CO-CURE: Myalgic Encephalomyelitis (ME) - Disapedia

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Date:    Sat, 8 Sep 2007 18:02:48 -0500

    LK Woodruff <lkw777

Myalgic Encephalomyelitis (ME) - Disapedia

 

Myalgic Encephalomyelitis (ME) - Disapedia

I had never heard of Disapedia until today. But I guess it started in May

2007, so I am not too far behind:)

 

While I would tweak or update a few things (below), overall it is quite

well-written and comprehensive.    LKW

 

- http://www.disapedia.com/index.php?title=Myalgic_Encephalomyelitis_(ME)

 

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Myalgic Encephalomyelitis (ME)

 

Myalgic Encephalomyelitis (abbreviated ME) is a chronic, inflammatory,

primarily neurological disease that is multisystemic, affecting the central

nervous system (CNS), immune system and cardiovascular system, the

endocrinological system and muscoskeletal system. ME can cause a wide

variety of symptoms, including changes in sensory tolerance, visual

problems, exertional muscle weakness, difficulties with coordination and

speech, severe fatigability, cognitive impairment, problems with balance,

subnormal or poor body temperature control and pain. ME will cause a degree

of impaired mobility and disability in all cases. The degree of impairment

and complexity depends on the degree of diffuse brain injury and end organ

involvement.

 

Myalgic Encephalomyelitis affects the brain and spinal cord which control

the body, allow thought and sensory processing, causing dysautonomia,

impaired thinking and loss of internal homeostasis, the process whereby the

body maintains a consistent internal environment in response to external

stressors. Cellular metabolism and communication is disrupted, causing

inefficiency in all biological processes. This includes the cellular

mitochondria which process fuel to make energy, resulting in a deficiency of

adenosine-triphosphate ATP with a chronic, severe, measurable loss of

sustainable strength on exertion. A hallmark of ME is intolerance to

previously trivial effort and deterioration through persistent or repeated

exertion.

 

Current theory suggests ME results from a persistent viral infection and/or

attacks by an individual's immune system on the nervous system,

muscoskeletal system and blood vessels. It has been classified by the World

Health Organisation as an organic brain disease since 1969. There is a

controversial view that ME is not a chronic infectious or autoimmune

disease, but rather a psychosocial illness triggered by infection or stress.

Usually proponents of this school disdain the term ME, claiming it to be

inaccurate. Although more than 50 years of research and clinical observation

informs knowledge of ME pathology, its exact cause remains unknown and more

research is required particularly for treatment. ME patients are barred from

donating blood or organs in the United Kingdom while symptoms persist.

 

Myalgic encephalomyelitis is a relapse-remitting disease with new symptoms

occurring either in discrete relapses (or " crashes " ) or slowly accruing over

time. Between relapses, symptoms may resolve completely with sufficient

rest, but permanent neurologic problems often persist, especially as the

disease advances. ME currently does not have a cure, though some treatments

such as antivirals are being trailed which may at least slow the appearance

of new symptoms.

ME affects all ages, with peak incidence typically between 20 and 40 years,

and is more common in women than in men.

 

Contents

 

1 Terminology

2 Signs and symptoms

3 Diagnosis

3.1 Differential Diagnosis

4 Disease course and clinical subtypes

4.1 Severity

5 =Comorbid Illnesses

6 Factors triggering a relapse

7 Pathophysiology

8 Causes

8.1 Environmental

9 Treatment

10 Prognosis

11 Epidemiology

12 History

12.1 The Formative Years

12.2 WHO Classification and Disgrace

12.3 CDC Intervention

12.4 Villified but Vindicated

12.5 ME Redux

13 References

13.1 External links

13.2 Organizations

 

 

Terminology

 

The name Myalgic Encephalomyelitis refers to the inflammation of the brain

and spinal cord accompanied by muscle pain.

In 1988 The US Centres for Disease Control (CDC) for reasons best known to

them dismissed fifty years of research and decided to treat the Lake Tahoe

outbreak as a new illness, which they christened chronic fatigue syndrome (CFS).

CFS is a highly contentious concept to patients and specialists alike. Because

of the similarity in terminology, CFS is often confused with " chronic

fatigue " . A study found that while most medical trainees consider the symptom

complex

of CFS to be a serious illness resulting in poor quality of life, the

" chronic fatigue syndrome " name may be regarded less seriously than the name

" myalgic

encephalopathy " . Another study found that nurses and physician assistants

viewed a patient's CFS symptoms as more severe and

disabling if they were told the patient had a more medical sounding diagnosis

of " chronic neuroendocrineimmune dysfunction syndrome " .

 

Patients and specialists alike had long lobbied for a name and definition

change or reversal of " CFS " . In January 2007 The American " CFS Name Change

Advisory Board " consisting of doctors Bateman, Bell, Cheney, Jason, Klimas,

Lapp,

and Peterson agreed that " " CFS downplays the severity of the disease and is

hurtful to patients " and publicised their deliberation that CFS should now be

termed ME.

 

Signs and symptoms

 

ME can cause a large variety of symptoms, including increased sensitivity to

light and sound (photosensitivity, hyperacusis) and general migraine-like

sensory intolerance, changes in sensation (hypoesthesia), muscle weakness

(myasthenia), muscle spasms (myclonus or fasciculation), or difficulty

initiating

movement (transient paralysis); difficulties with coordination and balance

(ataxia); problems in speech and verbalisation (Dysarthria, Dysphasia), visual

problems (Nystagmus, diplopia), easy fatigue]] and acute or chronic pain,

difficulty

standing (orthostatic intolerance), cardiopulmonary symptoms (papitations,

dysrhythmia and dyspnoea), sleep dysregulation (hypersomnia, insomnia or sleep

reversal), gastroenteric difficulties, cognitive impairment, or emotional

symptomatology (emotional lability or depression). More than 60 symptoms have

been

described and it is not unusual for severely affected sufferers to have more

than twenty.

 

Diagnosis

 

ME is diagnosed definitively using case history to look for a distinctive

pattern and type of symptoms and signs. Diagnosis necessitates involvement of

the

CNS and muscoskeletal symptomology.

 

Historically different criteria were used. The Ramsay criteria and Dowsett

criteria were both popular. Currently, Canadian Consensus criteria represents

international efforts to standardize the diagnosis of ME using clinical data and

laboratory data.

 

Generally Consistent findings of a novel low molecular weight antiviral

protein (Rnase-L) have shown promise as a potential diagnostic test. Another

test

which may become important in the future is an assay of genes for the immune

system and mitochondria, however, these tests are so far seen as discretionary.

 

Differential Diagnosis

 

The signs and symptoms of ME can be similar to other medical problems, such

as multiple sclerosis, Lyme disease, lupus, anemia, cancers, and other

autoimmune problems, such as lupus, sarcoidosis. Additional testing may be

needed to

help distinguish ME from these other problems.[edit]

 

Disease course and clinical subtypes

 

The initial acute phase illness most often occurs in summer with a 3-5 day

incubation period and during this period is said to be highly

infectious.Generally from then the initial presentation takes one of two forms:

a severe,

incapacitating prolonged illness or an apparent remission followed by increasing

relapses until the patient is forced to recognise exertional limitation. The

most

common initial symptoms reported are: pain in the spine, neck or head, mild

fever and 'flu-like symptoms, nausea or vomiting, flaccid muscle weakness and

muscle pain or tenderness Cite error 4; Invalid <ref> tag; refs with no name

must have content For some people ME is triggered by Hepatitis B vaccination,

blood transfusion or chemical poisoning, although it is now thought

organophosphate poisoning is a different illness.

 

The later course of ME is difficult to predict, and may either become

consistently severe, improve to a plateau or be markedly relapse-remitting. In

some,

even prolonged severe incapacitation can be relieved by unpredictable

remission, although relapse is always possible. The degree of impairment and

complexity depends on the degree of diffuse brain injury and end organ

involvement.

 

The evidence for subgroups is strengthened by research using heterogenous CFS

criteria, although this artificial heterogeneity also hampers consensus. It

is likely that subtypes exist within the ME mileu based on the clinical

findings, history and perhaps gender of patients.

 

 

Severity

Comorbid Illnesses

Commonly found comorbid disorders

 

Factors triggering a relapse

 

ME relapses are often unpredictable and can occur without warning with no

obvious inciting factors. Some attacks, however, are preceded by common

triggers.

In general, relapses occur more frequently during autumn and winter than

during spring and summer. Physical and emotional stress is the most reported

relapse trigger. Previously trivial effort, such as prolonged standing, aerobic

activity, multitasking activity or sensory stimulus are commonly reported.

Exposure to increased sensory information in light, sound, movement can provoke

a

sensory storm which has been termed " The Mall

Effect " due to it's particular provocation by the stimulus of a busy shopping

mall.

Infections, such as the common cold, influenza, and gastroenteritis, increase

the risk for a relapse. Heat and cold can transiently increase symptoms.

Pregnancy can directly affect the susceptibility for relapse. Later pregnancy

appears to offer a natural protection against relapses, and there are anecdotal

reports of post-partum remission. However pregnancy does not seem to influence

long-term disability.

 

Pathophysiology

 

Although much is known about abnormalities in myalgic encephalomyelitis, the

reasons why they occur is not known. There are two ME conferences held in the

UK each year attended by international research luminaries, and other

conferences held worldwide, organised for example by the AHMT.

 

Myalgic encephalomyelitis is a complex disease in which the immune and

neurological systems appear dysregulated and in conflict, producing a wide

variety

of findings. According to the view of most researchers, a special subset of

lymphocytes, called T cells, plays a key role in the pathology of ME.

 

According to a strictly immunological explanation of ME, the inflammatory

processes triggered by the T cells create leaks in the blood-brain barrier (a

capilar system that should prevent entrance of T-cells in the nervous system).

These leaks, in turn, cause a number of other damaging effects such as swelling,

activation of macrophages, and more activation of cytokines and other

destructive proteins such as Rnase-L. A reduced ability to move metabolites in

and

out of cells (channelopathy) has been implicated in this process

 

Some evidence shows viral infection of muscle and brain in at least a

proportion of sufferers. This triggers inflammatory processes, stimulating other

immune cells and soluble factors like cytokines and antibodies.A model for late

ME

has been proposed analogously to post-polio syndrome in which repaired nerve

tissue forms inappropriately. Radiological research shows punctate lesions

like those found in ME, brain hypometabolism and a reduced volume of grey matter

by an average of 11%.

 

An inquest into the death of Sophia Mirza from ME found inflammation of the

dorsal spine ganglia and liver abnormalities.

 

Hemodynamic abnormalities are widely found, including serum and RBC

hypovolemia, NMH, cerebral hypoperfusion. Vascular and endothelial abnormalities

have

been published by MERUK.

 

Some cardiological features such as cardiac insufficiency, inverted T-waves

and myofibre disarray have been reported and recently added to by findings of

reduced Q-value. This has lead clinician and researcher Dr Paul Cheney to posit

that ME is form of partially compensated cardiomyopathy in which orthostatic

intolerance and rapid fatiguability are secondary protective mechanisms.

 

Causes

 

Although risk factors for myalgic encephalomyelitis have been identified, no

single definitive virus has been found in all cases, which has lead to the

claim that ME is a common end path of a variety of infectious insults, perhaps

most commonly in the retroviral family. It is still possible ME involves some

combination of both environmental and genetic factors. Various theories try to

combine the known data into plausible explanations. Although most accept an

infectious explanation, several theories suggest that ME is an inappropriate

immune response to an underlying condition, a theory

bolstered by the observation that there is sometimes a family history of

autoimmune disease. 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.

 

Environmental

 

The most popular hypothesis is that a [viral infection or retroviral

reactivation primes a susceptible immune system for an abnormal reaction later

in

life. On a molecular level, this might occur if there is a structural similarity

between the infectious virus and some component of the central nervous system,

leading to eventual confusion in the immune system.

 

Other theories describe ME as an immune response to a chronic infection. The

association of ME with the Cocksackie-B and HHV-6 and HHV-7 viruses suggests

a potential viral contribution in at least some individuals.

 

Still others believe that ME may sometimes result from a chronic infection

with spirochetal bacteria. Another bacterium that has been implicated in ME is

'Chlamydiapneumoniae. Protein findings relating to several infections have seen

found in the oligoclonal bands ME patients.

 

Treatment

 

There is no known definitive cure for myalgic encephalomyelitis. However,

several types of therapy have been found helpful by sufferers. Different

therapies are used for patients experiencing greater neurological symptoms, for

patients who have greater muscle and/or cardiac symptoms, for patients who have

greater immune symptoms, for patients without an uncertain diagnosis, and for

managing the various consequences of ME. Treatment is aimed at reducing

disability, restoring sleep, reducing pain, reducing

relapses and preventing disability.

 

Mito cocktail

acetyl-L-carnitine

co-enzyme q10

D-ribose

magnesium

Antioxidants

L-glutathione

Disease-modifying treatments (in trial):.

Ampligen:

Imunovir

valganciclovir

Management

pacing

switching

avoiding relapse triggers

maintaining good hydration

dietary modification

Other

Neurontin (pain control)

EPA fatty acid

saline infusions

midodrine

 

Prognosis

 

The prognosis (the expected future course of the disease) for a person with

myalgic encephalomyelitis depends on severity and chronicity of the disease and

initial symptoms; the age; and the degree of disability the person

experiences. The life expectancy of people with ME is generally less than that

of

unaffected people. Fatalities occur mainly due to heart or pancreatic failure,

opportunist infection, neurodegeneration, cancer and suicide.

 

The degree of disability varies among individuals with ME. In general, 25%

are severelydisabled, though a number move in and out of categories due to

relapse-remission.Currently there are no clinically established laboratory

investigations available that can predict prognosis or response to treatment.

 

However, several promising approaches have been proposed. These include

measurement of the Rnase-L enzyme.

 

Epidemiology

 

ME has been found world-wide, in at least 63 epidemics documented in

published papers from the 1930's to the 1980s. Currently ME is less epidemic and

more

endemic than in previous decades. Epidemics have a penchant for enclosed

communities such as schools and hospitals, although not all of the outbreaks

have

occurred in enclosed commmunities.

 

As observed in many autoimmune disorders, ME is more common in females than

males; the mean sex ratio is about two to three females for every male. In

children the sex ratio is approximately equal. Some evidence suggests there may

be a higher incidence in ethnic minorities.

 

History

 

The Formative Years

 

The first definitive description of an illness resembling poliomyelitis was

by Gilliam after the 1930s Los Angeles outbreak. Careful clinical observation

in all the epidemics repeatedly found reproducible signs and a distinctive

pattern of CNS and sensory nerve involvement, muscle weakness with pain or

tenderness and emotional lability with a chronic relapsing course.

 

In the 1950s, the public eye was caught by several outbreaks of a mysterious

illness that incapacitated communities, often in hospitals. In the Iceland

epidemic it was noted patients who contracted the illness developed immunity to

poliomyelitis, suggesting confirmation of an association.

 

Autopsy findings, both on experimentally infected monkeys during the Adelaide

epidemic and on human casualties, led to the conclusion that the disorder was

caused by inflammation of the brain and the spinal cord. Accordingly names

such as atypical polio and Akiyuri disease were replaced in 1956 in the UK by

the term Myalgic encephalomyelitis.

 

 

WHO Classification and Disgrace

 

ME has been included in the classification of the World Health Organization

(WHO) as a disease of the central nervous system since 1969.In the ICD-10, ME

is the only disorder listed in the tabular classification under G93.3,

Post-viral fatigue syndrome (PVFS).

 

Despite the increasing prevalence of non-epidemic cases, the disorder was

soon dismissed by some as mass hysteria due to the 1970 McEvedy and Beard

speculative research, in which no patients were examined. Interest dropped, to

be

rekindled only after a similar outbreak at Incline Village, Lake Tahoe, Nevada

in

the mid-1980s.

 

CDC Intervention

 

Unaware or dismissive of the earlier findings, researchers from the Centers

for Disease Control & Prevention (CDC) now attached a different kind of name to

the phenomenon: Chronic Fatigue Syndrome (CFS), which is generally perceived

by ME researchers and patients as misleading and even insulting, as the

emphasis was now on non-specific fatigue as the only consistent symptom.

 

The Centers for Disease Control & Prevention published a first working case

definition for CFS in 1988,[240] even though by then the CDC were definitely

aware of ME. It has been suggested they preferred to see CFS as a new illness.

 

Around this time it was accepted that ME was now primarily found among the

general population and the epidemic form was the exception.

 

In 1993 the term Chronic fatigue syndrome (CFS) was added to the alphabetic

list of the WHO ICD classification.

 

Villified but Vindicated

 

Research increased, more so after the criteria were relaxed in 1994, but was

criticised for over-inclusiveness. With all objective signs now expunged, the

obvious possibility of misdiagnosis bedevilled clinical and research work.

Lacking a diagnostic laboratory test of any kind, CFS has frequently been

mis-diagnosed, for example in patients presenting CFS symptoms with similar

biological conditions or infections (such as Lyme or Epstein-Barr) (the latter

of which

is often the cause of glandular fever, or infectious

mononucleosis), or psychological conditions (ranging from depression to

hypochondria).

 

A lack of information and awareness has led to many patients being

stigmatised, sometimes as hypochondriac or lazy, yet at other times as

over-active and

perfectionistic. Because immune related symptoms are common in ME patients,

their immune system was suspected to be dysfunctional, or responding

inappropriately to specific viruses; this lead to the proposal of the

alternative name

" chronic fatigue immune dysfunction syndrome " (CFIDS).

 

Researchers in a study of patient perspectives have argued that the earlier

failure of Western medicine to demonstrate a viral etiology for ME led to a

paradigmatic shift to psychiatric and sociocultural research, which effectively

delegitimized CFS (ME) as a biomedical phenomenon within medical, academic,

governmental, and public arenas; they also suggest that the history of medical

attitudes toward ME may eventually parallel the transformations that occurred in

relation to multiple sclerosis, as the discovery of biological markers for ME

may lay to rest the categorization of ME as largely within the psychiatric

realm. Other researchers have stated that physicians have since minimized the

seriousness of ME and also interpreted the syndrome as being psychiatric, which

had negative consequences for the treatment of patients; and the revised CFS

case

definition might have produced heterogeneous patient groups which possibly

include some with pure psychiatric disorders. A major recurrent criticism of CFS

is that it does not make post-exertional malaise or muscle weakness an

essential criteria thus leading to the uncertainty and controversy over the

appropriatness of physical rehabilitation programmes.

 

ME Redux

 

More recently, additional evidence supportive of the ME paradigm has been

discovered, delineating; CNS inflammation, pathologically delayed recovery of

muscle strength, cardiac and vascular abnormalities and defects in cellular

metabolism. Neurocognitive dysfunction has been objectively observed; and

physiological abnormalities relating to immune activity, gene expression,

oxidative

stress and the nervous system have also been found, plus many psychological and

psychiatric studies have also been done.. The U.S. Centers for Disease Control &

Prevention (CDC) now recognized CFS as a serious illness but also list ME as

a differential diagnosis on their web site, reflecting the incompatibility of

the traditional definitions.

 

The CFS definition allowed sufficient laxity for US specialists including

those who had preceded the CDC at Lake Tahoe to customize the definition for

those patients they thought most representative of ME. Accordingly an

ideological

rift in CFS conceptualisation occurred, with biological (or " ICD CFS " ) being

perceived as similar to ME despite the CDC definition vagaries, while the

psychologists continued to research psychosomatic or affective disorders as CFS

despite the WHO classification.

 

In 2003 a group of international specialists published the consensus

definition of an illness now termed " ME/CFS " the criteria of which, including

CNS and

exertional signs, was more like that of ME than CFS. In January 2007 The

American " CFS Name Change Advisory Board " publicized their deliberation that CFS

should now be called ME, though no statement was made on definition. The CDC

continue to widen their CFS definition.

 

References

 

Wallis AL, " An investigation into an unusual illness seen in Epidemic and

Sporadic Form in a General Practice in Cumberland in 1955 and subsequent

years " , M.D. Thesis, Edinburgh University, 1957

 

Acheson E (1959). " The clinical syndrome variously called benign myalgic

encephalomyelitis, Iceland disease and epidemic neuromyasthenia. " . Am J Med

26 (4): 569-95. PMID 13637100.

 

Goldstein JE, Hyde BM (1992). The Clinical and scientific basis of myalgic

encephalomyelitis/chronic fatigue syndrome. Ogdensburg, N.Y: Nightingale

Research Foundation, 628-633. ISBN 0-9695662-0-4.

 

Carruthers BM, Jain AK, De Meirleir KL, Petersn DL, Klimas MD, Lerner AM,

Bested AC, Flor-Henry P, Joshi P, Powles ACP, Sherkey JA, van de Sande MI

(2003). " Myalgic encephalomyalitis/chronic fatigue syndrome: Clinical

working definition, diagnstic and treatment protocols " . Journal of Chronic

Fatigue Syndrome 11 (1): 7-36. DOI:10.1300/J092v11n01_02.

 

Gilliam AG. (1938) Epidemiological Study on an Epidemic, Diagnosed as

Poliomyelitis, Occurring among the Personnel of Los Angeles County General

Hospital during the Summer of 1934, United States Treasury Department Public

Health Service Public Health Bulletin, No. 240, pp. 1-90. Washington, DC,

Government Printing Office.

Jason LA, Helgerson J, Torres-Harding SR, Carrico AW, Taylor RR (2003).

" Variability in diagnostic criteria for chronic fatigue syndrome may result

in substantial differences in patterns of symptoms and disability. " . Eval

Health Prof 26 (1): 3-22. PMID 12629919.

 

Jason, LA, et al., " Chronic Fatigue Syndrome: The Need for Subtypes. "

Neuropsychology Review, Vol. 15, No. 1, March 2005, pp. 29-58 [PDF Format]

 

Crowhurst G, " Supporting people with severe myalgic encephalomyelitis. "

Nursing Standard. 19, 21, 38-43. 2005

 

Goudsmit E, Stouten B, Howes S, Illness Intrusiveness in Myalgic

Encephalomyelitis An exploratory study [1]

 

External links

 

A Hummingbird's Guide

MEactionUK

Memorial List

Dr Cheney on cardiac involvement

The HHV-6 Foundation

United Mitochondrial Disease Foundation

National Gulf War Resources Center (US)

[edit] Organizations

ME Research UK

The 25% ME Group (for the severely affected)

ME Society of America

Nightingale Research Foundation (Canada)

ME Association (UK)

The Young Sufferers' Trust {UK}

 

Retrieved from

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