Myalgic Encephalomyelitis Summary

Myalgic Encephalomyelitis (ME) is an acquired complex disorder characterized by a variety of symptoms and physical findings potentially affecting multiple systems of the body. Many cases are preceded by a viral infection, usually a flu-like or upper respiratory illness, although ME can also be preceded by a non-viral illness or other trauma such as chemical exposure. Onset is usually rapid (acute) but gradual onsets are also reported. Affected individuals do not recover from the infection and instead experience a wide variety of symptoms including an inability to produce sufficient energy to meet daily demands. Marked fatigue and weakness, sickness, cognitive dysfunction and symptom flare-up follows physical and cognitive exertion. Additional symptoms that may occur include headaches, pain, muscle weakness, neck pain, vision abnormalities (such as blurred vision), a sensation of tingling, burning or numbness of the extremities (paresthesia), bladder and bowel dysfunction, and sleep dysfunction. Cardiovascular abnormalities have also been reported. Myalgic encephalomyelitis is a chronic and disabling disorder. Severe cases often leave affected individuals bedridden or housebound. Myalgic encephalomyelitis may occur as an outbreak that affects a large group of people (epidemically) or may only affect an individual (non-epidemically).

Introduction                                                                                                      

There is significant controversy and debate in the medical literature about the relationship between Myalgic Encephalomyelitis. The first outbreak of Myalgic Encephalomyelitis was in 1934 and the term Myalgic Encephalomyelitis first appeared in the medical literature in 1956. Myalgic Encephalomyelitis is recognized as a distinct disorder and has been classified as a specific neurological disorder by the World Health Organization (WHO) since 1969.  Myalgic Encephalomyelitis should retain a strict definition as a distinct neurological disease that includes measurable abnormal changes in the brain and central nervous system. Individuals who meet the strict criteria of the ICC 2011 would be diagnosed with Myalgic Encephalomyelitis.

3 of the more common case definitions include the following                                               

Fukuda et al. (1994) case criteria for CFS:         

The Fukuda case definition was adopted by the Centers for Disease Control and Prevention (CDC), and stresses fatigue as a primary symptom. It also requires the presence of at least four of eight symptoms including:  memory and concentration impairment, sore throat, tender lymph nodes, muscle pain, joint pain, headaches, un-refreshing sleep, and post-exertional malaise). Research has indicated that individuals with a primary psychiatric illness (e.g. primary Major Depressive Disorder) may be misdiagnosed under the Fukuda criteria due to many overlapping symptoms including fatigue and sleep difficulties.                                                                               

Canadian Consensus Criteria for ME and CFS (Carruthers et al., 2003):                                                 

The Canadian Consensus Criteria defines ME/CFS as an acquired, organic, pathophysiological multi-systemic illness that occurs in both sporadic and epidemic forms and requires core symptoms including post-exertional malaise (PEM) and neurocognitive dysfunction, in contrast to the polythetic approach of the Fukuda case definition.             

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​Myalgic Encephalomyelitis International Consensus Criteria (ME-ICC 2011).                                                                    The Myalgic Encephalomyelitis – International Consensus Criteria (ME-ICC) advocates for removing fatigue as a characteristic symptom and defines the disorder as an acquired neurological disease with complex global dysfunctions. The ME-ICC also defines specific symptom requirements: post-exertional neuroimmune exhaustion, neurological impairments, immune, gastrointestinal, and genitourinary impairments, and energy metabolism impairments.  

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Dr Melvin Ramsay Defintion for Myalgic Encephalomyelitis  http://hfme.org/wramsay.htm

"The failure to agree on firm diagnostic criteria has distorted the data base for epidemiological and other research, thus denying recognition of the unique epidemiological pattern of myalgic encephalomyelitis."
-Dr. A. Melvin Ramsay-

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In 1956, M.E. pioneer Dr. A. Melvin Ramsay formally coined Sir Donald Acheson's selected name for the disease myalgic encephalomyelitis in a paper describing the 1955 epidemic among staff at Royal Free Hospital in London.   Dr. Ramsay investigated M.E. for more than 30 years, and his sound descriptions of the disease and its accurate name have stood the test of time and have earned him a place of honor in M.E. history.                                                                                       Dr. Byron Hyde notes that Dr. Ramsay was "much loved by patient or physician and all who had the privilege to meet him...."

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In Redefinitions of ME/CFS – A 20th Century Phenomenon, Dr. E.G. Dowsett summarizes historic ME and CFS definitions and emphatically states, "To Summarise: I would urge all our colleagues to look again at the literature prior

to 1988 before redefining this illness. Meantime, the Ramsay description of Myalgic Encephalomyelitis in 1986 with slight modifications to form a short definition still remains a useful guide to those new to this work:

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The Clinical Features of Myalgic Encephalomyelitis  - Melvin Ramsay, M.D., 1986

The onset of the disease is similar to those described in the various recorded outbreaks. Thus it may be sudden and without apparent cause, as in cases where the first intimation of illness is an alarming attack of acute vertigo, but usually there is a history of infection of the upper respiratory tract or, occasionally, the gastrointestinal tract with nausea and/or vomiting.

Instead of an uneventful recovery the patient is dogged by a persistent and profound fatigue accompanied by a medley of symptoms:

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• Headache

• Giddiness

• Widespread muscle pain, cramps or twitching

• Muscle tenderness and weakness

• Paraesthesiae (numbnessor tingling in the extremeties)

• Frequency of micturition (urination)

• Blurred vision and/or diplopia (double vision)

• Hyperacusis (sensitivity to noise sometimes alternating with deafness or normal hearing)

• Tinnitus (constant sound in the ears)

• General sense of feeling awful

Some patients report the occurrence of fainting attacks relieved by a small meal or just eating a biscuit; these attacks were the result of hypoglycaemia …  All cases run a low-grade pyrexia (fever), seldom exceeding 100°F (c. 38°C) and usually subsiding within a week.

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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.

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Disease in Chronic State
Once the syndrome is fully established the patient presents a multiplicity of symptoms which can most conveniently be described in three groups.

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Muscle Phenomena

•  Fatiguability: Muscle fatigability, whereby, even after a minor degree of physical effort, three, four or five days, or longer, elapse before full muscle power is restored and constitutes the sheet anchor of diagnosis. Without it I would be unwilling to diagnose a patient as suffering from ME, but it is most important to stress the fact that cases of ME or mild or even moderate severity may have normal muscle power in a remission. In such cases, tests for muscle power should be repeated after exercise.

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• Pain: In severe cases of ME, muscle spasms and twitching are a prominent feature and give rise to swollen bands of tissue which are acutely tender. In less severe cases, muscle tenderness may not be so readily elicited but careful palpation of the trapezii and gastrocnemii (the muscle groups most commonly involved) with the tip of the forefinger should enable the examiner to detect minute foci or exquisite tenderness.

• Clumsiness: In the aftermath of the disease patients frequently fumble with relatively simple maneuvers such as turning a key in a lock or taking the cork of a bottle. 

Circulatory Impairment. Most cases of ME complain of cold extremities, hypersensitivity to climatic change, Ashen grey facial pallor, 20 -30 minutes before the patient complains of feeling ill. 

Cerebral dysfunction

• The cardinal features:

• Impairment of memory

• Impairment of powers of concentration and

• Emotional lability

• [Other] common deviations from normal cerebral function:

• Failure to recall recent or past events,

• Difficulty in completing a line of thought . . .

• Becoming tongue-tied in the middle of a sentence, and a

• Strong inclination to use wrong words, saying “door” when they mean “table” or “hot” when they mean “cold” . . .

• Complete inability to comprehend a paragraph even after re-reading it

• Bouts of uncontrollable weeping . . .

• Alterations of sleep rhythm or vivid dreams, or both . . 

Accompanying features that can only be attributed to involvement of the Autonomic nervous system:

• Frequency of Micturition (urination)

• Hyperacusis (hypersensitivity to noise)

• Epsisodic Sweating

• Orthostatic Tachycardia

Variability and fluctuation of both symptoms and physical findings in the course of a day is a constant feature in the clinical picture of Myalgic Encephalomyelitis.

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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]

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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 occurrence 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.

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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 generalized 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.

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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 encephalo- myelitis 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.

I would like to suggest that in 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.

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References:

http://hfme.org/wramsay.htm

http://www.meassociation.org.uk/2011/02/london-criteria-for-m-e/

http://www.cfids-me.org/ramsay86.html

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​The Nightingale Research Foundation

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Canadian Charity dedicated to Myalgic Encephalomyelitis, uses a strict definition that states Myalgic Encephalomyelitis is an acute onset biphasic epidemic or endemic infectious disease process, where there is always a measureable and persistent diffuse vascular injury of the central nervous system in both the acute and chronic phases. For more information on specific case definitions, see the Resources and References sections of this report.

Byron Hyde's short videos provide an insightful concise perspective .

https://www.masscfids.org/more-resources-for-me-cfs/444-dr-byron-hyde-2012-fall-lecture-summary?showall=&start=20

or

https://www.youtube.com/watch?v=8rFLQ-StC5A

or

https://www.youtube.com/user/WetenschapvMEcvsVer/videos

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Dr Hyde had the opportunity to examine two physicians who had become ill during the 1934 polio epidemic outbreak.  At the Los Angeles (LA) County Hospital.  According to Dr Hyde’s slide, 198 healthcare workers, who were immunized With sera from recovering patients, fell ill with ME, but not Polio.

            He believes in this case that the combination of an immunization and viral infection triggered their  M.E.            The two doctors sued the Hospital and the city of LA and received about 2 million dollars each.

Dr Hyde’s hypothesis is that this was a wake up call for Insurance Companies to dismiss the illness and from then onward Anything resembling ME was mocked.  There were times when and even now, where ME patients were put into Psychiatric Hospitals and labeled as crazy  (plus given drugs that made them sick).  So, when CFS came along, it seemed to follow the same pattern.  Same illness, different name, same outcome.  
 

Unfortunately there is no consensus on nomenclature or classification for these disorders, and different countries, organizations, and researchers continue to use different names to describe these conditions. Until a global consensus is reached on how to name and classify these disorders, confusion will persist, and research will remain inconclusive. 

Causes                                                                                                                                                                                 The exact cause of Myalgic Encephalomyelitis (ME) is not fully understood, although there are several theories. Most investigators agree that the disease is most likely the result of an abnormal immune system and brain function in response to an infection or virus. Although the brain and immune system are most likely impaired or abnormal (dysregulated) in this disease, the exact underlying problems are unknown. A variety of additional factors that have been theorized as playing a role in the development of ME include genetic and environmental factors. Some studies have shown that ME occurs in greater frequency among relatives to the third degree (genetic predisposition). In contrast, some believe that environmental factors play a greater role than genetic ones. However, definitive evidence linking specific environmental factors to the development of Myalgic Encephalomyelitis is lacking.

​Some researchers believe that an enterovirus infection could be an underlying cause of the disease. Enteroviruses are small, contagious viruses consisting of ribonucleic acid and proteins. They are the second most common viral agents in humans, behind only rhinoviruses (the viruses that cause the common cold). Enteroviruses can affect anyone of any age. Individual susceptibility to enteroviruses varies. The reason why some individuals develop ME after infection with an enterovirus is unknown.

​Other viruses that have been speculated to be associated with ME include cytomegalovirus (CMV/HHV-5), Epstein Barr virus (EBV/HH-4), parvovirus B19, herpes simplex virus (HHV-1 or HHV-2), human herpes virus (HHV 6 or 7), and certain bacterial infections. It is not known whether these viruses caused ME or whether they developed due to an impaired immune system in affected individuals. It was once thought that the ability of the blood-brain barrier — the specialized capillaries that prevent blood contaminants from entering the brain–to block viral entry into the CNS was adequate; however, more recent evidence indicates entry through other routes, such as along the auditory nerve. Additionally, no one virus has been identified that explains all cases of ME. Some studies suggest that in individuals with ME the viruses can trigger cascading events in the central nervous system through chronic activation of the immune system which, in turn, can result in widespread (diffuse) neurological dysfunction, changes at the cellular level, and nerve cell injury and death.

​Even when not actively replicating, an infection can lead to profound dysregulation of the immune response, causing neuroinflammation which destabilizes overall brain function, and producing symptoms with widely fluctuating severity levels.  Viruses also do not continually replicate, but do so at times of immune vulnerability, such as at times of physical or psychological stress. Unfortunately, viruses go latent, then they reactivate, and repeat this pattern.  Once in your cells, any elevation of cortisol levels can cause the reactivation.

​Affected Populations                                                                                                                               

Because of The controversy regarding the definition and classification of Myalgic Encephalomyelitis (ME) and related disorders, determining their true frequency in the general population is difficult. The exact prevalence and incidence of ME is unknown, but one estimate places the prevalence at approximately 1 million affected individuals in the US general population. Approximately, three times as many women appear to be affected than men. Individuals of any race or ethnicity can be affected. Onset is most frequent between the ages of 30-50.

Disorders  thought to be related

A wide variety of disorders or conditions can have symptoms similar to those seen in Myalgic Encephalomyelitis (ME) including Multiple Sclerosis, Systemic Lupus Erythematous, Lyme Disease, Narcolepsy, Mononucleosis, Multiple Chemical Sensitivities, Gulf War Syndrome, and Chronic Epstein Barr infection. Comparisons may be useful for a differential diagnosis.   It is important to note that ME can not be self diagnosed.   

Diagnosis                

A diagnosis of Myalgic Encephalomyelitis (ME) is controversial and difficult. Because there are different case definitions for the disease, a specific set of symptoms for diagnosing ME does not exist.   Scientific Research are pursuing consistent and universally accepted biomarkers for ME.  Biomarkers are characteristics or substances that can be measured and evaluated in order to obtain a diagnosis or help obtain a diagnosis. A diagnosis of ME is ultimately based upon identification of characteristic symptoms (depending on the specific case definition used), a detailed patient history, a thorough clinical evaluation, and a variety of specialized tests to exclude other possible diagnoses. Process of elimination, referred to as diagnosis by exclusion, is used by physicians whenever scientific knowledge is scarce, objective methods are absent, and attempt is made to rule out all other known conditions that could potentially explain patient symptoms.

​Myalgic Encephalomyelitis is not Chronic Fatigue Syndrome  

The term CFS was first used in the medical literature during the 1980s in the United States. The criteria focused more on fatigue than the encephalitic (inflammation of the brain) features of the disorder. This was unfortunate, since there is more than sufficient robust evidence which illustrates the underlying biological process involving the central nervous system, immune system, energy metabolism and stress system. Consequently, the emphasis on fatigue unfortunately led to defining the disorder being seen as a psychiatric illness. Because little was known about the cause or physiology of CFS, a wide range of patients were diagnosed with CFS even though they may have had a variety of conditions and experienced different symptoms. CFS eventually evolved into a larger disease designation that overlapped with Myalgic Encephalomyelitis. Consequently, some researchers, patients, government organizations, and other organizations began to use the terms interchangeably or with the combined acronym ME/CFS, creating a broad disease category.

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Further, some researchers, physicians, and patient advocacy groups have pushed to abandon the illness label of CFS as they argue it is inaccurate and trivializes affected individuals. They want to reclassify these individuals as having Myalgic Encephalomyelitis. Other researchers, physicians, and many ME patient advocacy groups have argued against this change, noting that Myalgic Encephalomyelitis should retain a strict definition as a distinct neurological disease that includes measurable abnormal changes in the brain and central nervous system. Individuals who meet the stricter criteria would be diagnosed with Myalgic Encephalomyelitis.

The term CFS should be reserved for individuals who fail to meet the more stringent criteria for Myalgic Encephalomyelitis and in whom no other underlying disorder or condition can be identified. Many patients who have been diagnosed with CFS would meet the more stringent criteria for Myalgic Encephalomyelitis. Individuals who fail to meet the criteria should be retested for an underlying condition as many individuals initially diagnosed with CFS are eventually diagnosed with an underlying condition such as cancer, multiple sclerosis, lupus, brucellosis, or another condition.

​Standard Therapies & Treatment

There is no cure for ME. Treatment is aimed at relieving symptoms and preventing a worsening of symptoms. Decisions concerning the use of particular therapeutic interventions should be made by physicians and other members of the healthcare team in careful consultation with the patient and/or parents based upon the specifics of his or her case, a thorough discussion of the potential benefits and risks including possible side effects and long-term effects, patient preference, and other appropriate factors. A specific treatment plan will be highly individualized.

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Avoiding overexertion is extremely important in maintaining health in affected individuals. Depending on the individual, a variety of therapeutic options exist for alleviating ME symptoms which may include making changes to one’s diet, physical therapy, adjusting the pacing of activity levels, lowering overall exertion by getting a service dog, adjusting sleep parameters (regularizing sleep habits, changing pillows/blankets/mattress, room darkening, temperature, etc.), avoidance of substances (e.g. mold, chemicals) or situations prone to worsen one’s symptoms, and adjusting one’s lifestyle in ways that minimize the impact of physiological and psychological stress in general.

Some researchers have studied a treatment approach called “Pacing” as a potential therapy for some individuals with ME. This treatment option does not involve medications (non-pharmacologic) and strives to help affected individuals self-monitor and self-regulate their energy expenditures. By learning to pace their activity levels, affected individuals can stay within their “energy envelope.” Affected individuals are taught to balance expended energy with available energy to reduce the frequency and severity of some symptoms. Pacing can help affected individuals manage symptoms and, in some cases, can improve some quality of life.

Certain medications have been used to treat individuals with ME. However, many affected individuals are highly sensitive to medication. Additionally, because the underlying nature of ME is not fully understood, any specific medications or treatments should be considered cautiously. Initially, any medications should be given at low doses. No medications for ME are universally effective.

Affected individuals should be treated for any pathogens, toxins, or heavy metals as persistent exposure can worsen symptoms. Referral to an infectious disease specialist is recommended. Any antibiotics or antiviral drugs should be used cautiously.

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