CDC acknowledges Fukuda CFS is not Ramsay's ME

Discussion in 'Fibromyalgia Main Forum' started by tansy, Jun 15, 2008.

  1. tansy

    tansy New Member

    From the overview chapter of the CDC's CFS provider education course:

    ***The name myalgic encephalomyelitis (ME) was coined in the 1950s to clarify well-documented outbreaks of disease; however, ME is accompanied by neurologic and muscular signs and has a case definition distinct from that of CFS.***

    My thanks go to the ME advocate who posted this on another message board.

    tc, Tansy
    [This Message was Edited on 06/15/2008]
  2. Khalyal

    Khalyal New Member

    Well, that makes sense according to the CDC's own empirical, which basically says that CFS can't be anything identifiable, because then it would no longer be CFS.

    'Round and round and round it goes, where it stops, nobody knows! lol
  3. tansy

    tansy New Member

    that so little progress has been made by the CDC since the construct of CFS. CFS is just a group of vague symptoms including chronic fatigue with no apparent cause; that's why the psychobabblers have had it so easy.

    Victoria posted a list of tests that are recommended in the Canadian criteria; but the CDC insist they are not necessary. I have reposted them below.

    Byron Hyde lists the differences between CFS and ME.

    My Dx was confirmed by tests that were later used in Behan et al's research (Glasgow UK) in the early 90s; Prof Peter Behan described the research findings as gross abnormalities.

    tc, Tansy
    [This Message was Edited on 06/15/2008]
  4. tansy

    tansy New Member

    From: Mary Schweitzer

    re: Tests for ME or CFS patients
    CDC and Canadian Consensus

    I have put the list of tests that the CDC states patients with CFS should NOT have to compare with the list of tests that the Canadian Consensus Document SUGGESTS for ME/CFS patients (when appropriate) in two websites to make them both easy to download and compare side-by-side. In the case of the CDC list, I took a paragraph and opened it up to bullet points so it would be easier for PWC/ME's to read.

    The CDC list of tests NOT to give patients with CFS is here:

    (See below A )

    The Canadian Consensus Document's list of tests FOR patients with ME/CFS is here:

    (See below B)

    Mary Schweitzer

    A) List of tests the CDC insists that CFS patients should not get

    From the CDC's websites on CFS, as of 10 April 2008:

    "A number of tests, some of which are offered commercially, have no demonstrated value for the diagnosis of CFS. These tests should not be performed unless required for diagnosis of a suspected exclusionary condition (e.g., MRI to rule out suspected multiple sclerosis) or unless they are part of a scientific study. In the latter case, written informed consent of the patient is required. No diagnostic tests for infectious agents, such as:
    *) Epstein-Barr virus,
    *) enteroviruses,
    *) retroviruses,
    *) human herpesvirus 6 [HHV-6],
    *) Candida albicans,
    *) and Mycoplasma incognita,

    are diagnostic for CFS and as such should not be used (except to identify an illness that would exclude a CFS diagnosis, such as mononucleosis).

    "In addition, no immunologic tests, including cell profiling tests such as

    *) measurements of natural killer cell (NK) number or function,
    *) cytokine tests (e.g., interleukin-1, interleukin-6, or interferon), or
    *) cell marker tests (e.g., CD25 or CD16),

    have ever been shown to have value for diagnosing CFS.

    "Other tests that must be regarded as experimental for making the diagnosis of CFS include:

    *) the tilt table test for NMH, and
    *) imaging techniques such as MRI, PET-scan, or SPECT-scan.

    *) "Reports of a pathway marker for CFS as well as a
    *) urine marker for CFS

    are undergoing further study; however, neither is considered useful for diagnosis at this time."

    Taken from the CDC's websites on CFS,
    10 April 2008:


    B) **List of Tests from the Canadian Consensus Document for M.E./CFS**

    Tests for Abnormalities in ME/CFS.
    (See for sources of some specialized tests)

    While there is not one definite test for ME/CFS, many tests may indicate abnormalities. The standard battery of tests may be inadequate to reveal abnormalities in ME/CFS patients. Many of the following tests are not available in general medical laboratoris but may be available in reseach facilities or more generally available in the future.

    *) Virology, etc: viral antibodies, including Coxsackie B and HHV-6; bacteria, mycoplasma, etc.

    *) 37kDa 2-5A Rnase-L Immunoassay: protein, activity, PKR cleavage & elastase activity assays.

    *) Other immunological markers: NK [Natural Killer] cell levels and function per cell for low NK cell cytotoxicity; CD4-CD8 ratio; ANA; activated immune complexes - IgG sub-fractions including IgG1 and IgG3, circulating immune complexes IL2 and IL4; Th1-Th2 response to nitrogen stimulation (high levels of Th2 idicate autommunity), flow cytometry for activated/elevated lymphocytes; antilamin antibodies may autommunity and brain cell damage (lamin B antibodies are evidence of autoimmunity); humoral autoimmunity for polypeptides of the nuclear envelope (NE); antibodies in neuronel cells MAP2 (kinase regulators)

    *) Urinary markers: 24-hour urine free cortisol; elevated amino-hydroxy-N-methyl-pyrolidine corelate with quantity of symptoms; IAG-tryptopan metabolite, is usually positive and indicates a leaky gut, which in turn is indicative of a leaky blood brain barrier; urinary creatine and other muscle metabolites.

    *) Endocrine testing: CT scans may show reduced adrenal gland size; thyroid hormone levels with attention to bioavailability of T3 & those with reduced level should be checked for selenium as it regulates conersion of T4 to T3; reduced HPA function.

    *) Increased 5HT neurotransmission

    *) Chronic Orthostatic Intolerance: Use tilt-table test or monitor the pulse and blood pressure while standing. Note: This monitoring must be done with caution and someone standing beside the patient.

    *) Cardiac dysfunction: 24-hour Holtar monitoring - specifically ask to either view the results yourself or to report repetitive oscillating T-wave inversion and T-wave flats. This pattern is typical of many ME/CFS patients but may not be reported.

    *) Cardiopulmonary Exercise Testing: AMA Guide for Evaluation of Permanent Impairment. Lower cardiovascular and ventilatory values at peak exercise help determine functional capacity, and peak oxygen consumption levels determine disability categories. See caution in chart on page 4 [of the Consensus Document].

    *) Computer Science and Application (CSA): Actigraph is a small device that measures frequency and intensity of activity in one minute intervals for up to 22 days. Typically, less intense and shorter activity peaks followed by longer rest periods are identified. It is helpful to have the patient keep a daily diary of activities during this period and/or wear a speedometer.

    *) CNS, ANS: Romberg test; nystagmus test (may fluctuate from positive and negative throughout the day); altered sympathetic modulations; subnormal and/or fluctuating diurnal body temperature.

    *) Cognitive performance: decreased processing speed, working memory, information learning, etc.

    *) SPECT scans may reveal significantly lower cortical/cerebellar regional cerebral blood flow frequently in the frontal, parietal, temporal, occipital, brain stem and throughout the cerebral cortex.

    *) PET scans may reveal decreased glucose metabolism in the right mediofrontal cortex, and significant hypoperfusion and hypometabolism in the brain stem.

    *) MRI brain scans: Elevated numbers of punctuate lesions, particularly in the frontal lobes and subcortical areas, suggest demyelination or edema. Do spinal MRI for disc herneation and minor stenosis.

    *) qEEG brain topograpy: Elevated EEG activity in theta and beta frequencies and increased intracerebral electrical sources in left frontal region delta and beta frequencies in eyes closed condition may be identified. Reduced sources in right hemisphere (beta) may be noted during verbal cognitive processing.

    *) Hypercoagulability: flow cytrometry - fibrinogen, thrombin/anti-thrombin complexes, etc.

    *) Positive tests for fibromyalgia syndrome and myofascial pain syndrome should be noted.

    *) Skin conductivity and skin temperature: The combination of a lower ability of the skin to conduct electrical current in response to visual and auditory stimuli, and a higher skin temperature of fingers indicate a down-regulation of autonomic sympathetic tone.

    *) Sleep studies may idicate that there is insufficient time spent in the deeper stages of sleep, and alpha wave intrusion into delta waves within non-REM sleep

    *) Ocular test: slowed and marked jerkiness of saccades; difficulty with and slowed changing of visual fixation, constricted peripheral fields; low and/or incomplete blinking; small pupils; light hypersensitivity, tear film abnormalities such as low tear break-up time, inadequate productrion of the oil or mucous layer in tears, rose Bengal corneal staining; visual midline shift.

    *) Allergies or sensitivities; Lung function testing; Liver function: CPK and liver function.
  5. tansy

    tansy New Member

    In 1995 Prof Peter Behan described abnormalities in ME and tests that helped to confirm a diagnosis. Please note that well defined cases were used for his team's research illustrating the importance of a strict criteria for research as well as for diagnosis.

    tc, Tansy

    The following is an edited extract of a transcript of a talk given by Professor Peter Behan of the Institute of Neurological Sciences, University of Glasgow, to an audience of health professional at the Coventry and Warwickshire Post-Graduate Centre on the 23rd November 1995.

    Thanks must go to Julia Hamilton, who wrote the original transcript and Robert Ennis, Chairman of the Coventry and Warwickshire Support Group, for permission to reprint it.

    Professor Behan started by confirming that M.E. is an organic disease. He also confirmed that M.E. is not a new illness: it was well described in 1750 by Manningham in a book called 'Febricula' (little fevers), and was equally well described in the 18th, 19th and early 20th centuries.
    Although it remains essentially a diagnosis of exclusion, there are now laboratory techniques which will confirm the diagnosis.

    At first his team thought M.E. was precipitated by a virus, but there is now no question that some cases of the illness are precipitated by toxins.

    The challenge is to explain why minute doses of toxin re-exposure cause the illness, or why, if there is an acute precipitant such as a viral infection, the illness goes on for 20 years. The first exposure may have induced in the patient a lesion at the DNA level.

    Professor Behan then compared a condition known as myeloadenamate deaminase deficiency, from which patients they had taken a piece of muscle and had stained for this enzyme and found it to be missing. It is known that the enzyme is missing after a viral attack. Similarly, in M.E., there is a defect in that the enzyme is not present in muscle, which shows that there must be some persistant abnormality.

    He then went on to address the nature of the fatigue found in M.E.; he stated that it occurs acutely and is exactly the same fatigue which occurs in other conditions such as multiple sclerosis, even going so far as to state: "Patients with multiple sclerosis have chronic fatigue syndrome and the fatigue is exactly the same."

    Some patients with endogenous depression have exactly the same fatigue, as do patients with Gilbert's syndrome (a familial condition due to an inherited deficiency of an enzyme in the liver cells causing a form of jaundice). It is well documented that patients develop M.E.-like fatigue after stress, or after viral infection, or after exposure to toxins. Why, asked Professor Behan, should that lesion in the liver give patients fatigue?

    Post-polio syndrome is another condition in which fatigue is a prominent feature. In line with other recent research findings on the post-polio syndrome, Professor Behan stated catergorically that "PPS is identical in every way to chronic fatigue syndrome".

    Another condition in which fatigue occurs is idiopathic cyclic oedema, in which the woman is water-logged throughout the menstrual cycle due to hypothalamic disturbances. Also, there is classic fatigue in Parkinson's disease, a condition in which the fatigue is grossly incapacitating.

    He and his team at Glagow have been carrying out tests on M.E patients, along with a group of controls, in which participants are exercised until they are tired. The next day the exercise tests are repeated. In well-defined cases of M.E., by using refined techniques for measuring gait disturbance, and using an ergometer for measuring muscle power, there is a phenomenal drop off in maximum oxygen consumption.

    Professor Behan then mentioned single fibre EMG studies (1). In patients with M.E. there are gross abnormalities. About 80% suggest that something is wrong with the muscle.

    Professor Behan then observed that if the same thing that is demonstrably wrong with muscle may be wrong with other cells, it is necessary to come back to the concept of a primary stimulas. What might this be?

    He turned next to NMR imaging (2). He said NMR studies showed that in M.E. there is very early excessive intrcellular lactic acidosis with exercise and that this tends to persist, suggesting that there is something wrong with the glycolytic pathway (3).

    During strenuous exercise, pyruvic acid (a compound derived from carbohydrates) is reduced to lactic acid, which then accumulates in the muscles and causes cramp.

    In M.E., there are two indicators that there is undoubtably something wrong: one is nuclear magnetic resonance and nuclear imaging: the other is in the field of neuroendocrinology.

    Still on tests for muscle pathology, Professor Behan emphasised that when doing muscle biopsies on patients with M.E., it was necessary to look at them expertly. He showed a slide of a normal muscle biopsy in which the mitochondria (the sites of the cell's energy production) appeared as little red dots. Only careful and expert study revealed an increase in the mitochondria in M.E. The Glasgow team have now done about 400 such biopsies and they have found another abnormality in that cristae (the infoldings of the inner membrane of mitochondria) have gone, leaving honeycombed patterns. This honeycombing suggested to Professor Behan a toxic or a stress phenomenon in the mitochondria.

    When cells of M.E. patients are looked at in tissue culture, the lactic/pyruvic ratio of patients falls into two groups: patients are either producing too little or too much. Recently, Professor Behan has been interested in Syndrome X where an individual presents with what seems to be a coronary thrombosis. They may have very severe angina, but all the usual test results are normal: treadmill tests are normal. There is however, an abnormality of the lactic/pyruvic ratio, together with conspicuous abnormalities of carbohydrate metabolism. This Syndrome X has been reported from the Hammersmith Hospital in London, and also from Sweden. Professor Behan's team have discovered that these Syndrome X cases have gone on to develop chronic fatigue syndrome.

    The team at Glasgow has done thalium scans on patients with chronic fatigue syndrome, and in 100% of cases the scans are abnormal, yet again suggesting a cellular abnormality (4). Professor Behan showed a thallium scan of a young girl of 21 with M.E. He said he currently has a paper in press about these cases, all of whom have gross abnormalities of the myocardium. Referring to Syndrome X, Pr fessor Behan said that other data using PET scans (positron emission tomography) which measured the flow showed no ischaemia and no impairment and this is a metabolic abnormality.

    Resuming his review of tests which are abnormal in M.E., Professor Behan said that one of his lecturers had a special interest in liver function abnormalities, and had noted that patients with M.E. had raised cholesterol levels, so they did a study of 30 well-defined cases, looking not only at cholesterol levels but also doing a full lipid profile. Of the 30 patients in the study, 27 showed not only gross but grotesque abnormalities. These same abnormalities have also been observed by Professor Anthony Komaroff at Harvard Medical School. Professor Behan said that in M.E. there is not only abnormal carnitine metabolism, but abnormal lipid metabolism as well and that this has not so far been looked for in these cases.

    He then mentioned briefly that there is abnormal immune function in M.E. and that there is non-specific impairment of NK cells especially (natural killer cells are able to kill certain types of cancer cells), and this is another abnormality in which there are gross differences between these patients and normal controls.

    Professor Behan then moved on the SPECT scans, which his team have been doing for some years. They use serial SPECT scans to see if the abnormality which was present on one scan would have disappeared the next time. Patients with M.E. demonstrate that there are metabolic deficits in the temporal, occipital and fronto-parietal areas, all amounting to gross lesions within these patients.

    Another test used by the Glasgow team in M.E. patients is the water-loading test, which is given in the morning; the urinary output is measured over the next three hours, and in M.E. patients the results were grossly abnormal.

    This study done by the Glasgow team was to measure the serum osmolarity and the urine osmolarity and also to measure the pruduct of the posterior pituitary, argenine vasopressin (AGP) (5). The stimulus for AGP comes from the paraventricular nucleus of the hypothalamus, and when patients were given the water deprivation and water loading tests, there was an erratic, crazy production in these cases.

    At this point, Prfessor Behan stated that in his opinion, these test results bring home the fallacy of simply examining someone in a clinic with a tendon hammer and a stethoscope and pronouncing the patient to be normal.

    He then showed a slide of the paraventricular nuclei of a perfectly healthy ratt which was stained to look for activated receptors on neuroendoctrine cells, and also to measure a hormone, the presence of which is an index of the activity of that part of the gland. He told us that Professor Christiansen of Sweden had injected these normal rats with trypanosomes (mycroscopic parasites) and that the trypanosome does not get into the hypothalamus, but does get into other parts of the brain stem where the blood-brain-barrier is broken down (6). Having got into parts of the brain stem, an immune reaction is elicited. The activated T-cells produce cytokines (chemical messengers) and once these cytokines are produced, an enormous turn-on of the hypothalamus occurs; this is a selective turn-on of the paraventricular nuclei.

    Professor Behan then showed a slide of the brain stem demonstrating the reticular formation and various nuclei in the hypothalamus to which he had been referring, stating that these nuclei are the ones involved in viral infections, particularly polio infections. He said it is known that in the post-polio syndrome (PPS), if patients with severe fatigue have their growth hormone measured, it is low. Growth hormone has rapid daily fluctuations, but it is carried by a protein which does not fluctuate. The Glasgow team decided to measure growth hormone levels in patients with M.E., in patients with depression and in controls. They found that in M.E, at base line, the growth hormone levels are very low. Moreover, if patients are then stimulated by being given steroids (which should result in a massive up-swing), ther is no question that compared with controls, M.E. patients have no response. This work has been repeated in five different laboratories and the growth hormone abnormality in M.E has been absolutely confirmed. (Among other things, growth hormone increases protein synthesis.)

    To tie the whole thing up, Professor Behan explained that 5 H-T is particularly interesting. It is produced in the median eminance of the midbrain and sends fibres directly to the paraventricular nucleus and from there to the median eminance controlling the release of steroids. Thus if you give a 5 H-T agonist, there would be a rise in cortisol, so with this in mind, the team did an experiment with a pure 5 H-T agonist and found that in patients with M.E. there is a very blunted response. This demonstrates that there is something wrong between the 5 H-T axis and the production of cortisol (the hormone required for normal response to any stress). This test has also been done with prolactin; again, there is a conspicuous difference between patients with M.E., with depressives and with controls. The depressives react entirely differently from patients with this syndrome. Professor Behan noted that with any adrenal damage, there is supersensitivity to 5 H-T receptors.

    So what causes this illness? Is it a defect of carbohydrate metabolism? Is it a muscle abnormality? The illness cannot be due to all of these but if you have a central cellular deficit which was giving rise to a number of other abnormalities, that might explain the whole picture.

    The thinking at the moment is that in patients who are perhaps susceptiple, and depending on the stimulus and upon the time the stimulus is given, whether this is a virus or a toxin, damage occurs. This damage has to be fundamental because of the number of tissues involved, and is almost certainly at an enzyme level. this affects the subtle metabolism of the cell, probably in relation to potassium channels.

    At present, professional departments in Sweden, London, Harvard, and of course Glasgow are looking carefully to see if they can dissect out of this abnormality in very subtle ways, to see what the lesion is. This lesion will have enormous importance, not only for M.E., but particularly in multiple sclerosis and all those other diseases where fatigue is a feature. Until this particular lesion is understood, a rational mode of therapy cannot be brought about.

    Professor Behan concluded that in his own time of looking at M.E., he has seen far too many people who have been told that it's all in their head and that they are crazy. The end result has been that several committed suicide and others have been caused the most terrible distress.

    Electromyogram, is a continuous recording of the electrical activity of a muscle by means of electrodes inserted into muscle fibres.

    Nuclear magnetic resonance is a technique of chemical analysis used in the diagnosis of brain abnormalities based on the absorption of specific radio frequencies by atomic nuclei, enabling imaging of soft tissues anywhere in the body in any plane.

    Glycolysis is the conversion of glucose to lactic acid, which process involves the production of energy.

    Thallium scans are a method of studying blood flow theough the heart muscle using an injection of the radioosotope thallium-201.

    Argenine is an amino acid which plays an important role in the formation of urea (the main breakdown product of protein metabolism by the liver, and vasopressin is the anti-diuretic hormone, or ADH.

    Blood-brain-barrier (BBB) is the mechanism whereby circulating blood is kept separate from the tissue fluids surrounding the brain cells and which excludes solid particles and large molecules; this can break down after injuries such as whiplash.

  6. tansy

    tansy New Member

    Excerpts from:

    The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)

    "...what this definition does today is (a) separate clearly M.E. from CFS and (b) demonstrate that M.E. is an early diagnosable and provable disease - as are all true diseases, and (c) assist in the early treatment and cure of M.E. patients."
    -Dr. Byron Hyde-

    Primary M.E. is an acute onset biphasic infectious disease process, where there is always a measurable and persistent diffuse vascular injury of the Central Nervous System in both the acute and chronic phases. Primary M.E. is associated with immune and other pathologies.

    Primary M.E. is a chronic disabling, acute onset biphasic epidemic or endemic 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. 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. 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 its normal and pathological 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) patho-physiological 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 patho-physiological 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. are divided into two sections:

    (a) The clinical features and history of the ill patient that alert the physician to the initial diagnosis

    (b) The technological examinations that confirm to the physician proof of the diagnosis.

    Clinical Features

    The clinical features of Myalgic Encephalomyelitis are consistent with the following characteristics that can easily be documented by the physician.

    1. M.E. is an acute onset biphasic epidemic or endemic infectious disease: 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.... [see details about the types of immune stressors in the complete version of The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)]

    2. Primary Infection Phase: 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.

    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.

    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. 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 and occipital pain; (c) retro-orbital eye pain; (d) migratory muscle and arthralgia pain; (e) cutaneous hypersensitivity. Late Findings: Any of the early finding plus (f) 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 and chemical stressors.

    Testable & Non-testable Criteria

    The technological tests listed below can be used to (a) confirm the clinical diagnosis of Myalgic Encephalomyelitis and (b) to some degree gauge its severity and probability of persistence. The second and chronic phase that clearly defines M.E. 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: [see details about the types and degrees of brain injury in the complete version of The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)]

    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. [see details about the types of neuropsychological changes in the complete version of The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)]

    7. Testable Major Sleep Dysfunction: This can include all forms of sleep dysfunction. [see details about specific types of sleep dysfunction in the complete version of The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)]

    8. Testable Muscle Dysfunction: This feature may be due to vascular dysfunction or peripheral nervous or spinal dysfunction and includes both pain and rapid loss of strength of muscle function after moderate physical or mental activity. This feature tends to improve over a period of years but many patients frequently remain permanently vulnerable to new disease episodes. Unfortunately only a few major medical centres are equipped to study this type of dysfunction.

    9. Testable Vascular 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 scans and clinically most evident in patients with:

    a. POTS: severe postural orthostatic tachycardia syndrome. [More details]
    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. [More details]
    c. Raynaud’s Phenomenon [More details]
    d. Circulating Blood Volume Decrease: this is a nuclear medicine test in which the circulating red blood cell levels in some M.E. patients can fall to below 50%, preventing adequate oxygenation to the brain, gut and muscles. 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.[More details]
    e. Bowel Dysfunction: vascular dysfunction may be the most significant causal basis of the multiple bowel dysfunctions occurring in M.E. (See d. above.)
    f. Ehlers-Danlos Syndromes Group [More details]
    g. Persantine Effect in M.E. Patients [More details]
    h. M.E. Associated Clotting Defects [More details]
    i. Anti-smooth muscle Antibodies [More details]
    j. Cardiac Dysfunction: There are a large number of cardiac dysfunctions that can regularly appear in an M.E. patient. Without a clear understanding of these significant problem areas it is simply indefensible and potentially dangerous to place and unsuspecting patient in a graduated exercise program. [More details]

    [More in-depth details about the testable vascular dysfunction in #9 above can be found in the complete version of The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)]

    10. Testable Endocrine Dysfunction: These features are common and tend to be of late appearance. It is most obvious in:

    a. Pituitary-Thyroid Axis [More details]

    The following changes, while uncommon, may also be related to an M.E.disease process:
    b. Pituitary-Adrenal Axis Changes: where changes and findings are infrequent.
    c. Pituitary-Ovarian Axis Changes
    d. Bladder Dysfunction Changes [More details]

    [More details about testable endocrine dysfunction in #10 can be found in the complete version of The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)]

    [Further discussion on the foundations and implementation of this definition, as well as updated additions follow this list of criteria in the complete version of The Nightingale Definition of Myalgic Encephalomyelitis (M.E.) Treatment recommendations are also addressed in the Discussion section. References included.]

    As with all definitions, the Nightingale Research Foundation’s Definition of Myalgic Encephalomyelitis will have to be looked at by many clinicians and researchers and increasingly knowledgeable patients over the years, disagreed about, changed and improved upon. But what this definition does today is (a) separate clearly M.E. from CFS and (b) demonstrate that M.E. is an early diagnosable and provable disease - as are all true diseases, and (c) assist in the early treatment and cure of M.E. patients.

    This Nightingale Research Foundation’s Definition will be available with any updates or corrections, on the Nightingale Research Foundation’s Website, This definition may be copied, translated, distributed by electronic or hard copy and may be included, in whole or in part in any publication without permission from the Nightingale Research Foundation or the authors, provided that this last paragraph and referral back to our website are noted.

    Byron Marshall Hyde MD, Ottawa - January 29, 2007
  7. katte

    katte Member

    I get very leery of celebrating anything the CDC does.~~~~~What does this all actually mean,``````>>> for US patients <<<.```````Becasue of one TRICK after another, each move they make, worse for our ACTUAL LIVES than the one before.```````But also, the US and UK shrinks work hand in hand, so what does it mean for anyone?``````Many ways to view and question this, many contradictions.`````A) Technically, it does not say CFS is not ME. It say ME has *a different Case Definition*. ````Why did they word it this way? ```Why did they not say...```CFS is not ME? very simple, but no, they didn't say that...WHY?`````B) It says ME is muscular and neurologic. That *indicates*, of course that if you are in muscular, neurologic cat., you do not fit under CFS, period, even under wide umbrella. ```OK, we, w/ME have been saying that we have been defined out of the CFS def *utterly* for awhile. ```(Which is a CHANGE from earlier CFS defs, contrary to popular, incorrect opinion).If we have neurologic and muscular and do not have CFS under any umbrella def....`````WHERE DOES THAT LEAVE THE HUNDREDS OF THOUSANDS OF AMERICANS BEING TREATED, RECEIVNG PRESCRIPTIONS, AND BENEFITS, UNDER THE DIAGNOSTIC CODE OF CFS? YOU HAVE TO HAVE A DIAGNOSTIC CODE FOR MEDICAL TREATMENT.````C) THERE IS NO DIAGNOSTIC CODE FOR ME IN THE US````D) As it stands, w/the CDC's ever morphing, restrictive non-disease CFS def, For MANY people, they will not get to have ANY testsshowing abnormalities, even immune or suspected pathogens especially if your ME sees the CDC recommendations or your Ins catches up with it.```(already the case for many, or course, but not all) ````Since they state that TTT is *experimental*, this justifies it being denied, plus presumedly, not even be evaluated at all for OI. Which is what is keeping many people unable to sit or stand, and is TREATABLE.````{NOTE: Find out about "Poor Man's TTT"...can be done in office...and pray your DR. will do it}````I don't know if this is true, but my Dr., when I ask him to cahnge DX, says he can get more covered for me under "CFS". ```Hmmm doesn't sound like that will last for long, but I do get approval for tests, medications.```E) In the MYTHICAL lands which have Neurogenic ME as diagnosis, therefore better care ?! such as UK, the Psychs/Govt. are busy defining it out of existance also. ```They have woven a tale that it is an old disease, and an old name for CFS, which is a non-disease, with NO SIGNS OR SYMPTOMS, by definition, in the UK.```Look at the NICE guidelines, the UK Govt's recommendation ...*requirement*? for treatment. They are PSYCHIATRIC...CBT and GET..and for instance..discourage or deny adaptive aids, such as handicap sticker. ```THe NICE guidelines are now attached to the CDC CFS toolkit. THE UK itself increasingly says ME and CFS are the same thing. ```UK people should ask their Govt how can this be?...look at the CDC site! (Where the World looks for guidance, and codes for all research!) ```Grab the moment! ```*However*, the CDC site ONLY says they have a "different case definition", not "CFS is not ME", "ME is not CFS". ```If the CDC can keep changing the CFS case definition, why can't the UK change ME? ```THEY ALREADY ARE. ```MANY "scientific" papers are written stating this, CFS is ME, weaving an illusion which then becomes statement of fact``ie: ``"Studies now show"..."It is now well established"..."Todays's correct term is" "The case definition has changed has changed"````IMO, This, on the CDC site is a trick, of language, wording and intent, as is ALL else they do.```````````WHAT DOES IT ACTUALLY MEAN TO ANYONE'S LIFE and HEALTH, ANYWHERE?`````````What is it in prepration for?```Look at EVERYTHING done at the CDC or in the UK, with REEVES and WESSELY et al sitting, planning *together*.````Katrina
  8. Spinetti

    Spinetti New Member

    The CDC's "definition" of CFS pretty much boils down to saying it's something which can't be defined.

    How can any meaningful research, diagnosis, and treatment be conducted under this non-definition? It's down the rabbit hole - complete with smoke and mirrors.

    Thanks for posting, Tansy!

    Best wishes,

    [This Message was Edited on 06/16/2008]
  9. Spinetti

    Spinetti New Member

    From the report of the CDC's October 13, 1999 meeting:

    CFS Case Definition

    There was broad support among participants for reconsideration of the current CFS case definition.

    Several participants stated that the revised CFS case definition in 1994 had overly expanded the scope of the definition, and others expressed concern that the current definition fails to include some persons with CFS-like illnesses.

    Individual recommendations for revising the current CFS case definition included the following:

    include patient advocates as part of the review process, as was done in 1994;

    recognize that CFS is a contagious condition that can occur in clusters;

    recognize the effect of CFS among children and the occurrence of multiple pediatric and adolescent cases in families;

    recognize myalgic encephalomyelitis (ME) as a distinct clinical entity;

    specify the roles of several symptoms (e.g., postexertion malaise, dizziness, lightheadedness) in CFS;

    expand on the model showing concentric circles for fatigue (from the 1994 case definition) as a way of indicating overlapping forms of the illness.

    Dr. William Reeves, Chief of the Viral Exanthems and Herpesvirus Branch, stated that one of the proposed activities in the program's tentative work plan (see below) is to begin the process of reexamining the CFS case definition.

    CDC staff stated that changes in the case definition must be considered carefully because they can have important consequences for the specificity and sensitivity of various studies.

    I wonder what happened.
  10. Khalyal

    Khalyal New Member

    ..Dr. Byron Hyde and the other ME literate doctors walked out of the Holmes CFS definition study group because they were literally renaming ME. Since then, the definition has broadened and morphed to include so much stuff that the disease (ME) that became known as CFS got diluted right out of the description. Now if you have ME, you can't have CFS, because by definition CFS is a diagnosis of exclusion.

    Therefore, when studies come up with ways to measure our illness, our illness can no longer be CFS because according to the CDC there ARE no measurable biomarkers or definitive tests.

    It's a polite way to tell us we don't exist while at the same time appearing to be our champions.
    [This Message was Edited on 06/17/2008]
  11. Khalyal

    Khalyal New Member

    I'm sorry if I've confused you - my comment was regarding the political situation that CFS finds itself in, in the United States. What our doctors diagnoise may or may not be based on the CDC empirical.

  12. Khalyal

    Khalyal New Member

    Dr. Byron Hyde is one of the world's foremost authorities on ME. A good place to start learning is to read this portion of the Handbook of Chronic Fatigue Syndrome, called "The Complexities of Diagnosis" by Dr. Hyde:
  13. mezombie

    mezombie Member

    Katte--It's very clear from the phrasing that the reference is to Ramsay ME, not Oxford ME or any of the other watered down versions. What does it mean for patients? I don't think anything bad. There is no way a provider or insurance company can say, "Oh, you have ME, there is nothing to do". There are the Canadian Clinical Guidelines on ME/CFS, for example, to refer to. This reference is in the Provider Education program, which was put together with input from people like Drs. Klimas and Jason. I think that's why it is inconsistent with the other ME references on the CDC website.

    Spinetti--What happened? Ah, what happened is that all those good points were pretty much put forward by advocates, duly recorded, and then totally ignored. Except that Reeves and his helpers certainly were supportive of changing the case definition again--to make it fit anyone who reports feeling "unwell" for at least a month, as of 2005! Trying to get the CDC to do anything positive is like hitting one's head against a brick wall.

    [This Message was Edited on 06/20/2008]
  14. tansy

    tansy New Member

    only require chronic tiredness or fatigue (CF). The Tx for these are CBT and GET based on the psychobabblers' model; these rehabilition programmes are making patients with ME worse and in many cases permanently so.

    What we need is the restoration of ME and it's definition and more work done to look into the various causes of chronic fatigue and supposedly medically unexplained Sx. Atm everyone is losing out.

    tc, Tansy
  15. Spinetti

    Spinetti New Member

    Under the section "Basic Facts" for Patients & Care Givers, the CDC lists medical conditions similar to (and therefore different from) CFS.

    Similar Medical Conditions

    A number of illnesses have been described that have a similar spectrum of symptoms to CFS. These include fibromyalgia syndrome, myalgic encephalomyelitis, neurasthenia, multiple chemical sensitivities, and chronic mononucleosis. Although these illnesses may present with a primary symptom other than fatigue, chronic fatigue is commonly associated with all of them.

    [This Message was Edited on 08/18/2008]