Here is my response for all to read, regarding the recent CO-CURE post about the Pacific Fatigue Lab's 'CFS' work. LKW ***permission to repost***
2/16/2009 TO: ALL ADDRESSEES RE: Pacific Fatigue Lab studies on 'ME', G93.3, Neurogenic versus 'CFS', R53.82. This has turned out to be a very lengthy email. But I hope you will bear with me, and read it through to the end, as I have included a great deal of highly relevant and important illness information for your perusal. I wrote to Mr. Van Ness approx a year ago, about expanding the testings this group does to ME, G93.3 patients, rather than doing them on just 'CFS' (Fukuda, et al, R53.82) patients. I also urged him to contact the WPI (Whittemore Peterson Institute) and--I believe--a Dr. Byron Hyde in Canada, who is the world's pre-eminent authority on ME. Mr. Van Ness responded and expressed a willingness to do more, but explained the lack of funding, which still exists. This email response contains valuable and important information. For ME, G93.3 patients, it remains very disconcerting and troubling to read about the advancement and application of the 2003 'ME/CFS Canadian Criteria', which represents an illogical 'blend' of both ME (G93.3) and CFS (R53.82).
- It is this 'blending' and 'lumping together' of two disparate things that CFS patients like, because it makes their 'syndrome' (i.e., a group of symptoms) based on 'fatigue' sound more serious. - It is this 'blending' and 'lumping together' of two disparate things that infuriates those of us who are ME-defined, because it waters down and weakens our severely debilitating CNS (Central Nervous System) illness!!!
One would have to know the complete history of the past 20+ years to fully understand what's all taken place, but bascially, two entities, the USA CDC and the UK Wessely School (WS) have collaborated and done their utmost to turn CFS (or 'CFS/ME') into a 'psych' thing, and to help insurance companies deny claims. They have been well-compensated for their actions which saved the insurance ocmpanies many millions of dollars. And with the USA CDC's Reeve's 'empirical definition' for CFS since 2005 now, they are pushing hard to both expand the numbers (and funding) AND to get it classified under 'mental'.
So desperate CFS patients--who are often MISdiagnosed and actually have a myriad of other things wrong with them, many of which are treatable, like Lyme, thyroid, or 'fatigue' for a variety of reasons--have tried to make their illness sound more serious in an attempt to override Reeves and the WS's attempts. One of the ways they've done this is to latch onto ME. G93.3, and now start saying that ME and CFS belong together and are actually the same thing. - They most certainly are not! - ME, G93.3, is classified under Brain, CNS, Neurology.... It starts with a sudden onset viral event.... - And G's in the WHO vernacular, do not get mixed with R's (different bodily systems!) Read more below. It has all become a humungous MIXED MESS, made easier with the internet now, where large numbers of people can read all sorts of stuff and believe it's the gospel truth, rather than question or verify it:(
It also explains so well why your group--and others--continue to get confusing readings and are have trouble replicating study results. You are all doing studies on mixed patient groups, which always produce MIXED DATA, which really is quite irrelevant and helpful for NO ONE. The only way anyone is going to get pure data is to separate out the ME, G93.3, patients from this mixed nonsense 'ME/CFS' grouping, and study them separately. Then if you wish to compare the ME data with the CFS data, you may well find some interesting DIFFERENCES!
It is beyond time for the world to take ME, G93.3, seriously and stop subsuming it with, or under, 'CFS'. That is both absurd and completely UNscientific. Those presently diagnosed with 'CFS'--which the USA CDC has always classified under zoonotic, vector-borne, and designated as a 'DIAGNOSIS of EXCLUSION' only able to be made after 6 months--need to be better evaluated to determine precisely what it is that they have. -->Get them out of the mix. To read everything that 'CFS' is--and more importantly, ISN'T--as determined by the originators/authors (1988-1994) go to their site: www.cdc.gov/cfs/ ~ Below is: 1) Hyde's statement on the various incubation periods for proposed 'causes', followed by his 2) 'prodomal phase for ME', followed by his 3) newest (2006) ME Definition, which is excellent. And finally, 4) a paper on the many, many things 'CFS' patients are being diagnosed with when evaluated thoroughly and completely.
Please read it all very carefully and pay full attention to the details, as they do matter incredibly, and are much more important than the 'CFS &/or 'ME/CFS' proponents seem to realize:( Thank You, LaVonne K Woodruff, USA
I am a ME-defined patient who's done serious illness advocacy for 6+ years now. I got hit by ME 11 years ago (Feb 17th, 1998) and my health and my life as I knew them changed literally overnight, within a 12 hour period.
Hyde on incubation periods
By 1986 HHV6 was already known to have an incubation period of 9 days due to human experimentation when the actual virus was injected into several children. See (Gorbac, Second Edition, Infectious Diseases, page 1335). When acquired by random infection, the incubation period of HHV6 Roseola was more like 12 days. So once again anyone with access to a library or a computer would have soon dispelled any view that HHV6 was a cause of M.E. epidemics where the incubation was approximately 7 days or less. Is it possible that Steven Strauss and the other intelligentsia of the National Institute of Health (NIH) in Bethesda and CDC in Atlanta and elsewhere didn't have access to libraries and the Internet? Maybe we should start a public request to ask for donations for them. Dr Hyde M.D.
Associating the Lake Tahoe epidemic with Epstein Barr Syndrome was frankly ridiculous and you will see why almost immediately. Anyone who realizes that infectious mononucleosis is caused by the herpes family virus, Epstein Barr Virus (EBV), and that the incubation period of this illness is approximately 40 days, should have realized that you simply cannot have a rapidly spreading viral epidemic with a virus with a latent period of 40 days. Neither Dr Straus nor Dr Holmes, senior government physicians, should have fallen into such a trap. They only had to go to the excellent CDC library to realize that rather than spending half a million dollars or so on a publication that they should have known would not have incriminated EBV. Yet this epidemic somehow spread the myth that this illness was caused by EBV.
Such is the perseverance of error. - Dr Hyde M.D.
"[The] prodromal phase of ME, G93.3 is associated with a short onset or triggering illness.
This onset illness usually takes the form of either, or any combination, of the following (a) an upper respiratory illness, (b) a gastrointestinal upset, (c) vertigo and (d) a moderate to severe meningitic type headache. The usual incubation period of the triggering illness is 4-7 days. The second and third phases of the illness are usually always different in nature from the onset illness and usually become apparent within 1-4 weeks after the onset of the infectious triggering illness Hyde (1998 [Online])."
NOTE: highlights and underlines are mine. LKW http://www.nightingale.ca/documents/NightingalesDefinitionofME.pdf
The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)
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
(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
(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.
(d) If you are still not convinced, check the Internet for the Diagnostic and
Statistical Manual of Mental Disorder definition of: DSMIII Somatization
Disorder. You will find that there is little substantial difference to distinguish
the DSMIII definition from the 1988 and 1994 CDC definitions of CFS. It is
difficult to believe that the CDC medical bureaucracy is not aware of this
similarity. It is thus understandable why the insurance industry, as well as
some psychiatrists and physicians, have simply concluded that CFS is
somatization disorder. ~
I believe it essential to define clearly Myalgic Encephalomyelitis, G93.3. That is what the Nightingale definition of M.E. sets out to do. The definition is based upon two criteria:
(a) The excellent scientific work of respected physicians and scientists who
investigated the various M.E. epidemics
(b) Our Foundation's modern scientific testing techniques and the
knowledge resulting from examining thousands of M.E. patients using these techniques.
The proposed M.E. definition is designed to improve early diagnosis and
treatment for the 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.
What follows is the primary M.E. definition for adults.
The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)
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 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
As with any illness, the diagnostic criteria of M.E. are divided into two
(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
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 such as: (a) repetitive contact with a large number of infectious persons,
(b) unusually long hours of exhausting physical and / or intellectual work, (c) physical traumas, (d) immediate past immunizations, (e) epidemic disease cases whose onset and periodicity appear to occur cyclically in a susceptible population, (f) the effect of travel, as in exposure to a new subset of virulent infections, or (g) the effects of starvation diets. (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 agents. 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 Phase: The first phase is an epidemic or endemic
infectious disease generally with an incubation period of three to seven
days; in most, but not all cases, an infection or infectious process
(See B. Hyde and A Jain, Clinical and Scientific Basis of M.E./CFS,
Chapter 13, Nightingale Research Foundation, Ottawa, Canada, pp.
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: (f) fibromyalgia-like pain syndromes. When occurring, these various pain syndromes may include fibromyalgia-like 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. (See Clinical and Scientific Basis of M.E./CFS, Chapter 5, pp. 58-62)
Testable and 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: If the patient's illness is
not measurable using a dedicated brain SPECT scan such as a Picker
3000 or equivalent, then the patient does not have M.E. 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 Injury
Type 1: One side of the cortex is involved. Those patients labeled as 1A
have the best chance of recovery.
Type 2: Both sides of the cortex are involved. These patients have the least
chance of spontaneous recovery.
Type 3: Both sides of the cortex, and either one or all of the following:
posterior chamber organs, (the pons and cerebellum), limbic system, the
sub-cortical 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 injury
Type A: Anatomical integrity is largely maintained in the Brain SPECT scan.
Type B: Anatomical integrity is not visible in the CNS SPECT scan. Type 3B
are some of the most severely and chronically injured patients.
6. Testable Neuropsychological Changes: There are neuropsychological
changes that are measurable and demonstrate short-term memory loss,
cognitive dysfunctions, increased irritability, confusion, and perceptual
difficulties. There is usually rapid decrease in these functions after any
physical or mental activity. Neuropsychological changes must be measured
in relation to estimates of prior achievement. This feature may improve over
a period of years in patients with adequate financial and social support and
can be made worse by chronic stressors. The neurophysiological changes
are those observed by a qualified neuropsychologist with experience in
examining this type of disease spectrum. (See S. Bastien in Clinical and
Scientific Basis of M.E. / CFS, Chapter 51, pp. 453-460.)
7. Testable Major Sleep Dysfunction: This can include all forms of sleep
dysfunction. All or any of the following may be present: (a) impaired sleep efficiency, (b) significant fragmented sleep architecture, (c) movement arousals if there is an associated pain syndrome, (d) absence of type 3 and 4 sleep, (e) abnormal REM sleep pattern (f) changes in daytime alertness and (g) sleep reversals.
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. Few centres are equipped or funded to make these
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. 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. 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.
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.
c. Raynaud's Disease: vasoconstriction, blanching, coldness and pain of
extremities. This is in part the cause for temperature dysfunctions seen in
d. Circulating Blood Volume Decrease: this is a nuclear medicine test in
which the circulating red blood cell levels 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. Note: Body servomechanisms are genetically designed so
that blood flow and oxygen to the heart are always protected. Thus blood
flow to organs not necessary for short-term survival, such as the brain, the
gut and 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.
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 an infectious switch is turned on, usually in late teens to early thirties. 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, (iii) touch the floor readily with the full palm should be considered suspect for further examination. See S.I. Magalini, S.C. Magalini, Dictionary of Medical Syndromes, pp. 251-252, Lippincott-Raven Publishers, Philadelphia, 4th Edition, 1997.
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 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. 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
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 treat the
(i) genetic forms of vasculitis and 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 demonstrated when we do the "nuclear medicine circulating blood volume tests. It is important to do this test on all patients. POTS is poorly treatable and more often success in treatment presently escapes physicians' ability. Eventually, I have no doubt that these will be treatable causes of M.E. 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; 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 will allow the patient to return to normal range of activities (e.g. school, career, etc).
10. Testable Endocrine Dysfunction: This feature is common and tends to
be a late appearance. It is 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 can be followed by ultrasound of the thyroid gland, where
a steady shrinking of the thyroid gland may occur in some 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 to 23 cc.
volume in male patients to below a volume of 6 cc. (Mayo Clinic averages).
Serum analysis of M.E. patients for thyroid pathology is simply not
adequate. Repeat thyroid ultrasound must be performed for all M.E. patients
to ascertain 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.
The following changes, while uncommon, may also be related to an M.E.
b. Pituitary-Adrenal Axis Changes: where changes and findings are
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 an 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 articularly if the
cause of the individual disease is an enterovirus. Dr. John Richardson also
associated this finding with adrenal dysfunction that he measured.
To various degrees 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
who assisted in much of his later work), 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.
In varying degrees all of the following physicians have also noted the above
historical and the more recent investigational findings. They include
alphabetically, Doctors Peter Behan, David Bell, Dedra Buchwald, Paul
Cheney, Jay Goldstein, Seymour Grufferman, Anthony L Komaroff, Russell
Lane, Ismael Mena, Harvey Moldofsky, James Mowbray, Daniel Peterson,
Vance Spence and scores of others.
I have examined patients with M.E. since the late 1970s but only at the
urging of Dr. Charles Poser of Beth Israel Hospital at Harvard and John
Richardson in Newcastleupon- Tyne did I take up the study of these
unfortunate patients on a full time basis. The material in this definition is the cumulative result of my listening and interpreting the work of all of
the above clinicians and my evaluation of over 3,000 M.E. and CFS patients since 1984. The essential concept of the indepth medical evaluation that is the
basis of my work on M.E. and CFS since 1995 was crystallized in my
discussions in Seattle Washington State in 2002 with Dr. Leonard A. Jason,
Patricia A. Fennell and Renee R. Taylor. This discussion was set down as
Chapter 3, "The Complexities of Diagnosis", in their book, The Handbook of
Chronic Fatigue Syndrome, John Wiley and Sons, Hoboken, New Jersey,
2003. I would also like to thank Elizabeth Dowsett and Jane Colby whose
work with children in the UK as well as their advice have been instrumental
in this definition. I must also thank each and every one of the members of
John Richardson's Newcastle Research Group who have provided me with
so much valuable information over the years and who have all supported my
continued investigations of M.E. patients.
What is new and different about the Nightingale M.E. definition?
A: A Testable Definition
The definition is set out in both a clinical diagnostic and scientifically
testable fashion. This will allow the physician both an early diagnostic
bedside or office understanding of the 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 the 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) diagnosed and treated immediately following onset. The Nightingale Definition assists the physician in diagnosis and early treatment.
B: A Vascular Pathophysiology
The subject of vascular pathology is not new. The fact of the children dying of
a Parkinsonian-like vascular injury to the basal ganglia in Iceland during the
Akureyri Epidemic is an obvious indication of the CNS vascular effects.
Vasculitis has been well documented by Dr. E. Ryll in his description of the
epidemic in the San Juan Mercy, Sacramento California Hospital in 1975.
He described this M.E. epidemic as an epidemic vasculitis. In the late
1980s Drs. Jay Goldstein and Ismael Mena confirmed and proved this initial
description by examining the changed brain microcirculation using brain
SPECT imaging in M.E. patients. Following my over twenty years of
examining M.E. and CFS patients and sixteen years of subjecting the M.E.
and CFS patients to brain imaging techniques suggested by Goldstein and
Mena, it has become obvious to me that we are dealing with both a
vasculitis and a change in vascular physiology.
Numerous other physicians have supported this finding. Dr. David Bell, who
rediscovered the work of Dr. David Streeten and his book, Orthostatic
Disorders of the Circulation: Mechanisms, Manifestations and Treatment,
New York: Plenum Medical, 1986, advanced this understanding of M.E. The
work of Dr. Vance Spence and his colleagues in Scotland have started to
nail this CNS-vascular relationship down even further with a series of major
research papers. The recent interpretation of the cause of Multiple Sclerosis
(MS) as an injury of the microvasculization causing the injury of the schwann
cells that in turn causes the demyelination injuries of MS has been added to
that of paralytic poliomyelitis as an essential vascular injury. - Paralytic poliomyelitis was thought to be a primary injury to the anterior horn cells of the spinal cord but is now recognized as a vasculitis injuring the circulation to the anterior horn cells. Poliomyelitis is generally a non-progressive,
specific site injury, although post-polio syndrome has challenged that belief.
MS is a recurrent more fulminant physiological vascular injury.
M.E. appears to be in this same family of diseases as paralytic polio and
MS. M.E. is definitely less fulminant than MS but more generalized. M.E. is less fulminant but more generalized than poliomyelitis. This relationship of M.E.-like illness to poliomyelitis is not new and is of course the reason that Alexander Gilliam, in his analysis of the Los Angeles County General Hospital M.E. epidemic in 1934, called M.E. atypical poliomyelitis.
C: The Lack of Mention of Fatigue
Myalgic Encephalomyelitis is not CFS. Fatigue was never a major
diagnostic criterion of Myalgic Encephalomyelitis. Fatigue, loss of stamina,
failure to recover rapidly following exposure to normal physical or
intellectual stressors occur in most if not all progressive terminal diseases and in a very large number of chronic non-progressive or slowly progressive diseases.
Fatigue and loss of stamina are simply indications that there is something
wrong. They cannot be seriously measured, are generally subjective and do
not assist us with the diagnosis of Myalgic Encephalomyelitis or CFS or for
that matter any disease process.
D: Cause of Myalgic Encephalomyelitis
It is obvious that all cases of epidemic M.E. and all primary M.E. are
secondary to infectious / autoimmune phenomena. Many M.E. and M.E.-like patients' illness is complicated by multiple other causes. This is why
a complete technological investigation has to be made on each chronically ill
M.E. or M.E.-like patient. Under epidemic and primary M.E. there is no consensus as to the viral or infectious cause. Much of this lack of consensus may be due to the non-separation of acute onset from gradual onset patients in the M.E. and CFS groups of patients. Primary M.E. is always an acute onset illness. Doctors A. Gilliam, A. Melvin Ramsay and Elizabeth Dowsett, John Richardson of Newcastle-upon-Tyne, W.H. Lyle, Elizabeth Bell of Ruckhill Hospital, James Mowbray of St Mary's and Peter Behan all believed that the majority of primary M.E. patients fell ill following exposure to an enterovirus (Poliovirus, ECHO, Coxsackie and the numbered viruses are the significant viruses in this group).
I share this belief. Unfortunately, it is very difficult to recover polio and
enteroviruses from live patients. Dr. James Mowbray developed a test that
demonstrated enterovirus infection in many M.E. patients but I do not believe
he qualified his patients by acute or gradual onset type of illness.
In my tests in Ruckhill Hospital in Glasgow, I found confirmation of enteroviral infection only in acute onset patients and not in any gradual onset patients. Few physicians realize that almost all cases of poliovirus recovered from
poliomyelitis victims came from cadavers. At the very least, these
enteroviruses must be recovered from patients during their onset illness and
this has rarely been done. An exception is in the case of the
Newton-le-Willows Lancashire epidemic where Dr. W. H. Lyle's
investigation recovered ECHO enterovirus. Recent publications by Dr. J. R. Kerr have also identified the fact that enteroviruses are one of the
most likely causes of M.E. If this belief is correct, many if not most of the
M.E. illnesses could be vanquished by simply adding essential enteroviral genetic material from these enteroviruses to complement polio immunization.
I have not discussed non-infectious M.E.-type disease. Similar M.E.phenomena can occur due to diffuse Central Nervous System injuries from toxic chemical injury. I have seen this in police officers who have
fallen into toxic chemical ponds in pursuit of those suspected of criminal
activity. I have seen it in farmers, in hospital and industrial workers and in
military personnel in contact with toxic chemicals, specifically toxic gases. I plan to explore these in a future publication as Secondary M.E. They do have one thing in common, and that is the diffuse CNS injury as noted on brain SPECT scans. Often these Secondary M.E. diseases are more severe than the Primary M.E. cases.
E: Caution One
One should be careful in applying the diagnostic criteria discussed under
the Nightingale M.E. Definition without also completing a thorough
investigation. M.E., whether we are discussing primary or secondary forms,
involves a significant diffuse injury of the Central Nervous System and an
associated injury of the Immune System. This always implies the potential
for secondary injuries or secondary disease or pathology caused by a
dysfunctional brain and dysfunctional immune system. When the immune
system is injured there is an impairment of the patient's ability to resist the development of malignancy or other important organ and systemic injuries.
Due to funding limitations, we have only been able to demonstrate in our
work only two characteristics of this corollary injury. The first is the high
incidence of thyroid cancer in M.E. patients. In the general public, cancer of
the thyroid occurs in 1 case per 100,000. In our studies, in the case of the
M.E. patient, thyroid cancer has an incidence of 6,000 cases per 100,000.
We have already mentioned the pervasive vascular injuries. We believe that
other pathological associations also occur. Failure to evaluate fully the M.E.
patient may result in the physician missing important secondary pathology
and possibly giving rise to patient death.
All M.E. patients as well as all chronic illness patients deserve a systematic
and total body investigation. No individual should go through life, ill, disabled without knowing why he is ill. Simply offering a label, whether M.E., or CFS, without looking at the pathophysiology, is both unacceptable and potentially dangerous both for the patient and the patient's physician.
(See "The Complexities of Diagnosis" by Byron Hyde, in the Handbook of
Chronic Fatigue Syndrome, Chapter 3)
F: Caution Two
Insurance companies regularly employ reputedly independent psychologists
who demonstrate normal neuropsychological findings. This presents a grave
problem in that neuropsychological testing by a truly independent
neuropsychologist may be delayed for up to a year before the patient can be
properly tested. The conflicting results may tend to confuse any trial judge in
a legal case.
G: Depression, Anti-depressive Medications and Myalgic Encephalomyelitis
Myalgic Encephalomyelitis is not depression. Myalgic Encephalomyelitis is not hysteria. Myalgic Encephalomyelitis is not a conversion disorder nor is it a somatization disorder. Myalgic Encephalomyelitis is an acute onset diffuse injury of the brain. Psychiatrists should not ever be placed in charge of diagnosis and treatment of M.E. patients. It is simply not their area of expertise and their meddling has at times caused great harm to M.E. patients. Also, during the 20 years that I have investigated M.E. patients I have yet to see a single case of real M.E. that has responded to psychiatric pharmacological treatment such that the patient has recovered and been able to return to work or school.
This topic is a very large subject and demands a separate publication and
this is not the place for it. However I would like to note again the vascular
and cardiac pathologies that one encounters in M.E. patients and how M.E.
patients are often made worse by one antidepressive medication that is
considered benign. One of the most common antidepressive medications
employed by psychiatrists and physicians in general for M.E. patients is an
old pharmaceutical, Amitriptyline. Yet this medication may result in a
condition referred to as Torsade de Pointes, a cardiac irregularity giving
rise to resting tachycardia, QT interval prolongation and significant
orthostatic hypotension. Since there is already a high frequency of these
anomalies in M.E. patients, the use of Amitriptyline may assist sleep to
some degree but may also simply worsen existing M.E. symptomology. I plan to return to this subject in another publication.
Definition Changes and Improvements
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 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,
http://www.nightingale.ca 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 - November 18, 2006 ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
CFS is always a MISdiagnosis
Copyright © by Jodi Bassett December 2006 on ahummingbirdsguide.com
This version updated January 2008
The fact that a person qualifies for a diagnosis of Oxford Chronic Fatigue Syndrome (CFS), Fukuda (CDC) CFS, or either of the Australian CFS definitions:
(a) does not mean that the patient has Myalgic Encephalomyelitis (M.E.), and
(b) does not mean that the patient has any other distinct and specific illness named ‘CFS.’
A diagnosis of CFS--based on these or any of the other CFS definitions--can only ever be a MISdiagnosis.
The reason for this is that despite the fact that the new name and definition of CFS were created in a response to an outbreak of what was unmistakably M.E., this new name and definition did not describe the known signs, symptoms, history and pathology of M.E. It described a disease process which did not, and could not exist. (Hooper et al. 2001, [Online]) (Dowsett n.d.a. [Online]) (Hyde 2006, [Online]) As M.E. expert Dr Byron Hyde MD explains:
Do not for one minute believe that CFS is simply another name for Myalgic Encephalomyelitis. It is not.
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. It is:
(a) a partial mix of infectious mononucleosis /glandular fever,
(b) a mix of some of the least important aspects of M.E. and
(c) what amounts to a possibly unintended psychiatric slant to an epidemic and endemic disease process of major importance.
Any disease process that has major criteria, of excluding all other disease processes, is simply not a disease at all; it doesn't exist. The CFS definitions were written in such a manner that CFS becomes like a desert mirage: The closer you approach, the faster it disappears and the more problematic it becomes (2006, [Online]).
As Professor Malcolm Hooper (UK) explains, ‘As a basis for sound scientific research, [CFS] has been a disaster.’ (2001, [Online]) Today there are more than nine different CFS definitions. Just like the original definition of CFS produced in 1988 however, none of these definitions defines any distinct illness, including Myalgic Encephalomyelitis. (Hyde 2006, [Online]) All each of these flawed definitions ‘define’ is a heterogeneous (mixed) population of people with various misdiagnosed psychiatric and miscellaneous non-psychiatric states which have little in common but the symptom of fatigue. (Hooper et al 2001, [Online]) (Dowsett 2001b, [Online])
This is why being diagnosed with any of the definitions of CFS is not a useful or meaningful diagnosis and why a diagnosis of CFS should never be accepted – by doctor or by patient – as an end point of the process of diagnosis."
The creation of the flawed disease category of ‘CFS’ (and the equally flawed government policies that have gone along with it) have had a devastating effect on hundreds of thousands of M.E. sufferers around the world, including young children. These very ill patients are often denied appropriate medical treatment and care, denied appropriate insurance entitlements and other medical benefits and are often accused of malingering by doctors, welfare agencies and the media (and in turn even their own friends and family). M.E. patients are also routinely recommended or forced to participate in inappropriate or harmful psychologically based interventions while basic appropriate medical care is withheld. These harmful interventions (and the lack of basic medical care) have had disastrous and long-term physical effects on many sufferers. In some cases this has resulted in death. (Hooper et al. 2001, [Online]) (Hyde 2003, [Online])
Patients with M.E. are not the only patient group to be negatively affected however. Other patient groups misdiagnosed as CFS are also denied appropriate diagnosis and treatment. They may also be subjected to inappropriate psychological interventions. Doctors, researchers and the general public are also negatively affected in various ways by this subterfuge (As explained previously in Smoke and Mirrors). The only groups which gain from the ‘CFS’ confusion are insurance companies and various other organisations and corporations which have a vested financial interest in how these patients are treated, including the government.
The only way forward for every group involved is that the disease category of ‘CFS’ must be abandoned. (Hooper 2006, [Online]) Each of the patient groups involved must be correctly diagnosed and then treated as appropriate based on legitimate and unbiased science involving the SAME patient group. People with M.E. must be diagnosed and treated for M.E. Patients with depression should be diagnosed and treated for depression. Patients with cancer should be treated for cancer, and so on. Lumping these disparate patient groups together under a vague and meaningless category of ‘fatiguing illnesses’ (or CFS) only hinders each of the patient groups involved in their battle to regain their health. (Dowsett 2001b, [Online]) (Hooper 2006, [Online]) (Hyde 2003, [Online])
What a diagnosis of ‘CFS’ actually means is that the patient has a gradual onset fatigue syndrome which is usually due to a missed major disease. i.e. the patient has:
a. Missed cardiac disease, b. Missed malignancy, c. Missed vascular disease, d. Missed brain lesion either of a vascular or space occupying lesion, e. Missed test positive rheumatologic disease, f. Missed test negative rheumatologic disease, g. Missed endocrine disease, h. Missed physiological disease, i. Missed genetic disease, j. Missed chronic infectious disease, k. Missed pharmacological or immunization induced disease, l. Missed social disease, m. Missed drug use disease or habituation, n. Missed dietary dysfunction diseases, o. Missed psychiatric disease. (Hyde 2006, [Online])
Some of the illnesses commonly misdiagnosed as ‘CFS’ include:
- Various post-viral fatigue states/post-viral fatigue syndromes (eg. following glandular fever/mononucleosis, hepatitis, Ross river virus, Q fever, flu, measles, chickenpox, herpes and many other infections)
- Athlete over-training syndrome
- Multiple chemical sensitivity syndrome (MCSS)
- Multiple sclerosis
- Thyroid illness
- Adrenal insufficiency
- Localised and Metastatic malignancies
- Brain tumours, including astrocytomas, gliomas
- Transverse Myelitis
- Myopathic illnesses including:
- Myasthenia gravis
- Mitochondrial myopathies
- Post-infectious polymyositis
- Vitamin B12 deficiency disorders:
- Pernicious anaemia
- Intentional dietary deprivation
- Intestinal disease associated with or independent of M.E.
- Rheumatoid illness or lupus (SLE)
- Renal or liver disease
- Infectious illnesses including:
- Lyme disease (Borrelia burgdorferi)
- Various psychiatric and social psychiatric states including:
- Anxiety neurosis
- Uncomplicated endogenous or reactive depression
- Clinical depression
- Psychopathic personality disorder
- Post-traumatic stress disorder (PTSD)
- Schizophrenia and other psychiatric disease (Ramsay 1986, [Online]) (Ramsay 1988) (Hyde 1992, p 22) (Dowsett n.d.a. [Online]) (Hooper et al. 2001, [Online]) (Hyde 2003, [Online]) (Hyde 2006, [Online])
This is of course not a comprehensive list. M.E. expert Dr Elizabeth Dowsett explains that, ‘There are actually 30 well documented causes of ‘chronic fatigue.’’ (n.d.a. [Online]) It should also be remembered that although none of the CFS definitions define M.E., the majority of those with M.E. will be given a CFS diagnosis by default (due to the ignorance surrounding M.E., and the confusion with ‘CFS’). Therefore the possibility that a patient misdiagnosed with CFS has authentic Myalgic Encephalomyelitis should also be investigated, along with these myriad other possibilities.
- For details on the symptoms listed in the most commonly used CFS definitions, and the symptoms of many of the illnesses commonly misdiagnosed as CFS (as listed above), see part 2 of this text.
Today patients with all sorts of different illnesses are commonly misdiagnosed as having ‘CFS.’ Under cover of the bogus disease category of CFS, this diverse mix of patients are treated as if they each suffered the exact same specific illness. This is clearly unscientific, and unethical. These patients must be given the opportunity to be diagnosed correctly if they are to have any chance of appropriate treatment or recovery, not given a meaningless ‘CFS’ misdiagnosis. Patients with M.E. need this same opportunity. Treating this diverse and heterogenous patient group as if their illnesses each shared the same symptoms, aetiology, pathology and response to treatment is inappropriate and highly unlikely to benefit the health and wellbeing of any of the patient groups involved. Treating this ‘CFS’ group as if they each shared a specific psychological or behavioural illness is also clearly inappropriate. Aside from representing a heterogenous patient group, many (likely the vast majority) of those with the diagnosis are not mentally ill, and do not suffer from behavioural problems. (This includes of course, those patients with authentic M.E.) (Hooper 2006, [Online]) (Hyde 2006, [Online]) (Hooper et al. 2001, [Online])
For the benefit of all of the patient groups involved, doctors must return to the age-old medical principals of correct diagnosis (a) careful history, (b) detailed physical examination and (c) appropriate investigation. (Hyde 2006, [Online]) As Dr Byron Hyde MD explains:
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. (2006, [Online]) Thirty years ago when a patient presented to a hospital clinic with unexplained fatigue, any medical school physician would have told the students to search for an occult malignancy, cardiac or other organ disease, or chronic infection. The concept that there is an entity called chronic fatigue syndrome has totally altered that essential medical guideline. Patients are now being diagnosed with CFS as though it were a disease. It is not. It is a patchwork of symptoms that could mean anything. (2003, [Online])
Physicians who diagnose ‘CFS’ in any patient experiencing new onset fatigue without looking and testing for the true cause of the symptoms do their patients–and themselves–a great disservice. As Dr Elizabeth Dowsett explains,
"There is no such disease(s) as CFS’ (n.d.a. [Online]) Some of the conditions commonly misdiagnosed as CFS are very well defined and well-known illnesses and very treatable – but only once they have been correctly diagnosed.
Some conditions are also very serious or can even be fatal if not correctly diagnosed and managed, including Myalgic Encephalomyelitis."
Every patient deserves the best possible opportunity for appropriate treatment for their illness, and for recovery. This process must begin with a correct diagnosis if at all possible. A correct diagnosis is half the battle won.
From the article on the Pacific Fatigue Lab group, posted 2/16/2009: "Their results are both profound and disturbing. About
half of the ME/CFS patients they've tested do, in
fact, fail or significantly under perform in the first
single exercise test they cannot generate normal
amounts of energy even when theyre rested.
Its the rest of the patients that are so intriguing,
though. When you give these patients a second
test a day later many of them will fail as well -
and fail spectacularly." -->This is because ME, G93.3, Neurogenic, and 'CFS' patients (R53.82) are being illogically lumped together and studied as a group. -->Separate them apart again, and you will lead the way towards uncovering the etiology and pathophysiology of ME, G93.3, and the many, many MISdiagnoses of 'CFS. LKWoodruff ~ "Cracking the Foundations -
The Pacific Fatigue Lab and
Chronic fatigue Syndrome (ME/CFS)"
Phoenix Rising: An ME/CFS/FM Newsletter (Jan 09) by
Could a small lab in the Central Valley of California
shake the CFS research field with a quake of epic
proportions? Change how the disease is viewed?
How its defined? Legitimize the disease once and
for all? Its possible that given enough resources
the Pacific Fatigue Lab at the University of the
Pacific in Stockton, California may do all of
Run by three exercise physiologists, Dr. Christopher.
Snell (Ph.D), Dr. MarkVan Ness (Ph.D) and Staci
Stevens (M.A.), a former grad student and now a
researcher with chronic fatigue syndrome (ME/CFS),
the lab focuses on a very basic and still very
misunderstood aspect of CFS why patients have so
much trouble with exercise. Actually, that should be 'exertion', as mental and emotional effort also brings a ME patient to their knees. Also, with ME, G93.3, the full effects will be felt most 2-3 days after the exertion, not 24 hours! LKW
Staci Stevens, the founding Executive Director of the
Pacific Fatigue Lab explained. Many researchers look
at ME/CFS patients when theyre at rest- at baseline.
But as any ME/CFS patient knows, the real problems
occur when their systems are under stress due to too
much activity. Were taking a close look the
physiology of CFS patients as they undertake the
most stressful activity of all exercise.
Since oxygen plays a key role in energy production,
exercise physiologists use oxygen consumption
during exercise to tell how much energy a persons
body is capable of producing. Having people pedal a
stationary bicycle until they can pedal no more tells
researchers how much air their lungs can take in
(Ventilation Max) and therefore how much oxygen
they use to produce energy (VO2 Max) at their peak
level of effort. Since oxygen plays a key role in the
energy production process this test effectively tells
researchers how much energy is being produced.
Given the fatigue and post-exertional problems often
noted in ME/CFS one would think aerobic exercise
tests would have played a key role in legitimizing
this disease, but instead theyve given rise to further
skepticism. The ability of many patients to pass
them has added to confusion about a disease
characterized by the word fatigue. How could CFS
patients be so fatigued if theyre able to generate
normal amounts of energy?
A New Approach - The Pacific Fatigue Lab researchers
realized, however, that while researchers may have
been asking the right questions they were asking
them in the wrong way.
Many ME/CFS patients can, after all, get through a
single workout or a single day or single afternoon at
work okay only to crash afterwords.
Until now, though, no ones taken a close look at the
ME/CFS patients ability to produce energy when
theyre in a crash an odd oversight in a disease
whose symptoms are so tied to activity. (Indeed,
study after study is showing that many variables
which test out normal or near normal when ME/CFS
patients are at rest are abnormal when their systems
are put under stress).
With the Pacific Fatigue Lab doing a new exercise
testing regime, two exercise tests two days in a row
and other tests (now known as the Stevens Protocol)
theyve given the post-exertional problems ME/CFS
patients have reported for so many years a chance to
show up and they have.
Their results are both profound and disturbing. About
half of the ME/CFS patients they've tested do, in
fact, fail or significantly under perform in the first
single exercise test they cannot generate normal
amounts of energy even when theyre rested.
Its the rest of the patients that are so intriguing,
though. When you give these patients a second
test a day later many of them will fail as well--
and fail spectacularly.
The amount of impairment the Lab sees can be
astonishing - some patients suffer as much as a
50% drop in their ability to produce energy the next
Ms. Stevens spoke of a twenty-something man
whose next day exercise tests were worse that
those of a normal 85 year old. In a hospital setting
his cardiopulmonary exercise profile would suggest
he had heart failure.
Revolutionary Findings - According to modern
medical science this shouldn't occur. For decades
researchers have shown that human beings, under
virtually all conditions and in a variety of disease
states, can take an exercise test to exhaustion,
recover and return the next day and score the same
the next day.
It doesn't matter if she/he has heart failure or
end-stage kidney disease again and again
researchers have shown that the human body even in
extremely poor health - has an amazing ability to
quickly return to a baseline level of energy. That is
But its not just that chronic fatigue syndrome
(ME/CFS) patients are failing these tests, its also
the unique way they're failing them thats raising
eyebrows. Decades of research have shown if you a
take a female of W age and have her do X amount
of exercise at Y heart rate she will exhibit Z levels of
oxygen consumption. Researchers have believed
these algorithms are set in stone but they're not
holding up in chronic fatigue syndrome (ME/CFS)
patients. That they're not suggests that something
has gone awry in the basic physiological processes
the body uses to produce energy in this disease.
Even after 20 years in the field Staci Stevens
excitement was palpable. The implications of her
findings are profound not just for ME/CFS patients
but for the field of exercise physiology. She said We
are charting waters that have never been charted
before. Its an exciting time to be involved in CFS
The labs findings are so unusual that their peers
sometimes cant believe what theyre hearing. Since
decades of research have indicated theres no need to
do repeat exercise tests, they are simply not done.
Until recently the Pacific Fatigue Lab may be the only
lab in the world that regularly does them. I asked
Staci Stevens how her colleagues across the country
were reacting to this data were they excited? She
said some of them say, Its just not possible, they
think we must have imputed the data wrong but
others are enthralled. She said one colleague on the
east coast whos doing the tests said that after 30
years in the field, Id never seen anything like this.
A Quick Road To Legitimacy? - Their findings
undermine long held beliefs not only about chronic
fatigue syndrome (ME/CFS) but about exercise
physiology as well. Overturning paradigms is not
easy but the Pacific Fatigue Lab has an ace in the
hole in this regard. Many ME/CFS researchers and
patients have looked to the future for technological
breakthroughs that will legitimize the disease once
and for all. The new technologies coming to bear on
ME/CFS are exciting but new technologies take time,
sometimes long periods of time, to be assimilated
Theres nothing new, however, about the technology
the Lab is using; in fact its boringly well established.
The aerobic exercise tests they do form an essential
part of every cardiologists and pulmonologists tool
kit. Once the Pacific Fatigue Labs test results are
replicated and make it into the broader research
community acceptance should come relatively
quickly. In fact if one were to chart the quickest road
to legitimacy for this disease it would very much look
like the path the Pacific Fatigue Lab has embarked
on - charting gross abnormalities in well accepted,
well established tests. If the Pacific Fatigue Labs
findings hold up, the news couldnt be better for
chronic fatigue syndrome (ME/CFS) patients.
Redefining Chronic Fatigue Syndrome (ME/CFS) -
The Pacific Fatigue Labs results should also clarify one
of the key questions concerning the disease:
whether researchers have been mixing apples and
oranges in their studies. For decades researchers
have worried that the diseases vague definition
allows people with different illnesses to participate
in research studies. The most pressing question
concerns whether post-exertional malaise (PEM),
which signifies dramatically worsening symptoms
after physical or mental exertion, uniquely identifies
this disorder or is simply one symptom among
One side, lead by the producers of the Canadian
Consensus Definition of ME/CFS, believes that
post-exertional malaise (PEM) is a hallmark symptom
that reflects unique physiological processes. They
believe that allowing people without this problem to
participate in chronic fatigue syndrome (ME/CFS)
studies may have greatly hampered efforts to
understand this disease.
The other side, exemplified in the Center for Disease
Controls (CDC) empirical definition of 2005, believes
that post-exertional malaise (PEM) is one of many
symptoms present in the disease. They argue that
the most important feature of the disease is
unexplained degrees of unwellness that interfere
significantly with peoples work, personal, social, etc.
activities. They believe some different process is at
The Pacific Fatigue Labs results suggest that the
Canadian Consensus group is correct; during
either the first or second exercise test a large
subset of patients demonstrates significant
physiological abnormalities in their ability to
produce energy. Another subset of patients does
not. The Labs findings suggest that these two
groups should be separated in research studies.
Ms. Stevens could not say, however, how big the PEM
subset is. The Lab has derived most of its data from
three groups of patients research subjects in the
test/ re-test studies, those attempting to get
disability and participants in the Ampligen trials.
Many of the people they screen do exhibit PEM on
the exercise tests but others do not. It will take
statistically rigorous studies to determine how
prevalent the post-exertional malaise group is.
Demonstrating that this subset does exist and can
be differentiated by standard physiological tests
would go a long way toward breaking up the CFS
label, revamping the definition of the disease,
focusing researchers in on key abnormalities, and,
of course, creating a new name.
Answering the subset question would be
tremendously valuable but the Stevens Protocol
could also have an enormous impact on another very
bread and butter issue: disability.
A Comprehensive Disability Evaluation - CDC
studies indicate that the average annual financial
costs of CFS (@$25,000/year) impose an economic
burden that many families cannot sustain for long.
Getting disability can be the difference between
absolute poverty and at least a minimum amount of
financial comfort and medical attention. Without clear
diagnostic or functional tests, however, getting
disability has been a challenge.
To schedule a disability evaluation contact
Staci Stevens at (209) 946-7649 or email:
Chronic fatigue syndrome (ME/CFS) patients dont win
their disability cases because they have ME/CFS,
they win when they can demonstrate they cannot
function well enough to work.
Fortunately, measuring functioning is what the
Pacific Fatigue Lab is all about. The simplicity of
the exercise tests is their grace; patients who
cannot produce sufficient amounts of energy
cannot be expected to function its as simple as
that. Aerobic exercise tests have the added
advantage of a long history; they've been used to
demonstrate disability in heart patients and
others for decades. The Stevens Protocol has the
potential to produce a clarity that has been
strikingly missing in this arena.
The Pacific Fatigue Lab offers perhaps the most
extensive disability evaluation in the country. The
exercise tests dont take long 8-10 minutes with a
slow windup period. and they can have brutal
after-effects but, if successful, they are time well
spent. (The Pacific Fatigue Lab will not allow
severely disabled patients or those with moderate to
high cardiovascular risk to take the tests. If the first
test shows disability the next test is not needed).
Theyre not cheap, but even at $2,000 a pop, they
present a good value for those who can afford it.
(Single exercise tests typically run from $800-$1200
at a hospital. Some insurance companies will
reimburse for the testing though billing insurance is
the responsibility of the client).
The Stevens Protocol 8-12 minute aerobic exercise
tests, resting pulmonary function tests measuring
lung function, bioelectrical impedance exams
measuring hydration, acoustic nasal rhinometry
measuring sympathetic nervous system functioning,
reaction time testing evaluating cognitive processing
time, and a seven page written evaluation. Not every
patient who does the disability evaluation gets a
diagnosis of disabled, but for those who do it can be
The Stevens Protocol has the potential to rewrite the
disability rules for ME/CFS. The CFIDS Association of
America has already asked the Social Security
Administration to take them into account but they're
behind the game; the Fatigue Lab has already
notched its first of several wins in the long term
disability field. In fact, their first win holds a place of
honor in a frame on the wall of their office.
Education - With all the many ramifications of the
Labs work, its the day to day process of educating
students about ME/CFS that may be the most
fulfilling for Staci. She, Dr. VanNess and Dr. Snell all
incorporate their latest findings into their classes;
Here is a normal exercise stress test they say and
here is a CFS patients test.
The students are enthralled and they should be;
they are being exposed to cutting edge data that
the textbooks say shouldnt be happening. Its
exciting to be a young (or old) student on the cusp
of research that has the possibility of overturning
accepted paradigms. Ms. Stevens laughed and said
They love working with CFS patients. Theyre always
asking to see the results on the last patient.
When these students leave the University of the
Pacific theyll be ambassadors for this disease and
spread the word about the unusual findings.
Currently the PFL has four graduate students and a
handful of undergraduates working with them.
They also provide hope for a field that is not
attracting many new faces. In fact, the lack of
young researchers may be the biggest long-term
problem the research field faces. The researchers
that got engaged in the field when it was new and
not subject to so much controversy will be retiring in
the not so distant future. Ms. Stevens lamented the
lack of young faces at the Symposium on Viruses in
CFS in Baltimore in May, 2008.
The chronic fatigue syndrome (ME/CFS) research
world is catching onto the implications of the Pacific
Fatigue Labs work. A repeat exercise study by Ellie
Stein in Canada recently opened and one is
reportedly underway in Europe. Ms. Stevens readily
acknowledged that replicating results has been
difficult in ME/CFS, but shes confident that their
results will hold up. She's done 1,000s of single
cardiopulmonary exercise tests on chronic fatigue
syndrome (ME/CFS) over the years and close to a
hundred with the Stevens Protocol at the Pacific
Whether in Stockton, Stanford, Incline Village or
Ithaca, New York they see the same general
pattern again and again, a unique metabolic
dysfunction that characterizes and objectifies the
most mystifying symptom in the disease, post
(Research, education, treatmentdoes this sound
familiar? Advocates have been asking for the federal
government to produce Centers of Excellence that
combine research, treatment and education. The
Pacific Fatigue Lab is a COE in miniature. )
Opportunity - The Pacific Fatigue Lab is a remarkable
accomplishment; a testament to one grad student's
persistence and a small coterie of advisors and
mentors who made her passion their own. University
affiliated chronic fatigue syndrome facilities are
Aside from the Whittemore-Peterson Neuro-Immune
Institute in Reno, Nevada (which won't open its
doors on the university campus for another two
years) there may be no other University sponsored
Chronic Fatigue Syndrome lab in the country. Special
thanks must go to the Sport Sciences Department
Chair Dr. Christopher Snell and to the University of
the Pacific for having the vision to recognize the
opportunity the Lab presents and backing it despite
of the controversy still surrounding this syndrome. NOTE: There are NO USA research groups for ME, G93.3, even tho the WHO has formally acknowledged it since 1969. LKW
The opportunities the Lab presents for this
disease are staggering. Yet the contrast between
the opportunity present and the resources
available is a little heartbreaking.
The Pacific Fatigue Lab is entirely volunteer run by
three people who are trying to analyze their data,
get grants and publish on their off-time. Somehow,
theyve managed to create a beautiful lab but theyre
still missing key ingredients. Their papers have
mostly been published in less well known journals,
they don't have a website to get the word out, and
they don't have a strong funding base. Indeed the
theme of overworked (and unpaid) researchers trying
to make do on a shoestring is a constant one in the
ME/CFS research community.
I asked Staci Stevens about doing heart rate
variability (HRV) studies. Given their ability to
provide data on how the autonomic nervous system
is functioning which appears to be a key player in the
disease HRV studies seem like a perfect fit for the
She said Id love to do HRV but we don't have the
funding. Staci noted that this doesn't need to be
rocket science. We could go a long way just by
focusing on some simple areas that the research
community has basically ignored One gets the idea
that there are many things the Pacific Fatigue Lab
could do to advance the science of ME/CFS if they
just had a bit more money.
But theres only so much money and so much time in
the day. The Pacific Fatigue Lab has been able to
produce what it has through two private grants from
the CFIDS Association of America and from funds it
gathers from doing its comprehensive disability
studies and firefighter fitness testing on the side.
Currently the Labs researchers are focused on
analyzing the results from the Stanford Montoya
Valcyte study and the data from their latest repeat
exercise study plus a new study, all while they're
teaching full loads.
The Next Level - One wonders what these
researchers could achieve if they had more time and
money to focus on a subject that theyre obviously so
I asked Staci how much money would it take to move
the Lab to next level? She said For sixty thousand
dollars we could hire a Ph.D in exercise physiology
to write grants, run the studies and write up the
data. There are plenty of people who would love to
get a job to do that. Hiring a full time clinical
testing supervisor who could take over the grunt
work of data input would allow them to focus more
on the big picture. Monetarily speaking this is
chicken feed in the medical world; theyre not far at
all from creating a lab that could start turning out
study after study.
Ms. Stevens was reluctant to delve into the thorny
issue of federal financing for CFS research but it was
clear that she felt that whatever semblance of a
spigot that had once been turned on has been
mostly turned off. The loss of the Cooperative
Research Centers at the NIH in 2002 was a severe
blow. The Pacific Fatigue Labs efforts to get an NIH
grant failed. When I asked if the Centers for
Disease Control had shown an interest in her work
she said Interest and funding are two different
matters and they are struggling with funding as well.
One would think that somewhere in a community of
1,000,000 patients a way could be found to assist
them in their work.
Advocacy - When the federal system fails to assist
people in need one must turn to advocates to put
pressure on the government. Ms. Stevens agreed
that advocacy was critical but noted that the
problems with exhaustion chronic fatigue syndrome
(ME/CFS) patients faced made them ill-equipped for
advocacy. Still she noted that when she served on
the federal advisory committee for CFS (CFSAC) they
typically had less than 5 patients show up for the
meetings and they tended to be the same five
patients - not a strong signal to the government to
move on these issues.
Having a University support an ME/CFS
laboratory is a rare thing. In fact, aside
from the Whittemore-Peterson Institute
there doesn't appear to be another
University laboratory devoted to ME/CFS in
the U.S. The University of the Pacific
deserves our heartfelt thanks for their
leadership in this area. Let's help out the
PFL in their work. Please e-mail the people
below and say Thank You!
NOTE: 'ME/CFS' and 'CFS/ME' have no WHO classifications nor ICD Codes. LKW
# Thomas W. Krise, Ph.D., Dean of the
College of the Pacific: email:
# Edith Sparks, Ph.D., Senior Associate
Dean: email: email@example.com
# Jin Gong, Ph.D., Dean of Graduate
Studies: email: firstname.lastname@example.org
The Future - The Pacific Fatigue Lab is creating a
body of work that has the potential to revolutionize
the medical community’s understanding of this
disease. The possibilities are impressive; legitimize
ME/CFS, rewrite the diseases disability rules, create
viable subsets, focus the attention of the research
community on the post-exertional period to
determine how this disease is defined and guide
both non-pharmacological and pharmacological
treatment to improve quality of life for patients.
How well it will be able to achieve these goals will in
good part depend on the resources it has and how
well it can get the word out about its findings.
Indeed the Lab is still mostly a secret in the ME/CFS
community. Ms. Stevens said that as theyve been
accumulating data and analyzing it that Weve been
kind of underground but she also felt it was about
time for them to come out. Chronic fatigue
syndrome (ME/CFS) patients can only hope they
come out in a big way indeed.
Pacific Fatigue Lab at the University of the Pacific:
3601 Pacific Avenue, Stockton, CA 95211; (209)
946-7649. email: email@example.com
Contribute to the Pacific Fatigue Lab through the
Workwell Foundation; a non-profit foundation created
by Staci Stevens to advance research into chronic
fatigue syndrome (ME/CFS). Phone: (209)599-7194.
NOTE: That would be 'CFS' (R53.82), to-date. LKW