​ A full and comprehensive  CFS report can be viewed (on the full website) here http://cfshelp.info/cf2 which includes such topics as diagnosis nomenclature and categorization of cfs M.E., CFS, GWS and FM also formerly known as systemic exertion intolerance disorder (SEID), chronic fatigue immunity deficiency syndrome (CFIDS), or post-viral fatigue syndrome (PVFSquoted below regards the different diagnosis and etiology of CFS and consistent abnormalities found in CFS patients, etc review of 'Chronic fatigue syndromes and vasoactive neuropeptide autoimmunity' https://www.amazon.com/Chronic-syndromes-vasoactive-neuropeptide-autoimmunity/dp/0977552802#customerReviews "book show that that author has done some genuine research into the early outbreaks of Myalgic Encephalomyelitis (M.E.) and on the genuine M.E. research of the 50s, 60s and 70s - before M.E. became conflated with the bogus disease category of 'Chronic Fatigue Syndrome.' Considering all the genuine information the author had, that he has somehow been unable or unwilling to see the vast differences between M.E. and 'CFS' is baffling and disappointing. The author has the information which shows that M.E. is a distinct, organic, neurological disease which occurs in epidemic forms yet thinks this is the same as 'CFS' which is a wastebasket diagnosis based on medically unexplained fatigue. The two are apples and oranges. The author could have busted the myths about 'CFS' but has chosen instead to reinforce them. This book is just gibberish. 'CFS' is made up of patients with hundreds of different diseases. Seriously analysing 'CFS' studies to try and come up with a single cause or treatment for this very diverse groups of patients is unscientific. There will never be one cause of 'CFS' as it is not a distinct disease. Saying you have found the most likely cause of 'CFS' is just silly. Like if you claimed to have the sole cause of itching say, or sleeplessness. There are so many causes of all these things that even trying to find a single cause is just ridiculous. Even worse this book says M.E., CFS, GWS and FM are all basically the same thing. But M.E. is not a fatigue syndrome and is also not medically unexplained. To explain a bit further:M.E. patients were treated appropriately and correctly diagnosed until around 1988, when there was an increase in the number of M.E. patients and outbreaks in the US. Some medical insurance companies (and others) decided that they would prefer not to lose many millions of dollars on so many new claims and so they created a new vague fictional disease category called 'Chronic Fatigue Syndrome' to try to confuse the issue of M.E. and to hide M.E. in plain sight. Under the cover of 'CFS' certain vested interest groups have assiduously attempted to obliterate recorded medical history of M.E.; even though the existing evidence has been published in prestigious peer-reviewed journals around the world and spans over 70 years. M.E. is a distinct, scientifically verifiable and measurable, acute onset, organic neurological disease. 'CFS' in contrast, is not a distinct disease. 'CFS' doesn't exist. Every diagnosis of CFS - based on any of the CFS definitions - can only ever be a misdiagnosis. A watebasket diagnosis. The fact that a person qualifies for a diagnosis of 'CFS' (a) does not mean that the patient has M.E., and (b) does not mean that the patient has any other distinct illness named CFS.' M.E. and 'CFS' are not the same. Far fewer than 0.5% of the population has the distinct neurological disease known since 1956 as Myalgic Encephalomyelitis. Chronic Fatigue Syndrome is an artificial construct created in the US in 1988 for the benefit of various political and financial vested interest groups. It is a mere diagnosis of exclusion based on the presence of gradual or acute onset fatigue lasting 6 months. If tests show serious abnormalities, a person no longer qualifies for the diagnosis, as 'CFS' is 'medically unexplained.' A diagnosis of 'CFS' does not mean that a person has any distinct disease (including M.E.). According to the latest CDC estimates, 2.54% of the population qualify for a 'CFS' (mis)diagnosis. The patient population diagnosed with 'CFS' is made up of people with a vast array of unrelated illnesses, or with no detectable illness. However, while 'CFS' is not a genuine diagnosis, those given this misdiagnosis are in many cases significantly or even severely ill and disabled. 'CFS' is made up of people with cancer, MS, Lyme disease, depression and hundreds of other unrelated conditions. Sub-grouping different types of 'CFS,' refining the bogus 'CFS' definitions further or renaming 'CFS' with some variation on the term M.E. (such as 'ME/CFS') would achieve nothing and only create yet more confusion and help to continue and further entrench the mistreatment and abuse. The problem is not that 'CFS' patients are being mistreated as psychiatric patients; some of those patients misdiagnosed with CFS actually do have psychological illnesses. There is no such distinct disease/s as 'CFS' - that is the entire issue. Due to outrageous political influences on medicine and govermnent policy, the vast majority of M.E. patients will not be able to be correctly diagnosed with M.E. Most M.E. patients will unfortunately be misdiagnosed with 'CFS.' It is extremely important to note, however, that only a very tiny percentage of those told they have 'CFS' will be M.E. patients. The overwhelming majority of those misdiagnosed with 'CFS' do NOT have M.E. 'CFS' is NOT just another term for M.E. The bogus disease category of 'CFS' must be abandoned. All those misdiagnosed with 'CFS' must immediately reject this harmful misdiagnosis and begin the search to find their correct diagnosis whether this be M.E., PVFS, depression, cancer, or any other disease. Correct diagnosis is vital in obtaining the correct treatment. This book should be avoided, as should the International Consensus Criteria the author is involved with - new definition of 'CFS' which (appallingly, unscientifically and unethically) tells patients that fit this vague non-M.E. definition that they should start telling everyone that what they have is M.E. Good intentions (which the author seems to have) are just not enough when the most basic facts, history and logic are ignored. Sadly it is the patients that pay the price for such poor work and lack of political guts and nous - both M.E. patients and those misdiagnosed with 'CFS' that do not have M.E. See books by Dr Hyde or articles by Dr Dowsett and others to learn more about M.E. and the politically motivated disease category of 'CFS.' Jodi Bassett, The Hummingbirds' Foundation for M.E. (HFME The Nightingale Definition of Myalgic Encephalomyelitis (M.E. https://www.hfme.org/whydepapers.htmThe Nightingale Definition of Myalgic Encephalomyelitis (M.E.) by Dr Byron Hyde 2007 Download the English 2007 PDF The Nightingale Definition of M.E.Download the 2006 HTML English version of The Nightingale Definition of M.E.Download the Norwegian PDF version of The Nightingale Definition of M.E.Download the French PDF version of The Nightingale Definition of M.E.Download the Danish PDF version of The Nightingale Definition of M.E.'The Nightingale defintion of M.E.' and 'The complexties of diagnosis' are now also available together in book form from Lulu. The second edition includes one extra paper. This book is also now available at Amazon. (Buy the book using this link and a percentage of the purchase price will be donated to the HFME.) An excerpt: Preface Since the Nightingale Research Foundation's publication in 1992 of its textbook, The Clinical and Scientific Basis of Myalgic Encephalomyelitis / Chronic Fatigue Syndrome, there has been a tendency by some individuals and organizations to assume that M.E. and CFS are the same illness. Over the course of two International Association of Chronic Fatigue Syndrome (IACFS, formerly the American Association of CFS) conferences, there have been suggestions that the name CFS be changed to M.E., while retaining the CFS definitions as a basis for such change. This does not seem to me to be a useful initiative: it would simply add credence to the mistaken assumption that M.E. and CFS represent the same disease processes. They do not. M.E. is a clearly defined disease process. CFS by definition has always been a syndrome At one of the meetings held to determine the 1994 U.S. Centers for Disease Control and Prevention (CDC) definition of CFS, in response to my question from the floor, Dr. Keiji Fukuda stated that numerous M.E. epidemics he cited the Los Angeles County Hospital epidemic of 1934, the Akureyri outbreak of 1947-48 and the 1955-58 Royal Free Hospitals epidemics-- were definitely not CFS epidemics. Dr. Fukuda was correct. The Psychiatric Label Unfortunately many physicians and some senior persons in governments, including Great Britain, Norway and to a lesser degree the USA and Canada treat CFS as a psychiatric illness. This view has been arrived by some physician's readings of the CFS definitions from CDC. Indeed, despite clear signals in the 1994 CDC definition that CFS is not a psychiatric disease, each of the CDC definitions and their addenda referring to CFS remain open to interpretation as a psychiatric rather than a physical illness. This is not a view to which I subscribe. It is the CFS definitions themselves that give rise to this inaccuracy. Consider the following: (a) What other physical disease definitions essentially state that if you discover the patient has any physical injury or disease, then the patient does not have the illness CFS? In other words if you have CFS then it does not result in or cause any major illness. What else could CFS then be but any number of various psychiatric, social, hysterical or mendacious phenomena? (b) The various CDC administrations dealing with the subject have clearly stated that CFS is a physical, not a psychiatric disease. However, is there any other definition of any physical disease that is not provable by  scientific and clinical tests? Only psychiatric diseases are not clearly verifiable by physical and technological tests. (c) What other physical disease definition requires a six month waiting period before the illness can be diagnosed? Any physician knows that to treat a disease adequately you have to be able to define the disease at its onset and treat it immediately in order to prevent chronic complications from arising. There are simply no other disease definitions that have ever been assembled similar to the CFS definitions. I believe it essential to define clearly Myalgic Encephalomyelitis. That is what the Nightingale definition of M.E. sets out to do   A simplified definition of Myalgic Encephalomyelitis Myalgic Encephalomyelitis is:  1  A variable and biphasic acute onset disease  2  Primary Infection Phase: The first phase is an epidemic or endemic infectious disease generally with an incubation period of 4 to 7 days, where in most, but not all cases, an infection is evident. 3  Chronic Phase: The second and chronic phase follows closely on the first phase, usually within two to seven days, and is characterized by a measurable diffuse change in the function of the CNS. This is the persisting disease that most characterizes M.E. and is demonstrated by the following: 4  Testable Brain Changes: This second phase becomes chronic and is characterized by various measurable and clinical dysfunctions of the cortical or cortical and sub cortical brain. If the patient's illness is not persistently measurable using SPECT, PET or QEEG and/or Neuropsychological changes then it is not M.E. These changes can be roughly characterized as to severity: 1. Type 1: where one side of the cortex is involved. These patients have the best chance of spontaneous recovery. 2. Type 2: where both sides of the cortex are involved: These patients have the least chance of spontaneous recovery. 3. Type 3: where both sides of the cortex, and either one or all of the posterior chamber organs, the Pons and Cerebellum, the sub cortical and brain stem structures are involved. Type 3 are the most severely affected patients and the most likely to be progressive or see little or no improvement with time. 5  Pain Syndromes: The pain syndromes associated with the acute and chronic phases of M.E. may include (a) severe headaches of a type never previously experienced, (b) often associated with neck rigidity and occipital pain, (c) retro-orbital eye pain, (d) migratory muscle and arthralgia pain, (e) cutaneous hypersensitivity and (f) fibromyalgia type pain. These pain syndromes tend to decrease over time. 6  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. This feature may improve over a period of years in patients with adequate financial and social support. 7  Major Sleep Dysfunction: including all forms of sleep dysfunction and day time alertness and sleep reversals. 8  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. 9  Vascular Dysfunction: This is the most obvious dysfunction when looked for and probably is the cause behind a significant number of the above complaints. Vascular change is most evident in patients with: a. POTS: severe postural hypotension. b. Cardiac irregularity: on minor positional changes or after minor physical activity, including inability for the heart to increase or decrease in speed and pump volume in response to increase or decrease in physical activity. c. Raynaud's Disease: vasoconstriction, blanching, coldness and pain of extremities. This is in part the cause for temperature dysfunctions seen in M.E. d. Bowel Dysfunction: vascular dysfunction may be the single most causal basis behind bowel dysfunction when it occurs 10  Endocrine Dysfunction: This feature is common and tends to be a late appearance and is most obvious in the: a. Pituitary-thyroid axis: This is common. Changes in serum TSH, FTI, FT4, Microsomal Ab., PTH, Calcium and phosphorus rarely occur until one or more years after illness onset and usually only after several years. This can be followed by ultrasound of the thyroid gland where a steady shrinking of the thyroid gland occurs with or without the development of non-serum positive Hashimoto's thyroiditis (a seeming contradiction of terms) and a significant increase in thyroid malignancy. Serum positive changes occur only after years. b. Pituitary-adrenal axis changes: this finding is infrequent. c. Pituitary-ovarian axis changes: d. Pituitary-Bladder dysfunction: occurs frequently in the early disease in some people. It is unknown if the cause is due to this link. *HIGHLY RECOMMENDED* This paper by Dr Hyde, and the two other papers below are probably the three most important papers on M.E. available. They are absolutely essential reading for everyone with any interest in Myalgic Encephalomyelitis (or 'CFS'). A New and Simple Definition of Myalgic EncephalomyelitisA New and Simple Definition of Myalgic Encephalomyelitis and a New Simple Definition of Chronic Fatigue Syndrome & A Brief History of Myalgic Encephalomyelitis & An Irreverent History of Chronic Fatigue Syndrome by Dr Byron Hyde 2006 View/download/print the 2006 PDF of A New and Simple Definition of Myalgic Encephalomyelitis and a New Simple Definition of Chronic Fatigue Syndrome & A Brief History of Myalgic Encephalomyelitis & An Irreverent History of Chronic Fatigue SyndromeAn excerpt: ‘Do not for one minute believe that CFS is simply another name for Myalgic Encephalomyelitis (M.E.). It is not. Though CFS is based upon a typical M.E. epidemic, in my opinion it has always been a confused and distorted view of reality. The invention of Chronic Fatigue Syndrome has to be one of the most curious cases of inventive American scientific imperialism that one could imagine. It is my opinion that the CDC 1988 definition of CFS describes a non-existing chimera based upon inexperienced individuals who lack any historical knowledge of this disease process. The CDC definition is not a disease process.’ *HIGHLY RECOMMENDED* The Complexities of DiagnosisThe Complexities of Diagnosis by Dr Byron Hyde MD 2003 View/download/print the 2003 PDF The Complexities of DiagnosisThe Nightingale defintion of M.E.' and 'The complexties of diagnosis' are now also available together in book form from Lulu This book is also now available from Amazon. (Buy the book using this link and a percentage of the purchase price will be donated to the HFME.) An excerpt: The physician and patient alike should remember that CFS is not a disease. It is a chronic fatigue state as described in four definitions starting with that published by Dr. Gary Holmes of the CDC and others in 1988 (Holmes, Kaplan, Gantz, et al., 1988; Holmes, Kaplan, Schonberger, et .al., 1988). The definition created by Lloyd, Hickie, Boughton, Spencer, and Wakefield (1990) is also widely used in Australia. There are two subsequent definitions. The Oxford definition of 1991 (Sharpe et al., 1991) and the 1994 NIH/CDC definitions (Fukuda et al., 1994) are basically, with a few modifications, copies of the first definition. Where the one essential characteristic of ME is acquired 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 definition and few are scientifically testable. Despite the list of signs and symptoms and test exclusions in these definitions, patients who conform to any of these four CFS definitions 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 Nightingale Research Foundation definition https://me-pedia.org/wiki/Nightingale_Research_Foundation_definition#:~:text=myalgic%20encephalomyelitis%20(M.E.)%20%2D%20A,synonym%20for%20chronic%20fatigue%20syndrome. 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[1], published in 2007[2], and updated in 2016[3].  Primary M.E. 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.[2] 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 patho-physiological 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, and (b) The technological examinations that confirm to the physician proof of his diagnosis. Clinical FeaturesThe 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 (sporadic) infectious disease processBoth 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: repetitive contact with a large number of infectious persons,unusually long hours of exhausting physical and / or intellectual work,physical traumas,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,epidemic disease cases whose onset and periodicity appear to occur cyclically in a susceptible population,the effect of travel, as in exposure to a new subset of virulent infections, orthe effects of starvation diets.(It should be noted that subsets c, d, e, f and g are all stressors associated with decreased immune adaptability plus an associated infection with an appropriate neurovascular infectious virus or other infectious agent. This may be due either to an immediate preexisting infectious disease or to a closely following infection, either of which may or may not be recognized.) 2. Primary Infection PhaseThe 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./CFS, Chapter 13, pps. 124-126) 3. Secondary Chronic PhaseThe 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 variableThe pain syndromes associated with the acute and chronic phases of M.E. may be described as Early and Late findings. Early Findings: severe headaches of a type never previously experienced;these are often associated with neck rigidity and occipital pain;retro-orbital eye pain;migratory muscle and arthralgia pain;cutaneous hypersensitivity.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./CFS, Chapter 5, pps. 58-62) Testable & Non-testable CriteriaThe 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 SPECTIf 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. 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. Extent of InjuryType 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. Degree of injuryType 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. 6. Testable Neuropsychological ChangesThere 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: word-finding problems,Subtle problems with receptive and expressive aphasia,Decreased concentration,Distractibility and the decreased ability to process multiple factors simultaneously,Dyscalculia,Decreased fine and gross motor problems,Dysfunction of spatial perception,Abstract reasoning,Compromised visual discrimination,Sequencing problems.In Cochran’s Q Neuropsychological tests there is an increased observation of significant problems in both immediate and delayed verbal recall. In Dr Sheila Bastien’s investigations, over 50% of M.E. patients have delayed visual recall, TAP dominance, TPT N-Dominance and 40% or more have abnormalities of Immediate visual recall, Tap N-Dom, Grip N Dominance, & grip dominance problems. (Bastien, Sheila. The Clinical and Scientific Basis of M.E. / CFS. Chapter 51, pps. 453-460) 7. Testable Major Sleep DysfunctionThis can include all forms of sleep dysfunctions. All or any of the following may be present: impaired sleep efficiency,significant fragmented sleep architecture,movement arousals, particularly if there is an associated pain syndrome,absence or significant decrease of type 3 and 4 sleep,abnormal REM sleep patternchanges in daytime alertness andsleep reversals. 8. Testable Muscle DysfunctionThis 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. Few centres are equipped or funded to make these examinations. Unfortunately only a few major medical centres are equipped to study this type of dysfunction. 9. Testable Vascular & Cardiac DysfunctionThis 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. 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. 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. 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. 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. This phenomenon is found in many other conditions than M.E. 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. (See Magallni, S. for more detail.) 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. These patients do not generally have aenemia 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. 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. 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: This is a group of illnesses with a genetic predisposition to M.E. 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. 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. 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. 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. patients. Severe pain and fatigue can be intolerable and persist for minutes to days in some M.E. 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. 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. pain. To my knowledge, no testing of M.E. 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. patients are due to a pathological vascular physiology. h) M.E. Associated Clotting Defects: M.E. 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 patho-physiology 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 demonstratedwhen 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. type disease. However there is a significant group of M.E. patients who are ill due to a treatable form of vasculitis and can be treated if the physician takes the time to diagnose the subgroup. 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 Ab.,(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. 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. 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. 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. 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. 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. 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./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 DysfunctionThese features are common and tend to be of late appearance. They are most obvious in: 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. 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. 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. patients. Repeat thyroid ultrasound must be performed for all M.E. 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 its 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. disease process: b) Pituitary-Adrenal Axis Changes: where changes and findings are infrequent. c) Pituitary-Ovarian Axis Changes d) 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. CriticismJohn Chia reportedly feels that the SPECT scans required by the Nightingale Research Foundation definition are not conclusive, as insufficient research has been done regarding the use of SPECT in ME/CFS. Reportedly, he also feels that the hypoperfusion shown in SPECT could be seen in other conditions as well.[4] Learn more2006, A new and simple definition of Myalgic Encephalomyelitis[1]2007, The Nightingale Myalgic Encephalomyelitis (M.E.) Definition[2]2016, The Nightingale Research Foundation Definition of Myalgic Encephalomyelitis (M.E.) Missed Diagnoses Myalgic Encephalomyelitis & Chronic Fatigue Syndrome by Byron Hyde MD https://www.hfme.org/booksbest.htm#420114714This book is essential reading for doctors and patients alike, and those interested in M.E. as well as those interested in 'CFS' or that have been misdiagnosed as 'CFS.' (As this book explains, there is no such distinct disease as 'CFS' - and every diagnosis of 'CFS' is a MISdiagnosis. This book also explains that M.E. is not a similar disease to 'CFS' nor a mere 'fatiguing disorder.') The Nightingale Definition of Myalgic Encephalomyelitis paper in particular cannot be recommended highly enough. Finally this is a modern and TESTABLE definition of Myalgic Encephalomyelitis, created by the world's leading and most experienced M.E. expert, Dr Byron Hyde. This is NOT a redefinition of CFS but is instead a pure M.E. definition. It draws on the long history of M.E., collates the evidence from each of the world's leading M.E. experts (past and present) and combines this with details of the most modern medical tests. This definition also rightly gives no importance at all to the bogus notion of mere `fatigue' having any importance in the diagnosis/definition - unlike each of the `CFS' definitions, including unfortunately the Canadian `ME/CFS' definition which just mixes in a few M.E. facts with what is still primarily a `CFS' redefinition. Dr Hyde explains that: "I believe it essential to define clearly Myalgic Encephalomyelitis, returning the definition to its clinical and historic roots and complementing this information with the certitude of modern scientific testing. That is what the Nightingale definition of M.E. sets out to do. But let me first ask you a very important question. What is the purpose of any medical definition? What is the purpose of any disease definition if it is not to allow the physician to rapidly and accurately diagnose a specific illness in order to attempt to effectively treat the patient before the illness becomes chronic or to call in the appropriate specialists? Our definition solves this problem." "There is a third purpose for any disease definition. That is to clearly define the disease so that various physicians and researchers can clearly understand that they are talking about the same illness spectrum and so launch research into what will become an effective treatment. Our definition gives a clear baseline for investigation. The Nightingale definition is based upon the following two criteria: (a) The excellent scientific and clinical work of respected physicians and scientists who investigated the various M.E. epidemics. (b) The results of modern scientific testing techniques and the knowledge accruing from examining thousands of M.E. patients using these and more historical techniques. The proposed M.E. definition is designed to improve early diagnosis and treatment for the tens of thousands of patients stricken with M.E. It is not a new definition of CFS nor should it be conceived as a rewording of any previous CFS definition. The definition is set out in such a fashion as to enable the physician to make a bedside or office clinical diagnosis and then to scientifically test the hypothesis. This will allow the physician an early diagnostic understanding of this complex illness and a scientific and technological method to investigate and confirm the diagnosis. It is well known by all serious physicians that in order to assist any patient in a partial or full recovery the illness must be (a) prevented from occurring by either immunization or understanding and avoiding the causes, (b) or diagnosed and treated immediately following onset. The Nightingale Definition assists the physician both in diagnosis and early treatment. What follows is the primary M.E. definition for adults. I believe it essential to define clearly Myalgic Encephalomyelitis. That is what the Nightingale definition of M.E. sets out to do........ To various degrees many if not all of the above historic findings have been observed and discussed by Doctors Alexander Gilliam, Bjorn Sigurdsson, Alberto Marinacci, Andrew Lachlan Wallis, A Melvin Ramsay (Elizabeth Dowsett), John Richardson, Elizabeth Bell, Alexis Shelokov, David C Poskanzer, W.H. Lyle, Sir E. Donald Acheson, Louis Leon-Sotomayor, J. Gordon Parish and many others."  'The Complexities of Diagnosis' is also very, very good overall and is also recommended. (This piece does very unfortunately use the misleading and confusing term 'ME/CFS' throughout, but the content of the paper makes it crystal clear that M.E. and 'CFS' are not at all the same.) Buy this book, and an extra copy for your doctor. See also the free downloads of some parts of it available online on the Dr Hyde page. This book is available from Lulu M.E. symptoms (in brief https://www.hfme.org/mesymptoms.htmM.E. is primarily neurological, but also involves cognitive, cardiac, cardiovascular, immunological, endocrinological, metabolic, respiratory, hormonal, gastrointestinal and musculo-skeletal dysfunctions and damage. M.E. affects all vital bodily systems and causes an inability to maintain bodily homeostasis. More than 64 individual symptoms of M.E. have been scientifically documented. M.E. symptomsWhat defines M.E. is a specific type of viral damage to the brain. M.E. represents a major attack on the CNS by the chronic effects of a viral infection which targets the brain: an enterovirus. The onset of M.E. is acute or sudden. More than 60 symptoms have been authentically documented in M.E. M.E. is associated with signs and symptoms including (but not limited to): Neurological signs and symptoms: Inconsistent central nervous system function Vertigo, disequilibrium and proprioception difficulties (e.g. lack of sense of 'up' and 'down' with eyes closed)Temperature dysregulation and poor tolerance for hot or cold environmentsHyperacusis (sensitivity to noise) and photophobia (pain/relapse on exposure to light)Pain and pressure at the back of the head (where the head meets the neck) and behind the eyesBlurred vision, blacked-out vision, nystagmus, wavy visual field, and other visual disturbancesStroke-like or coma-like episodesSeizures and 'sensory storms' (while conscious)Sleep paralysis, fragmented sleep, difficulty initiating sleep, lack of deep-stage sleep and/or a disrupted circadian rhythmMany other varied neurological symptoms and abnormalities Vascular and cardiovascular signs and symptoms: A very high heart rate, chest pressure, heart pain and a fluttering/straining heartVery low blood pressure particularly when upright (e.g. 84/48 or less in an adult at rest), orthostatic tachycardia/POTS and reduced circulating blood volume (up to 50%)Feet burning painfully and turning blue/purple on standing (Reynaud's phenomenon)Pain/discomfort/poor digestion following meals Muscular signs and symptoms: Muscle weakness and paralysis (affecting all muscles including the heart, eyes, digestive system etc.)Muscle pain, twitching and uncontrollable spasmsDifficulty breathing and air-hunger, difficulty swallowing/chewingParesthesias, polyneuropathy or myoclonus Cognitive signs and symptoms: Word-finding difficulty, scanning or disjointed speech, speech reversals, difficulty or an inability to speakDifficulty comprehending speech or delayed speech comprehensionHandwriting changes, difficulty writing or comprehending textDifficulty with even basic mathematics (dyscalculia)Difficulty with simultaneous processing, concentration, spatial perception and with sequencingDifficulty making new memories, recalling formed memories and with immediate and delayed visual and verbal recall (e.g. facial agnosia). There is often a marked loss in verbal and performance IQ Other signs and symptoms: Nausea, vomiting and feeling 'poisoned' and very illThroat and gland pain/tenderness, chills and low grade feversFood allergies, alcohol intolerance, hypoglycaemia and sensitivity to common drugs/chemicalsGhastly pallor of face with frequent lupus-like submaxillary mask or facial vasculoid rashParkinsonian rigidity of facial expression What characterises M.E. every bit as much as the individual symptoms is the way in which people with M.E. respond to physical and cognitive activity, sensory input and orthostatic stress, and so on. It is unique in a number of ways and must be present for a correct diagnosis of M.E. to be made, and includes the following: People with M.E. are unable to maintain their pre-illness activity levels. This is an acute, sudden change. M.E. patients can only achieve 50% or less of their pre-illness activity levels. People with M.E. are limited in how physically active they can be but are also limited in similar ways with cognitive exertion, sensory input and orthostatic stress. When a person with M.E. is active beyond their individual limits, there is a worsening of various neurological, cognitive, cardiac, cardiovascular, immunological, endocrinological, respiratory, hormonal, muscular, gastrointestinal and other symptoms. The level of physical activity, cognitive exertion, sensory input or orthostatic stress (being upright) that is needed to cause significant relapse varies from patient to patient, but is often trivial compared to pre-illness tolerances and abilities. The severity of M.E. waxes and wanes throughout the hour/day/week and month. The worsening of the illness caused by overexertion often does not peak until 24 - 72 hours or more later. The effects of overexertion can accumulate over time and lead to disease progression The activity limits of M.E. are not short term: an increase in activity levels beyond a patient's individual limits, even if gradual, causes relapse, disease progression The symptoms of M.E. do not resolve with rest. There is also a base level of illness which can be quite severe even at rest. Repeated overexertion can harm the patient's chances for future improvement in M.E. Patients who are able to avoid overexertion have repeatedly been shown to have the most positive long-term prognosis. Not every M.E. sufferer has 'safe' activity limits within which they will not exacerbate their illness: this is not the case for very severely affected patients. 30% of M.E. patients are housebound and/or bedbound and are severely limited with even basic movement and communication. Cognitive disability can be very pronounced in M.E., just as much as can physical disability. This information is based upon an enormous body of clinical information and research. Although M.E. can cause many different symptoms the major features of epidemic and sporadic M.E. are distinct and almost identical from one patient to the next. M.E. is a severely disabling, distinct, easily recognisable and testable disease entity. To read or download an extended and fully referenced version of the above text, please see the The comprehensive M.E. symptom list page. Additional relevant links: For more information on all aspects of M.E. please see the (fully referenced) What is M.E.? A historical, medical and political overview paper. For more information on the political issues facing M.E. patients please see: M.E. vs MS: Similarities and differences and Who benefits from 'CFS' and 'ME/CFS'? and M.E.: The shocking disease. Patients given a diagnosis of 'CFS' are advised to read the following papers: The misdiagnosis of CFS, Where to after a 'CFS' (mis)diagnosis? and Why the disease category of 'CFS' must be abandoned and Who benefits from 'CFS' and 'ME/CFS'?To read a list of all the articles on this site suitable for different readers, see the Information guides page. Guides available so far include the following: severe M.E. patients, M.E. patients, patients given a 'CFS' diagnosis (but that do not have M.E.), doctors, carers looking after M.E. patients, friends and family of M.E. patients, parents of children with M.E., members of the public who would like to know a little more about the disease, media and politicians and human rights groups To view a list of all HFME papers and resources, see the HFME site map page. Extra information: Is 'fatigue' an essential M.E. symptom?Because of the vast amount of inaccurate information being propagated about Myalgic Encephalomyelitis by various vested interest groups (helped immeasurably by the creation of the bogus disease category of ‘CFS’ as well as a number of vague and misleading umbrella terms such as ‘ME/CFS’ ‘CFS/ME’ ‘CFIDS’ and Myalgic ‘Encephalopathy’ etc.) it is important to explain briefly what are the myths about M.E., and the symptoms of M.E. M.E. is not synonymous with being tired all the time. If a person is fatigued for an extended period of time this does not mean they are having a ‘bout’ of M.E. To suggest such a thing is no less absurd than to say that prolonged fatigue means a person is having a ‘bout’ of multiple sclerosis or Parkinson’s disease. Fatigue is a symptom of many different illnesses – but it is not a defining symptom of M.E., or an essential symptom of M.E. Some patients with M.E. may suffer with fatigue as a minor symptom, but many will not. There are a number of post-viral fatigue states or fatigue syndromes which may follow common infections such as mononucleosis/glandular fever, hepatitis, Q fever, Ross river virus and so on. M.E. is an entirely different condition to these self-limiting fatigue syndromes however, the science is very clear on this point. M.E. is also not the same condition as Lyme disease, athletes over-training syndrome, burnout, depression, somatisation disorder, candida, multiple chemical sensitivity syndrome or Fibromyalgia, or indeed any other illness. What defines M.E. is not ‘chronic fatigue’ but a specific type of damage to the brain. M.E. is an infectious neurological illness of extraordinarily incapacitating dimensions that affects virtually every bodily system – not a problem of unexplained ‘fatigue' or exhaustion. For more information on this topic please see: The comprehensive M.E. symptom list and  What is Myalgic Encephalomyelitis? Many M.E. experts (and M.E. sufferers) have spoken out about against 'fatigue' being the defining features of M.E., see: M.E. is not defined by 'fatigue' and also the Quotes section for more information plus What it feels like to have Myalgic Encephalomyelitis: A personal M.E. symptom list and description of M.E. The Fatigue Schmatigue paper explains how the fraudulent 'fatigue' construct came into being and how the M.E. community can and MUST play an active part in debunking this myth. This paper is aimed not at the public but at M.E. sufferers and other members of the M.E. community and is highly recommended. Extra information: A warning on misdiagnosing M.E.It should not be assumed that because one may have some of the symptoms on the list that one necessarily has M.E. - many of them are common in a variety of other disorders and it is the pattern of symptoms which enables a M.E. diagnosis to be made, as well as the presence of a number of core characteristics and symptoms which are always present in the illness, and without which a diagnosis of M.E. should never be made. (For example, damage to the brain, the CNS, which is visible on brain scans, and so on.) Even having a large number or percentage of the symptoms on this list does NOT necessarily mean a M.E. diagnosis is likely or even possible. M.E. cannot be accurately diagnosed merely on the presence of a certain percentage of possible M.E. symptoms. Those with Lyme disease may see many of their symptoms listed in M.S. or M.E. symptom lists, but this does not mean that Lyme disease is the same as M.S. or M.E. The same is true of many different diseases. Many diseases share a few symptoms, but what is important is the very different causes of these symptoms and the very different pathology and response to treatment seen in each of these patient groups. None of these patient groups has the same cause of symptoms as seen in M.E. as none of these patient groups share the pathology of M.E. (For example, most of the symptoms of M.E. are caused by cardiac insufficiency and the associated reduced circulating blood volume of up to 50%. This can be so severe as to lead to death in M.E., in some cases. Yet this problem of cardiac insufficiency and reduced circulating blood volume simply does NOT OCCUR in these non-M.E. diseases.) M.E. patients can be separated very easily and clearly from those with Lyme disease, various post-viral fatigue syndromes, candida, Bechet's disease, vitamin deficiencies, depression and other mental disease and so on when the onset of the disease is taken into consideration (unlike most of these diseases, the onset of M.E. is always sudden or acute) and when an evaluation of the core and unique symptoms of M.E. is done along with some of the tests used to confirm a M.E. diagnosis. M.E. should never be diagnosed based on a superficial analysis of non-core M.E. symptomatology. See: Testing for M.E. for more information on the diagnosis of M.E. M.E. tests (in brief https://www.hfme.org/metests.htmM.E. tests (in brief)M.E. is a distinct, recognisable disease entity with several unique features that is not difficult to diagnose within just a few weeks of onset.  Although there is as yet no single test which can be used to diagnose M.E. there are (as with Lupus, multiple sclerosis and ovarian cancer and so on) a series of tests which can confirm a suspected M.E. diagnosis with confidence. Virtually every M.E. patient will also have various abnormalities visible on physical exam. If all tests are normal then a person does NOT have M.E. M.E. testsM.E. is a distinct, recognisable disease entity that is not difficult to diagnose and can in fact be diagnosed relatively early in the course of the disease, within just a few weeks, providing that the physician has some experience with the disease. There is just no other disease that has all the major features of M.E. Objective evidence of quantifiable organic abnormalities in M.E. patients has existed since the 1950s. As with a wide variety of illnesses – lupus, multiple sclerosis, and ovarian cancer for example – there is as yet no single test which can diagnose M.E. in all patients. Therefore, like these other illnesses, M.E. must be diagnosed by taking a detailed medical history, noting the type and severity of symptomatology and other characteristics of the illness and the type of onset of the symptoms. (An acute or sudden onset of symptoms is always seen in M.E. and this onset type rules out a wide variety of other illnesses associated with gradual onset). A series of tests may also then be necessary to rule out or confirm a suspected M.E. diagnosis. One cannot test for ‘CFS’ but M.E. is not the same thing as ‘CFS’ (or ‘ME/CFS.’) The presence or absence of ‘fatigue’ is largely irrelevant in determining an M.E. diagnosis except in that its presence may of course make the diagnosis of a large number of well-known fatigue causing illnesses considerably more likely (depression, vitamin deficiency or malignancy for example) (Hyde & Jain, 1992). M.E. is not a diagnosis of exclusion or an untestable disease. Tests will only all be normal in M.E. patients – as with all illnesses – if the wrong tests are conducted, or if those tested do not in fact have M.E. (Hyde 2007, [Online]) (Hyde 2006, [Online]) (Chabursky et al. 1992, p.22). Contrary to common disinformation erroneously linking M.E. with ‘CFS,’ it is not mere ‘fatigue’ that defines M.E. but central nervous system (CNS) dysfunction. M.E. represents a major attack on the CNS by the chronic effects of a viral infection which targets the brain: an enterovirus. As M.E. expert Dr Byron Hyde explains: The one essential characteristic of M.E. is acquired CNS dysfunction. A patient with M.E. is a patient whose primary disease is CNS change, and this is measurable. We have excellent tools for measuring these physiological and neuropsychological changes: SPECT, xenon SPECT, PET, and neuropsychological testing (2003, [Online]). Tests which together can be used to confirm an M.E. diagnosis include: SPECT and xenon SPECT scans of the brain.MRI scans of the brain.PET scans of the brain.EEG/QEEG brain maps.Neurological examination. Neuropsychological testing.The Romberg test.Immune system tests.Insulin levels and glucose tolerance tests.Erythrocyte Sedimentation Rate (ESR) tests.Circulating blood volume tests.24 hour Holter monitor testing.Tilt table examination and standing/sitting/reclining blood pressure tests.Exercise testing and chemical stress tests.Physical exam. These tests are the most critical in the diagnosis of M.E., although various other types of tests are also useful. M.E. expert Dr Byron Hyde’s Nightingale Definition of M.E. also now makes diagnosis easier than ever before even for those with no prior experience in diagnosing M.E. This is a pure M.E. definition and, most importantly, it defines M.E. as testable  (Hyde 2007, [Online]) (Hyde 2006, [Online]) (Hyde 2003, [Online]) (Dowsett 2001a, [Online]) (Dowsett 2000, [Online]) (Hyde 1992 p. xi) (Hyde & Jain 1992 pp. 38 - 43) (Hyde et al. 1992, pp. 25-37) (Dowsett et al. 1990, pp. 285-291) (Ramsay 1986, [Online]) (Dowsett n.d., [Online]) (Dowsett & Ramsay n.d., pp. 81-84) (Richardson n.d., pp. 85-92). More informationTo read or download an extended and fully referenced version of the above text, please see the Testing for M.E. page. Additional note for patients: Despite the existence of the tests for M.E. described in this paper, the unfortunate reality is that many people who suspect they have M.E. do not have access to the appropriate tests or to doctors who are able to make the diagnosis due to political interference in science (helped immeasurably by the creation of the bogus disease category of 'CFS').  See Testing for M.E.: Plan D for discussion of the ways in which patients seek a diagnosis in practice. Additional relevant links: For more information on all aspects of M.E. please see the (fully referenced) What is M.E.? A historical, medical and political overview paper.For more information on the political issues facing M.E. patients please see: M.E. vs MS: Similarities and differences and Who benefits from 'CFS' and 'ME/CFS'? and M.E.: The shocking disease.Patients given a diagnosis of 'CFS' are advised to read the following papers: The misdiagnosis of CFS, Where to after a 'CFS' (mis)diagnosis? and Why the disease category of 'CFS' must be abandoned and Who benefits from 'CFS' and 'ME/CFS'?To read a list of all the articles on this site suitable for different readers, see the Information guides page. Guides available so far include the following: severe M.E. patients, M.E. patients, patients given a 'CFS' diagnosis (but that do not have M.E.), doctors, carers looking after M.E. patients, friends and family of M.E. patients, parents of children with M.E., members of the public who would like to know a little more about the disease, media and politicians and human rights groups.To view a list of all HFME papers and resources, see the HFME site map page.Extra information: Medical science vs politicsM.E. is not difficult to diagnose, or to distinguish from ‘CFS’ or any other fatiguing illnesses. M.E. is also not ‘difficult to define’ or ‘mysterious’ or ‘medically unexplained’ or a mere ‘diagnosis of exclusion.’ These are characteristics of ‘CFS’ but not of M.E. M.E. is no more difficult to diagnose through using a series of tests than is MS. In fact, it has been suggested that M.E. diagnosis is significantly less difficult and more reliable than that of MS! We can also be a lot more certain about the cause of M.E., compared to MS. The cause of MS is hotly debated, while the fact that M.E. is caused by a virus is well established beyond doubt and there is overwhelming evidence that M.E. is caused by an enterovirus. On a purely scientific level, we have more than enough information to reliably diagnose patients with M.E. using objective tests (and by taking detailed case notes and conducting a detailed physical exam etc.) within just a few weeks of the onset of the disease. If the will and the funding were there, scientists could right now very easily make sure that studies contained a 100% M.E. population – just as they do with MS patients or patients with Lupus and so on. Scientifically, it would be no more difficult to do this for M.E. than with these other diseases. The problem is not that these tests don’t exist, but that doctors – and many patients – are unaware of this information on testing, that it is not generally accepted due to the nefarious influence of political and financial vested interest groups, and that there are overwhelming financial and political incentives for researchers to IGNORE this evidence in favour of the bogus ‘CFS’ (or ‘subgroups of ‘ME/CFS’) construct, and so on. For more information see: Testing for M.E. and Dr Hyde's The Nightingale Definition of M.E. plus Are we just 'marking time?' Why are we waiting to act when tests for M.E. exist RIGHT NOW, and the need for activism/action is so very urgent? See also: See M.E. vs MS: Similarities and differences  

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