Historical Facts of M.E.

Note that this is an ongoing work in progress


History of Myalgic Encephalomyelitis.  ME was added to the World Health Organization in 1969.      

Please note that “Chronic Fatigue Syndrome” was constructed in the mid 1980’s in the United States so any

historical facts and/or inclusion of CFS prior to that date is a public relations agenda and is incorrect.  

Myalgic Encephalomyelitis is not the same as Chronic Fatigue Syndrome.


Several descriptions of illness resembling those of chronic fatigue syndrome have been reported for at least two hundred years.   In the 19th century, neurologist George Miller Beard popularized the concept of neurasthenia, with symptoms including fatigue, anxiety, headache, impotence, neuralgia and depression. This concept remained popular well into the 20th century, eventually coming to be seen as a behavioral rather than physical condition, with a diagnosis that excluded post-viral syndromes.   Neurasthenia has largely been abandoned as a medical diagnosis.  The World Health Organization ICD-10 system now categorizes neurasthenia under (F48 Other neurotic disorders) which specifically excludes chronic fatigue syndrome.


What ME used to be called in the past? (Answer: Superior Polio: Medin Type & Neurasthenia)


Ivar Wickman and 10 types of Polio from 1905 Epidemic - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3782271/

Wiliam Osler's 1914 Description of Neurasthenia - https://archives.library.tmc.edu/991618713505007;dacs?sf_culture=ja

How did the patient get sick ? What type of Flu-like Illness ? What symptoms did they have ? https://www.enterovirusfoundation.org/the-symptoms


Onset Symptoms

  • an upper respiratory track infection, which may include "rhinosinusitis", a "sore throat", (laryngitis), (pharyngitis) or (tonsillitis - Viral Replication) or (herpangina), "croup" (breathing difficulty and harsh cough), blisters or ulcers may develop on roof of mouth, cheeks or on tongue  - Cold/Flu-like Onset

  • lower respiratory track infection like (bronchitis or bronchiolitis) so a persistent "cough" (pneumonia), (pleurisy) or (pulmonary edema) - Respiratory-like Onset

  • gastrointestinal disturbances including (gastroenteritis) and "nausea" and/or "vomiting" and "diarrhea" and "abdominal pain" including (gastritis) and (enterocolitis "Peyer Patches" - Viral Replication) - Gastroenteritis Onset

  • acute vertigo" and "ataxia" accompanied by a "fever", "hyperhidrosis - excessive sweating", severe "headache", "myalgia - muscle pain" and "malaise & fatigue" and leading to "rhombencephalitis", "post-infectious encephalomyelitis" and "tinnitus: pulsatile, tonal, neurological".

  • leading onto "sympathetic nervous system dominance" and "tertiary adrenal insufficiency", insomnia", "hypersomnia" and "sleep reversal" and "weight loss" then "headaches", a "stiff neck - whiplash, neck pain and crepitus", "post-infectious encephalitis, and neuroinflammation - hypersensitive primed microglia and oxidative stress" (brain fog), "myelitis", "lower back pain", "syncope post exertion crashes", "post-infectious myositis", "arthralgia", "arthritis", "myalgia", "muscle stiffness", "muscle weakness", "spastic paraplegia" and "flu-like muscle fatigue after exertion": 2020 NICE guidelines call this "profound malaise".

  • Syncope Post-Exertion Crashes and Fear of Approaching Death (Impending Doom) (Video) - Dr. Byron Hyde

  • Spots or Rashes may or may not develop around the mouth. Exanthems of the extremities may appear in red spots, which develop into blisters, on either the hands or the feet in some cases but not in others.

  • Sensitivities to light known as Photophobia, to sound known as Hyperacusis or Misophonia, and to touch known as Allodynia may develop in some but not in others.

  • Since the disease is so very protean in its manifestations it may masquerade as influenza, respiratory catarrh, tonsillitis, gastroenteritis, rheumatism or as some transient virus infection" - Melvin Ramsay ("Infectious Diseases" 1967 book, page 142)

  • Fibromyalgia, Dysautonomia's including PoTS and Mast Cell Activation Syndrome tend to be common comorbidities as well as Irritable Bowel Syndrome, Enterocolitis, Eosinophilic Colitis, Gasteroparisis, Dysmotility, Paralytic Ileus or Elhers Danlos Syndromes.

1930 to 1940

In 1932, there were epidemics in New Jersey, Pennsylvania and Los Angeles.  Los Angeles epidemic was so bad that the city’s public health services began to break down.  Ambulances and stretchers blocked the streets in front of the country hospital, where frightened hospital workers turned people away.  100,000 people in Los Angeles became ill.  5% had Polio but others were ill with other diseases and illnesses.  In 1934, blood serum from the victims of the outbreak was used on the staff of LA Hospital.  Although some who never had this serum injected into them did get sick, many more injected with the serum became ill with an unknown disease which was polio-like.   

The 1934 Los Angeles County General Hospital epidemic is the first known recorded cluster outbreak resulting in what is now known as Myalgic Encephalomyelitis.  Los Angeles County General Hospital was a public hospital that served the people of Los Angeles city and county, in California, US. It served an average of 2,000 in-patients and 2,500 out-patients daily.

Between May 1934 and December 15, 1935, one hundred ninety-eight (198) employees of Los Angeles County Hospital came down with an acute onset neurological illness. This accounted for 4.5% of hospital personnel becoming ill including about 10.7% of the nurses and 5.4% of the physicians.

As a poliomyelitis epidemic was occurring in California at this time, the first impression from the medical community was that the illness was polio, especially since the illness presented with similarities including febrile onset and flaccid weakness.[1]

In a short time, striking deviations from polio began to emerge in five areas:

  • relatively high attack rate (4.5% of all employees fell ill compared to the incidence of 0.07% of polio in the Los Angeles community)

  • low fatality rate (there were 0 deaths compared to a 1.39% fatality rate with polio)

  • low paralytic rate, both in terms of weakness at any time or in residual paralysis (an estimate of 7% of polio cases resulted in residual paralysis in the Los Angeles community)

  • high transmission/communicability rate

  • age selection of adults (only adults were afflicted, whereas polio is predominantly a childhood disease with the highest incidence in those under six years of age)

Seventy-five percent of those who became ill were women, and rates of illness were higher in adults under 30. Rates of illness were 2.5 times higher for staff working in the communicable diseases ward. Investigators determined that the infection was spread by direct personal contact with cases and carriers and not by contamination of the hospital milk or food supply.


The disease onset included the following cluster of symptoms: painheadachemuscle tendernessnauseasensory disturbancesstiff neck or back, localized muscular weaknessvomitingmuscle twitchingsore throatconstipationfevercoughdiarrheaurinary retentionvertigophotophobia, and double vision.

Patients also experienced fatigue on walking short distances and on the least exertion, loss of concentration and lapses of memory, and sleep disturbances. Recurrences of both systemic and neurological symptoms were frequent, and some patients were more disabled by these recurrences than by the original illness.

There was no mortality but compared to polio, morbidity was high: 55% of the staff were still off duty six months after the peak of the epidemic.

In 1936, Novices and convent candidates at a Wisconsin convent were diagnosed with "encephalitis"   


In 1938, Alexander Gilliam described an illness that resembled poliomyelitis, interviewing patients and reviewing records of one of several clusters which had occurred in Los Angeles, United States in 1934. The Los Angeles County Hospital outbreak included all or most of its nurses and doctors. Gilliam called the outbreak "atypical poliomyelitis" and described the symptoms as: rapid muscle weakness, vasomotor instability, clonic twitches and cramps, ataxa, severe pain (usually aggravated by exercise), neck and back stiffness, menstrual disturbance and dominant sensory involvement. 


The following year two towns in Switzerland had outbreaks of "abortive poliomyelitis" , and 73 Swiss soldiers were given the same diagnosis in 1939. Outbreaks in Iceland were called "Akureyri disease" or "simulating poliomyelitis" and were later called "Iceland disease."


1940 & 1950





Eight hundred people in Adelaide, Australia became ill during 1949-1951 with a disease "resembling poliomyelitis." Two smaller clusters in the United States during 1950 were diagnosed as "Epidemic Neuromyasthenia" and "resembling Iceland disease simulating acute anterior poliomyelitis." Additional outbreaks of poliomyelitis-like "mystery diseases" occurred from the 1950s through the 1980s, in Denmark, the United States, South Africa, and Australia, among others.

Several outbreaks of a polio-resembling illness occurred in Britain in the 1950s.  A 1955 outbreak at the Royal Free Hospital Group was later called Royal Free Disease or Benign Myalgic Encephalomyelitis.  After the Royal Free Hospital outbreak, a disorder with similar symptoms was found among the general population and the epidemic form came to be considered the exception.  Pathology findings, from both monkeys intentionally infected with biological fluids from patients and from rare human casualties, led to the conclusion that the disorder was caused by inflammation of the brain and the spinal cord, particularly the afferent nerve roots, perhaps with neuroimmune etiology.

A record of fifty-three patients admitted to the Infectious Diseases Department of the Royal Free Hospital between April 1955 and September 1957 suffering from 'epidemic neuromyasthenia' establishes the fact that the condition was endemic in the general population before, during and after the outbreak among the staff of the hospital.

Introduction 'Epidemic neuromyasthenia' occurred in Dalston, Cumberland, in February 1955 but the author and his colleagues were not aware of that when they began to admit a series of very puzzling cases in April of that year. An account of the first eight of these was published (Ramsay and O'Sullivan, 1956). After an onset which took various forms but chiefly upper respiratory catarrh, gastro-intestinal disturbances (with nausea and vomiting), or acute vertigo, there followed severe headache accentuated by movement, nuchal pain, pain in the limbs, back, or chest, giddiness, extreme lassitude and paraesthesiae. Muscular cramps and twitchings, pain referred to the ears and transient or persistent tinnitus were features of many cases. Cervical gland enlargement was found in seven cases, various degrees of neck stiffness, pareses and exaggerated tendon reflexes in six; objective sensory impairment and muscle tenderness in five; cranial nerve palsies in five, extensor plantar responses in three, nystagmus in two and diplopia in two. Later, the details of the first thirty-four cases admitted to the Unit (with very similar findings) were reported (Ramsay, 1957). Records have been traced of fifty-three patients of whom sixteen were seen in 1955, eighteen in 1956 and nineteen in 1957. Only thirteen of these were from the hospital staff, namely nurses, ward maids or students from the geographically adjacent preliminary training school. Despite difficulty in deciphering the names and addresses of all the doctors who referred these cases with diagnosis of poliomyelitis, meningitis and pyrexia of unknown origin it was possible to identify nineteen whose practices ranged from Highbury to Chelsea. This surely establishes the endemicity of the disease.

Symptoms and physical signs in terms of percentage incidence; Headache was the most frequent symptom; sometimes both frontal and occipital and accentuated by movement.  Acute vertigo was the presenting feature of five cases: in others it occurred intermittently in the course of the illness. A combination of headache, dizziness, nausea, vomiting and extreme lassitude was common. Some patients complained of a sense of 'deadness' in a limb. Muscle cramps, twitchings and extreme muscle tenderness were common. Visual phenomena generally took the form of blurring of vision but diplopia was not infrequent. 'Paresis' occurred in 67% of cases. This is not a satisfactory term as the weakness is the result of an unusual form of muscular fatigability which is the predominant clinical feature of the disease.  Lymphadenopathy affecting chiefly the cervical glands, and exaggerated tendon reflexes were found in at least 5000 of cases. Sensory impairment generally presented as areas of hyperaesthesia (often corresponding with the distribution of deep muscle tenderness) interspersed with patches of hypoalgesia. Acute myalgia was present in 40-50°/0 of cases. This was sometimes obvious as the patient winced even on light palpation of the affected muscle; but much more frequently it took the form of minute foci of muscle tenderness which had to be carefully sought and for no ostensible reason were generally found in the trapezii and gastrocnemii. Muscle involvement sometimes took the form of severe and painful spasm, tremor, twitchings, cogwheeling or fasciculation. Extensor plantar responses were found in 16% of cases and in two instances persisted after discharge from hospital. Cranial nerve palsies were present in just under 100 of cases, the third, fifth, seventh and eighth nerves being chiefly affected.

The increased frequency of these outbreaks during the 1950’s brought greater interest to M.E.  Dr Melvin Ramsay and others further defined the illness and Myalgic Encephalomyelitis became the recognized term for this neurologic infectious disease.

A number of distinguished doctors continued to study and report on ME outbreaks, including Wallis, Acheson, Richardson, Parish, Henderson, Shelokov, Dowsett, Ryll, Behan and Hyde.  Their science have brought us a wealth of information about ME and a continuous historical record of ME over many decades.  Perhaps the most impressive among them, Dr Richardson could attest that the cases he saw in the year 2000 have the same disease as patients he and Dr Ramsay encountered in the 1950’s.  The neurological disease defined as Myalgic Encephalomyelitis.


1960 & 1970’s  


In the 1960s and 1970s, chronic fatigue symptoms were often attributed to chronic brucellosis, but typically people were seen as having psychiatric disorders, in particular depression.  Epidemic cases of benign myalgic encephalomyelitis were called mass hysteria by psychiatrists McEvedy and Beard in 1970, provoking criticism in letters to the editor of the British Medical Journal by outbreak researchers, attending physicians, and physicians who fell ill. The psychiatrists were faulted for not adequately investigating the patients they described, and their conclusions have been refuted.   

                                                                                                                                                                                                                      A further outbreak occurred in North Finchley between 1964 and 1967 and sporadic new cases are still being encountered. The majority of these patients show evidence of involvement of the central and sympathetic nervous systems and the reticulo-endothelial system. Abnormal muscular fatigability is the dominant clinical feature and it is suggested that mitochondrial damage may provide an explanation for this phenomenon. Enzyme tests carried out in seven cases show pathologically high levels of lactic dehydrogenase, and glutamic oxalo-acetic transaminase. A follow-up study suggests that there is one group of patients that recovers completely or nearly completely, a second that recovers but is subject to relapses and a third that shows little or no recovery, these patients remaining incapacitated.

Myalgic encephalomyelitis (ME) was recognized by WHO as a neurological disease since at least 1969, when it published the ICD-8 classification of diseases. The ICD-8 did not include any alternative names for Myalgic Encephalomyelitis; or fatigue-related alternative names were only added in later revision.


Chronic fatigue symptoms were often attributed to chronic brucellosis, but typically people were seen as having psychiatric disorders, in particular depression.  Epidemic cases of Benign Myalgic Encephalomyelitis were called mass hysteria by psychiatrists McEvedy and Beard in 1970, provoking criticism in letters to the editor of the British Medical Journal by outbreak researchers, attending physicians, and physicians who fell ill. The psychiatrists were faulted for not adequately investigating the patients they described, and their conclusions have been refuted.  In 1978 a symposium held at the Royal Society of Medicine (RSM) concluded that "epidemic Myalgic Encephalomyelitis" was a distinct disease entity with a clear organic basis.


The World Health Organization's (WHO) International Classification of Diseases (ICD), mandates the international classifications of diseases to allow comparison of health and health fields across countries and throughout the world.  Not all terms appear in the tabular list (Volume 1), and many more terms are listed in the alphabetic index (Volume 3) of the ICD.


ICD-8:  Since its introduction into the eighth edition of the WHO ICD-8 in 1969 (code 323), (Benign) myalgic encephalomyelitis has been classified as a disease of the central nervous system.


ICD-9:  The term "Benign Myalgic Encephalomyelitis" appears in the 1975 ICD-9 alphabetic index, and references code 323.9, Encephalitis of unspecified cause. The code 323.9 did not include reference to postviral syndrome. The term “postviral syndrome” was classified to code 780.7, Malaise and fatigue, in Chapter 16, Symptoms, signs and ill-defined conditions.


The name Chronic Fatigue Syndrome has been attributed to the USA Centers for Disease Control 1988 research case definition for the illness, "Chronic fatigue syndrome: a working case definition". Chronic Fatigue Syndrome (CFS) was added to ICD-9 after 1988 and listed under code 780.71, Symptoms Signs and Ill-defined Conditions.


ICD-9-CM:  (CM is American) Since 1979 the U.S. has used a clinical modification of WHO's ICD 9th revision (ICD-9-CM), and ME is under index: "Encephalomyelitis (chronic) (granulomatous) (hemorrhagic necrotizing, acute) (myalgic, benign) (see also Encephalitis) 323.9


For CFS, a modification to the alphabetic index was made, effective on October 1, 1991, to direct users to code 780.7, Malaise and fatigue, the same code used to identify cases of postviral syndrome. In 1998, a new five-digit code included 780.71, Chronic fatigue syndrome, consistent with the WHO version of ICD-9.  Chronic fatigue syndrome is classified in tabular list: "Symptoms, Signs and Ill-Defined Conditions," under the sub-heading of "General Symptoms".


ICD-10:  CFS is not included as a coded term in the 1992 ICD-10, WHO created a new category G93, Other disorders of brain, in Chapter VI, Diseases of the Nervous System, and created a new code G93.3, post-viral fatigue syndrome (PVFS), a condition which was previously in the symptom chapter of ICD-9.  WHO also moved Benign Myalgic Encephalomyelitis to G93.3, subordinate to PVFS.  The alphabetic index contains other terms, such as chronic fatigue syndrome, to which WHO assigned the same code.


ICD-10-CM (American version)  The proposed U.S. classification ICD-10-CM (2010 Update replaces July 2009 version) separates CFS and Postviral fatigue syndrome into mutually exclusive categories. "Chronic fatigue, unspecified | Chronic fatigue syndrome not otherwise specified" appears in Chapter XVIII under R53.82. "Postviral fatigue syndrome | Benign Myalgic Encephalomyelitis" appears in Chapter VI under G93.3.  The Chronic Fatigue Syndrome Advisory Committee (CFSAC) had previously recommended CFS to be placed under the same neurological code as ME and PVFS, G93.3.


1970 & 1980: 


The Impact of Persistent Enteroviral Infection by Dr Elizabeth Dowsett. 

By 1972, a distinguished group of clinicians and scientists had set out to share information, form research groups and hold national and international conferences related to the problems of ME. Following successful vaccination against the three polio viruses during the early 1960s over 60 epidemics of atypical, non paralytic polio had been recorded in the UK alone. It was obvious that (since Nature abhors a vacuum) the non polio enteroviruses were naturally filling the gap, and demonstrating their potential for inducing a serious neurological disease of considerable chronicity, mainly affecting school children and middle aged adults in the most important and productive years of their lives. Most of the famous London teaching hospitals were involved, at that time in investigating epidemics and in subsequent research while links were forged with international institutions in USA, Canada, Europe and Australasia, facing the same problems.

Research first published in 1975 indicated that the enteroviruses (which triggered the illness) belonged to a vast group of viruses (many of them at that time yet to be discovered) which were able to survive persistently in the human body as an uncoated form of intracellular genetic material, thus avoiding direct challenge from the immune system. Simple (indirect) laboratory confirmation of their presence based on blood tests, was available in most NHS laboratories without let or hindrance, while the European enterovirus reference centre at Ruchill Hospital in Glasgow, provided expert identification. It was clear from their work that epidemics occurred at 10 year intervals and pandemics (world wide spread) were approximately 20 years apart.  By 1987, famous research workers, including Drs Ramsay, Richardson and (from Canada and the USA) Byron Hyde and David Bell, Professors Mowbray and Banatvala and scientists of the status of Len Archard and (from the USA) Roger Loria and Richard Bruno and Nancy Frick, were able to enlighten and to back up the hundreds of GPs and NHS consultants dealing with an ever increasing number of seriously disabled patients. The potential of this disease to disable children and interrupt their education was realised and (in the early 1980’s) the late effects of polio were rediscovered (earlier reports dated from the late 19th century).

1980 to 1990



MYALGIC ENCEPHALOMYELITIS : A Baffling Syndrome With a Tragic Aftermath. By A. Melvin Ramsay M.D., Hon Consultant Physician, Infectious Diseases Dept, Royal Free Hospital. [Published 1986]

Myalgic Encephalomyelitis leaves a chronic aftermath of debility in a large number of cases. The degree of physical incapacity varies greatly, but the dominant clinical feature of profound [paralytic muscle] fatigue is directly related to the length of time the patient persists in physical effort after its onset; put in another way, those patients who are given a period of enforced rest from the onset have the best prognosis.

Although the onset of the disease may be sudden and without apparent cause, as in those whose first intimation of illness is an alarming attack of acute vertigo, there is practically always a history of recent virus infection associated with upper respiratory tract symptoms though occasionally there is gastro-intestinal upset with nausea and vomiting. Instead of making a normal recovery, the patient is dogged by persistent profound fatigue accompanied by a medley of symptoms such as headache, attacks of giddiness, neck pain, muscle weakness, parasthesiae, frequency of micturition or retention, blurred vision and/or diplopia and a general sense of 'feeling awful'. Many patients report the occurence of fainting attacks which abate after a small meal or even a biscuit, and in an outbreak in Finchley, London, in 1964 three patients were admitted to hospital in an unconscious state presumably as a result of acute hypoglycaemia. There is usually a low-grade pyrexia [fever] which quickly subsides. Respiratory symptoms such as sore throat tend to persist or recur at intervals. Routine physical examination and the ordinary run of laboratory investigations usually prove negative and the patient is then often referred for psychiatric opinion. In my experience this seldom proves helpful is often harmful; it is a fact that a few psychiatrists have referred the patient back with a note saying 'this patient's problem does not come within my field'. Nevertheless, by this time the unfortunate patient has acquired the label of 'neurosis' or 'personality disorder' and may be regarded by both doctor and relatives as a chronic nuisance. We have records of three patients in whom the disbelief of their doctors and relatives led to suicide; one of these was a young man of 22 years of age.

The too facile assumption that such an entity - despite a long series of cases extending over several decades - can be attributed to psychological stress is simply untenable. Although the aetiological factor or factors have yet to be established, there are good grounds for postulating that persistent virus infection could be responsible. It is fully accepted that viruses such as herpes simplex and varicella-zoster remain in the tissues from the time of the initial invasion and can be isolated from nerve ganglia post-mortem; to these may be added measles virus, the persistence of which is responsible for subacute sclerosing panencephalitis that may appear several years after the attack and there is a considerable body of circumstantial evidence associating the virus with multiple sclerosis.


There should surely be no difficulty in considering the possibility that other viruses may also persist in the tissues. In recent years routine antibody tests on patients suffering from Myalgic Encephalomyelitis have shown raised titres to Cocksackie B Group viruses.  It is fully established that these viruses are the aetiological agents of 'Epidemic Myalgia' or 'Bornholm's Disease' and that, together with ECHO viruses, they comprise the commonest known virus invaders of the central nervous system. This must not be taken to imply that Cocksackie viruses are the sole agents of myalgic encephalo- myelitis since any generalised virus infection may be followed by a period of post-viral debility.  Indeed, the particular invading microbial agent is probably not the most important factor. Recent work suggests that the key to the problem is likely to be found in the abnormal immunological response of the patient to the organism.

A second group of clinical features found in patients suffering from myalgic encephalomyelitis would seem to indicate circulatory disorder. Practically without exception they complain of coldness in the extremities and many are found to have abnormally low temperatures of 94 or 95 degrees F. In a few, these are accompanied by bouts of severe sweating even to the extent of waking during the night lying in a pool of water. A ghostly facial pallor is a well known phenomenom and this has often been detected by relatives some 30 minutes before the patient complains of being ill.

The third component of the diagnostic triad of Myalgic Encephalomyelitis relates to cerebral activity. Impairment of memory and inability to concentrate are features in every case.  Many report difficulty in saying the right word and are conscious of the fact that they continue to say the wrong one, for example 'cold' when they mean 'hot'. Others find that they start a sentence but cannot complete it, while some others have difficulty comprehending the written or spoken word. A complaint of acute hyperacusis is not infrequent; this can be quite intolerable but alternates with periods of normal hearing or actual deafness. Vivid dreams generally in colour are reported by persons with no previous experience of such a phenomenom.  Emotional lability is often a feature in a person of previous stable personality, while sudden bouts of uncontrollable weeping may occur. Impairment of judgement and insight in severe cases completes the 'encephalitic' component of the syndrome.


All patients suffering from chronic debility for which a satisfactory explanation is not forthcoming a renewed and much closer appraisal of their symptoms should be made. This applies particularly to the dominant clinical feature of profound fatigue. While it is true that there is considerable variation in degree from one day to the next or from one time of the day to another, nevertheless in those patients whose dynamic or conscientious temperaments urge them to continue effort despite profound malaise or in those who, on the false assumption of 'neurosis', have been exhorted to 'snap out of it' and 'take plenty of excercise' the condition finally results in a state of constant exhaustion.


This has been amply borne out by a series of painstaking and meticulous studies carried out by a consultant in physical medicine, himself an ME sufferer for 25 years. These show clearly that recovery of muscle power after exertion is unduly prolonged. After moderate excercise, from which a normal person would recover with nothing more than a good night's rest, an ME patient will require at least 2 to 3 days while after more strenuous excercise the period can be prolonged to 2 or 3 weeks or more. Moreover, if during this recovery phase, there is a further expenditure of energy the effect is cumulative and this is responsible for the unrelieved sense of exhaustion and depression which characterizes the chronic case. The greatest degree of muscle weakness is likely to be found in those muscles which are most in use; thus in right- handed persons the muscles of the left hand and arm are found to be stronger than those on the right. Muscle weakness is almost certainly responsible for the delay in accommodation which gives rise to blurred vision and for the characteristic feature of all chronic cases, namely a proneness to drop articles altogether with clumsiness in performing quite simple manoeuvres; the constant dribbling of saliva which is also a feature of chronic cases is due to weakness of the masseter muscles. In some cases, the ‘Myalgic’ element is obvious but in others a careful palpitation of all muscles will often reveal unsuspected minute foci of acute tenderness; these are to be found particularly in the trapezii, gastrocnemii and abdominal rectii muscles.


The clinical picture of Myalgic Encephalomyelitis has much in common with that of multiple sclerosis but, unlike the latter, the disease is not progressive and the prognosis should therefore be relatively good. However, this is largely dependent on the management of the patient in the early stages of the illness. Those who are given complete rest from the onset do well and this was illustrated by the aforementioned three patients admitted to hospital in an unconscious state; all three recovered completely. Those whose circumstances make adequate rest periods impossible are at a distinct disadvantage, but no effort should be spared to give them the all-essential basis for successful treatment. Since the limitations which the disease imposes vary considerably from case to case, the responsibility for determining these rests upon the patient. Once these are ascertained the patient is advised to fashion a pattern of living that comes well within them. Any excessive physical or mental stress is likely to precipitate a relapse.  

In the controversy of the 1980s and '90s, the topic of epidemics of ME was often sidelined. Broadly, two types of account of the genesis of ME as organic disorder have prevailed (Cooper, 1997: 189). The first attributes the condition to persistent viral infection: it is considered an endemic disease subject to outbreaks of epidemic prevalence (Ramsay, 1986: 28).

A contending account is that, although ME may be triggered by a virus, its underlying cause is a damaged immune system. The latter explanation allows for the preponderance of sporadic cases, which later came to constitute the majority of those diagnosed with the condition (Aronowitz, 1992: 161), and it underlies many of the constructions of ME widespread in the media in the 1980s and 1990s.

However, Dr Melvin Ramsay (1989: 20), who treated the victims of the 1955 outbreak, inveighed against immunological views of ME, demanding to know how 200 nurses at the Royal Free Hospital could have developed abnormalities of their immune system within three months. Whether the Royal Free nurses of the 1950s were afflicted by a disorder of the same aetiology as the patients of the 1980s, 1990s and 2000s – or indeed, whether the symptoms of the latter all result from the same underlying pathology - remains uncertain.

Melvin Ramsay's "Epidemic" Myalgic Encephalomyelitis (M.E.) - Atypical Poliomyelitis" should be it's own distinct disease category; which is separate from "Chronic Fatigue Syndrome".    Acute Disseminated Encephalomyelitis-Post- Infectious & Post Infectious & Post Vaccination ‘Inflammatory’ Encephalomyelitis


Post-Infectious "Inflammatory" Encephalomyelitis has been linked to Enteroviruses and particularly Coxsackie B, Epstein Barr Virus, Cytomegalovirus, Human Herpes Virus 6, Varicella Zoster Virus, Influenza, Adenovirus, Measles, Mumps, Rubella, Borrelia and Mycoplasma in the medical literature; which have all been connected to the terms Myalgic Encephalomyelitis within the UK and Chronic Fatigue Syndrome within the US; which has erroneously made these two terms synonymous with each other.

Myalgic Encephalomyelitis (M.E.) is a chronic, inflammatory, physically and neurologically disabling immune mediated disease that presents with symptoms involving multiple bodily systems. It is frequently triggered by a viral infection or as in the case of the Incline Village outbreak a flu-like illness, it affects the central nervous system (CNS), autonomic nervous system (ANS), immune system, cardiovascular system, endocrine system, digestive system, and (neuro) musculoskeletal system.


"Melvin Ramsay's "Epidemic" Myalgic Encephalomyelitis (M.E.) - Atypical Poliomyelitis)" is caused by an "enteroviral" infection of central nervous system; which can lead to Aseptic Meningitis, Encephalitis or Meningoencephalitis, Brainstem Encephalitis, Encephalomyelitis, Hypothalamic Dysfunction, Autonomic Nervous System Disorder or Postural Orthostatic Tachycardia Syndrome (PoTS) as well as a host of other outcomes. 



Canker Sores, Mouth Ulcers, Facial Rash around Mouth & Nose, Bornholm Disease, Myocarditis, Pericarditis, Enteric Hepatitis, Acute Flaccid Myelitis, Spastic Paraplegia, Whiplash, Fibromyalgia, Trapezius Myalgia, Infectious Myositis, Post-Infectious Reactive Myositis, Small-Fiber Peripheral Neuropathy, Paresthesia, Raynard's


"It should be noted that ME/CFS symptoms are comparable to those of "Post-Poliomyelitis Syndrome" (Bruno et al 1995) https://nyaspubs.onlinelibrary.wiley.com/doi/abs/10.1111/j.1749-6632.1995.tb27536.x and that viral injury to excitable tissues, such as muscle and nerve, has the potential to alter their crucial metabolic functions.


These metabolic functions include ion channel transport, mitochondrial function (Mitochondrial Encephalopathy & Myopathy) and the response to circulating neurotransmitters and neuro-hormones (Hypothalamic Hypopituitary) - the alterations are capable of persisting well after apparent recovery from a precipitating infection.

Dr. Charles Shepherd & Dr. Abhijit Chaudhuri) https://www.frontiersin.org/articles/10.3389/fimmu.2019.00796/full

The descrepency between Chronic Fatigue Syndrome and Myalgic Encephalomyelitis continued to widen.


CDC 1988 criteria - a clinical criteria only 

The initial chronic fatigue syndrome definition was published in 1988. It is also called the "Holmes definition", after the manuscript's first author.  The Holmes criteria exclude patients with psychiatric diagnoses and require the presence of eight secondary symptoms.


Fukuda Case Definition for CFS (1994) (clinical & research criteria)

In 1994, Fukuda and colleagues published a case definition for CFS and idiopathic chronic fatigue that was intended to guide research in adult populations.  The Fukuda definition defines chronic fatigue as “self-reported persistent or relapsing fatigue lasting 6 or more consecutive months” and requires a clinical evaluation to identify or rule out medical or psychological conditions that could explain the chronic fatigue's presence. A diagnosis of CFS requires the absence of exclusionary conditions, severe chronic fatigue, and at least four of eight minor symptoms.  The definition has been criticized for being overly inclusive, particularly of patients whose symptoms may be caused by a psychiatric disorder.  NOTE; Michael Sharpe, UK Psychiatist and author of the pace Trial Study was an author of the Fukuda. Because many of the minor symptoms overlap with the symptoms of major depression.  Many have argued that the Fukuda definition fails to sufficiently operationalize the major and minor symptoms, leading to variations in the way these symptoms are interpreted.  The Fukuda definition indicates that patients who fail to meet its criteria for fatigue severity and at least four minor symptoms should be diagnosed with idiopathic chronic fatigue. The research guidelines recommend subgrouping cases of CFS or idiopathic chronic fatigue by the presence or absence of comorbid conditions, level of fatigue, duration of fatigue, and level of physical function (Fukuda et al., 1994). Despite the challenges noted above, the Fukuda case definition is the most widely used definition in ME/CFS research, and it is also used for clinical evaluation of patients.


Canadian Consensus Criteria for ME/CFS (2003)  (Clinical Criteria only)

Carruthers and colleagues (2003) published the CCC as a clinical working case definition to assist physicians and other clinicians in making a diagnosis of ME/CFS. Because fatigue can be present in many other illnesses, the CCC requires for a diagnosis of ME/CFS the presence of four cardinal symptoms—fatigue, PEM, sleep dysfunction, and pain—as well as minor symptoms grouped by region of pathogenesis. Thus, for a diagnosis of ME/CFS, the CCC requires that symptoms be present from the following six symptom categories for 6 months or longer: fatigue, including substantial reduction in activity level; PEM and/or post-exertional fatigue; sleep dysfunction; pain; neurologic/cognitive manifestations; and autonomic, neuroendocrine, or immune manifestations.





This is some of what research funding for ME has paid for over the years. Careful what you endorse.

There's an agenda at work to increase prevalence which cannot provide the help we need.