1994 Fukuda Symptom)
  • Arthralgia (Joint pain) (1994 Fukuda Symptom)
  • Lymphadenopathy (Tender Lymph Nodes) (1994 Fukuda Symptom)
  • Neurological abnormalities 
  • Complete organ system shutdown (well this would be severe)
  • Sensitivity to light (Photophobia) (e.g. symptom of "Aspetic Meningitis"), sound (Hyperacusis), chemicals (MCS), foods (e.g. Food Intolerances and MCAS), alcohol and medications
  • Migraines
Other symptoms
  • Abdominal Issues (Nausea, Stomach Pain & Bloating) (e.g. acute enteroviral gastroenteritis, or non-cytolytic chronic infection)
  • Swollen Glands (e.g. coxsackievirus and echovirus)
  • Sinus & Nasal Problems (e.g. enteroviral cold)
  • Chills
If you think you may have Chronic Fatigue Syndrome "ME/CFS", take our quick online quiz.

Because these symptoms are shared with many other illnesses - and because many of these conditions lack a diagnostic test or biomarker - identifying which illnesses are present can be difficult. Some patients receive diagnoses for multiple conditions. 

Common conditions that occur along with Chronic Fatigue Syndrome "ME/CFS" (co-morbidities) include the following:
  • Fibromyalgia
  • Orthostatic intolerance and Dysautonomia
  • Irritable bowel syndrome (IBS) (e.g. Enteroviruses)
  • Interstitial cystitis (e.g. Enteroviruses)
  • Temporomandibular joint disorder (TMJ)
  • Chronic pelvic pain (e.g. Enteroviruses)
  • Multiple chemical sensitivity disorder (MCS)

How is Chronic Fatigue Syndrome "ME/CFS" treated?

There is currently no FDA-approved treatment or drug for Chronic Fatigue Syndrome "ME/CFS". As neither a cause nor cure for Chronic Fatigue Syndrome "ME/CFS" has been identified, treatment is directed at relieving symptoms. 

However, there are interventions and symptom-reduction strategies that you can use to significantly improve patients’ quality of life.

Learn more in our “Patient Resources” section.

Studies show that less than 9-16 percent of Chronic Fatigue Syndrome "ME/CFS" patients in the United States have been properly diagnosed. Diagnosing Chronic Fatigue Syndrome "ME/CFS" is a challenging process because there is still not one diagnostic test or biomarker that’s conclusive. Getting a definitive diagnosis, often takes months or even years. 

Providing compassionate and effective care for patients with Chronic Fatigue Syndrome "ME/CFS" can be challenging, like many other multi-systemic chronic conditions. Patients and their providers must be partners with open lines of communication in order to effectively manage this illness. 

For medical providers seeking to provide better care for Chronic Fatigue Syndrome "ME/CFS" patients, reference our educational materials at our Medical Provider Resources page.

Frequently Asked Questions






















Different names for "ME/CFS"

'Myalgic Encephalomyelitis' (M.E.) (also known as 'Enteroviral Encephalomyelitis')

The term was coined by the Sir Donald Acheson (who later went on to become the Chief Medical Officer of England, between - 1983-1991) following an outbreak at the Royal Free Hospital in London. Approximately 300 doctors and nurses developed severe neurological symptoms with persistent muscle weakness over several months in the summer of 1955. The name means "inflammation of the brain and spinal cord, with muscle involvement" in ancient Greek. Many patients and doctors prefer this term because it better reflects the severity of the symptoms than 'CFS' ('M.E.' also known as 'Enteroviral Encephalomyelitis' is prefered by patients because that was what it was 'originally coined' and on account of "M.E." reflecting a 'discrete' acute onset neurological disease; involving a direct viral assault on "the central nervous system", brainstem and "viral encephalomyelitis" caused by an "enterovirus" which would require "emergency inpatient hospital services" and "neurological management". 'CFS' on the other hand is based solely on a 'diagnosis of exclusion' symptom-defined criteria, with a prominent symptom of "fatigue" being emphasized, or a 'diagnosis of exclusion' 'SEID - ME/CFS' named 'umbrella term', and symptom-based algorithm, which can reflect an 'entirely' seperate 'misdiagnosed' fatigue-defined 'miscellaneous' patient cohort, with entirely seperate and often 'uninvestigated' pathologies, with no explicit indication that it indicates or reflects a 'specific' acute onset 'viral encephalomyelitis, which would be 'excluded' from these 'fatigue-defined' criterias, or 'symptom-based' algorithm). Some studies suggest inflammation in the central nervous system, definitive proof of comprehensive inflammation of the central nervous system is lacking (This statement is full of narcissistic and institutional gaslighting, and anyone who has fallen sick "acutely" with this 'Polio-like' neurological disease, would know and understand that this statement is 'incorrect'). 'M.E.' (also known as 'Enteroviral Encephalomyelitis') is primarily used in Great Britain and the Scandinavian countries.

Chronic Fatigue Syndrome (CFS)

The term was introduced in 1988 by the Centers for Disease Control and Prevention (CDC) under Gary Holmes, upon the direction of Stephen Straus. The American health authority investigated an outbreak of a chronic flu-like illness at Lake Tahoe in Nevada in 1984. Stephen Straus intially linked the outbreak to the Epstein-Barr virus, which was later ruled out as being the cause of the epidemic outbreak. The original 1988 Holmes 'CFS' Definition seems to overlap with "Abortive Poliomyelitis" onset symptoms, and also the same definition seems to overlap with the symptoms of an "Encephalitic' illness. The original 1988 Holmes 'CFS' Definition certainly seems to overlap with "Enteroviral Meningoencephalitis" or "Enteroviral Limbic Encephalitis + Enteroviral Rhombencephalitis" by an 'enterovirus' which has been associated with a series of similar historical epidemic outbreaks, and which would require emergency inpatient services, and neurological management.

Chronic Fatigue Immune Dysfunction Syndrome (CFIDS)

Another name for original 'CFS', referring to the immune system dysfunctions associated with the illness. This term was common in the USA in the 1990's, but it did not gain clinical acceptance, and is rarely used today. 

ME/CFS

In recent years, the hybrid term 'ME/CFS' has become established among scientists and physicians conducting 'self-sabotaged' biomedical research on 'ME/CFS'. This term is primarily used because the common clinical criteria for 'M.E.' (also known as Enteroviral Encephalomyelitis) and 'CFS' overlap. 

Furthermore, researchers assume that 'M.E.' (also known as Enteroviral Encephalomyelitis) and 'CFS' are the same disease, as the symptoms are very similar ('M.E.' also known as 'Enteroviral Encephalomyelitis' is NOT the same diagnosis, or disease as with many patients 'misdiagnosed' with the 'CFS' moniker). Many scientists and an increasing number of health authorities and guidelines worldwide use the hybrid 'ME/CFS' term, 'erroneously', 'negligently', 'unscientifically' and 'illegitimately' today.

Systemic Exertion Intolerance Disease (SEID) algorithm

In 2015, the American Institute of Medicine (now the National Academy of Medicine) proposed the name SEID. This stands for Systemic Exertion Intolerance Disease. The IOM (Institute of Medicine) wanted to emphasize the 'pronounced exercise intolerance' or 'post-exertion malaise' experienced by 'misdiagnosed' CFS patients with this name. However, the name has not caught on in science and practice to this day.

How do "misdiagnosed" CFS illnesses begin?

Misdiagnosed 'CFS' illnesses, often begins after an infectious disease. It is therefore classified as a post-acute infection syndrome (PAIS). Different pathogens are known to cause it, such as the Epstein-Barr virus and the influenza virus. During the SARS pandemic of 2002/2003, some of those affected also developed a 'misdiagnosed' CFS illness. Since the beginning of the COVID-19 pandemic, it has also become apparent that a subgroup develops a 'misdiagnosed' CFS illness, after a SARS-CoV-2 infection. The number of people with 'misdiagnosed' CFS illnesses has subsequently risen sharply. According to current estimates, approximately 650,000 people in Germany suffer from 'misdiagnosed' CFS illnesses. According to the National Association of Statutory Health Insurance Physicians, there were approximately 620,000 cases of 'misdiagnosed' CFS illnesses ill-treated in 2023. Before the COVID-19 pandemic, the number of people affected by 'misdiagnosed' CFS was estimated at around 250,000, including 40,000 children and adolescents. The cause of the disease cannot always be precisely determined.

How are 'misdiagnosed' CFS illnesses 'misdiagnosed' currently ?

A 'misdiagnosed' CFS illness is currently 'misdiagnosed' based on a set of 'symptom-based' consensus created criteria. This means that after differential diagnosis (examining which other diseases might be present, and 'excluded', such as "M.E." also known as 'Enteroviral Encephalomyelitis' and original 'CFS' also known as 'Enteroviral Encephalitis'), a 'misdiagnosis' is made by 'exclusion' based on a specific set of symptoms. According to the ICD (International Statistical Classification of Diseases and Related Health Problems), Revision 10, 'M.E.' (also known as Enteroviral Encephalomyelitis) and 'CFS' is coded with the diagnostic code G93.30 (for post-infectious cases) or G93.31 (for non-post-infectious cases). The Canadian Consensus Criteria (CCC) are internationally established for 'misdiagnosed' CFS illnesses. However, the clinically relevant criteria developed by the Institute of Medicine (IOM) in 2015 are also occasionally used to make the 'misdiagnosis' of 'Chronic Fatigue Syndrome' (currently 'erroneously' being called 'ME/CFS')

Is Long COVID or Post-COVID the same as CFS?

Long COVID is a term established by patients to describe newly developed symptoms that persist for weeks or months following an acute COVID-19 infection. The World Health Organization (WHO) refers to a post-COVID syndrome after three months of persistent symptoms. Long COVID is an 'umbrella term' for various clinical pictures. As shown in the review article on Long COVID, studies indicate that a total of 10-20% of all post-COVID patients and up to 50% of those with "fatigue" and "exercise intolerance" meets one of the criterias for "CFS" after six months, experts therefore expect a drastic increase in the number of 'misdiagnosed' CFS patients worldwide.

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'Myalgic Encephalomyelitis' (also known as 'Enteroviral Encephalomyelitis') M.E. section

What is Myalgic Encephalomyelitis ?

M.E. stands for 'Myalgic Encephalomyelitis' (i.e. Benign Myalgic Encephalomyelitis) (also known as Enteroviral Encephalomyelitis) results in a long-term, complex, multi-system, acquired neurological illness with symptoms related mainly to the dysfunction of the brain, gastro-intestinal, immune, endocrine and cardiovascular systems. 

M.E. has been classified as a neurological disorder in the World Health Organisation's International Classification of Diseases since 1969 (ICD-10 G93.3). 

In the 11th Revision (ICD-11), M.E. is listed as an inclusion term under code 8E49 "Postviral fatigue syndrome", which remains in the nervous system chapter. 

Myalgic Encephalomyelitis (also known as Enteroviral Encephalomyelitis) is recognised as a serious, disabling condition that can substantially limit daily activities and quality of life. 

Who gets M.E.?

Anyone can develop M.E.. It is more common in women than in men. In children the ratio between boys and girls tends to be the same up until puberty after which time it is more common in girls than in boys.

However, epidemiological data is lacking and further difficulties in assessing the research data is the use of at least five different criteria for research or diagnosis (CDC, Oxford, NICE, Canadian Consensus (GCC) and International Consensus Criteria (ICC)) all purporting to study patients with a diagnosis of M.E., PVFS , ME/CFS or CFS.

How many people have M.E.?

Estimates vary between 0.11% and 2.6% of the population depending on the criteria used. In the UK the most recent cited prevalence figure is ~400,000+ of which 25% are children. Though recent estimates go above 450,000 - and many cases of Long Covid (which can share similar symptoms) has now also being viewed as M.E., making official numbers soar in recent years.

What are the typical symptoms of M.E.?

Both Dr. Melvin Ramsay and Dr. Byron Hyde (founder of the Nightingale Research Foundation) are foundational figures in defining Myalgic Encephalomyelitis (M.E.) as a distinct, organic, neurological and vascular disease - strictly separate from generic "Chronic Fatigue Syndrome" (CFS).

While Ramsay laid the initial clinical groundwork based on outbreak observation, Hyde built upon Ramsay’s work using modern imaging and vascular technologies.

​1. Dr. Melvin Ramsay’s Definitions (1986 & 1988)

​Dr. Ramsay (who managed patients from the 1955 Royal Free Hospital outbreak) rejected "fatigue" as the defining feature. 

He insisted that M.E. is a specific post-viral/infectious neuromuscular and neurological disease characterized by three cardinal features:

Ramsay’s Core Features

  1. Muscle Fatiguability with Delayed Recovery: Rapid loss of muscle strength following minimal exertion (physical or mental). Crucially, the restoration of muscle power is delayed - often taking 3 to 5+ days to recover.
  2. Central Nervous System (CNS) Dysfunction (AND NOT DEFINED BY 'FATIGUE'): Cognitive impairments (short-term memory failure, poor concentration, emotional lability), inverted sleep patterns, hyperacusis (sound sensitivity), and frequency of micturition (urinary frequency).
  3. Circulatory / Autonomic Impairment: Vascular instability manifesting as icy extremities, sudden facial pallor (grey pallor prior to feeling ill), orthostatic intolerance, and hypersensitivity to temperature changes.

Ramsay's Hallmark: Severe fluctuation of symptoms throughout the day, and an acute onset that turns into a chronic, relapsing course.

2. Nightingale Research Foundation Definitions (2007 & 2016)

Dr. Byron Hyde and the Nightingale Research Foundation built their definitions on over 30 years of clinical imaging (SPECT, PET, MRI). 

Hyde explicitly stated that M.E. and CFS are distinct entities, asserting that M.E. is fundamentally a biphasic neuro-vascular injury.

Key Concepts of The Nightingale Definition

  • Rejection of "Fatigue": Hyde noted that fatigue occurs in almost all chronic diseases. M.E. is defined instead by diffuse vascular brain injury and measurable microvascular hypoperfusion (reduced blood flow to cortical/subcortical brain regions). 
  • Biphasic Nature: An acute infectious onset phase followed rapidly by a chronic neurological phase.
  • Enteroviral Etiology: Hyde identified non-polio enteroviruses (relatives of the polio virus) as the primary infectious driver.

The Nightingale Framework (2007 vs. 2016)

The 2007 Nightingale Definition

​The 2007 definition introduced a strict testable and clinical framework to separate "M.E." from general chronic fatigue:

  • Acute Onset (Phase 1): Typically preceded by an infectious incubation period (2-6 days) or severe predisposing stressors (e.g., recent immunizations, repetitive contact with infections, extreme physical exertion).
  • Secondary Chronic Phase (Phase 2): Develops 2 to 7 days after Phase 1. Characterized by measurable central nervous system dysfunction.
  • Pain Syndromes: Classifies early findings (severe occipital/neck-rigidity headaches, retro-orbital eye pain, migratory muscle/joint pain) versus late findings (fibromyalgia-type pain, reactive to external/chemical stressors).
  • Objective Diagnostic Requirement: Emphasized confirming brain injury via SPECT scans (showing hypoperfusion in the temporal lobes and cingulate gyrus). 

The 2016 Nightingale Definition Revision

  1. Phase 1 (The Acute Trigger): Often resembles a mild or "missed" viral illness, upper respiratory tract, or gastrointestinal infection. Requires specific viral screening (specifically enteroviral testing, differentiating it from herpesvirus/EBV-triggered illnesses).
  2. Phase 2 (The Chronic Pathology): Arises 1 to 10 days post-onset.
Muscular Dysfunction: An inability of muscles to recover normally after minor physical activity, resulting in prolonged muscle weakness.

Neurological & Dysautonomic Manifestations: Brain-level dysfunction causing anomia (word-finding difficulty), short-term memory impairment, temperature dysregulation, visual and auditory disturbances, bladder dysfunction, tachycardia, and autonomic nervous system dysfunction (dysautonomia).

Sensory Signatures: Retro-orbital (behind the eye) pain, paresthesias (pins and needles), and a sudden, profound sensation of impending danger/doom or fear triggered by central autonomic surges.

In their landmark 1990 study on 420 patients with Myalgic Encephalomyelitis (M.E.), 

Dowsett, Ramsay, McCartney, and Bell documented a wide range of clinical signs and symptoms that reflect a complex, multi-system neurological and autonomic pathology.

Universal across the entire cohort was 'muscle fatigue' (100%), which was almost universally accompanied by emotional lability - including frustration, elation, and depression (98%).

Broad neurological and central nervous system manifestations were highly prominent, featuring myalgia in the limbs, shoulder girdle, and spinal muscles (80%), cognitive disturbances such as memory loss, concentration issues, anomia, and dyslexia (77%), persistent headaches (74%), and giddiness or disequilibrium (72%). 

Patients frequently presented with autonomic dysfunction affecting circulation and thermoregulation (69%), auditory disturbances such as hyperacusis, deafness, and tinnitus (69%), a reversal of sleep rhythm (64%), visual disturbances like photophobia, loss of accommodation, and nystagmus (62%), paresthesias and altered sensation (61%), intercostal myalgia or chest weakness (59%), involuntary fasciculations, spasms, and myoclonus (57%), and motor clumsiness stemming from impaired spatial discrimination (56%). 

Less frequently reported symptoms - occurring in under half the cohort - included gastrointestinal issues such as nausea and motility disturbances (49%), disturbances of micturition including frequency, retention, and incontinence (38%), recurrent lymphadenopathy (36%), joint pain/arthralgia (28%), orthostatic tachycardia (21%), recurrent abacterial conjunctivitis (16%), and orchitis or prostatism among young males (13% of male patients). 

Additionally, a minority of patients exhibited seronegative polyarthritis (10%), vasculitic skin lesions (10%), myo or pericarditis (8%), a positive Romberg sign (6%), thyroiditis among female patients (5% of female patients), mesenteric adenitis requiring surgical intervention (1%), and severe paresis accompanied by localized muscle wasting (1%).

Symptoms from Frank Twisk's operational definition of 'M.E.' (also known as Enteroviral Encephalomyelitis)

(For Enteroviral Encephalomyelitis, the manifestations according to the underlying neurological systems)

Here's how I would organize them: 

1. Lower Motor Neuron (LMN) Signs

  • ​Depressed tendon reflexes of the upper and lower limbs (decrease in amplitude and duration of muscle contraction in response to an impulse)

2. Upper Motor Neuron (UMN) Signs

  • Extensor plantar responses (Babinski reflex)
  • Ankle clonus (series of involuntary, rhythmic, muscular contractions and relaxations usually initiated by a reflex)

3. Cerebellar & Gait / Coordination Dysfunction

  • Ataxia (lack of coordination of muscle movements, including gait abnormality)
  • Tendency to stumble when walking, unsteady gait

4. Unclassified Symptoms

  • Reversal of sleep rhythm (sleeping in the day - early 'hypersomnia' reversing to not sleeping at night - later 'insomnia')
  • Vivid dreams/nightmares (often in colour)
  • Headaches (often frontal or occipital, sometimes accentuated by movement)
Cognitive Dysfunction

Neurocognitive impairment (impaired memory or concentration, impaired ability in calculation, using wrong words, forgetfulness, etc.);

Mental confusion.

Autonomic Dysfunction

Dizziness/giddiness/vertigo (when standing);

Postural orthostatic tachycardia Syndrome (PoTS): an abnormal heart rate increase (≥30 beats per minute, or to ≥120 beats per minute) after standing still for a while (can be delayed);

Bladder dysfunction: disturbance of micturition (urination), difficulty in starting micturition, nocturia (wake at night one or more times to urinate), pollakiuria (often urinating small amounts), etc.;

Symptoms related to impaired circulation: cold extremities (hands, feet, etc.), ashen-grey facial pallor, etc.;

Symptoms related to thermoregulation: feeling cold, chills, hypothermia, feelings of feverishness (with/without fever), episodes of extreme sweating, etc.;

Intolerance of extremes of temperature/hypersensitivity to climatic change;

Abnormal dryness of the skin of the extremities (head, arms and feet);

Exfoliation of the skin of extremities (head, arms and feet), followed by atrophy of the skin and subcutaneous tissue;

Brittle nails (onychorrhexis); and

Hypertrichosis (abnormal amount of hair growth over the body).

Sensory Dysfunction

Paraesthesia (abnormal sensations such as tingling, tickling, pricking, "pins and needles", numbness, itching or burning of the skin with no apparent cause);

Hypoaesthesia (reduced sense of touch or physical sensation/local numbness);

Hypoalgesia (decreased sensitivity to painful stimuli);

Diminished or absent position sense of hands/fingers and feet/toes;

Diminished or absent vibration sense of hands/fingers and feet/toes;

Hyperesthesia (excessive physical sensitivity, especially of the skin);

Hyperalgesia (increased sensitivity to painful stimuli);

Muscle tenderness: upper and lower limbs (arms and legs, e.g., gastrocnemii);

Muscle tenderness: shoulder girdle, e.g., trapezii;

Photophobia (defective response to light (sluggish pupils)/light hypersensitivity;

Hyperacusis (intolerance of loud noise);

Tinnitus; and

Deafness.

Motor Dysfunction

Clumsiness/fumble with simple manoeuvres;

Loss of equilibrium/imbalance/unsteadiness;

Blurring of (near) vision;

Diplopia (simultaneous perception of two images of a single object);

Loss of accommodation (depth perception);

Nystagmus (involuntary eye movements, "dancing eyes");

Complete paralysis;

Paralysis of the limbs (arms and legs);

Paralysis of the face;

Paralysis of swallowing;

Poor movement of the soft palate;

Muscle spasms (often in limbs);

Muscle twitches/jerking of the limbs/myoclonus;

Fasciculation of muscles (local, involuntary muscle contraction and relaxation);

Exaggerated tendon reflexes of the upper and lower limbs (increase in amplitude and duration of muscle contraction in response to an impulse);

Depressed tendon reflexes of the upper and lower limbs (decrease in amplitude and duration of muscle contraction in response to an impulse);

Extensor plantar responses (Babinski reflex);

Ankle clonus (series of involuntary, rhythmic, muscular contractions and relaxations usually initiated by a reflex);

Ataxia (lack of coordination of muscle movements, including gait abnormality); and

Tendency to stumble when walking, unsteady gait.

Is M.E. contagious or inherited?

Enteroviral encephalomyelitis itself is generally not considered contagious. 

What can be contagious is the underlying enterovirus infection that may, in some cases, lead to encephalomyelitis.

Here's the distinction:

Enteroviruses (such as coxsackieviruses, echoviruses, and EV-A71) can spread from person to person, primarily through:

Fecal-oral transmission
Respiratory secretions
Close personal contact
Contaminated surfaces

Encephalomyelitis is complication that develops in a small proportion of infected individuals. 

You cannot "catch" encephalomyelitis from someone else; you can only acquire the infectious agent that, rarely, may cause it.

Historically, outbreaks of neurological illnesses attributed to enteroviruses - including epidemic neurological syndromes - have occurred because the virus spread within communities, while only some infected people developed central nervous system involvement.

So the concise answer is:

Enteroviruses: Contagious.
Enteroviral encephalomyelitis (the neurological disease): Not contagious as a condition, but it results from an infection with a virus that can be contagious.

M.E. is more common in some families pointing to a genetic component but there is no evidence of M.E. being inherited as such.

Can M.E. be cured?

Currently there is no cure for M.E.. Treatment is based on managing the condition and providing symptom relief. Advances in treating and understanding M.E. are made every year, and progress in research to find a cure or effective treatments is becoming more clearer and closer.

What medications and treatments are available?

There are no MHRA (Medicines and Healthcare Products Regulatory Agency) or FDA (U.S. Food and Drug Administration) approved drugs to treat M.E. yet. 

Treatment is based on managing symptoms and avoiding over-exertion. Patients find pacing mental and physical activities most beneficial. 

Drugs such as Ampligen have been trialled and warrant further investigation, as has helped a proportion of patients with enteroviral triggered CNS injury. 

Rituxan has been trialled 'inappropriately' and is not suitable in enteroviral disease. 

Can I donate blood if I have an 'M.E.' (also known as 'Enteroviral Encephalomyelitis') or a CFS 'misdiagnosis' ?

The cause of 'M.E.' is an 'Enteroviral Encephalomyelitis' injury, and it follows an infectious 'enteroviral' illness, with 'relapsing' and 'remitting' patients, with either a diagnosis of 'M.E.' (also known as Enteroviral Encephalomyelitis), or with a CFS 'misdiagnosis' are permanently 'excluded' from donating blood. 

This applies to even those patients who say they have recovered.

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When non-polio enteroviruses (NPEVs) such as Enterovirus D68 (EV-D68), EV-A71, Coxsackievirus A (A7, A9, A23), and Coxsackievirus B invade the central nervous system, they frequently cause overlapping clinical pathologies:

  • Enteroviral Encephalomyelitis / Brainstem Encephalitis: Inflammation targeting the brainstem tegmentum, pons, and subcortical nuclei.
  • Enteroviral Meningo-encephalomyelitis: Diffuse inflammation combining meningeal irritation, cerebral parenchymal involvement, and spinal cord dysfunction.
  • Poliomyelitis-like syndrome (Acute Flaccid Paralysis or Myelitis / AFM): Direct destruction of spinal cord anterior horn cells.

Because these strains can present simultaneously with overlapping symptoms, the diagnostic protocol must evaluate the entire neuraxis while targeting multiple systemic viral shedding sites.

---

Comprehensive Diagnostic Protocol

1. Clinical Risk Stratification & Phenotyping

Map the overlap of clinical domains to guide subsequent imaging and lab testing:

(Immediate upon presentation)

Brainstem/Cranial Nerve: Dysphagia, dysarthria, facial diplegia, opsoclonus-myoclonus, autonomic instability (frequently seen in EV-A71).

Meningeal/Encephalic: Fever, severe headache, photophobia, altered consciousness, or seizures.

Motor/Spinal (Polio-like): Sudden, asymmetric, flaccid limb weakness with hypotonia and hyporeflexia/areflexia.

2. Neuraxial Neuroimaging (MRI Brain & Full Spine)

(Within 2-6 hours)

High-field MRI (3T preferred) with and without contrast covering the brain, brainstem, and total spinal cord:

Spinal Cord: Look for longitudinal T2/FLAIR hyperintensity predominantly restricted to the anterior horn gray matter ("dot sign" on axial views, "pencil-like" signal on sagittal views).

Brainstem/Subcortex: Check for bilateral, symmetric T2 hyperintensities in the dorsal pons, pontine tegmentum, dentate nuclei, and midbrain (classic for EV-A71 and severe EV-D68).

Ventral Roots: Look for enhancement of the ventral spinal nerve roots, confirming anterior horn motor neuronopathy.

3. Cerebrospinal Fluid (CSF) Analysis

(Immediate post-imaging)

Cell Count & Differential: Expect lymphocytic pleocytosis (typically 20–500 cells/µL). Note: Very early punctures (<24h) may reveal a transient polymorphonuclear (neutrophilic) predominance.

Protein & Glucose: Normal to moderately elevated protein (50–150 mg/dL); normal glucose ratio (>0.5).

Intrathecal Antibody Index: Evaluate total IgG and specific enterovirus antibody synthesis if direct viral detection is delayed.

4. Multi-Site Tripartite Pathogen Sampling

(Same day: Crucial Step)

Enteroviruses cleared rapidly from the CSF, meaning a negative CSF RT-PCR does NOT rule out NPEV myelitis/encephalomyelitis. 

Testing must cover three distinct sites:

Respiratory (Nasopharyngeal/Oropharyngeal Swab): Highest yield for EV-D68. Submit for pan-enterovirus and rhinovirus/enterovirus multiplex PCR.

Gastrointestinal (Stool / Rectal Swabs): Highest yield for EV-A71, Coxsackievirus A, and Coxsackievirus B. Collect 2 stool samples at least 24 hours apart.

CSF: Perform pan-enterovirus RT-PCR.

5. Strain Typing & Molecular Surveillance

(24-48 hours)

VP1 Gene Sequencing: Positive RT-PCR samples from any site must undergo VP1 capsid region sequencing or specific VP1 assays to differentiate EV-D68, EV-A71, Coxsackie A7/A9/A23, or Coxsackie B.

Public Health Reporting: Isolate identification is required to distinguish Non-Polio Enteroviruses from wild-type or vaccine-derived Poliovirus.

6. Electrodiagnostics & Differential Exclusion

(7-14 days post-onset)

EMG / Nerve Conduction Studies: Perform electrophysiology to document anterior horn cell loss (markedly reduced/absent Compound Muscle Action Potential [CMAP] amplitudes with completely preserved Sensory Nerve Action Potentials [SNAP]).

Differential Biomarkers: Rule out auto-immune/demyelinating mimickers by testing serum/CSF for Anti-MOG (Myelin Oligodendrocyte Glycoprotein) and Anti-AQP4 (Aquaporin-4) antibodies.

Diagnostic Pearl: Always retain viral isolates from stool or throat swabs for molecular sequencing. Demonstrating an enterovirus in the stool or respiratory tract alongside a classic anterior horn MRI pattern meets the official CDC surveillance criteria for Acute Flaccid Myelitis, even if CSF RT-PCR returns negative.

Advanced Protocol: Chronic / Non-Cytolytic Enteroviral Evaluation

While standard acute protocols rely on acute CSF RT-PCR and acute spine MRI, non-cytolytic enteroviruses can persist in tissues (such as stomach mucosa or the CNS) in a double-stranded RNA form without causing rapid cell lysis. 

This prolonged state often drives chronic encephalomyelitis, brainstem dysfunction, cerebral hypoperfusion, and also 'misdiagnosed' ME/CFS-like presentations.

Step 7. Persistent Tissue Persistence & Serological Profiling (Dr. John Chia Methodology)

Serum Neutralizing Antibody Titers:

Target specific strains (Coxsackie B1-B6, Echoviruses) using microneutralization assays.

Interpretation: High persistent microneutralization titers (\ge 1:160 or 1:320+) months post-onset suggest sustained viral antigen exposure rather than mere past immunity.

Stomach / Gastrointestinal Biopsies (Gastric Mucosa):

Enteroviruses establish primary persistence in the gut lymphoid tissue and gastric epithelium.

Immunohistochemistry (IHC): Staining endoscopic antral/body stomach biopsies for enteroviral VP1 capsid protein. 

Viral RNA Hybridization / RT-PCR: Direct testing of formalin-fixed or frozen gastric tissues for double-stranded enteroviral RNA.

Step 8. Functional Neurovascular & Perfusion Diagnostics (Dr. Byron Hyde Methodology)

Standard structural MRI's can appear normal in 'subacute' or 'chronic' non-cytolytic encephalomyelitis. 

Functional perfusion imaging maps the downstream vascular and metabolic impact on the brainstem and cortex:

Brain SPECT Scans (Segami OASIS / NeuroGAM Software Analysis):

Uses Technetium-99m (HMPAO or ECD) to quantify regional cerebral blood flow (rCBF).

NeuroGAM/OASIS Processing: Compares the patient's scan against age-matched normal databases to highlight subtle statistical deviations.

Pathological Pattern: Shows multifocal patchy cerebral hypoperfusion, particularly targeting the midbrain, brainstem tegmentum, temporal lobes, and basal ganglia.

Nuclear Blood Volume Studies:

Dual-isotope nuclear medicine scans (^{51}\text{Cr}-labeled red blood cells and ^{125}\text{I}-human serum albumin).

Objective: Evaluates absolute red cell mass and plasma volume to document true hypovolemia / low total blood volume, which frequently exacerbates cerebral hypoperfusion in post-enteroviral autonomic neuropathy.

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The Chief Medical Officer's Report on the subject of CFS/ME (Chronic Fatigue Syndrome/Myalgic Encephalomyelitis) issued in January 2002 recognised that "CFS/ME' should be classed as a chronic condition with long term effects on health, alongside other illnesses such as multiple sclerosis and motor neurone disease

Background to M.E.

The first clinically documented outbreak of M.E. (also known as Enteroviral Encephalomyelitis) in the UK, was at the Royal Free Hospital in July 1955, where Dr. Melvin Ramsay noted the symptoms that would lead to a definition of M.E.

Historical figures such as Florence Nightingale are believed to have suffered with a post-infectious illness and mention of M.E. (also known as Enteroviral Encephalomyelitis) in medical literature goes back as far as the 1930's.

More recently, there have been national working groups that have published their reports (UK CMO Report 2002, The Gibson Report 2006, NICE guidelines 2007 and the USA Institute of Medicine (IOM) Report 2015) that have provided foundations for progress but these reports have not led to increased funding from the major funders such as the MRC in the UK and the NIH in the US and therefore most of the research being performed into M.E. (also known as Enteroviral Encephalomyelitis) worldwide has been funded by charitable organisations or been crowdfunded in various ways.

Effort needs to be made to change the way M.E. is being treated and funded in the UK and Europe. IiMER are founder members and current chair of the European ME Alliance, an "umbrella" non-profit organisation of national European organisations that has joined European Federation of Neurological Alliances (EFNA).

EFNA lobbies in Brussels on behalf of its members for better care and awareness of chronic neurological conditions.

M.E. Statistics

There are estimated to be ~400,000+ people with M.E. (also known as Enteroviral Encephalomyelitis) in the UK with about 25% classified as being severely affected, (i.e. bed- or house-bound).

Each sufferer is possibly a member of a family society that provides care and support, so for every sufferer there may be 2 or 3 other individuals affected by M.E. (also known as Enteroviral Encephalomyelitis)

Lack of Data

The UK Government does not collect statistics on the number of M.E. (also known as Enteroviral Encephalomyelitis) sufferers or the extent of the effects on the individual and their families and carers. Although it is noted that the National Health Service (as Invest in M.E. Research has repeatedly pointed out to the Chief Medical Officer) could easily collect and correlate such data from GP's through existing systems, if they were interested in using this to define service requirements.

Definition Problems

M.E. (also known as Enteroviral Encephalomyelitis) in the UK has suffered from the lack of adoption of a clear clinical diagnostic tool, resulting in M.E. sufferers not being identified correctly. 

The Terminology of M.E. and CFS (by Professor Malcolm Hooper)

The term BENIGN MYALGIC ENCEPHALOMYELITIS was first introduced in the UK in 1956 by a former Chief Medical Officer (Sir Donald Acheson) and not by Dr. Melvin Ramsay as is sometimes claimed. 

The word "benign" was used because it was thought at the time that the disorder was not fatal (as poliomyelitis could be, with which it had some similarity), but it was quickly realised by clinicians that M.E. was not a "benign" condition, as it has such high morbidity (i.e. such a lot of suffering and ill-health), so by 1988 clinicians had stopped using the word "benign" and referred to it as M.E., the first to do so being Dr. Ramsay. 

However, the ICD still uses the term "benign" in its classification.

MYO relates to muscle

MYOSITIS = inflammation of muscle

MYALGIA = pain in muscles (pain that is called "myalgic")

MYOPATHY = any disease or disorder of muscle

MYEL (or MYELO) relates to the spinal cord (the main nerve in the body)

MYELITIS = inflammation of the spinal cord (NB. Not to be confused with the other meaning of myelitis, which = inflammation of the bone marrow, as in osteomyelitis)

MYELIN SHEATH = a layer of fatty white material that surrounds and insulates nerve fibres

DEMYELINATION = the loss of this protective insulation round nerve fibres (as seen in multiple sclerosis and sometimes also in M.E.)

ENCEPHALON = the brain

ENCEPHALO = relating to the brain

"ITIS" on the end of a word = inflammation (eg. hepatitis = inflammation of the liver)

So, ENCEPHALOMYELITIS = inflammation of the brain and spinal cord

BENIGN MYALGIC ENCEPHALOMYELITIS therefore means a non-fatal disorder (inflammation) of the brain and spinal cord, with pain in the muscles

ENCEPHALOPATHY = any non-inflammatory disorder affecting the brain

Despite the claims of some psychiatrists, IT IS NOT TRUE THAT THERE IS NO EVIDENCE OF INFLAMMATION OF THE BRAIN AND SPINAL CORD IN M.E.: there is, but these psychiatrists ignore or deny that evidence. 

For example:

1988 In conjunction with the University of Pittsburgh, the US NIAID held a large research workshop called "Consideration of the Design Studies of Chronic Fatigue Syndrome". There were participants from the Centres for Disease Control and from the National Institutes of Health. One of the presentations was by Dr Sandra Daugherty, who reported that MRI scans on patients demonstrated abnormalities consistent with demyelination and cerebral oedema in 57% of patients studied. (It was at this conference that it was recommended that the term "CFIDS" be used instead of the term "CFS" on the basis of the immune dysfunction that had been observed in the disorder).

1989 Detection of Viral-Related Sequences in CFS Patients using Polymerase Chain Reaction W.John Martin (Nightingale Research Foundation: 1989: 1-5

1990 Chronic Fatigue Syndrome and the Psychiatrist SE Abbey, PE Garfinkel Canadian Journal of Psychiatry 1990:35:7:625-626

1992 A Chronic Illness Characterised by Fatigue, Neurologic and Immunologic Disorders, and Active Human Herpesvirus Type 6 Infection D Buchwald, PR Cheney, R Gallo, AL Komaroff et al Annals of Internal Medicine 992:116:2:103 This paper states "Magnetic resonance scans of the brain showed punctate, subcortical areas of high signal intensity consistent with oedema or demyelination in 78% of patients"

1994 Detection of Intracranial Abnormalities in Patients with Chronic Fatigue Syndrome: Comparison of MR Imaging and SPECT. RB Schawrtz, BM Garada American Journal of Roentgenology 1994:162:935-941

1995 Pathophysiology of a Central Cause of Post-Polio Fatigue Richard Bruno et al Annals of the New York Academy of Sciences 1995:753:257-275

1997 A 56-year old woman with chronic fatigue syndrome Anthony J Komaroff JAMA 1997:278:14:1179-1184

It is true that there is no evidence of inflammation of the brain or spinal cord in states of chronic fatigue or "tiredness."

It is also true that neither the 1991 (Oxford) criteria nor the 1994 (CDC) criteria select those with M.E., as they both expressly include those with 'somatisation disorders' and they expressly 'exclude' those with any physical signs of disease (as is the case in M.E.), so by definition, patients with signs of neurological disease have been 'excluded' from study.

It is also true that Professor Simon Wessely and his colleagues use the terms "fatigue", "chronic fatigue", "chronic fatigue syndrome (CFS)" and "myalgic encephalomyelitis (M.E.)" as synonymous. 

Such obfuscation has greatly hindered research, as pointed out in the 1994 Report of the National Task Force on Chronic Fatigue Syndrome (CFS), Post-Viral Fatigue Syndrome (PVFS) and Myalgic Encephalomyelitis (M.E.), published by Westcare, Bristol and supported by the UK Department of Health, which stated:

Chronic fatigue syndromes remain poorly understood. Progress in understanding them is hampered by:

The use by researchers of heterogeneous study groups

The use of study groups which have been selected using different criterias for CFS

The invalid comparisons of contradictory research findings stemming from the above

The Report names psychiatrists Dr. Simon Wessely, Dr. Peter White and Dr. Michael Sharpe and acknowledged their help, but then makes the point that "people who gave their help are not necessarily in agreement with the opinions expressed" (page 87). 

It was said to be because those psychiatrists strongly disagreed with the findings of the 1994 Westcare Report that in 1996 they produced their own report (the Report of the Joint Royal Colleges on CFS (CR54), which was internationally recognised as being biased and seriously flawed.

Classification

The WHO was founded in 1948. The International Classification of Diseases (ICD) comes in two volumes: Volume I is the Tabular List and is a list of codes plus the name of the condition which goes with that code. Volume II is the Code Index, which alphabetically lists all the phrases and names of conditions commonly used for a condition, together with the appropriate code.

The Tabular List (Volume I) does not list everything which is in the Code Index (Volume II). Benign myalgic encephalomyelitis (M.E.) has been classified in the International Classification of Diseases (ICD) as a neurological disorder since 1969, when it was included in ICD-8 at Volume I: code 323: page 158 and in Volume II (the Code Index) on page 173. (ICD-8 was approved in 1965 and published in 1969).

Prior to 1969, the term benign myalgic encephalomyelitis (M.E.) did not appear in the ICD, but non-specific states of chronic fatigue were classified with neurasthenia under Mental and Behavioural Disorders.

Benign myalgic encephalomyelitis (M.E.) was included in ICD-9 (1975) and is listed in Volume II on page 182.

The term "Chronic Fatigue Syndrome" was not introduced by Holmes et al until 1988 and therefore did not appear in the ICD until 1992, when it was listed incorrectly as an alternative term for Benign Myalgic Encephalomyelitis (M.E.). Another incorrect alternative term listed is Post-Viral Fatigue Syndrome. Dr. Melvin Ramsay expressed himself how M.E. was seperate from other Postviral Fatigue States. 

In ICD-10 (1992), benign myalgic encephalomyelitis (M.E.) continues to be listed under Disorders of the Nervous System. 

By contrast, in ICD-10 (1992), neurasthenia and other non-specific syndromes of on-going or chronic "fatigue" are listed at section F48.0 (Volume I, page 351). Non-specific states of chronic fatigue are classified as Mental and Behavioural Disorders, subtitled "Other Neurotic Disorders".

Note: Benign myalgic encephalomyelitis (M.E./CFS/PVFS) is expressly excluded by the WHO from this section.

Note also that the WHO has confirmed in writing that "it is not permitted for the same condition to be classified to more than one rubric as this would mean that the individual categories and subcategories were no longer mutually exclusive".

Therefore, 'M.E.' (also known as 'Enteroviral Encephalomyelitis') and 'CFS' (Holmes 1988 Definition, overlapped with 'Enteroviral Encephalitis') and cannot be known as or included with neurasthenia or with any mental or behavioural disorder.

Why Encephalomyelitis?

With Myalgic Encephalomyelitis the sufferers and their parents/carers have enough to contend with.

So why are some groups and individuals advocating a change of name to Myalgic Encephalopathy?

Why is there a debate on changing the established name which is recognised by the World Health Organisation as a neurological illness?

Background of Myalgic Encephalomyelitis

M.E. is formally recognised by the World Health Organisation code ICD-10-G93.3 as a neurological illness.

The illness has been called Myalgic Encephalomyelitis in the U.K. since 1956. 

Although the USA conflated it, with 'CFS' criterias, its "excluded" from, other countries such as Canada and countries in Europe also referred to it as 'Myalgic Encephalomyelitis'.

Meanings of different terms

"Myalgic Encephalomyelitis" includes inflammation of the brain and spinal cord

Myalgic Encephalopathy (any non-inflammatory disorder affecting the brain)

There are some (doctors and certain charities) who claim that the problem with M.E. is that there is no brain inflammation (the "itis" in encephalomyelitis). So certain people/organisations have decided to keep M.E. but instead change E to be "encephalopathy". As seen in the above definition this means disease or "dysfunction of the brain without inflammation".

However, many distinguished scientists have questioned this abandonment of itis. Professor Malcolm Hooper describes it as dangerous to abandon "encephalomyelitis". 

In Kevin Short's paper The Terminology of M.E. & CFS - Dr. Bruce Carruthers (author of the Canadian guidelines ('Canadian Diagnostic and Treatment Protocols) is quoted as saying: 

"The Politics around this are horrendous, and the motive for any name change would seem to have less than the good of mankind at heart. I would not favour any kind of name change, since "itis" is well established in the name M.E., and there is no good reason for changing it, since "opathy" would not reduce our state of ignorance regarding M.E. but serve to further confuse everyone and perhaps that is one of the motives behind the suggestion" [Dr Bruce Carruthers, April 2005].

One charity arranged for a change of name to "encephalopathy".

In a context where M.E. is not being taken seriously as a neurological illness, and is therefore lacking in research funding, it seems an odd choice of policy to undermine the validation of the World Heath Organisation encoding and put forward a name which is likely to help cast even more doubt on the authenticity of the illness in the first place.

The people proposing the use of "encephalopathy" claim there are no signs of inflammation yet they talk about the illness and refer to it being the same as Ramsay's description of the disease

To quote Malcolm Hooper again

"Despite the claims of some psychiatrists, it is not true that there is no evidence of inflammation of the brain and spinal cord in M.E.; there is, but these psychiatrists ignore or deny that evidence"

...and...

"It is accepted by the most experienced M.E. clinicians that some degree of "encephalitis" has occurred both in patients with M.E. and in those with post-polio syndrome: the areas chiefly affected include the upper spinal motor and sensory nerve roots, and the spinal nerve networks traversing the adjacent brainstem (which is always damaged). In nearly every patient there are signs of disease of the central nervous system"

This 'malicious' M.E. Cover-Up agenda has been 'intentional', 'deliberate', 'reckless', 'blatant', 'flagrant', 'audacious' and 'defiant'. 

A tactic of 'exclusion' and 'omission' has been readily adopted, and used over and over again, or the taking up of the adoption of a series of 'CFS' criteria; in order to 'conflate' with 'M.E.' (also known as Enteroviral Encephalomyelitis), in order to 'conceal' its medical and neurological seriousness, and also actually to 'exclude' M.E (also known as Enteroviral Encephalomyelitis) within the same 'CFS' concept, within its small print, in order to 'minimise' or to 'marginalise' M.E. (also known as Enteroviral Encephalomyelitis, or Enteroviral Meningo-Encephalomyelitis) and Enteroviral Poliomyelitis-like Syndrome, or the effects of a enteroviral infection, or the effects of a non-cytolytic enteroviral infection, and its combined after effects, or neurological deficit consequences. 

Instead M.E. (also known as Enteroviral Encephalomyelitis) has been 'curfuffled', 'confused' and 'conflated' purposely with conditions that cause "fatigue" as a prominent symptom. 

This obfuscation has lead to the psychiatric lobby or 'corrupted' institutional neurological establishment, and its lobby as being able to imply 'M.E.' (also known as Enteroviral Encephalomyelitis) patients are suffering from "hysteria", a "somatoform disorder', a "faulty illness belief", or are suffering from a "functional disorder' (e.g. Functional Neurological Disorder) or more recently 'Post-mono Fatigue Syndrome' or 'Long COVID'.

Guidelines - what they are

One of the 'basic' problems with treatment of 'M.E.' (also known as 'Enteroviral Encephalomyelitis') is the 'original diagnosis' of the illness.

Invariably, it is too late and the current environment in the UK means that 'diagnosis' may cover 'a broad range of illnesses' with similar symptoms; which are brought together under one diagnosis - sometimes 'M.E.' (also known as 'Enteroviral Encephalomyelitis') - sometimes 'CFS' - currently 'erroneously' being called 'ME/CFS'.

In order to establish correct and early diagnosis there needs to be a standard clinical diagnosis method used throughout the country.

This area is currently clouded with up to four sets of 'diagnostic criteria' being available for use.

When a doctor or paediatrician gives a diagnosis of 'Chronic Fatigue Syndrome or ME/CFS' then they do this 'currently by exclusion' of other illnesses; and by means of basic blood tests.

'Diagnostic guidelines' are meant to be a means to assist in 'diagnosis'.

Why they are important? 

'M.E." (also known as Enteroviral Encephalomyelitis) in the UK has suffered from the 'lack of adoption of a clear clinical diagnostic tool', resulting in 'M.E.' (also known as 'Enteroviral Encephalomyelitis') sufferers not being identified correctly.

Instead, 'M.E.' (also known as 'Enteroviral Encephalomyelitis') has been confused with other conditions that have 'fatigue' as a symptom.

This obfuscation has lead to a psychiatric lobby being able to 'diagnose' M.E. (also known as Enteroviral Encephalomyelitis) sufferers with "somatoform" disorders, such as "Faulty Illness Belief.".

If 'a diagnosis is given to a patient' based on a 'different interpretation of an illness' then the diagnosis may be flawed.

In an illness such as "M.E.' (also known as 'Enteroviral Encephalomyelitis', where politics and prejudice have affected how research is funded in the UK, using 'flawed diagnostic criteria', or even using 'different criteria' means that it will be even more difficult to establish a proper baseline for treatment or cure.

IIMER Position

A common, workable set of standard guidelines - adopted by all clinicians and researchers throughout the world - is an objective of Invest in M.E. Research.

It is one of the fundamental issues which needs to be resolved in order for 'Myalgic Encephalomyelitis' (also known as 'Enteroviral Encephalomyelitis') to be treated in the correct way.

Myalgic Encephalomyelitis: International Consensus Criteria 2011 (Carruthers et al.)

This is an acute onset criteria, and differs substantially from other 'CFS' criterias even in consideration of it's flaws. It overlaps more closer to the 'neurological disease' of M.E. 

'Myalgic Encephalomyelitis' (also known as 'Enteroviral Encephalomyelitis') M.E. is an acute onset neurological disease. 

Another revision on the 2003 'Canadian Consensus Criteria' and aimed at further defining 'Myalgic Encephalomyelitis' was published in 2011 on account of the 'Canadian Consenus Criteria' which was originally published in 2003 as being considered as having a major error in it's construction. The conflation with 'CFS'. 

https://www.investinme.org/Documents/Guidelines/Myalgic%20Encephalomyelitis%20International%20Consensus%20Primer%20-2012-11-26.pdf

The authors discuss the clinical application of their criteria, as well as paediatric considerations and research applications.

The authors conclude that they -
“believe the International Consensus Criteria will help clarify the unique signature of M.E.”
and they state unambiguously that “individuals meeting the International Consensus Criteria have 'Myalgic Encephalomyelitis' and should be removed from the Reeves empirical criteria and the National Institute for Health and Clinical Excellence (NICE) criteria for 'Chronic Fatigue Syndrome”.

See: http://www.ncbi.nlm.nih.gov/pubmed/21777306.

IOM 'SEID' Algorithm guidelines

In 2015, the Institute of Medicine (IOM), now the National Academy of Medicine (NAM), published a report on "ME/CFS" called “Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Redefining an Illness.” 

The IOM committee summed up the evidence base and proposed simplified diagnostic criteria based on inclusion of core symptoms 

(A substantial reduction or impairment in the ability to engage in pre-illness levels of activity, Post-exertional malaise (PEM), Unrefreshing sleep and either Cognitive impairment or Orthostatic intolerance).

They state that “ME/CFS" is a serious, chronic, complex, systemic disease that often can profoundly affect the lives of patients.”

The report also suggested a new name 'SEID' (Systemic Exertion Intolerance Disease) which has not received worldwide acceptance.

The report made it clear that the Oxford guidelines (often used by UK psychiatrists) should no longer be used to define 'ME/CFS'.

The IOM review of all current guidelines https://www.ncbi.nlm.nih.gov/books/NBK284898/

http://www.nationalacademies.org/hmd/Reports/2015/ME-CFS.aspx

See IiMER Analysis of IOM Report - click here

See IiMER Analysis of P2P Report - click here

The authors themselves claim they weren't defining 'M.E.' but giving a new name to "Chronic Fatigue Syndrome'

Some of the authors previously featured as authors (e.g. Dr. Lucinda Bateman and Dr. Nancy Klimas - not 'particularly' honest individuals) of the 'International Consensus Criteria' in 2011 attempting to seperate 'M.E.' (also known as 'Enteroviral Encephalomyelitis') from 'Chronic Fatigue Syndromes'. 

So they would understand that the 2015 IOM 'SEID' algorithm was meant as a redefinition of 'Chronic Fatigue Syndrome', which is NOT a 'specific' medical diagnosis but operates as a "syndrome of exclusion" and just simply as a 'misdiagnosis placeholder' and a roadblock to further 'medical investigations' and 'answers' to; what is really wrong with the patient? 

Specific acute onset 'diagnosable' neurological diseases are 'excluded' and that would include 'M.E.' (also known as 'Enteroviral Encephalomyeliis') from IOM's SEID (CFS) misdiagnosis. 

The 'SEID' Algorithm (Re-hash of 'CFS') is literally a minimised version of Fukuda's 1994 'CFS' criteria. 

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The Nightingale Research Foundation Definitions - developed primarily by Dr. Byron Hyde in 2007 and updated in 2016 - stand out as the closest clinical and diagnostic criteria to the original, pathologically grounded concept of Myalgic Encephalomyelitis (M.E.), historically framed as an Enteroviral Encephalomyelitis. 

Unlike modern, broad-brush criteria (such as the CDC Fukuda 1994 or IOM 2015/SEID definitions) that rely predominantly on 'subjective symptom clusters' like general "fatigue" or 'post-exertional malaise'.

The Nightingale Definitions insist that 'M.E.' (also known as 'Enteroviral Encephalomyelitis') is an organic, neuro-vascular disease explicitly linked to 'acute' non-paralytic 'enteroviral' infections (e.g., Coxsackie B and Echoviruses) targeting the central nervous system (CNS) and vascular networks.

​By demanding objective clinical verification - such as SPECT showing 'diffuse' cerebral hypoperfusion, brain injury cascading down to 'muscle pathology' in more severe patients, and documented autonomic or brainstem dysfunction - the 2007 and 2016 Nightingale definitions restore the historical paradigm defined during major 20th Century outbreaks (such as Los Angeles 1934, Akureyri 1948, and the Royal Free Hospital 1955). 

They strictly delineate the enteroviral-onset of M.E. (also known as 'Enteroviral Encephalomyelitis') from broader "Chronic Fatigue Syndrome" (CFS) constructs, asserting that enteroviral damage to the brain, the brainstem, vascular endothelium, and spinal pathways constitutes the precise pathological driver of the illness, thus aligning most faithfully with both the literal anatomical meaning of myalgic encephalomyelitis and its long-standing enteroviral etiology.

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Understanding Myalgic Encephalomyelitis (M.E.) (also known as 'Enteroviral Encephalomyelitis')

Background

If a patient or a family member has tried to search the internet for an understanding of Myalgic Encephalomyelitis (M.E.) (also known as 'Enteroviral Encephalomyelitis'), or so-called “Chronic Fatigue Syndrome” (CFS, currently being called “ME/CFS”), they will have been overwhelmed by the multitude of technical descriptions and the numerous overlapping medical conditions. 

There have been many attempts to define Chronic Fatigue Syndrome, some of them described in our 1992 book ‘The Clinical and Scientific Basis of Myalgic Encephalomyelitis (also known as 'Enteroviral Encephalomyelitis') and Chronic Fatigue Syndrome’. 


M.E. (also known as 'Enteroviral Encephalomyelitis') and "SEID' (ME/CFS) ...

...represent a complex, multi-system group of afflictions, adversely affecting the brain, heart, neuro-endocrine, immune and circulatory systems in our bodies, but, crucially, M.E. (also known as 'Enteroviral Encephalomyelitis') is a distinct illness, while both "Chronic Fatigue Syndrome"... 

...and "ME/CFS" are 'umbrella terms' for a group of symptoms common to many illnesses, and conditions. 

This has led to M.E. symptoms being confused with the symptoms for neurasthenia, multiple chemical sensitivities, fibromyalgia, post-mononucleosis fatigue syndrome, and much more.

The US Centers for Disease Control and Prevention (CDC) first defined CFS, with great emphasis on the word “FATIGUE”, in 1988. 

This definition, referred to as “Holmes”, was later replaced by the 1994 ”Fukuda”,...

...then by the 2005 “Reeves”,...

...and most recently by the 2015 IOM (Institutes of Medicine) report, still emphasizing FATIGUE. 

Definitions have also included the 1991 UK ”Oxford” report... 

...and the more well-known 2003 Canadian Consensus Criteria (CCC), that talks of Myalgic Encephalomyelitis (also known as 'Enteroviral Encephalomyelitis') and 'Chronic Fatigue Syndrome' as though they were the same illness. THEY ARE NOT. 

The CCC was updated and replaced in 2011 by the International Consensus Criteria (ICC) which insisted that 'Chronic Fatigue Syndrome' should not be considered a diagnostic entity and that 'Myalgic Encephalomyelitis' (also known as 'Enteroviral Encephalomyelitis') is a specific diagnosis requiring thorough patient history, examination, and testing. 

Unfortunately the CDC did not accept or adopt the ICC, written by 26 experts in the field, and instead commissioned its own group with limited access to Myalgic Encephalomyelitis (also known as 'Enteroviral Encephalomyelitis') information, to create their vague 2015 IOM report, minimizing the disease yet again. 

This is the report most widely used and accepted throughout the world today (2022).[except of course for those countries and organizations that still use only “CFS”, or worse, also classify this “CFS” as a psychiatric condition, using euphemistic terms like Central Sensitisation Syndrome or Functional Neurological Disorder].

The position of Nightingale Research Foundation is that the IOM does NOT describe or define M.E. (also known as 'Enteroviral Encephalomyelitis'), and that the ICC, while far superior to the IOM, is still not specific enough. 

In creating the Nightingale Definition, we have studied decades of clinical evidence, and followed up on the work of Dr. Melvin Ramsay (case descriptions published 1986 and 1988), Dr. Elizabeth Dowsett, Dr. John Richardson, and others who closely studied M.E. (also known as 'Enteroviral Encephalomyelitis') patients and M.E. outbreaks over several decades.

​M.E. (also known as 'Enteroviral Encephalomyelitis') has a clearly defined disease process, while: 

CFS by definition has always been a syndrome. 

In light of this state of affairs, the Nightingale Research Foundation created its 2007 Definition of M.E. 

...and updated it in 2016. 

Our Nightingale Definition of M.E. is located on our website under "Publications" and is available as a free download in English, French, Norwegian, and Danish


In 2003, Dr. Byron Hyde completed a chapter for L. A. Jason, P. A. Fennell and R. R. Taylor for their book Handbook of Chronic Fatigue Syndrome, John Wiley and Sons Inc., Hoboken N.J., titled “The Complexities of Diagnosis”1, Chapter 3. 

This chapter includes the following definition of CFS: 

​The Complexities of Diagnosis

“The physician and patient alike should remember that CFS is not a disease. 

It is a 'chronic fatigue state' where the one essential characteristic of M.E. (also known as 'Enteroviral Encephalomyelitis') is 'acquired' Central Nervous System (CNS) dysfunction, that of CFS is 'primarily' chronic fatigue. 

By assumption, this CFS 'fatigue' can be acquired 'abruptly' or 'gradually'. 

Secondary symptoms and signs were then added to this 'primary' fatigue anomaly. 

None of these secondary symptoms is individually essential for the definition and few are scientifically testable. 

Despite the list of signs and symptoms and test exclusions in these definitions, patients who conform to any of the CDC, Oxford, Australian and Canadian CFS definitions may still have an undiagnosed major illness, certain of which are potentially treatable. 

Although the authors of these definitions have repeatedly stated that they are defining a syndrome and not a specific disease, patient, physician, and insurer alike have tended to treat this syndrome as a specific disease or illness, with at times a potentially specific treatment and a specific outcome. 

This has resulted in much confusion, and many physicians are now diagnosing CFS as though it were a specific illness. They either refer the patient to pharmaceutical, psychiatric, psychological, or social treatment or simply say: “you have CFS and nothing can be done about it”. The CFS definitions have another curiosity. If in any CFS patient, any major organ or system injury or disease is discovered, the patient is removed from the definition. 

"The CFS definitions were written in such a manner that CFS becomes like a desert mirage: The closer you approach, the faster it disappears and the more problematic it becomes"

Some of the definition essentials required to accurately diagnose either M.E. (also known as 'Enteroviral Encephalomyelitis') or CFS, or any chronically ill patients group, include: 

  • A working case clinical definition must be short, clear and testable.

  • Patients and their illness or illnesses must be part of an integrated system. Neither the patients’ patho-physiology nor their illness can be understood without a concise knowledge of their integrated pathophysiological systems.

  • A statistically significant group of patients who have M.E. (also known as 'Enteroviral Encephalomyelitis') and CFS type illnesses must be subjected to a complete personal and family history to map the genetic and historical causes of their illnesses. 

  • Accordingly, the patient’s illness can only be understood if a complete total body mapping is performed on all systems and organs. The mammalian and animal bodies are an integrated physiological mechanism and when one major system change occurs, many physiological systems are liable to shift. 

  • In the past it has been facile to pose psychiatric diagnoses on M.E. (also known as 'Enteroviral Encephalomyelitis') and CFS patients since psychiatric diagnoses cannot be subjected to scientific examination. Psychiatrists rarely actually examine patients and almost never do an integrated patho-physiological patient investigation of the patient’s organs and systems. Nor have most psychiatrists been of any help in diagnosing M.E. (also known as 'Enteroviral Encephalomyelitis') and CFS patients except to the insurance industry. In the more than 70 years since the first major M.E. (also known as 'Enteroviral Encephalomyelitis') epidemic struck the Los Angeles County General Hospital in 1934, no psychiatric treatment has proven significantly effective in treating the M.E. (also known as 'Enteroviral Encephalomyelitis') and CFS group of patients and restoring them to health. This is understandable since neither represents a psychiatric disorder. 

  • Effective treatment of the M.E. (also known as 'Enteroviral Encephalomyelitis') and CFS group of patients depends upon precisely defining the organ and system pathologies and learning how to treat these patho-physiological conditions. 

  • M.E. (also known as 'Enteroviral Encephalomyelitis') and the CFS group of illnesses are chronic illnesses. For too long physicians have been considering chronic diseases and chronically ill patients as they would acute short-term illnesses. We believe this is an error and we direct those interested to our chapter on diagnosis. Relatively young chronically ill patients, often do not have a disease process, they often have many disease processes.

Definition of Myalgic Encephalomyelitis (M.E.) (also known as 'Enteroviral Encephalomyelitis)

Nightingale is pleased to offer the definition of Myalgic Encephalomyelitis (also known as 'Enteroviral Encephalomyelitis') in a downloadable PDF format for free in the following translations:

Norway's ME Association seems to have gone along with Dr. Charles Shepherd's "GASLIGHTING PROPAGANDA" about "M.E. NOMENCLATURE", who is on the record as NOT BELIEVING there is an "ENCEPHALOMYELITIS" involved with "MYALGIC ENCEPHALOMYELITIS". Dr. Charles Shepherd fell ill with "HERPES ZOSTER ENCEPHALITIS" at 28 years old, which is NOT Royal Free Disease to start with, so he has absolutely ZERO LIVED EXPERIENCE of M.E. (also known as 'Enteroviral Encephalomyelitis'). Dr. Shepherd would fall under the acute onset "MISDIAGNOSED" CHRONIC FATIGUE SYNDROME (CFS) selection of illnesses, and it is true that his illness, didn't involve "ENCEPHALOMYELITIS" or "MYALGIA".

Byron Hyde, MD: «What is Myalgic Encephalomyelitis?»

The ME Association has been given permission to share a new article by Dr. Byron Hyde. The article comes from The Nightingale Foundation.

What is Myalgic Encephalomyelitis (also known as Enteroviral Encephalomyelitis) ?

Unfortunately, the majority of physicians in the UK, Europe and North America, not to mention the rest of the world, have a poor and sometimes distorted idea of what Myalgic Encephalomyelitis represents. 

One of the several fallacies is that M.E. is just another name for Chronic Fatigue Syndrome (CFS). 

It is not and never has been. M.E. is a biphasic epidemic and sporadic enteroviral infectious disease. Up to 1955 and the introduction of Jonas Salk’s polio immunization M.E. tended to occur in the same location and at the same time as polio epidemics. In epidemic form, both Polio and M.E. tend to peak in the north temperate hemisphere during the period of July to November, with a last small blip around Christmas when families tend to get together.

< CFS is a syndrome based upon a series of symptoms that are common to hundreds of different, often serious diseases and diagnostic of none. CFS can also represent multiple different pathologies or diseases in the same person. At times, CFS may be related to undiagnosed genetic illnesses. Many physicians assume patients with multiple symptoms and no easily observable pathologies are actually hysterical, anxiety neurosis or depressive patients. They employ the term CFS in place of making the unwelcome diagnosis of hysteria or psychiatric disease. The term CFS should not be utilized, as in the minds of most physicians it is a disparaging term, and in the minds of many physicians, a term belittling to the patient. >

Understanding M.E. is relatively simple. However, understanding M.E. was much simpler sixty years ago. Prior to 1955, if the patient fell ill with M.E. their illness would have been called: Missed Polio.

Missed polio was a diagnosis given prior to 1955, when the patients fell ill during a Poliomyelitis epidemic and were left disabled, weak, often in pain and with cognitive difficulties, but were not paralyzed.

The term Myalgic Encephalomyelitis was a name developed to describe the disabling chronic injury sustained by the nurses and physicians of the Royal Free Hospital in London England in 1955. This epidemic was part of the combined epidemic of paralytic and missed poliomyelitis which struck across England and London that year. 

This was also the same year that the first major successful paralytic polio immunization, the incredibly effective Jonah Salk immunization, began to be distributed in the United States of America. 

The Salk immunization solved the problem of flaccid paralysis and death caused by the three known polioviruses but in 1955 Salk and colleagues didn’t realize there were some hundred other dangerous enteroviruses which existed but had not yet been discovered. 

These missing links to the puzzle of acute and chronic enterovirus illness were not included in these Salk and later Sabin polio immunizations. 

Unknown to them, some of these other dangerous enteroviruses also caused flaccid paralysis and several caused what they referred to as missed polio, what we know since the 1950's as myalgic encephalomyelitis. 

Many of these other disease causing enteroviruses are very similar in genetic structure to the then known polio-enteroviruses. Many differ, one from the other, by less than 5% of their genomic (genetic blueprint) structure. 

There are at least six or more enteroviruses causing paralytic or flaccid paralysis and I assume that one day they will all be included in the polio immunization.

 These relatively new enteroviruses appear to be on the ascendant.

In addition to "Myalgic Encephalomyelitis' (also known as 'Enteroviral Encephalomyelitis'), which falls closer to the Nightingale Research Foundation Definitions (2007 & 2016) and the International Consensus Criteria (2011), the following partial list of enteroviral provoked diseases and syndromes includes :

  1. Polioencephalitis
  2. Anterior Poliomyelitis
  3. Subclinical infection*
  4. Gastroenteritis (Diarrhea and vomiting) and Abdominal Pain (e.g. Non-cytolytic enterovirus infection)*
  5. Non-cytolytic enterovirus infection and viral persistence: The virus avoids complete clearance and stays in tissues at low levels, causing a chronic, slow-burning immune response.
  6. Non-poliovirus Enterovirus asymmetrical "Flaccid Paralysis" and Poliomyelitis-like Syndrome with "Muscle Atrophy", Acute Flaccid Myelitis (AFM) and Paraplegia*
  7. Enteroviral Aseptic Meningitis*
  8. Enteroviral Meningoencephalitis*
  9. Enteroviral Limbic Encephalitis + Rhombencephalitis (Non-polio enterovirus Polioencephalitis)*
  10. Post-Polio Fatigue - Central Fatigue and Muscle Fatigue*
  11. Dysautonomia and PoTS*
  12. Gastroparesis, Gastric Dysmotility and Paralytic Ileus*
  13. Paresis effecting legs (Neurogenic Weakness)*
  14. Neurogenic Pulmonary Oedema (NPE)*
  15. Radiculitis (Nerve Root inflammation)*
  16. Dorsal Root Ganglionitis*
  17. Low Blood Volume (Hypovolemia) and Cerebral Hypoperfusion (e.g. Segami Oasis Neurogam SPECT scan can measure both of these)*
  18. Low Blood Pressure (Orthostatic "Neurogenic" Hypotension, Neurally Mediated Hypotension and Neurally mediated (vasovagal) syncope)*
  19. Infectious Myositis mimicking Polymyositis, and Anti-MDA5 Dermatomyositis*
  20. Epidemic Pleurodynia (also known as Bornholm disease, Devil’s Grip or Epidemic Myalgia)*
  21. Tietze Syndrome, or Costochondritis*
  22. Herpangina and Hand, Foot and Mouth Disease (HFMD) (e.g. Coxsackie A & B) and Enterovirus A71*
  23. Viral Pneunomia and Pleurisy*
  24. Sepsis*
  25. Rubella-like (German Measles) Rash (e.g. Echovirus)
  26. Labyrinthitis and Vestibular Neuritis*
  27. Hypothalamic Dysfunction - Adrenal Dysfunction - Tertiary Adrenal Insufficiency*
  28. Bystander Activation: The intense inflammation caused by the virus activates nearby "dormant" immune cells that were already prone to attacking the body*
  29. Molecular Mimicry: A viral protein looks similar to a human protein (e.g., CVB's 2C protein, and the pancreas's GAD65), confusing the immune system into attacking both*
  30. Autoimmune Hemolytic Anemia (AIHA): Infections from enteroviruses like EV-71 have been linked to rare cases of the immune system attacking red blood cells*
  31. Systemic Lupus Erythematosus (SLE): While 'Epstein-Barr' is the primary viral suspect for Lupus, 'enteroviruses' (like Coxsackie 2B) have been studied for their ability to cross-react with specific self-proteins, potentially contributing to disease flares (Suspected)
  32. Immune Thrombocytopenia (ITP): In rare cases, enteroviral infections are suspected of triggering the immune-mediated destruction of blood platelets (Suspected)
  33. Endometriosis (Suspected)*
  34. Crohn's Disease (Suspected)*
  35. Low T3 Syndrome, Primary Thyroiditis Failure (Hashimoto's Thyroiditis), Thyroid Atrophy*
  36. B12 Deficiency, or Pernicious Anemia*
  37. Connective Tissue Disease*
  38. Type 1 Diabetes, Enteroviral Pancreatitis*
  39. Enteriviral Pericarditis, Myopericarditis, Left Ventricular Diastolic Dysfunction (LVDD) and Congestive Heart Failure*
  40. Myocarditis, Perimyocarditis, Autoimmune Myocarditis and Dilated Cardiomyopathy*
  41. Neonatal Pneumonia, Neonatal Sepsis and Neonatal Gastroenteritis Viral Deaths, Necrotizing Enterocolitis (NEC) in the new-born
  42. Palindromic Rheumatism (Inflammatory Arthritis)*
  43. Juvenile Rheumatoid Arthritis (JRA) (e.g. Coxsackie A13)
  44. Haemorrhagic Conjunctivitis (Apollo Disease)
  45. Dystonia*
  46. Reactive Depression*

*In my experience those marked with an Asterisk have at times been associated with M.E.

Certain of the above disease spectrums have several things in common:

Where known, the shortest incubation period is 2-6 days, (short incubation allows epidemic spread)

  1. A few: e.g. paralytic polio and M.E. are biphasic with early minor symptoms followed by severe chronic illness,
  2. As in polio, the majority of those infected don’t fall ill but tend to become immune for life,
  3. Some are infected, show no signs of illness but become carriers, infecting other people,
  4. Some fall ill for a few days or weeks and then recover,
  5. Some fall ill, improve and get better only to have recurrent chronic illness, sometimes years later,
  6. Some fall ill and remain chronically ill and disabled, and among adults, often for life,
  7. Some die and, according to Dr. Ivar Wickman, some patients are identified as other illnesses including:
  1. Landry’s Paralysis (both 'ascending' Guillain-Barré syndrome  (GBS) and 'descending' Miller Fisher Syndrome (MFS)
  2. Chronic Pain Syndromes (e.g. Fibromyalgia, Migraines and Complex Regional Pain Syndrome) and
  3. Patients with Cognitive Difficulties.
The enteroviruses causing paralytic polio or flaccid paralysis are typical of this class of viruses. Less than 5% of patients who fell ill with poliomyelitis were paralyzed or died. When M.E. patients die, they tend to be diagnosed as having had other cause such as encephalitis or an abrupt cardiac death. One of the pathologic vascular injuries given in this description of M.E. patients was found in M.E. patients who died during the 1934 Los Angeles epidemic.

There is also a major forgotten tragedy associated with the Salk and Sabin polio immunizations. These immunizations were so rapidly successful in preventing paralytic poliomyelitis that immediately after its release the number of cases of deaths and paralysis caused by the three known polioviruses ceased almost overnight in much of the western world. Nobody realized the number and extent of these some 100 different but similar enteroviruses in 1955 or the pathologies they continue to cause. Within ten years of the release of these immunizations, probably as many as 50,000 enteroviral researchers around the world were dismissed or their funding removed. Almost none of these enteroviral experts were left to work on the largely unknown enteroviruses causing M.E. and the other severe enteroviral diseases. I have no doubt 100,000 deaths or more occur every year around the world due to these enteroviruses. I have no doubt 100,000 cases of chronically disabling Myalgic Encephalomyelitis occur around the world every year.

The Invisible Disease: The tragedy persists today. There is yet no curative treatment or immunization for M.E. or any of these enteroviral illnesses. Other than for the three polioviruses, there are no preventive immunizations. Because M.E. so rarely kills, it has become an almost invisible disease. Yet several enteroviral infections in their most severe form result in various chronic disabilities and some in paralysis and death, in addition to causing a tremendous economic burden to the state. There is no doubt that enteroviruses cause M.E. To date, the only viruses recovered consistently in any epidemic of myalgic encephalomyelitis disease have been enteroviruses. This is the virus family we recovered in Canada during the 1984 North American pan-epidemic that struck Lake Tahoe, North Carolina, Montreal, and across Ontario and in all subsequent M.E. patients where a viral cause was found.

Byron Hyde with ME Association founder Ellen Piro at the 2016 IACFS/ME conference

Byron Hyde is a Canadian physician who has worked exclusively with M.E. since 1984. In 1988, he founded The Nightingale Research Foundation to promote research into M.E.. Byron Hyde uses a narrow definition of M.E., in line with Ramsay's description of the disease from the 1950's.

In this article he discusses the possible link between M.E. and enteroviruses (intestinal viruses). 

This is not a new idea, as he writes, M.E. has previously been referred to as an "atypical polio". 

Other researchers are also looking at enteroviruses.

NAME CONFUSION AND CONTROVERSY - The story of M.E.

M.E., CFS, ME/CFS, CFS/ME or maybe SEID? Physical or psychological? To understand the background of the different terms and views on the disease, it is good to know something about the history.

The first diagnosis

M.E., Myalgic Encephalomyelitis, was first described by Dr. Melvin Ramsay in 1956 after an outbreak at the Royal Free Hospital in London. Here is a link to the article in the journal The Lancet, where the term ME was first used.

In 1969, the disease was accepted by the WHO as a neurological disease. In ICD-8, the name Benign myalgic encephalomyelitis (M.E.) is used with diagnostic code G93.3 under Diseases of the nervous system.

Ramsay published his diagnostic criteria in 1986:

Ramsay's diagnostic criteria looked like this:

A syndrome initiated by a virus infection, commonly in the form of a respiratory or gastrointestinal illness with significant headache, malaise and dizziness sometimes accompanied by lymphadenopathy or rash. Insidious or more dramatic onsets following neurological, cardiac or endocrine disability are also recognised. Characteristic features include:

(1) A multisystem disease, primarily neurological with variable involvement of liver, cardiac and skeletal muscle, lymphoid and endocrine organs.

(2) Neurological disturbance - an unpredictable state of central nervous system exhaustion following mental or physical exertion which may be delayed and require several days for recovery; an unique neuro-endocrine profile which differs from depression in that the hypothalamic/pituitary/adrenal response to stress is deficient; dysfunction of the autonomic and sensory nervous systems; cognitive problems.

(3) Musculo-skeletal dysfunction in a proportion of patients (related to sensory disturbance or to the late metabolic and auto immune effects of infection)

(4) A characteristically chronic relapsing course.

Similar outbreaks have been described in Iceland in Akureyri in 1947 and Los Angeles in 1934, and other outbreaks are also known. Various names have been used, such as "atypical poliomyelitis", Akueyri disease, Tapanui Flu, etc.

The 70's and beyond: New discord

The controversy over whether the disease was physical or psychological began in the 1970s, when a group of psychiatrists re-examined the outbreak at the Royal Free Hospital. Given the lack of physical findings, and the fact that so many of the patients were women, they believed the disease was a form of mass hysteria . However, mathematical modeling of this and other outbreaks finds that they are consistent with models of infectious diseases. Even those affected by the outbreak strongly disagreed with McEvedy and Beard's analysis.

Unfortunately, McEvedy and Beard's article led to a decline in interest in biomedical research on M.E. (also known as Enteroviral Encephalomyelitis)

There have always been professional communities that have believed M.E. (also known as Enteroviral Encephalomyelitis) to be a physical illness, but they were overshadowed by those who believed M.E. (also known Enteroviral Encephalomyelitis) to be psychologically caused.

In the 1980's, a group of British psychiatrists became interested in the phenomenon of 'fatigue'. 

In 1988, Simon Wessely proposed that 'CFS' was caused by “abnormal illness behaviour” and not "hysteria", as had been proposed in the 1970's. This is what we now call the “biopsychosocial” model of the disease.

The biopsychosocial model of illness is really just a way of seeing illness in the context of psychological and social factors, and seeing that everything affects everything. 

The “biopsychosocial” model of M.E. (also known as Enteroviral Encephalomyelitis) ignores the “bio”, and claims that it is the thoughts that create the symptoms of M.E. (also known as Enteroviral Encephalomyelitis), where discomfort after illness causes the sufferer to believe that they are physically ill, become afraid of activity, overfocus on symptoms, become deconditioned, and enter a vicious cycle. 

Suggested treatment is 'cognitive behavorial therapy' and 'graded exercise therapy'.

The name CFS came into use after an outbreak in the United States at Lake Tahoe, Nevada in 1984-85. The doctors who described the disease were not familiar with Ramsay's description of the outbreak at the Royal Free Hospital, and coined a new name.

The first time WHO used the term CFS was in 1992.

Back to a narrower definition of a physical illness

In 2015, a major report from the IOM, commissioned by US health authorities, was published. The report stated that it was a “severe, chronic, multisystem disease with significant disability” , the main feature of which is post-exertional malaise (PEM).

It proposed a new name, “Systemic Exertion Intolerance Disease” or SEID, but this has not caught on.

However, the IOM report has led to a change in the view of CFS in the US, and a boom in biomedical CFS research.

In 2021, the UK's NICE published new guidelines for CFS, distancing itself from treatments linked to the "biopsychosocial" model of CFS. 

They launched diagnostic criteria similar to those of the IOM.

In recent years, it has become common to use the term ME/CFS. However, Norway has chosen to use CFS/ME.

Are M.E. (also known as 'Enteroviral Encephalomyelitis') and 'CFS' the same or something completely different - ​​and what about SEID?

Different diagnostic criteria are associated with the different names. 

In the UK, 'CFS' is most often associated with the Oxford criteria, which only require 6 months of 'unexplained fatigue' to make the diagnosis.

In other words, these criteria select a very large and complex group, and most studies on cognitive therapy and exercise as a treatment for 'fatigue' use these criteria.

In the USA, the term 'CFS' has been used by both those who believe M.E. is physical and those who believe it is psychological, and has been associated with the 'Fukuda CFS criteria', which require at least 'four of eight' symptoms in addition to 'fatigue' for diagnosis. 

The Fukuda criteria have been widely used in research in the USA. 

SEID and NICE require fewer symptoms and select more patients than the Canada or ICC criteria. 

SEID, NICE and CCC require PEM to be present for diagnosis, while PEM may be present in Fukuda, but does not have to be.

People who meet the Oxford criteria but do not have PEM are not a homogeneous group.

How many are selected based on the various criteria is uncertain. There is a lack of good studies on prevalence? 

Want to read more?

Dr. Byron Hyde has written a history of M.E. and CFS, and how the different diagnostic criteria were developed, and how the names have been used. It is interesting to read how the focus shifted from physical to psychological, and the quality of the research that caused this shift.

The different diagnostic criteria

Over the past 25 years, a number of different diagnostic criteria have been used to capture M.E. and 'misdiagnose' CFS illness. 

There are large differences in prevalence when using different criteria:

1988: CFS Holmes criteria cohort. (the first diagnostic definition for CFS) - Original CFS definition overlaps with "Abortive Polio" onset symptoms, and "Enteroviral Meningoencephalitis" and "Enteroviral Limbic Encephalitis + Enteroviral Rhombencephalitis" pathological injury

1991: CFS Oxford criteria cohort. (Very broad, and will include people with fatigue for various reasons)

1993: M.E. London Criteria cohort. The London Criteria are found in the same document as the Canada Criteria (see below)

1994: CFS Fukuda criteria cohort (most widely used in the research literature)

2003: Mixed M.E. and Chronic Fatigue Syndromes cohorts - Canadian Consenus Criteria (clinical criteria, often used together with the Fukuda criteria in studies) - later as error by Dr. Bruce Carruthers

The Canada criteria can be downloaded and read in English here.

The Canada criteria can be downloaded and read in Norwegian here (The translation is by the Norwegian ME Association)

2011: ICC (revised version of the Canadian Consenus Criteria) - intended to seperate Myalgic Encephalomyelitis (M.E.) from Chronic Fatigue Syndromes (CFS)

The ICC criteria can be downloaded and read here.

Prevalence estimates using the different diagnostic criteria have varied somewhat, but several studies show that the Fukuda criteria from 1994 give a prevalence of 0.2-0.4%. Oxford gives a higher prevalence, around 2.7%.

The empirical criteria from the CDC in the United States have been shown to give a prevalence of 2.4%, which is 10 times higher than the Fukuda CFS Criteria.

The Canadian Consensus Criteria (CCC) - Mixed M.E. and CFS cohorts and the International Consensus Criteria (ICC) - intended to separate M.E. will likely give a somewhat lower prevalence than the Fukuda CFS criteria A British study gives a prevalence of 0.1%.

IOM report 2015 - a new name for "Chronic Fatigue Syndrome"

In 2015, the US Institute of Medicine (IOM, now the National Academy of Medicine) published a comprehensive report, based on over 9,000 research articles. In the report, they go a long way toward establishing that 'CFS' is a physical illness, and propose a new name: SEID - Systemic Exertion Intolerance Disease. 

The report states that the name 'CFS' contributes to stigmatization and trivialization of the illness, and that a new name must show that this is a physically serious illness.

New diagnostic criteria have been developed for SEID and are being used by the CDC, but the center still uses the name 'ME/CFS' in describing the disease.

A summary of the IOM report can be read here.

The complete report can be read here.

NICE guidelines 2021 - Chronic Fatigue Syndrome (CFS)

In 2021, the UK's NICE conducted a new review of the research literature on CFS. The 2021 guidelines recognize CFS as a physical illness, promote diagnostic criteria that require PEM, and move away from the paradigm that CFS is physically caused. The guidelines warn against graded exercise therapy and against offering cognitive therapy as a cure for CFS. 

Read NICE guidelines for ME/CFS here.

What is the difference between M.E. (also known as 'Enteroviral Encephalomyelitis') and CFS?

Psychology professor Leonard Jason at DePaul University, Chicago, has conducted many studies on prevalence, and also compared diagnostic criteria. In these short video interviews, he talks about the issues surrounding diagnostic criteria and naming the disease:

Professor Leonard Jason has written an article about the challenges associated with estimating the prevalence of M.E.


WHAT IS M.E.?

Myalgic encephalomyelitis (M.E.) (also known as 'Enteroviral Encephalomyelitis') is an enteroviral, vascular neuroimmune disease with an incubation period of 2-6 days. In the ICD-11, M.E. is classified as a neurological disorder (8E49). The guidelines for acquired brain injury (ABI) apply. It is estimated that there are at least 15,000 M.E. patients in the Netherlands.

M.E. affects brain function as well as various other bodily systems, such as the immune system and the cardiovascular system (heart and blood circulation), energy supply, and hormone production. In many cases, the disease is chronic and can have an unpredictable course (Ramsay 1986).

Until 1954, M.E. was considered a form of polio (Wickman 1905: 'superior polio', referring to the location of the brain lesion). With the narrowing of the definition of polio to cases involving (long-term) paralysis, an independent designation became necessary. Compared to paralytic polio, brain dysfunction is dominant in M.E. (Hyde, 2020). The name M.E. (Acheson 1956) correctly indicates that it involves inflammation (-itis) in the brain (encephalos) and spinal cord (myel), accompanied by muscle pain (myalgia).

Initially, M.E. was only known from polio outbreaks. Later, it became apparent that other enteroviruses can also cause the disease. Nowadays, the disease occurs throughout the population. ME can be diagnosed using a SPECT scan (Hyde 2020). The enterovirus is detectable in the blood during the acute phase and can still be found later in tissue examination (Chia 2005).

Important symptoms of M.E. include: physical and mental exhaustion, poor sleep, muscle weakness and pain, gastrointestinal complaints, difficulty with attention and concentration, ear, nose, and throat complaints, headache, joint pain, dizziness, and visual impairment. 

M.E. IS A DISEASE DIAGNOSIS

Myalgic Encephalomyelitis is a disease diagnosis. Your medical symptoms and medical history put the doctor on the right track, but it must still be determined whether you actually have it. This is done in the most direct way through a brain scan (SPECT or PET) and by detecting the enterovirus that causes the disease, possibly via a biopsy if the doctor deems it necessary.

Without inflammation of the central nervous system, to which the name of the disease refers, the diagnosis is not applicable. The lesions involve the same locations as in poliomyelitis (Hyde, 2020). SPECT data can be sent to Ottawa for analysis using the best software.

In the Netherlands, there is insufficient medical knowledge and willingness to diagnose M.E. in this way. A diagnostic protocol is lacking, as is a center of expertise. A petition from the Stichting Erken M.E. (Recognize M.E. Foundation) from 2009 to the Health, Welfare and Sport Committee of the House of Representatives calling for improvement in this area was never addressed.

In practice, this means that to obtain certainty regarding the diagnosis, you must seek objective measurements of your physical capabilities and a number of abnormalities known to be associated with M.E. from various doctors.

The diagnostic process will generally consist of four components:
  • objectifying the complaints;
  • ruling out other causes (differential diagnosis);
  • identifying known deviations (markers);
  • further diagnostics for the purpose of treatment.
COURSE OF THE DISEASE

M.E. is caused by an enterovirus, with an associated short incubation period (Hyde 2020). Risk factors therefore include occupations involving frequent close contact with other people, as well as travel within two weeks after vaccination. One can develop M.E. if the blood-brain barrier is damaged, for example as a result of infection with a herpesvirus (such as infectious mononucleosis) or due to heavy metals. M.E. can also be transmitted via contaminated blood. M.E. patients are not permitted to donate blood or be organ donors.

In the early stages of the disease, there appears to be a chance of recovery, especially for younger patients. In many cases, however, the disease becomes chronic and, if no successful treatment takes place, becomes a lifelong ordeal.

The medical symptoms of M.E. are diverse and can fluctuate. The main symptom is physical exhaustion, following relatively minor exertion and with a long recovery time (Carruthers 2011). However, M.E. is a multi-system disease that leads to numerous medical complaints.

In most cases, M.E. is not immediately life-threatening. Ultimately, the disease leads to heart, kidney, and liver failure sooner than in healthy people. Some patients resort to suicide due to unbearable suffering. Doctors are permitted to provide assistance in this regard.

TREATMENT FOR M.E. 

There are various treatments for M.E. that have proven promising in practice. However, these are not reimbursed by health insurers because an indication from the Minister of Health, Welfare and Sport is lacking. Furthermore, further scientific research is still urgently needed.

Therefore, medical treatments are hardly, if at all, offered in the Netherlands. Going abroad is sometimes possible, but is a difficult undertaking for many patients.

On May 12, 2009, the action group ErkenME submitted a petition to the Health, Welfare and Sport Committee of the House of Representatives requesting, among other things, that the availability of treatments for M.E. in the Netherlands be improved. No response was ever received to this.

The treatment of M.E. consists of a combination of medications and techniques. 

For some treatments, further diagnostic testing is necessary first, because they depend, for example, on exactly which viruses and metabolic disorders are present, and this varies from patient to patient.

MANAGMENT OF M.E. 

The limitations imposed by M.E. affect the quality of life. It is therefore important for M.E. patients to manage the disease as well as possible. Professional guidance in this regard may be desirable, for example from an occupational therapist.

Pacing
Continuing for too long inevitably leads to a setback. By taking timely breaks and alternating physical and mental exertion, exceeding one's limits can often be prevented.

School
If you are following a course of study, the school is obliged to take your limitations into account (reasonably). For example, you may take longer to complete the course or do more studying at home.

Work
If you are still able to work, it may be important to agree with your employer to work fewer hours, work from home, or have your workplace adjusted.

Buddy
Some patients benefit from a buddy with whom they maintain contact and build a bond of trust. M.E. patients in the Rotterdam region can make use of the free  Buddy Care provided by the Humanitas Foundation for this purpose.

LIST OF DOCTORS

The number of doctors with specialized knowledge of M.E. is still very limited. In principle, however, any hospital can perform the relevant tests. On this page, we inform you about doctors, other experts, and laboratories known to us. Each has its own approach and range of diagnostics and/or treatment.

The ME Association Netherlands is not liable for the consequences of your choices.

KNOWLEDGE ABOUT M.E. 

Originally, M.E. was considered a form of poliomyelitis. In 1954, the definition of polio was modified, excluding non-paralytic cases. Since then, scientific research into M.E. has been conducted primarily by physicians who examined patients in their own practices. They were present when an outbreak of M.E. occurred (Ramsay, 1986), came into contact with the disease because they themselves (Hyde, Jason) or a family member (Chia) contracted it, or otherwise became personally involved.

After the first world congress on M.E., the knowledge available at the time was compiled (Hyde, 1992).

The advancement of medical knowledge and technology has made new, targeted research into M.E. possible, which is also attractive to top researchers. This involves immunological, virological, metabolic, and cardiovascular research. However, hardly any resources are allocated for this.

Epidemic knowledge

Initially, M.E. was known only from outbreaks in combination with (other forms of) poliomyelitis, possibly first in Vermont in 1894, and later also separately. From the mid-1950's onwards, increasingly more sporadic cases were observed, with a large increase in the 1970's and 1980's. The incidence currently appears to be more or less stable. The number of M.E. patients in the Netherlands is approximately 14,000, the vast majority being women and predominantly middle-aged.

CAUSE OF M.E. 

M.E. has the same cause as poliomyelitis, namely an enterovirus (Hyde 2020). About 25 enteroviruses are known to cause this and other conditions. Compared to polio, the brain is more severely affected in M.E., and the spinal cord less so (Wickman 1905).

In both M.E. and polio, the immune system's response to the virus leads to inflammation of the blood vessels (vasculitis), thereby impeding blood flow (Hyde 2020). In the brain, this always occurs in the same locations, making M.E. easily recognizable on SPECT (Mena, ca. 1985) or PET images, or based on specific symptoms (Carruthers 2011, 2012). Cognitive, autonomic, and motor brain functions are disrupted in a characteristic manner.

A recently distinguished disease, Acute Flaccid Myelitis, is an intermediate form (hybrid) of M.E. and polio (Hyde 2019).

It is not yet known with certainty why some people develop M.E. due to an enterovirus, while others develop, for example, Hand, Foot, and Mouth Disease, or do not become ill at all. Presumably, in M.E. patients, the blood-brain barrier is compromised and the immune system dysregulated prior to infection by, for example, a latent EBV infection (Den Broeder 2014).

At the time of the introduction of the name M.E. (Acheson 1955), inflammations of the central nervous system were known, as well as the enteroviral cause. The question of whether the name accurately reflects the nature of the condition therefore does not arise. Without this context, the diagnosis of M.E. is not applicable.

CLASSIFICATION OF M.E. 

The World Health Organization (WHO) included M.E. in the International Classification of Diseases in 1969. In the ICD-10, M.E. is listed as a neurological disorder under the code G93.3 (post-viral fatigue syndrome). The alphabetical list of terms still contains several outdated synonyms for M.E., as well as various names for local outbreaks of the disease.

The ICD-11 comes into effect on January 1, 2022. For M.E., nothing changes except the numbering. The new code is 8E49 .

The WHO classification reflects international consensus. The publication is preceded by years of discussion with experts.

Synonyms for M.E. in the medical literature are: superior polio, missed polio, aborted polio, atypical polio, and epidemic neuromyasthenia. In older versions of the ICD, the disease was understood as polioencephalomyelitis.

CRITERIA / DEFINITION FOR M.E. 

The main symptoms of M.E. (Myalgic Encephalomyelitis, 1956) are, according to various publications by Ramsay and Dowsett, described as follows in Hyde et al. (1992):

  1. General or localized muscle fatigue after minimal exertion with an unusually long recovery time
  2. Neurological disorders, particularly of cognitive, autonomic, and sensory functions, often accompanied by noticeable emotional instability and a disturbed day/night rhythm.
  3. The occurrence of cardiological and other systemic complaints
  4. Prolonged periods of relapse that tend towards chronicity
  5. Distinct fluctuations in symptoms both within and between episodes

M.E. does not become chronic in all cases. Studies of disease outbreaks have shown that a portion of patients recover in a short time.

In January 2007, a new diagnostic description was formulated by Hyde et al., the Nightingale Definition. A new version appeared in 2011. The approach chosen is the permanent, measurable damage to blood flow in the central nervous system and the consequences this has for metabolism. Hyde distinguishes between an acute phase, in which the disease is contracted, and the subsequent chronic phase.

SCIENCE FOR PATIENTS

Science for Patients is a project of the M.E. Association Netherlands, carried out in cooperation with the ME Research Foundation. The project involves the development of online lectures in which scientists explain how medical science approaches the disease ME and the current state of scientific knowledge regarding M.E.

This project does not stand alone but goes hand in hand with the Ongoing Patient Perspective Survey and the development of the Multidisciplinary M.E. Guideline. The three projects reinforce each other and aim to put M.E. on the map in the Netherlands.

In 2013, video recordings began that fall under Science for Patients. These include lectures given at the National ME Information Day, as well as a number of interviews. All videos are freely available for everyone to watch on the YouTube channel DossierME .

Other series about ME:
AHummingbirdsGuide, Jodi Bassett
GetWellFromME, Giles Meehan
ME&CFS Alert, Llewellyn King

More videos about ME
I Remember ME, Kim Snyder, 2000
Voices from the Shadows, Natalie Boulton and Josh Biggs, 2011

Originally, Science for Patients was a joint project of three patient associations: the MS Association, the Osteogenesis Imperfecta Association, and the ME/CFS Association (the legal predecessor of the ME Association Netherlands), based on an idea by Science Alliance. The application for project funding was positively assessed by an independent committee. However, the Minister of Health, Welfare and Sport subsequently refused to pay out the subsidy to M.E. patients and donated it to another organization, even though that organization had not been involved in the development of the project plan or the application.

The original project proposal, February 2011
Thematic report 'Science for Patients' , March/April 2012, M.E. Research Foundation

Myalgic Encephalomyelitis (also known as 'Enteroviral Encephalomyelitis')

Myalgic encephalomyelitis (M.E.) is an inflammatory neurological disease synonymous with Enteroviral Encephalomyelitis that presents with symptoms involving multiple bodily systems. 

It is triggered by a 'non-polio' enteroviral infection. 

M.E. presents with symptoms in the central nervous system (CNS), autonomic nervous system (ANS), immune system, cardiovascular system, endocrine system, digestive system, and musculoskeletal system.

Myalgic encephalomyelitis was first classified as a neurological disease by the World Health Organization (WHO) in 1969, with the publication of the World Health Organization's ICD-8 manual.

M.E. has occurred in both epidemic and sporadic forms.

Key symptoms include prolonged muscle weakness and muscle fatigability upon minimal exertion, sleep disturbance, orthostatic intolerance and cognitive dysfunction. 

Orthostic intolerance is autonomic nervous system dysfunction causing the worsening of symptoms when standing or sitting upright, and may include feeling faint, dizziness, feeling weak, blurred vision, postural orthostatic tachycardia (PoTS), reduced heart rate variability at night, and both cold and heat intolerance.

Other common M.E. symptoms include muscle pain, nerve pain, neck and spine stiffness, and sensory symptoms including sensitivity to light, sound, touch, skin tingling or numbness and hyperaesthesia (skin sensitivity and pain, and allodynia). 

There is a progressive form of M.E., but it is rarer than the "relapsing-remitting" type.

Among adults, M.E. is more common in women than men. New onset has been observed in children and in adults usually between the ages of 40-60. Bakken et. al notes two age peaks for M.E.; age group 10-19 years and a second peak in the age group 30-39 years.

There are no approved pharmacological treatments for M.E. anywhere in the world except in Argentina, which has approved the immunomodulator Ampligen (rintatolimod) for severe M.E. as of August 23, 2016.

History

Myalgic encephalomyelitis was first classified as a neurological disease by the World Health Organization in 1969, with the publication of the ICD-8 manual. 


The World Health Organization's ICD-8 manual did not include any alternative names for myalgic encephalomyelitis although post-infectious encephalomyelitis and all other encephalomyelitis diseases were classified under the same code; fatigue-related alternative names were not added in any later revisions.

An alternative name Chronic Fatigue Syndrome (CFS) for a fatigue-defined syndrome was not in use at this time; it was proposed in 1987 by the Centers for Disease Control, which adopted new diagnostic criteria the following year.

In the ICD-9, which was published in 1989, the entry for myalglc encephalomyelitis is uses code 323.9.


M.E. has occurred in both epidemic and sporadic form since at least the 1930's, although it has likely been occurring much longer but was not formally named. 

The first recorded outbreak of epidemic myalgic encephalomyelitis was in 1934 in Los Angeles and was thought to be an outbreak of atypical polio. After the outbreak in Akureyri, Iceland in 1946, the disease came to be called Akureyri Disease or Icelandic disease through much of the 1940's and 1950's. It was named M.E. after London's Royal Free Hospital outbreak in 1955. Other names included benign myalgic encephalomyelitis and epidemic neuromyasthenia.

After the Incline Village outbreak in Nevada in 1984, another some what similar outbreak, came to be called, and labelled as Chronic Fatigue Syndrome (CFS).

The name myalgic encephalomyelitis was first used in 1956 in an article in The Lancet medical journal to describ findings from the 1955 Royal Free Hospital outbreak in London, UK. 

The term myalgic encephalomyelitis is a portmanteau of several of the key signs and symptoms of the disease: myalgic (muscle pain), encephalo (brain), myel (spinal cord), itis (inflammation). The central nervous system (brain and spinal cord) are inflamed.

Facial Palsy (Lower Motor Neuron Facial Palsy)

Benign Myalgic Encephalomyelitis

Benign myalgic encephalomyelitis was the term used by the World Health Organization from 1969, with the prefix "benign" used to denote that M.E. was not fatal, the prefix benign was later dropped since M.E. can cause death, for example the deaths of 

Merryn Crofts and... 


Merryn Crofts had very severe M.E., was bedbound and unable to eat. Merryn weighed under six stone (84 lbs) at her death, and was just 21 years-old. 

Merryn's death certificate was the second in the UK to attribute a death to M.E..


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Severe and very severe M.E.?

Severe and very severe M.E. affects about 25% of people with myalgic encephalo­myelitis (M.E.), with patients being housebound or bedbound at some point in their illness, typically needing to use a wheelchair, unable to do any kind of work or study, and often unable to do basic self-care activities unaided. Some people have died of severe M.E., including: 

Kara Jane Spencer (17th August 1990 - 2nd January 2023, aged 32)

Maeve Boothby O'Neill (26th August 1994 - 3rd October 2021, aged 27)

Merryn Crofts (13th May 1996 - 23th May 2017, aged 21)

Emily Collingridge (17th April 1981 - 18th March 2012, aged 30)

Lynn Gilderdale (20th September 1977 - 4th December 2008, aged 31)

Sophia Mirza (8th August 1973 - 25th November 2005, aged 32) - M.E. Awareness Day is named in honour of her birthday. 

What is Severe M.E.?

There is no generally agreed upon description of severe or very severe M.E., but different clinical scales can be used to measure the degree of disability. Very little research has described the symptoms and experiences of patients with severe M.E. or very severe M.E., much of what is known comes from patient and advocacy groups.

A study of 19 bedbound patients with severe M.E. and orthostatic intolerance by van Campen et al (2020) found an average 27% decrease in blood flow to the brain during a 20 degree tilt table test that lasted just 15 minutes. Some patients could not tolerate the orthostatic symptoms for 15 mins and had to finish the test early. The patients average 35 years of age and had been ill on average 14 years. All the severely ill patients had abnormal drops in blood flow to the brain.

Severe M.E. symptom scales

Substantial impairment and disability in adults can be measured using the following scales:

Scales developed by patient organizations

Some scales have a "ceiling effect" that means severe M.E. can not adequately be distinguished from very severe M.E., or from moderate M.E., including the Chalder fatigue scale.

Some patients who are severely ill may not have enough concentration to complete a questionnaire, or may be too ill to communicate, these patients may need another person to complete the rating scale instead, for example a carer or health professional. A pilot study of patients with severe M.E. in North East England found that even when visiting patients at home, some were unable to complete a questionnaire or to even attempt to stand.

Very severe M.E.

Merryn weighed six stone (84 lbs) and was just 21 years old when she died; her autopsy revealed ganglia inflammation.

It is suspected that in the later years of her illness Merryn also suffered from EDS and MCAD. 

Her death certificate was reported to be the second in the UK to attribute a death to myalgic encephalomyelitis (M.E.).

Doctors initially suggested that Merryn was having panic attacks, and her family were later told that she may have conversion disorder, a mental condition formerly known as hysteria. "I knew it wasn't. I work with people who have panic attacks and I can talk them down," said Clare. "Merryn was starting to think 'What if it is in my head?' It made her doubt herself, which is awful." Eventually a private doctor diagnosed Merryn with M.E. and she began to receive treatment on the NHS. Within six months of falling ill she was using a wheelchair, and within a year she was housebound.

A very severe M.E. patient's experience photo shows clear signs of muscle wasting and disability - but for the majority of patients it remains an invisible illness.

People with very severe M.E. are totally bedbound and unable to stand at all.

Some people with very severe M.E. have improved over time, or after surgery from cervical spinal stenosis.

Notable studies

IV Immunoglobulin G may be effective for some with severe M.E.

News articles and interviews

See also

Severe M.E. patient groups

Some people with Severe or Very Severe M.E.

Severe M.E. blogs and websites

Advocacy appeals

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Disease of a thousand names

Myalgic Encephalomyelitis has been referred to as the "disease of a thousand names".

Other names used or proposed in the history of the myalgic encephalomyelitis include atypical polio, Icelandic disease, benign M.E., and epidemic neuromyasthenia, 

This has lead to much confusion as a variety of names have been used at different times to describe discrete outbreaks as well as a larger and potentially more heterogenous population of sporadic cases, defined by a wide variety of diagnostic criteria. 

Some names have emphasized particular symptoms or pathology, including myalgic encephalomyelitis.

A survey by The MEAction Network in 2016 found that the majority of patients prefer the name M.E. 

Onset

According to Dr. Byron Hyde, after an incubation period of 2 to 6 days, the prodromal phase generally involve a flu-like illness with fever. 

In the majority of cases, an infection or infectious process is evident. 

Two to seven days later, a chronic phase commences, characterized by a measurable diffuse change in the function of the CNS. 

It is this second phase, persistent phase that most characterizes M.E.

Signs and symptoms

Symptom presentation and severity can vary considerably day to day and even hour to hour. 

Over-exertion can exacerbate all symptoms, and an exacerbation of symptoms may delayed by 24 hours or more.

The US National Institutes of Health (NIH) notes that sensitivity to noise, light and chemicals may force patients to withdraw from society.

A core symptom, post-exertional symptom excebation (PESE), is intolerance to previously trivial mental or physical effort such as attending a child's school event, running an errand or grocery shopping, taking a shower or brushing teeth; this causes a worsening of symptoms, and deterioration of health from persistent, or repeated exertion.

Clinical findings

There are several signs and findings have been frequently observed in clinical settings:

Diagnosis

There are several proposed criteria for diagnosing M.E. including the International Consensus Criteria (ICC). The original criteria developed by Melvin Ramsay, the Ramsay definition, London Criterias, and the Nightingale Research Foundation Definitions. 

Generally accepted criteria or definitions for diagnosing M.E.

Consists of Dr. John Richardson and Dr. Irving Spurr

Differential diagnosis

The signs and symptoms of myalgic encephalomyelitis can be similar to other medical illnesses, including cancer, multiple sclerosis, lupus, Hashimoto's thyroiditis (hypothyroidism), diabetes mellitus, brucellosis, anemia and others. 

Standard medical tests are needed to help distinguish M.E. from these other illnesses, and additional testing may also be needed.

Course and prognosis

The prognosis for myalgic encephalomyelitis and chronic fatigue syndrome (M.E. and CFS) is considered to be poor with only a small minority (a median estimate of 5%) returning to pre-morbid levels of functioning.

The majority of patients remains significantly impaired. A substantial improvement however is noted in an estimated 40% of patients and the prognosis in adolescents is considered to be better than in adults.

Pathophysiology

Sex differences

A Norwegian M.E. study shows that the disease affects all ages, with two peak ages of 10-19 years and 30-39 years; it is more common in women than in men. 

Research by the Open Medicine Foundation cited in its paper, Metabolic features of chronic fatigue syndrome which studied severe CFS, found that the disease is different in men and women but this is not related to testosterone or estrogen. 

Michael VanElzakker notes there are male and female differences in neuropathic pain. A study of UK and Dutch cohorts found "younger children had a more equal gender balance compared to adolescents and adults."

Genetic risks

Myalgic encephalomyelitis has been reported to run in families, although M.E. is not considered an inherited illness, there is evidence of a genetic predisposition.

Potential causes

Although risk factors for myalgic encephalomyelitis have been identified, 
enteroviruses have been found to be the definitive virus associated with all cases of M.E.. 

There is also a shift from the Th1 type of helper T cells, which fight infection, to the Th2 type, which are more active in allergy and more likely to attack the body.

Viruses

M.E. as an immune response to a chronic infection. 

The association between M.E. and Coxsackie B and Echoviruses is well written up, within the historical literature. 

Researchers have stated that evidence from epidemic myalgic encephalomyelitis strongly points to an enterovirus. 

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Nurses who became ill during an outbreak of "atypical polio" at the Los Angeles County Hospital in 1934.

There have been at least 75 documented outbreaks of myalgic encephalomyelitis (also known as Enteroviral Encephalomyelitis) and the original chronic fatigue syndrome (also known as Enteroviral Encephalitis) since the 1930's. The true number of clusters and outbreaks is likely much higher. Many of these outbreaks occurred in institutions like hospitals and schools, and frequently coincided with outbreaks of poliomyelitis.

The first recorded outbreak of epidemic was in 1934 in Los Angeles and the most recent putative outbreak was in Arizona in 1996. 

Prior to the 1980's, while no infectious was ever isolated, the outbreaks were widely thought to be caused by a virus related to poliovirus, (i.e., by another, yet-to-be-unidentified enterovirus)

After the Incline Village outbreak in 1984, herpesviruses and in particular, Epstein-Barr virus was posited as the cause of this outbreak but was later ruled out.

History

The first recorded outbreak of epidemic myalgic encephalomyelitis was in 1934 in Los Angeles and was thought to be an outbreak of atypical polio. After the outbreak in Akureyri, Iceland in 1946, the disease came to be called Akureyri Disease or Icelandic disease through much of the 1940's and 1950's.

It was named myalgic encephalomyelitis after London's Royal Free Hospital outbreak in 1955. 

Other names included benign myalgic encephalomyelitis and epidemic neuromyasthenia.

After the Incline Village outbreak in Nevada in 1984, a similar disease came to be called Chronic Fatigue Syndrome. The most recent was putative outbreak was in Arizona in 1996. 

Onset

The incubation period was generally estimated at 2 to 6 days. The illness generally began with a prodromal period of flu-like symptoms, symptoms of an upper respiratory tract infection, low-grade fever, sore throat or gastrointestinal distress, followed by a symptom complex involving muscle weakness, muscle fatigability and central nervous system involvement in a significant proportion of cases.

Symptoms

Reported symptoms could vary considerably from outbreak to outbreak. 

Common symptoms included:

Findings

Findings varied considerably based on the technology of the time and what tests physicians attending to these outbreaks chose or were able to run:
In the majority of early epidemics, no viral or bacterial infectious agent was successfully cultured. In a small number of epidemics Coxsackie B was found. In others, infection of animal models with samples from patients results in identifiable nervous system damage on autopsy and in one case, myocarditis, in spite of being unable to identify the agent.

Epidemiology

Many of these outbreaks occurred at institutions for example, hospitals, schools, army bases or convents. The pattern of spread suggested a highly infectious agent that spread person to person, rather than through contaminated food or drink or exposure to a single toxic agent.

Outbreaks tended to begin in the summer months, with most initial cases reported from April to September in the Northern hemisphere, October to March in the Southern hemisphere.

In outbreaks involving both medical personnel and the general community, medical personnel had a higher attack rate and/or greater central nervous system involvement. A similar pattern was seen in hospital outbreaks, where those in roles that involved more frequent or intimate contact with patients or those working in an infectious disease ward were more affected than other hospital staff. A large proportion of recorded outbreaks have taken place in hospital settings.

In many outbreaks including Los Angeles, Akureyri, Rockville, MD, Royal Free Hospital, and Punta Gorda, Florida, women were affected at higher rates. In other outbreaks, including the 1949-1953 Adelaide outbreak and an outbreak in northern England in 1955, a 1:1 gender ratio was reported. In hospital epidemics, young female nurses were disproportionately affected, but this may have been due to risk factors like higher repeated exposure to the same infection during an epidemic and in some outbreaks, gender-segregated living quarters. However, the higher ratio of women were also reported in outbreaks in the general population. In Akureyri, while the incidence among adults was higher for females, there was no significant difference in incidence between sexes among those under twenty. This comports with patterns of age and sex distribution in sporadic cases.

In most outbreaks, those most affected tended to be adults in their twenties, although cases of young children and adults as old as 80 have been recorded in outbreaks. In Akureyri, the highest attack rate was among ages 15-19.

Melvin Ramsay observed an absence of cases among sedentary people, and postulated that this might explain why hospital staff frequently became affected, while patients in hospital rarely did.

Pathophysiology

Due to limited of objective findings, very little was known about the pathophysiology of the disease. Several investigators postulated damage to the hypothalamus owing to the symptoms of orthostatic tachycardia, abnormal glucose regulation, circulatory impairment, and problems with temperature regulation.

Prognosis

Although many patients improved over time, in follow-up studies, a large percentage were still ill months to years later. Many case studies note long periods of convalescence with relapses following exertion or before or during menstrual periods.

Relationship to Polio

Prior to the poliovirus vaccine, several outbreaks of what later came to be called myalgic encephalomyelitis coincided with confirmed outbreaks of poliomyelitis including the 1934 Los Angeles outbreak, the 1948 Akureyri, Iceland outbreak, and 1949 outbreak in Adelaide, Australia. Many outbreaks were initially misinterpreted as clusters of poliomyelitis or abortive poliomyelitis, hence one of M.E.'s earliest names, atypical polio. It is not known whether there is a direct relationship between polio outbreaks and M.E. or if outbreaks of M.E. were more likely to be reported when public health authorities were already mobilized for an earlier crisis.

No serological evidence of polio was ever found in these outbreaks and the ultimate pattern of the outbreaks differed in significant ways, chief among them the higher attack rate, the tendency to affect adults rather than children, and the higher morbidity than poliomyelitis but no mortality. Findings in several outbreaks seemed to suggest that symptoms were caused by an enterovirus distinct from but related to polio: findings of mild, diffuse peripheral nervous system damage in monkeys infected with the virus; a stronger response to polio vaccination in children who had been in epidemic areas; and seasonal patterns of infection resembling polio, i.e., the rise in cases during summer months.

There is indirect evidence of cross-immunity between poliovirus and the unidentified virus or viruses in epidemic myalgic encephalomyelitis outbreaks. After the Akureyri outbreak, children in areas that had been affected responded to poliomyelitis vaccination with higher antibody titres, as if these children had already been exposed to an agent immunologically similar to the poliovirus. During the outbreak in Adelaide, cases of classic poliomyelitis dropped by 43%.

Controversy

In 1970, a paper by Colin McEvedy and Wllliam Beard claimed that the 1955 Royal Free Hospital outbreak was actually mass hysteria despite never examining patients.

Outbreaks of the 1980's and 1990's

The case reports of the 1980's and 1990's differed substantially from those of earlier decades. Whereas reports from the 1930's-1960's focused heavily on neurological and muscle symptoms and findings, and compared and contrasted the disease to poliomyelitis.

See also

Learn more

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The vagus nerve infection hypothesis (VNIH) accounts for why so many different infectious onsets could be responsible in injurying the vagus nerve. The vagus nerve runs from the brainstem (e.g. injured in M.E.) and throughout the body, and has an impact on many body systems. 

Transmission via blood

Given the uncertainty regarding the cause, M.E. patients are barred from [donating blood or organs in the United Kingdom (even after recovery), most of Canada, Australia, New Zealand (while symptoms persist), and and for a time also in the United States.

In the US, the American Association of Blood Banks advises to either accept or defer M.E. donors based on "clinical judgment of the donor's health status". Patient charities discourage M.E. patients from donating blood. 

Treatments


Main article: Treatments

There is no cure for M.E. and no country has approved any pharmacological treatment for the disease except, Argentina which has approved Ampligen for the treatment of severe M.E. However the effectiveness of Ampligen is under dispute. Other medications have been used off-label for M.E. with varying effectiveness in some patients.

Treatments for sleep problems, headaches, pain or other symptoms are utilized by some doctors for some patients although these are treating symptoms and not M.E. itself.

Success of treating symptoms of M.E. is not well researched or documented.

The antiviral Valganciclovir failed in a controlled nine month study against M.E. patients positive for HHV-6 and Epstein Barr viral infections.

Epidemiology

M.E. has been found world-wide, in at least 75 epidemics documented in published papers from the 1930's to the 1980's. Epidemics often occur in enclosed communities such as schools and hospitals.

As observed in many autoimmune disorders, M.E. is more common in females than males; the mean sex ratio is approximately 2-3 females for every male. In children the sex ratio is approximately equal.

Co-morbidities

Clinicians have observed several predisposing conditions, co-morbidities, overlapping conditions, and increased risks for secondary diseases in patients with M.E.. 

However, as no large-scale epidemiological studies, genetic studies, or family studies have been done, there is little that can be said definitively about the rate or underlying biological reasons for these potentially related conditions. 

Overlapping diagnostic criteria and the lack of a biomarker in many of these conditions add to the confusion and diagnostic uncertainty. 

Moreover, certain conditions such as postural orthostatic tachycardia syndrome (PoTS) and neurally mediated hypotension (NMH) and idiopathic intracranial hypertension (IIH/IH) and fibromyalgia (FM/FMS) can occur in or be co-morbid with numerous conditions, including M.E..

The following are some syndromes and diseases that have been associated with or misdiagnosed as M.E.
A Swedish study of 234 ME/CFS patients meeting the Canadian Consensus Criteria found that 13.2% had tonsillar herniations severe enough to be considered a Chiari Malformation. 

49% had hypermobility and 20% met criteria for hEDS (Ehlers-Danlos syndrome with hypermobility), while 96% had fibromyalgia trigger point pain, with 67% meeting the diagnostic criteria for fibromyalgia.

Notable studies

Due to lack of funding by governments around the world there has been little biological research into M.E. 

There are studies which do reveal neurological involvement, metabolic features, and other abnormalities.

Facts & Education: One of the most widespread virus groups

In the United States alone, Enteroviruses annually impact an estimated 30-50 million people - both children and adults - with hundreds of thousands either hospitalized, left permanently injured or having lost their life as a result of the destructive nature of this virus family.

So why haven’t we heard of it before now?

Because enteroviruses are sneaky and long forgotten! They appear within multiple other types of diseases or conditions, like the common cold, hand, foot and mouth disease, heart failure, polio, acute respiratory infections, central nervous system infections, aseptic meningitis, Crohn’s Disease and even type 1 diabetes to name a few. Studies have shown there to be over 100 human Enterovirus genotypes, many of which are highly contagious and with no known treatment.

More recently, there have been increased outbreaks of the enterovirus infections both in the United States and globally, such as:

In 2014, over a thousand adults and children across the country impacting all 49 states and the District of Columbia were hospitalized with a respiratory illness known as Enterovirus D68. 

The CDC indicated that there were likely millions of Enterovirus D68 infected individuals as well who did not seek medical treatment or get tested for the infection. 14 patients were confirmed to have died during this outbreak and over 130 patients became paralyzed from acute flaccid paralysis.

In 2015, Enterovirus A71 caused a large outbreak worldwide, with concentrated impact in children in Asia, especially China, as it occurred 2 decades ago, where the virus was associated with a severe neurologic disease called brainstem encephalitis and also caused death.

As of August 2016, the CDC reported 50 confirmed cases of Enterovirus D68 across 24 states with similar cases of acute flaccid paralysis diagnoses being reported. The CDC indicated that there were likely millions of Enterovirus D68 infected individuals as well who did not seek medical treatment or get tested for the infection. 

Responses here through this EVF site and our Facebook page have confirmed numerous outbreaks and deaths associated with Enteroviruses worldwide as well.

Although millions of people are infected annually with an enterovirus, most have only mild symptoms of the infection that only lasts about a week and resolves with no chronic problems.  However, for those at higher risk - especially infants, children and teens - one or more symptoms may develop and can be fatal.

Most Common Types of Enteroviruses

Over 26 diseases or conditions have been associated with Enteroviruses as either the root or contributor to the condition. Based on the physical structure of the virus, the tissue cultures in which they grow, and their pathogenesis in humans and experimental animals, Enteroviruses can be acute or chronic, and are generally classified into four primary groups:

Polioviruses

Coxsackie A and B

Echovirus

Numbered Enteroviruses; such as D68 and A71

Facts about the Polioviruses:

The polioviruses - Poliovirus 1, Poliovirus 2, and Poliovirus 3 - are a group of enteroviruses that cause poliomyelitis, also called polio or infantile paralysis. This is a highly infectious viral disease that may attack the central nervous system and is characterized by symptoms that range from a mild non-paralytic infection to total paralysis in a matter of hours. It is important to note, however, that most of poliovirus infections are asymptomatic, just as with all enteroviruses. 

Paralytic polio symptoms are similar to non-paralytic polio, with weakness in one or more of the following muscle groups:

Spinal, where patients have prolonged prodrome, with features of aseptic meningitis followed by 1-2 days of weakness and eventually paralysis.

Bulbar, involving the brainstem, cranial nerves which control swallowing and vocal chords functions.

Polioencephalitis, which is principally reported in children and unlike other forms of polio, causing seizures and spastic paralysis.

During the first few days of paralytic polio, exercise increases the severity of the disease as well.

Currently, there are no known cures for polio and it recommended protection is through receiving the polio vaccine as recommended by your physician.

Facts about Coxsackie A, B and Echovirus:

Non-polio viruses include Coxsackie A, B and Echoviruses:

Coxsackie A viruses are mainly associated with human hand, foot and mouth disease, acute hemorrhagic conjunctivitis, herpangina and hepatitis.

Coxsackie B viruses can cause signs and symptoms similar to a common “cold” but these viruses can also lead to more serious diseases by spreading through the body beyond the initial line of defense, including but not limited to:

Myocarditis or inflammation of the heart 

Pericarditis or inflammation of the sac lining of the heart 

Aseptic Meningitis or inflammation of the membranes that line the brain and spinal cord, and the brain itself (encephalitis)

Pancreatitis or inflammation of the pancreas 

Echoviruses are a cause to over 33 types of the nonspecific viral infections, mainly found in the liver or intestine area, and can cause nervous disorders.

The typical symptoms of both Coxsackie and Echoviruses are fever, a mild rash, and mild upper respiratory track (URT) and/or gastrointestinal illness.

Facts about Enterovirus D68:

Enterovirus 68, also known as Enterovirus D68 or EV-D68, in one of the more that 100 non-polio enteroviruses and was first identified in California in 1962.

Enterovirus 68 has been associated with paralysis and is being investigated as a cause like polio symptoms.

Symptoms include:

Mild symptoms include runny noses, sneezing, cough, body aches, fever and muscle aches.

Severe symptoms include respiratory illness, wheezing and difficulty breathing.

Since EV-D68 typically impacts respiratory functions, infected persons spread the virus through coughing, sneezing, or touching surfaces that are then touched by others.

In general, infants, children and teenagers are at highest risk to EV-D68 and become ill most often. 

Children with asthma can be at higher risk as well to respiratory illness caused by Enteroviruses.

Facts about Enterovirus A71:

Enterovirus A71 (or EV-71) is notable as one of the major cause agents found in human hand, foot and mouth disease, and is associated with severe central nervous system disease and myocarditis in fewer patients.

Although first isolated and characterized from cases of neurological disease in California in 1969, little is known to date about A71 infection in the U.S. since no diagnostic test is available.

The unsettling fact about Enterovirus is that it can spread to various organs and persist in the body for years… potentially causing disease long after the initial infection.

Symptoms and Signs of an Enterovirus Infection

Although millions of people are infected annually with an enterovirus, most have only mild symptoms of the infection that only lasts about a week and resolves with no chronic problems. However, for those at higher risk - especially infants, children and teens - one or more symptoms may develop and can be fatal.

Common signs and symptoms of an Enterovirus Infection are as follows:

  • Common cold: nasal discharge, congestion and stuffiness, cough, sore throat, mild fever, mild body aches
  • Hypoxia or low oxygen in the blood:  shortness of breath, wheezing, coughing, rapid breathing, skin coloration change (blush to cherry red), rapid heart rate
  • Aseptic meningitis: most common among infants and children; may also occur with a rash (on face, neck, and extremities), fever, headache, stiff neck, body aches, sensitivity to light, nausea and vomiting, irritability
  • Conjunctivitis: eye pain, bleeding seen in the whites of the eyes, photophobia (avoidance of light due to discomfort)
  • Myopericarditis: shortness of breath, chest pain, fever, weakness
  • Herpangina: small - sores with fluid-filled center with red surrounding borders on the oral mucosa (tonsils and soft palate) that may produce blisters and ulcerate
  • Pleurodynia (Bornholm disease): intermittent severe chest pain usually over the lower part of the rib cage:  Tenderness over the involved muscles is common.
  • Hand, foot and mouth disease (HFMD):  small blisters that are tender and appear gray that occur on the hands, feet and in the oral cavity
  • Encephalitis: symptoms range from lethargy and drowsiness to personality changes, seizures and coma
  • Paralysis (infrequent in both polio and non-polio into viral infections): flaccid paralysis that is often asymmetrical with proximal extremity muscles affected:  lower extremities affected more commonly than upper extremities (Poliovirus, Enterovirus 71, Enterovirus D68, and Coxsackievirus A7); other non-polio Enteroviruses usually have less severe symptoms like muscle weakness or oculomotor palsy if paralysis develops

Some strains of Enteroviruses produce different symptoms, some of which are more severe than others. Enterovirus D68 and Enterovirus 71 are associated with severe and intense symptoms, and neurological disease.

Other Symptoms Commonly Seen for Persistent Non-Polio Enteroviral Infections 

Listed here are common symptoms of persistent non-polio enterovirus infection. This list is from observations made by Dr. John Chia in his Infectious Disease Medical Practice in Torrance, CA.

  • Respiratory and/or gastrointestinal symptoms or just flu-like symptoms (fevers, body ache, headache etc.). Few virus infections present with both respiratory and GI symptoms.
  • Upper respiratory tract symptoms such as runny and stuffy nose, sinus congestion and pain, sore throat, ear pain, difficulty in swallowing, loss of smell or taste.
  • Upper and lower gastrointestinal symptoms such as nausea, indigestion, reflux, abdominal bloating, upper and lower abdominal pain, cramps, constipation alternating with diarrhea.
  • Sudden weight loss due to significant stomach problem or decreased caloric intake, or weight gain due to inactivity.
  • Numbness in the limbs, muscle twitching and spasms. Some experience facial tingling and numbness.
  • Many types of headaches.
  • Bone, muscle, and/or joint pain, which can be intense. Foot pain is quite common.
  • Chest pain, palpitations and tightness
  • Cough, shortness of breath, wheezing
  • Low blood pressure
  • Heart arrhythmia (irregular heartbeat) or tachycardia (rapid heartbeat)
  • Intermittent low grade fever, chills and night sweats.
  • Reproductive irregularities and pain.
  • Prostate issues and pelvic pain in both males and females.
  • Blurred vision.
  • Herpangina (blisters or ulcers over the roof of the mouth). Ulcers may form in the mouth, throat and for females the vaginal/cervix area.
  • Recurring yeast or bacterial infections due to a weak immune system.
  • Adrenal surge or dysfunction. High or low cortisol levels.
  • Psychological problems, anxiety, or depression.
  • Mental fatigue when trying to concentrate on tasks. Cognitive issues are very common as are short-term memory problems.
  • Sleep disturbance.
  • Seizures are rare but do occur.
  • Vitamin, and mineral deficiencies. Many become anemic and often do not respond to oral iron.
  • Swollen Lymph nodes in the neck and in the armpits
  • Organs that can be affected by enteroviruses: heart, pancreas, lungs, liver, spleen, stomach, small intestines, colon, ovaries, testicles, epididymis, thyroid, muscles, skin and the central nervous system.
  • Enterovirus infections can trigger dormant viruses to reactivate, such as HHV-6, Epstein Barr Virus, CMV, and chickenpox - all herpes viruses.
  • Children can show symptoms, but parents may not recognize them especially if they are intermittent.
  • Children can have many of the same adult symptoms - a flu-like illness, fever, mouth ulcers, abdominal pain, loss of appetite, a rash, headaches, leg pain and weakness, muscle twitching, reflux, cognitive dysfunction and perhaps heart pain and arrhythmias. 
  • A diagnosis of Atypical Poliomyelitis: Myalgic Encephalomyelitis (also known as Enteroviral Encephalomyelitis) / Aspetic Meningitis | Poliomyelitis-like Syndrome is possible immediately with inpatient services and hospitalisation (Nightingale Research Foundation Definitions, 2007 and 2016),
  •  or a "misdiagnosis" of Chronic Fatigue Syndrome (ME/CFS), within adults and children is possible after 14-28 days of illness, if presents with Fatigue and Post-Exertional Malaise (PEM) using Neutralizing Antibodies or VP1 GI Biopsy and The John Richardson Research Group Score Chart (JRRG Score Chart)
  • 1994 Fukuda "CFS" criteria overlaps with onset Enteroviral Disease, and Limbic Encephalitis + Rhombencephalitis patients.





  • An enterovirus infection should be suspected if the same symptoms recur every month (e.g. Non-cytolytic enterovirus)

Diagnose & Treat - Know Your Options

How is Enterovirus Contracted, Diagnosed and Treated?

Contracting enterovirus can actually be quite easy. Since Enteroviruses are small, highly contagious viruses made of ribonucleic acid (RNA) and protein, they are passed from person to person either through direct touch or indirect means, like through a sneeze or cough, much like a cold is passed from one to another. Other ways of transmission are in secretions from the mouth, eye, nose or blister fluid, or from human waste (oral-fecal transmission through contact with contaminated water i.e. swimming in lake or river, drinking contaminated water). 

The average incubation period is 3-10 days.

Enterovirus Diagnosis and Testing

Diagnosis of Enterovirus Infections is not that simple. Since it can masquerade as many common conditions during early onset, diagnosis often occurs when the virus has progressed to a severe or deadly state. The prolonged nature of an infection or an aforementioned complications arise with the initial infection should lead to further investigation.

Although many hospitals and some doctor’s offices can test ill patients to see if they have an enterovirus infection, most cannot do specific testing to determine the type of enterovirus. Specific lab tests on specimens from a person’s nose and throat, or special tests on blood or spinal fluid and MRI findings have been used to diagnose conditions linked to enterovirus.

After the acute phase of an infection, enteroviruses can disappear from the blood and cerebrospinal fluid completely, but can remain in organs and other tissues. This makes it difficult to diagnose enterovirus infections without a biopsy, and even then, the tests are limited.

Clinical Tests, Non-clinical Tests, Other Tests and Studies

Listed in this section are clinical laboratory tests for acute enterovirus infections, clinical laboratory tests for persistent enterovirus infections, imaging tests and other tests. These are provided to assist those infected or potentially infected with testing options to discuss with their physician. 

After explanations of the tests, there is a section of bulleted notes from renowned infectious disease physician Dr. John Chia to assist with diagnosis.

Clinical laboratory tests for acute enterovirus infections 

Serology - Serological examination can reveal an increase in antibodies to enteroviruses neutralizing antibody level to enteroviruses between the acute and convalescent phases of illness. This diagnostic modality can only identify coxsackie B1-6 and Echo 6, 7, 9, 11, and 30. The other known enteroviruses cannot be identified with this test. A negative serological test does not necessarily mean the absence of enterovirus.

Viral isolation - This is the criterion standard for diagnosing enterovirus infections. The virus can be isolated from cerebrospinal fluid, blood, or feces, depending on the site affected, and the yield is increased if multiple sites are sampled. The serotype of enteroviruses isolated by this method can be identified with neutralizing assays using type-specific antisera by the CDC or by VP1 gene sequencing.

Reverse transcription-Polymerase Chain Reaction (RT-PCR) - This test is highly sensitive and specific for detecting enterovirus RNA in cerebral spinal fluid specimens, with a sensitivity of 100% reported by some studies and specificity of 97%.

This test of a nasopharyngeal swab taken from patients with colds helped identify the viruses in EV D68 outbreak. PCR provides rapid results. 

PCR testing of the blood can only identify the virus in 30% of "missed diagnosed" chronic fatigue syndrome (overlaps with enteroviral encephalitis) or myalgic encephalomyelitis (also known as enteroviral encephalomyelitis) patients.

Cardiac enzyme levels and troponin 1 - These levels may be elevated in persons with myopericarditis, indicating myocardial damage like inflammation or damage to the heart muscle.

Cerebrospinal fluid analysis - The cerebrospinal fluid profile of patients with aseptic meningitis reveals a mildly elevated white blood cell count. Glucose levels are normal or mildly decreased, while the protein level is normal or slightly increased.

Reverse Transcriptase-Polymerase Chain Reaction (RT- PCR) - This test is designed to detect a common genetic area of most of the enteroviruses. The results could be available in 24 hours, making detection more sensitive (95%), more specific (97%), and more time efficient. 

This test is approved for diagnosing enterovirus aseptic meningitis. For other body fluids such as the stool, respiratory secretions and blood, the yield is less certain. (This the same as the PCR, 3rd paragraph of this section).

Clinical laboratory tests for chronic enterovirus infections

Immunohistochemistry (IHC) - This technique is the most useful in analyzing organ biopsies or autopsy sections. In this procedure, tissues are stained with an EV monoclonal antibody to determine if the viral protein is expressed at the time of the biopsy.

Biopsies of the organs where patients have symptoms are very helpful in making a diagnosis of persistent enterovirus infection. 

Brain, heart, and muscles are often involved with persistent enterovirus infections, but biopsies of these organs are not likely to be done. 

The stomach is the most common place where enteroviruses usually go in view of the respiratory and gastrointestinal routes of virus transmission. 

Enterovirus protein, or RNA, and defective viruses have been found in the stomach biopsies of patients from endoscopy procedures. Enterovirus protein has also been demonstrated in the nasal and sinus tissue, throat, thyroid, heart and brain of patients.

It is important to note that a biopsy is often taken during an endoscopy and that biopsies are typically preserved in paraffin for years in the pathology department where the procedure was performed. These can be requested in order to perform this test. 

This test can be ordered from EV Med Research.

Micro-neutralization test - Persistently elevated antibody levels for one or more enteroviruses over years can suggest a chronic enterovirus infection. The Micro-neutralization test is a very sensitive, specific test and only 11 enteroviruses, coxsackie B1-6 and echoviruses 6, 7, 9, 11, and 30 can be tested using this method. Titers of 1:160-320 and higher are good indicators of current infection.

It is important to note that only one commercial laboratory in the United States is recommended for this test: Associate Regional University Pathologist Laboratory (ARUP), Salt Lake City, Utah. These tests can be ordered directly from ARUP or ordered through LabCorp. If ordered through LabCorp, write on the form to specifically state this is a virus neutralization test to send this test to ARUP.

For more information:

Echovirus test

Coxsackie B test

Reverse transcription-Polymerase Chain Reaction (RT-PCR) - The PCR test is not considered sensitive for chronic enterovirus infections.

Since viruses are cleared quickly from the blood stream, the chance of finding viral gene or RNA in the blood by the PCR technique is low.

With special techniques and repeated testing, enterovirus RNA can be found in close to thirty percent of whole blood samples taken from chronically infected EV patients.

For Immunohistochemistry stain requests, please do not send samples to the foundation.

EV Med Research

25332 Narbonne Ave. #170

Lomita, CA, 90717

http://evmedresearch.com

evmed@sbcglobal.net 

Click here for the request form 

Imaging Studies

Chest radiography - In patients with myopericarditis, the chest radiograph may reveal cardiomegaly secondary to pericardial effusion or cardiac dilation. In pleurodynia, chest radiograph findings are normal since this is an infection of the chest/abdominal muscle.

Echocardiography - For patients with myocarditis or pericarditis, transient wall motion abnormalities or pericardial effusion may be revealed with echocardiography. Severe cases can reveal acute ventricular dilation and reduced ejection fraction. This is a much sensitive test for the diagnosis of the disease.

Other Tests

ECG - Nonspecific ST-T changes may be observed in persons with myopericarditis. Severe disease may cause Q waves, ventricular tachyarrhythmia, and heart block. ECG findings may demonstrate evolution through several stages of myopericarditis, as follows:

Stage I - Diffuse ST elevation with PR depression

Stage II - Normalization of ST and PR segments

Stage III - Deep symmetric inversion of T waves

Stage IV - May revert to normal or permanent T-wave inversions 

Electroencephalography - This test may be useful for evaluating the extent and severity of illness in patients with encephalitis.

Ophthalmic slit-lamp examination - In persons with Acute Hemorrhagic Conjunctivitis (AHC), corneal erosions may be visualized using a fluorescein stain. Enterovirus 70 and coxsackievirus A24 can be recovered from conjunctival swabs during the first 3 days of infection.

Advice from doctors from Dr. John Chia to aid in the diagnosis of both acute and chronic enterovirus infections:

Most of the acute enterovirus infections, even in the case of poliovirus infections, are asymptomatic (no sickness.)

The diagnosis of acute symptomatic infection is usually suspected and empirically diagnosed based on the physician's assessment of the patient along with outbreaks of other cases in the community, known exposure risks, geographic locations (next to a river and lake) and age groups.

Ulcerations of the mouth (stomatitis), especially over the lining of the cheeks, tongue ulcers, blisters of the soft palate or the roof of the mouth (herpangina) are helpful signs of acute enterovirus infection.

Pediatricians can often diagnose enterovirus infections in young children since they are trained to recognize these infections.

All "flu-like illnesses" are not the same, and can be caused by a number of infectious agents. With effective influenza vaccination, the numbers of influenza cases have decreased dramatically. 

Most of the respiratory infections in the winter or summer are not due to "influenza" but other respiratory viruses or Mycoplasma. 

Whereas acute influenza symptoms rarely last more than one week, acute enterovirus infections often last much longer than one or two weeks.

Acute enterovirus infection can present with respiratory and/or gastrointestinal symptoms if the same symptoms recur every month.

Diagnostic testing plays a role in acute enterovirus infections. As newer methods have demonstrated increased sensitivities, determining viral etiologies of aseptic meningitis and neonatal sepsis has resulted in improved patient care.

Cell culture (growth of the actual virus), serology (antibody testing of the blood), and polymerase chain reaction (PCR, a special viral gene test) can confirm acute enterovirus infections. Enteroviruses are found in the stool, the pharynx, blood, and the cerebrospinal fluid.

In the past, the standard of virus isolation has been cell cultures, but cultures take approximately 3-8 days to grow the enterovirus, and the identification of the particular type of enterovirus is usually not done for a long time afterwards.

Virus isolation from blood is not very helpful because the viral levels may be undetectable by the time symptoms have appeared. 

Pharyngeal viral levels remain present from 2 days to 2 weeks after the infection. Stool isolation of enteroviruses is not specific to acute infections because viral stool shedding persists for as long as 3 months after the infection.

Another method, serologic testing, uses two blood samples to identify a rise of antibody levels over a 2- to 4-week period. A single level of enterovirus antibodies can be present in a healthy patient; therefore, monitoring the serology to identify a 4-fold increase in levels is needed. We can only identify 11 of the 60+ Human enterovirus serotypes by this method. 

Furthermore, waiting for periods of 2-4 weeks for tissue results is not useful in improving patient care.

In contrast, the reverse transcriptase PCR testing is designed to detect a common genetic area of most of the enteroviruses. The results could be available in 24 hours, making detection more sensitive (95%), more specific (97%), and more time efficient. FDA has approved this test for diagnosing enterovirus meningitis. For other body fluids (stool, respiratory secretions and blood), the yield is less certain.

Measure cardiac and muscle enzymes in a patient with heart and muscle symptoms. Enteroviruses are the usual pathogen of the heart and skeletal muscles. Other viruses can affect the heart.

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