Understanding "Myalgic Encephalomyelitis" (also known as Enteroviral Encephalomyelitis) and how it's not the same as "Chronic Fatigue Syndrome" criteria's or the SEID "ME/CFS" algorithm, which reflect "missed diagnosed" Chronic Fatigue Syndromes. "M.E." is actually EXCLUDED.
"At the first meeting on the 27th of October 2005, the Chairman of the Joint Committee, Dr. Ian Gibson, asked me to prepare a report and definition that might assist the committee in its further deliberations. The following are my original recommendation.
Dr. Bruce Carruthers, who chaired the 2003 Canadian Clinical Case Definition for ME/CFS, was also present when I gave this definition.
I strongly disagreed with Dr. Bruce Carruthers in the merging of the definitions of M.E. (also known as Enteroviral Encephalomyelitis) and CFS since on basis of the physical total body assessment of both M.E. (also known as Enteroviral Encephalomyelitis) and CFS patients; these two names represent two entirely different spectrums of illnesses. The present 2016 definition is confined to the defining of Myalgic Encephalomyelitis (M.E.)."
"The term CFS is mentioned from time to time to clarify differences. It is increasingly obvious that too much importance was being placed upon the definitions of Chronic Fatigue Syndrome (CFS), and not enough upon the actual disease, Myalgic Encephalomyelitis (M.E.) (also known as Enteroviral Encephalomyelitis). These two illness spectrums are not the same and shouldn't be considered the same. Nor is there any doubt in my mind that the various definitions of CFS actively impede physicians' ability to make a rapid and rational diagnosis as well as a scientific confirmation of any testable illness. Such is not true of M.E. (also known as Enteroviral Encephalomyelitis) where a rapid and rational diagnosis can be confirmed by laboratory and other technological testing."
"In my 27-year investigation of M.E. (also known as Enteroviral Encephalomyelitis) and CFS patients, I can state with clarity that there is less psychiatric among M.E. (also known as Enteroviral Encephalomyelitis) or CFS patients than in the general public"
"Garbage Bag Disease: Unfortunately, many physicians appear to be using CFS (currently erroneously labelled ME/CFS) as a convenient garbage bag disease, simply telling patients whom they have no time to investigate, "Oh, you have Chronic Fatigue Syndrome". It is most unfortunate that the Americans, who have now promoted the idea that CFS is the same as M.E. (also known as Enteroviral Encephalomyelitis) have only compounded the disaster. Due to this garbage bag phenomena mentality many CFS patients are never properly investigated for serious disease and most CFS patients have significant and often treatable pathologies."
In creating the Nightingale Definition, we have studied decades of clinical evidence, and followed up on the work of Dr. Melvin Ramsay (case descriptions published 1986 and 1988),...
...Dr. Elizabeth Dowsett,
...Dr. John Richardson,
M.E. (also known as Enteroviral Encephalomyelitis) has a clearly defined disease process, while CFS by definition has always been a syndrome. In light of this state of affairs, the Nightingale Research Foundation created its 2007 Definition of M.E. and updated it in 2016. Our Nightingale Definition of M.E. is located on our website under "Publications" and is available as a free download in English, French, Norwegian, and Danish.
The Complexities of Diagnosis
In 2003, Dr. Byron Hyde completed a chapter for L. A. Jason, P. A. Fennell and R. R. Taylor for their book Handbook of Chronic Fatigue Syndrome, John Wiley and Sons Inc., Hoboken N.J., titled “The Complexities of Diagnosis” 1, Chapter 3. This chapter includes the following definition of CFS:
“The physician and patient alike should remember that CFS is not a disease. It is a chronic fatigue state where the one essential characteristic of M.E. is "acquired" Central Nervous System (CNS) Dysfunction, that of CFS is primarily Chronic Fatigue. By assumption, this CFS fatigue can be "acquired" abruptly or gradually. Secondary symptoms and signs were then added to this primary fatigue anomaly. None of these secondary symptoms is individually essential for the criteria and few are 'scientifically' testable. Despite the list of signs and symptoms and test exclusions in these definitions, patients who conform to any of the CDC, Oxford, Australian and Canadian CFS criterias may still have an undiagnosed major illness, certain of which are potentially treatable. Although the authors of these definitions have repeatedly stated that they are defining a syndrome and not a specific disease, patient, physician, and insurer alike have tended to treat this syndrome as a specific disease or illness, with at times a potentially specific treatment and a specific outcome. This has resulted in much confusion, and many physicians are now diagnosing CFS as though it were a specific illness. They either refer the patient to pharmaceutical, psychiatric, psychological, or social treatment or simply say: “you have CFS and nothing can be done about it”. The CFS criterias have another curiosity. If in any CFS patient, any major organ or system injury or disease is discovered, the patient is removed from the definition. The CFS criterias were written in such a manner that CFS becomes like a desert mirage: The closer you approach, the faster it disappears, and the more problematic it becomes.”
Definition Essentials
Some of the definition essentials required to accurately diagnose either M.E. (also known as Enteroviral Encephalomyelitis) or CFS, or any chronically ill patients group, include:
A working case clinical definition must be short, clear and testable.
Patients and their illness or illnesses must be part of an integrated system. Neither the patients’ pathophysiology nor their illness can be understood without a concise knowledge of their integrated pathophysiological systems.
A statistically significant group of patients who have M.E. (also known ss Enteroviral Encephalomyelitis) and CFS-type illnesses must be subjected to a complete personal and family history to map the genetic and historical causes of their illnesses.
Accordingly, the patient’s illness can only be understood if a complete total body mapping is performed on all systems and organs. The mammalian and animal bodies are an integrated physiological mechanism and when one major system change occurs, many physiological systems are liable to shift.
In the past it has been facile to pose psychiatric diagnoses on M.E. (also known as Enteroviral Encephalomyelitis) and CFS patients since psychiatric diagnoses cannot be subjected to scientific examination. Psychiatrists rarely actually examine patients and almost never do an integrated pathophysiological patient investigation of the patient’s organs and systems. Nor have most psychiatrists been of any help in diagnosing M.E. (also known as Enteroviral Encephalomyelitis) and CFS patients except to the insurance industry. In the more than 70 years since the first major M.E. (also known as Enteroviral Encephalomyelitis) and original CFS (also known as Enteroviral Encephalitis) epidemic struck the Los Angeles County General Hospital in 1934, no psychiatric treatment has proven significantly effective in treating the M.E. (also known as Enteroviral Encephalomyelitis) and heterogeneous CFS group of patients and restoring them to health. This is understandable since neither represents a psychiatric disorder.
Effective treatment of the M.E. (also known as Enteroviral Encephalomyelitis) and heterogeneous CFS group of patients depends upon precisely defining the organ and system pathologies and learning how to treat these pathophysiological conditions.
M.E. (also known as Enteroviral Encephalomyelitis) and the hetrogeneous CFS group of illnesses are chronic illnesses. For too long physicians have been considering chronic diseases and chronically ill patients as they would acute short-term illnesses. We believe this is an error and we direct those interested to our chapter on diagnosis. Relatively young chronically ill patients, often do not have a disease process, they often have many disease processes.
ep·i·dem·ic my·al·gic en·ceph·a·lo·my·e·lop·a·thy
Nightingale is pleased to offer the definition of Myalgic Encephalomyelitis in a downloadable PDF format for free in the following translations:
Nightingale Research Foundation - MEPedia
The Nightingale Research Foundation Definition is a definition of Myalgic Encephalomyelitis that was developed by the Nightingale Research Foundation. It was first presented as a preliminary draft in 2006, published in 2007, and updated in 2016.
Definitions, Abbreviations and Acronyms
EV = Enterovirus: (incubation period circa 3-7 days) (illness beginning most frequently in late summer and autumn in the north temperate world) (these infections first enter the body through the gastric portal, hence the name: entero.
Enteroviruses cause paralytic polio, other paralytic enteroviral diseases, type 1 diabetes, major gastric diseases.
Genome - The complete set of genes or genetic material which defines a micro-organism.
M.E. - Epidemic Myalgic Encephalomyelitis: a complex epidemic and sporadic biphasic disease state caused by a chronic enteroviral infection, which injures the GIT system and the upper CNS brain function. CNS dysfunction, in turn, causes generalized body dysfunctions.
CFS = Chronic Fatigue Syndrome: CFS is not a disease. It is a non-specific group of poorly investigated chronically disabling and major illnesses, diseases and pathologies.
EBV = Epstein Barr Virus is the primary cause of Mononucleosis (Glandular Fever in the UK): This is an easily diagnosed viral illness that due to its circa 40 day incubation period does not cause epidemic diseases. Unlike Enteroviral infections there is no specific season when it is more common.
CNS = Central Nervous System: (brain, brainstem, spinal cord and appendages).
MRI = Magnetic Resonance Imaging: Used as brain imaging technology. This technique visualizes anatomy not function. Routine MRI cannot demonstrate most physiological brain dysfunction.
SPECT = Single Photon Emission Computed Tomography: This technique visualizes physiological function or vascularization, not anatomy. SPECT can document major brain dysfunction.
HMPAO = A nucleotide (Hexa-Methyl-Propylene-Amine-Oxime) used in SPECT imaging and the essential product for brain mapping employing Segami Oasis NeuroGam software.
Dysautonomia = a malfunction of the autonomic nervous system seen in many severe M.E. patients, specifically Insular hypoperfusion. (Several brain areas are responsible for normal blood pressure, efficient body and CNS circulation, and normal heart rate.)
PoTS = Postural Orthostatic Tachycardia Syndrome: (This is a variety of dysautonomia.)
Insular Lobe = a hidden lobe covered by the operculum (the junction of the temporal, parietal, frontal lobes). The insular lobe is the brain area significantly responsible for autonomic control. Hypoperfusion of the operculum is consistently found in patients with Dysautonomia.
GIT = Gastrointestinal Tract: (oesophagus, stomach, small and large intestines)
CDC = Centers for Disease Control and Prevention: (Atlanta, Marietta Georgia)
NIH = National Institutes of Health (Bethesda, Maryland) One of the world’s foremost medical research centres, an agency of the USA Department of Health.
To the reader,
The following information explains how physicians can diagnose clinically & test scientifically for Myalgic Encephalomyelitis (M.E.) (also known as Enteroviral Encephalomyelitis).
But, first a word about M.E. (also known as Enteroviral Encephalomyelitis) and EnteroViral (EV) infections.
M.E. is not Chronic Fatigue Syndrome (CFS).
M.E. (also known as Enteroviral Encephalomyelitis) is an epidemic and sporadic illness caused by many E.V.s. The best known E.V.s are Polio 1, 2 & 3 but the genomes of the approximately 100 different E.V.s are identical to the polio genome except for a 5% difference in the 5’ (prime) untranslated area.
Most interesting is that the first-year symptoms of M.E. (also known as Enteroviral Encephalomyelitis) are identical to Dr. Ivar Wickman’s description of the Polio symptoms in the 1905 Stockholm-area polio epidemic, which maimed and killed over 1031 patients.
a. E.V.s injure the CNS, primarily above the spinal cord; whereas Polio E.V.s injure the spinal cord, brainstem, & to a lesser extent the brain itself.
b. Certain E.V.s have always caused paralysis but not usually as frequently nor as severely as polio 1 & 3, although many of these E.V.s can cause muscle weakness as in M.E. In addition, E.V.s cause a large number of other serious and often fatal illnesses, both in children and adults.
c. Polio immunization researchers didn’t know about E.V. until after the first successful Salk polio vaccine. In effect, they built the polio-immunization on the basis of the 5’ prime area of the genome (at the left of the following diagram). If they had built the immunization on the basis of the VP3 section of the genome below, were it possible, there would be no M.E. (also known as Enteroviral Encephalomyelitis) today, nor would there be any paralytic polio either.
Epidemic Myalgic Encephalomyelitis (also known as Enteroviral Encephalomyelitis) M.E. is described in this booklet and is caused by enteroviruses.
Acute Onset missed diagnosed Chronic Fatigue Syndromes can be associated with any CNS (neurotropic) injuring or infectious agent. Childhood infections in adults (usually adults over 20 yrs.) such as varicella (chicken pox), measles, EBV, can cause death or chronic brain dysfunction, which can provoke the so-called CFS-type patients. But EBV can never cause rapidly-spreading epidemics.
Chronic Fatigue Syndrome (CFS): in our experience the diagnosis of CFS only means the investigating physicians have not thoroughly investigated the patient.
We routinely find in US, Canadian and European CFS patients diagnosed by physicians in their country, a variety of missed diseases. These include: toxic & chemical injuries, genetic injuries, cardio and cardio-vascular injuries, collagen diseases, adverse medication reaction, mitochondrial disease, adverse immunization caused illness, Ehlers-Danlos Syndrome, rarely M.S., missed thyroid malignancy and thyroid diseases. CFS in general implies a serious missed disease. I have found up to 20 significant pathologies in a single CFS patient, none of them caught by any physician. Yet they are diagnosed as CFS. Fibromyalgia is also a legitimate symptom in over 10 different classically-accepted illnesses.
See our book: Missed Diagnoses at Lulu.com.
I believe CFS is not a disease or a syndrome, but is a mixed group of undiagnosed significant illnesses.
The CDC 1988 CFS publication, based on the summer 1984 Lake Tahoe epidemic, was a classic enterovirus epidemic & not an EBV infection. The authors of the 1988 CDC definition quoted EBV research publications almost exclusively, believing this to be an Epstein Barr epidemic. They also appear to have crafted the CFS diagnostic criteria to fit their EBV prejudice. One rarely ever found swollen cervical glands in M.E. (also known as Enteroviral Encephalomyelitis) patients. The CFS authors should have known, EBV, with an incubation period of 40 days, can never have caused the rapidly spreading epidemic across Nevada & North America. Also, EBV does not have a late summer early autumn peak. Late summer and autumn is enterovirus territory.
The so-called Oxford Guidelines were created primarily by a large group of UK psychiatrists, in attempt to receive NIH funds. However, they crafted their CFS definition as a psychiatric illness. This intentional prejudice has been disastrous for many M.E. (also known as Enteroviral Encephalomyelitis) patients in the UK, as it succeeded in the psychiatric-ization of this epidemic post-infectious CNS-injuring illness. The dangerous practices of CBT, GET and PACE treatment do not result in recovery in true M.E. (also known as Enteroviral Encephalomyelitis) brain-injured patients any more than if CBT had been used to treat paralyzed polio patients. In our experience, CBT & GET are often employed to nullify disability pensions since true M.E. (also known as Enteroviral Encephalomyelitis) patients cannot continue such treatments without further damage.
Today, many UK, Northern American & European patients are routinely dismissed, rarely correctly investigated and too often placed on a psychiatric treatment, or hospitalized against their will due to the Oxford & CDC definitions. They base their diagnosis upon the fallacious concept: a patient with only symptoms and no physical or positive test findings is a psychiatric patient. This is why correct tests for M.E. (also known as Enteroviral Encephalomyelitis) must be performed as described in this booklet.
I am in turn critical of the New England Journal of Medicine, one of the world’s best medical journals, for making the late Dr. Stephen Straus...
This Nightingale Research Foundation Definition for M.E. is particularly important to physicians since the cause of M.E. (also known as Enteroviral Encephalomyelitis) is related to chronic enteroviral infections, close cousins of paralytic poliomyelitis. At the August Europic 2016 meeting on picornaviruses & enteroviruses in Switzerland, several new anti-enteroviral medications were discussed, including: Pirodavir, Vapendavir, Pocapavir, Pleconaril & Rupintrivir. Although at an early stage, some have shown success in animal models. Help may yet be on the way for chronically-disabled M.E. (also known as Enteroviral Encephalomyelitis) patients. Prevention is always better than treatment. Prevention can only occur with a new enterovirus immunization which would not only stop M.E. and polio from occurring, but would prevent many type 1 diabetes and and many deaths in millions of children world wide who die every year due to EV diarrhea and pneumonia.
Nightingale Research Foundation Definition (2007)
M.E. (also known as Enteroviral Encephalomyelitis) is a chronic disabling, acute onset biphasic epidemic or endemic (biphasic) infectious disease process affecting both children and adults.
There are both central and peripheral aspects to this illness.
A) The Central Nervous System (CNS) symptoms, as well as the clinical and technological abnormalities, are caused by a diffuse and measurable injury to the vascular system of the Central Nervous System. These changes in the organization of the CNS are caused by a combined infectious and immunological injury and their resulting effect on CNS metabolism and control mechanisms. Much of the variability observed in an M.E. (also known as Enteroviral Encephalomyelitis) patient’s illness is due to the degree and extent of the CNS injury and the ability of the patient to recover from these injuries.
B) A significant number of the initial and long-term peripheral or body symptoms, as well as clinical and technological body abnormalities in the M.E. (also known as Enteroviral Encephalomyelitis) patient, are caused by variable changes in the peripheral and CNS vascular system. The vascular system is perhaps the largest of the body’s organs and both it's normal and pathophysiological functions are in direct relationship to CNS and peripheral vascular health or injury, to CNS control mechanisms and to the difficulty of the peripheral vascular system and organs to respond to CNS neuro-endocrine and other chemical and neurological stimuli in a predictable homeostatic fashion.
C) When pain syndromes associated with M.E. occur, they are due to a combined injury of
(i) the posterior spinal cord and / or posterior root ganglia and appendages,
(ii) pathophysiological peripheral vascular changes, and
(iii) CNS pain reception homeostasis mechanisms.
Depending upon the degree and extent of the ongoing CNS and peripheral vascular injuries, these pathophysiological changes in turn may give rise to both transient and in many cases permanent systemic organ changes in the patient.
As with any illness, the diagnostic criteria of M.E. (also known as Enteroviral Encephalomyelitis) are divided into two sections:
(a) The clinical features and history of the ill patient that alert the physician to the initial diagnosis, and
(b) The technological examinations that confirm to the physician proof of his diagnosis.
Clinical Features
The clinical features of Myalgic Encephalomyelitis (also known as Enteroviral Encephalomyelitis) are consistent with the following characteristics that can easily be documented by the physician.
Biphasic Epidemic or Endemic (Sporadic) Infectious Disease Process
Both Epidemic and Non-Epidemic cases are often preceded by a series of repeated minor infections in a previously well patient that would suggest either a vulnerable immune system, or an immune system subject to overwhelming stressors such as:
a. Repetitive contact with a large number of infectious persons,
b. Unusually long hours of exhausting physical and / or intellectual work,
c. Physical traumas,
d. Immediate past immunizations, particularly if given when the patient has concurrent allergic or autoimmune or infectious disease or if the patient is leaving for a third world country within three weeks of receiving the immunization,
e. Epidemic disease cases whose onset and periodicity appear to occur cyclically in a susceptible population,
f. The effect of travel, as in exposure to a new subset of virulent infections, or
g. The effects of starvation diets.
The first phase is an epidemic or endemic (sporadic) infectious disease generally with an incubation period of 4 to 7 days; in most, but not all cases, an infection or infectious process is evident. (See Clinical and Scientific Basis of M.E. and CFS, Chapter 13, pps. 124-126)
3. Secondary Chronic Phase
The second and chronic phase follows closely on the first phase, usually within two to seven days; it is characterized by a measurable diffuse change in the function of the Central Nervous System. This second phase is the persisting disease that most characterizes M.E. (also known as Enteroviral Encephalomyelitis)
4. The Presence or Absence of Various Pain Syndromes is highly variable
The pain syndromes associated with the acute and chronic phases of M.E. (also known as Enteroviral Encephalomyelitis) may be described as Early and Late findings.
Early Findings:
a. Severe headaches of a type never previously experienced;
b. These are often associated with Neck Rigidity (Stiff Neck) and...
...Occipital Head Pain and Headache;
c. Retro-Orbital Eye Pain;
d. Migratory Muscle Pain (Myalgia)
...and Arthralgia (Joint Pain);
e. Cutaneous Hypersensitivity (Muscle Tenderness).
Late Findings: Any of the early findings plus:
- Fibromyalgia-like Pain Syndromes. This is only a partial list of the multiple pain syndromes. Many of the pain features tend to decrease over time but can be activated or increased by a wide range of external & chemical stressors. (See Clinical and Scientific Basis of M.E. and CFS, Chapter 5, pps. 58-62)
Testable & Non-Testable Criteria
The technological tests listed below can be used to :
(a) Confirm the clinical diagnosis of Myalgic Encephalomyelitis (also known as Enteroviral Encephalomyelitis) and
(b) To some degree gauge it's severity and probability of persistence. The second and chronic phase that clearly defines M.E. (also known as Enteroviral Encephalomyelitis) is characterized by various measurable and clinical dysfunctions of the cortical and/or sub-cortical brain structures.
5. Diffuse Brain Injury Observed on Brain SPECT
If the patient’s illness is not measurable using a dedicated brain SPECT scan such as a Picker 3000 or equivalent, then the patient does not have M.E. (also known as Enteroviral Encephalomyelitis) For legal purposes these changes may be confirmed by PET brain scans with appropriate software and /or QEEG. These changes can be roughly characterized as to severity and probable chronicity using the following two scales:
A) Extent of injury and
B) Degree of injury of CNS vascular function.
Initial Disease Severity:
Extent of Injury
Type 1: One side of the cortex is involved. Those patients labeled as 1A have the best chance of recovery.
Type 2: Both sides of the cortex are involved. These patients have the least chance of spontaneous recovery.
Type 3: Both sides of the cortex, and either one or all of the following: posterior chamber organs, (the pons and cerebellum), limbic system, the subcortical and brainstem structures are involved.
Type 3B are the most severely affected patients and the most likely to be progressive or demonstrate little or no improvement with time.
Type A: Anatomical integrity is largely maintained in the Brain SPECT scan.
Type B: Anatomical integrity is not visible in the CNS SPECT scan. Type 3B are some of the most severely and chronically injured patients.
Psychological Symptoms:
a. Psychological despair and reactive depression set in, particularly if the patient does not have support or disability pension access. The symptoms can be so severe, the fear the doctors are missing some terminal illness is a common patient sentiment. This becomes more evident when the patient’s physicians, due to unfamiliarity, are unable to find anything to explain the patient’s now chronic illness and their inability to return to the normal activity expected. Why? The illness has been mistakenly diagnosed as a typical short-term viral infection or influenza.
b. A sense of abandonment often occurs when friends and family members begin to drift away, and physicians begin to talk of a psychological diagnoses, depression and suggest antipsychotic medications, which if taken, often make the patient worse and if abruptly stopped by the patient due to side effects or lack of funds, has provoked many suicides.
6. Testable Neuropsychological Changes
There are neuropsychological changes that are measurable and demonstrate short-term memory loss, cognitive dysfunctions, increased irritability, confusion, and perceptual difficulties.
There is usually rapid decrease in these functions after any physical or mental activity. Neuropsychological changes must be measured in relation to estimates of prior achievement. This feature may improve over a period of years in patients with adequate financial and social support and can be made worse by chronic stressors.
The neurophysiological changes are those observed by a qualified Neuropsychologist with experience in examining this type of disease spectrum.
Some of the deficits that a Neuropsychologist should consider examining include:
a. Subtle problems with receptive and expressive aphasia,
This can include all forms of Sleep Dysfunctions.
All or any of the following may be present:
1. Impaired sleep efficiency,
2. Significant fragmented sleep architecture,
3. Movement arousals, particularly if there is an associated pain syndrome,
4. Absence or significant decrease of type 3 and 4 sleep,
5. Abnormal REM sleep pattern
6. Changes in daytime alertness and
9. Testable Vascular & Cardiac Dysfunction
This is the most obvious set of dysfunctions when looked for and is probably the cause behind a significant number of the above complaints. All moderate to severe M.E. patients have one or more and at times multiple of the following vascular dysfunctions. As noted, the primary vascular change is seen in abnormal SPECT brain scans and clinically most evident in patients with:
a) PoTS: severe Postural orthostatic Tachycardia Syndrome.
Note: This group can be confused with diabetes insipidus due to the fact that they may have polydipsia from their attempt to increase their circulating blood volume by consuming large amounts of fluids. This group can be verified by the absence of pituitary adenoma or pathology and the fact that they can sleep through the night without waking to drink fluids. (Streeten, David)
Despite the great steps forward in the understanding of this relatively common pathophysiology seen routinely in M.E. (also known as Enteroviral Encephalomyelitis) patients, a pathology which is really related to either an autonomic injury to the CNS, injury to the vascular receptors or both, very little of the present treatment protocol is of much use. The situation is so bad that few major centres have any well-funded expertise in either autonomic or vascular receptor injury. Many of the M.E. (also known as Enteroviral Encephalomyelitis) patients that are dismissed by physicians as suffering from lack of activity have significant proprioceptive injuries in these areas. Nor can we always rely on the few autonomic laboratories and their tilt table testing abilities. Many of the tilt table examination reports return as normal, many as grossly abnormal. Yet all the physician has to do is have each M.E. (also known as Enteroviral Encephalomyelitis) patient stand for 8-12 minutes to realize that a large number of these normal tilt table patients simply cannot maintain a normal blood pressure and normal heart rate. Compare this to non-M.E. patients and one immediately can tell the difference. A large number of M.E. (also known as Enteroviral Encephalomyelitis) patients have significant autonomic difficulties.
b) Cardiac Irregularity: on minor positional changes or after minor physical activity, including inability of the heart to increase or decrease in speed and pump volume in response to increase or decrease in physical activity. (Hyde, B., Chapter on Cardiac Aspects): (Montague, T.,) Cardiac irregularity is closely related to the above discussion. In many M.E. patients there is an unusual daytime tachycardia, particularly since these patients are often very sedentary. In doing a 24-hour Holter monitor this may be missed since the 24 hour average is usually given. One should always ask for wake time and sleep time heart rates.
c) Raynaud's Phenomenon: vasoconstriction of small arteries or arterioles of extremities, with change in colour of the skin, pallor and cyanosis. It is associated with coldness and pain of extremities. This is in part, the cause for temperature and pain dysfunctions seen in M.E. (also known as Enteroviral Encephalomyelitis). This phenomenon is found in many other conditions than M.E. (also known as Enteroviral Encephalomyelitis) Some of the associations are post-traumatic, neurogenic conditions, occlusive arterial diseases, toxic chemical associations and a wide range of rheumatoid conditions. Many of these conditions have associations with M.E. (also known as Enteroviral Encephalomyelitis) (See Magallni, S. for more detail.)
d) Circulating Blood Volume Decrease (Hypovolemia) : This is a nuclear medicine test in which the circulating red blood cell levels in some M.E. (also known as Enteroviral Encephalomyelitis) patients can fall to below 50%, preventing adequate oxygenation to the brain, gut and muscles. These patients do not generally have anemia and are not blood deficient. This is undoubtedly a subcortical dysregulation. It is associated with serum and total blood volume measurements. This is a concept that many physicians have difficulty understanding.
I have heard physicians repeatedly tell the patient they are not aenemic and therefore dismiss this important finding.
Note: So where does the blood go? Body servomechanisms are genetically designed so that blood flow and oxygen to the heart are always protected. Thus, when the body of the M.E. (also known as Enteroviral Encephalomyelitis) patient is stressed, the blood flow to organs not necessary for short-term survival, such as the brain, the gut and skeletal muscles, can be temporarily decreased. This of course gives rise to many of the M.E. symptoms.
Gastroenterological, GIT Symptoms and Dysfunctions:
a. Pain, uncomfortable change of bowel habitus often occurs both at onset and in chronicity. 'Autoimmune bowel illnesses' have been seen.
Beware: M.E. (also known as Enteroviral Encephalomyelitis) patients may have unrelated GIT illnesses not associated with M.E. (also known as Enteroviral Encephalomyelitis) such as bowel malignancy and ulcers. The physician must be aware of more traditional illnesses.
e) Bowel Dysfunction: vascular dysfunction may be the most significant causal basis of the multiple bowel dysfunctions occurring in M.E. (also known as Enteroviral Encephalomyelitis) (See d. above.)
f) Ehlers-Danlos Syndromes Group: This is a group of illnesses with a genetic predisposition to M.E. (also known as Enteroviral Encephalomyelitis) or M.E.- like illness. In fact it probably represents a spectrum of illnesses that start with (i) hyper-reflexia syndrome, moving through any of the (ii) various Ehlers-Danlos Syndromes and climaxing in (iii) Marfan Syndrome where there tends to be early death if the aortic and cardiac changes are not repaired. Ehlers-Danlos Syndromes can go undetected until what appears to be a switch is turned on, usually in late teens to early thirties. The “switch” may be viral or possibly age or hormonal related. Raynaud’s Phenomenon is usually associated.
Diagnosis: briefly, patients over the age of 16 who can
(i) Touch their nose with their tongue,
(ii) Touch their forearm with the thumb of the same extremity (joint laxity),
(iii) Touch the floor readily with the full palm should be considered suspect for further examination. There are several fascination variations of Ehlers-Danlos. They are generally considered to be a group of genetic illnesses but in my examination of M.E. (also known as Enteroviral Encephalomyelitis) patients most often are not manifested until well past puberty and in adulthood. Additional generalized features of this spectrum of illnesses include
(v) India rubber or hyperelastic skin,
(vi) Easy bruisability (vascular fragility),
(vii) Arachnodactyly (long spiderlike fingers). Many of the patients with a more severe form tend to be tall, slender with a dolichocephalic skull, high palate and long narrow feet with hammertoes verging on Marfan Syndrome. (See Magalini, S. I., Magalini S. C. for both E-D Syndrome and Marfan 1 and Marfanoid hypermobility.)
g) Persantine Effect in M.E. (also known as Enteroviral Encephalomyelitis) Patients: Persantine is a chemical manufactured by Boehringer Ingelheim. It is employed to perform chemical cardiac stress testing when a patient cannot exercise sufficiently to stress the heart. It is a particularly safe medication but when employed with many M.E. (also known as Enteroviral Encephalomyelitis) patients it can cause severe muscle pain over the extremities and entire musculature. Normally this can be reversed by injection of an antidote but this does not always work rapidly in M.E. (also known as Enteroviral Encephalomyelitis) patients. Severe pain and fatigue can be intolerable and persist for minutes to days in some M.E. (also known as Enteroviral Encephalomyelitis) patients following Persantine use. Persantine works by dilating both peripheral and cardiac blood vessels and causing the heart rate to increase as in a PoTS patient. Obviously one major pain and fatigue factor in M.E. (also known as Enteroviral Encephalomyelitis) patients is caused by abnormal dilatation of peripheral blood vessels. The resulting pain may be related to reflex vasospasm as in severe Raynaud’s Phenomenon that I note elsewhere is one of the causes of M.E. (also known as Enteroviral Encephalomyelitis) pain. To my knowledge, no testing of M.E. (also known as Enteroviral Encephalomyelitis) patients with Persantine has ever been published by Boehringer Ingelheim or others. It is one of the reasons I believe that pain syndromes in M.E. (also known as Enteroviral Encephalomyelitis) patients are due to a pathological vascular physiology.
h) M.E. (also known as Enteroviral Encephalomyelitis) Associated Clotting Defects: M.E. (also known as Enteroviral Encephalomyelitis) represents both a vasculitis and a central and peripheral change in vascular physiology.
All such vascular illnesses should be potentially treatable.
We do not yet know how to adequately treat the
(i) Genetic forms of vasculitis & vascular pathophysiology mentioned here, nor
(ii) The probable viral triggered genetic vascular pathologies also mentioned. Nor do we know how to treat those
(iii) Centrally caused injuries causing the circulating blood volume defects that are demonstrated when we do the “nuclear medicine circulating blood volume tests".
It is important to do this test on all patients.
PoTS is poorly treatable and more often success in treatment presently escapes physicians’ ability. Eventually, I have no doubt that these will be treatable causes of M.E.-like disease.
However there is a significant group of M.E. (also known as Enteroviral Encephalomyelitis) patients who are ill due to a treatable form of vasculitis and can be treated if the physician takes the time to diagnose them.
These patients are the clotting defect patients. Some of these clotting defects are genetic and some appear to be genetic with an age or viral switching mechanism, as I have mentioned elsewhere with Ehlers Danlos Syndromes; although they may develop in childhood, they are more frequently noted well after puberty and before the age of 40.
Many of these patients can be diagnosed by the following tests:
(1) Serum viscosity test,
(2) Antiphospholipid Syndrome (Hughes Syndrome),
(3) Protein C defects,
(4) Protein S defects,
(5) Factor V Leiden defect, to name the most common that we have uncovered.
However, there are others for which we also test. These conditions are all potentially treatable and when treated adequately may allow the patient to return to school or work. Although any physician can order these tests, a haematologist should review all M.E. (also known as Enteroviral Encephalomyelitis) patients for these and other possible clotting anomalies.
Most clotting defects are treatable and treatment has resulted in recovery in some cases.
Remember M.E. (also known as Enteroviral Encephalomyelitis) is essentially a problem of microcirculation and any improvement in this area can have dramatically positive effects.
It is well worthwhile for all physicians reading this definition who have an interest in M.E. (also known as Enteroviral Encephalomyelitis) to examine the Internet for Hughes Syndrome. Curiously, Hughes Syndrome was first outlined in St. Thomas’ Hospital London, the home of the Nightingale School of Nursing. Hughes Syndrome, a vascular syndrome also called Sticky Blood Syndrome, closely parallels the definition of M.E. (also known as Enteroviral Encephalomyelitis)
i) Anti-Smooth Muscle Antibodies: This is an antibody to the muscle tissue in the arterial bed. It is elevated in about 5% of M.E. (also known as Enteroviral Encephalomyelitis) patients but whether this is different in non-M.E. patients is unknown but unlikely. It rarely is over 1:40.
j) Cardiac Dysfunction: There are a large number of cardiac dysfunctions that can regularly appear in an M.E. (also known as Enteroviral Encephalomyelitis) patient.
Certain are obvious and discussed under Ehlers-Danlos Syndrome and...
...Marfan Syndrome.
I also discussed cardiac dysfunction in Chapter 42, The Clinical and Scientific Basis of M.E. and CFS.
Since that chapter was written a large number of other cardiac pathologies and pathophysiologies have been noted by various researchers and clinicians, particularly by Dr. Paul Cheney.
Without a clear understanding of these significant problem areas, it is simply indefensible and potentially dangerous to place an unsuspecting patient in a graduated exercise program.
This is particularly true if the patient is not being tested in a cardiac unit. Although in our clinic we have performed what we believe to be a complete cardiac assessment on all patients seen, what the Ottawa Cardiac Institute and I believed was a complete assessment may be wanting.
Over the next year we will reassess these patients, with a more detailed cardiac examination and report on it in these diagnostic criteria.
10. Testable Endocrine Dysfunction
These features are common and tend to be of late appearance.
Would you recommend that M.E. Patients get their Thyroid checked up?
They are most obvious in:
24-Hour Holter Monitor for Arrhythmia (Irregular Heart Rates)
a) Pituitary-Thyroid Axis: Changes in serum TSH, FT3, FT4, Microsomal Ab., PTH, calcium and phosphorous rarely occur until several years after illness onset. This anomaly can best be followed by serial ultrasounds of the thyroid gland, where a steady shrinking of the thyroid gland may occur in some M.E. (also known as Enteroviral Encephalomyelitis) patients with or without the development of non-serum positive Hashimoto’s Thyroiditis (a seeming contradiction in terms)...
...and a significant increase in thyroid malignancy.
What treatments would you recommend to an M.E. Patient with Thyroid Atrophy?
Thyroid Ultrasound - measurements and size changes,...
...malignancy thyroid check with Ultrasound-guided fine needle aspiration (FNA) biopsy if abnormality suspected.
In cases of thyroid wasting, serum positive changes tend to occur only after years and often not until the thyroid gland shrinks from the normal 13 to 21 cc. volume in an average adult female and 15-23 cc. volume in male patients to below a volume of 6 cc. (Mayo Clinic averages) (Rumack, Carol). The normal serum analysis of patients for thyroid dysfunction, TSH, FT4, microsomal antibodies etc., the golden rule of most physicians and endocrinologists, is simply not an adequate means of ascertaining thyroid dysfunction in most M.E. (also known as Enteroviral Encephalomyelitis) patients. Repeat thyroid ultrasound must be performed for all M.E. (also known as Enteroviral Encephalomyelitis) patients to observe the presence of dystrophic changes. It is also inadequate simply to accept the radiologist’s report of a normal thyroid. The volume of each lobe and it's homogenicity must be requested and documented. Radiologists simply report normal thyroids when in effect they are hypo and hyper-trophic. Although the Mayo Clinic averages cited above may be criticized they are as good as any in ascertaining normal thyroid size.
The following changes, while uncommon, may also be related to an M.E. (also known as Enteroviral Encephalomyelitis) disease process:
Hypothalamic Damage / Dysfunction and Tertiary Adrenal Insufficiency (Adrenal Dysfunction) as a consequence - Mount Sinai
b) Pituitary-Adrenal Axis Changes: where changes and findings are infrequent.
c) Pituitary-Ovarian Axis Changes
d) Neurogenic Bladder (Bladder Dysfunction) Changes: This dysfunction occurs frequently in the early and in chronic disease in some people. In some instances this may be due to a form of diabetes insipidus, in other cases it is related to PoTS-type illness where the patient is compensating for the inability to maintain vascular pressure by attempting to increase fluid volume.
In other cases this may be due to interstitial cystitis...
...or a form of polio-type-bladder particularly if the cause of the individual disease is an enterovirus.
Dr. John Richardson also associated this finding with adrenal dysfunction that he measured.
Myalgic Encephalomyelitis : Guidelines for Doctors - Dr. John Richardson, MB, BS
Medical Journal: Journal of Chronic Fatigue Syndrome, Vol. 10(1) 2002, pp. 65-80
Abstract
Introduction
Aim of the work
Patients
Methods
Results
Conclusion
The Terrible Tale of Amy Brown (Nightingale PDF)
Sources: Understanding M.E. from Nightingale Research Foundation website and Nightingale Research Foundation Definition
Comments
Post a Comment