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Dr. Byron Hyde
describes M.E./CFS
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"Where M.E. and
CFS overlap, they undoubtedly represent the same illness, however,
due to the considerable definitional and conceptual differences,
CFS and M.E. should not be considered the same illness."
-Dr.
Byron Hyde-
Dr. Byron Hyde, founder of the
Nightingale Research
Foundation, Ottawa, Canada, has written some of the most
insightful articles on the clear distinctions between
historically described M.E. and the current CFS definitions.
He has also been vocal in criticizing the methods, creation of,
and flaws in the CDC CFS definitions (see sidebar).
Excerpts
from:
The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)
"...what this
definition does today is (a) separate clearly M.E. from CFS and (b) demonstrate that M.E.
is an early diagnosable and provable disease - as are all true
diseases, and (c) assist in the early treatment and cure of M.E.
patients."
-Dr. Byron Hyde-
Primary
M.E. is an acute onset biphasic infectious disease process, where
there is always a measurable and persistent diffuse vascular
injury of the Central Nervous System in both the acute and chronic
phases. Primary M.E. is associated with immune and other
pathologies.
Primary M.E.
is a chronic disabling, acute onset biphasic epidemic or endemic
infectious disease
process affecting both children and adults. There are both central
and peripheral aspects to this illness.
A:
The Central Nervous System (CNS) symptoms, as well as the clinical
and technological abnormalities, are caused by a diffuse and
measurable injury to the vascular system of the Central Nervous
System. These changes in the organization of the CNS are caused by
a combined infectious and immunological injury and their resulting
effect on CNS metabolism and control mechanisms. Much of the
variability observed in an M.E. patient’s illness is due to the
degree and extent of the CNS injury and the ability of the patient
to recover from these injuries.
B: A
significant number of the initial and long-term peripheral or body
symptoms, as well as clinical and technological body abnormalities
in the M.E. patient, are caused by variable changes in the
peripheral and CNS vascular system. The vascular system is perhaps
the largest of the body’s organs and both its normal and
pathological functions are in direct relationship to CNS and
peripheral vascular health or injury, to CNS control mechanisms
and to the difficulty of the peripheral vascular system and organs
to respond to CNS neuro-endocrine and other chemical and
neurological stimuli in a predictable homeostatic fashion.
C: When pain syndromes associated with M.E. occur, they are
due to a combined injury of (i) the posterior spinal cord and / or
posterior root ganglia and appendages, (ii) patho-physiological
peripheral vascular changes, and (iii) CNS pain reception
homeostasis mechanisms.
Depending
upon the degree and extent of the ongoing CNS and peripheral
vascular injuries, these patho-physiological changes in turn may
give rise to both transient and in many cases permanent systemic
organ changes in the patient.
As with any
illness, the diagnostic criteria of M.E. are divided into two
sections:
(a) The
clinical features and history of the ill patient that alert the
physician to the initial diagnosis
(b) The
technological examinations that confirm to the physician proof of
the diagnosis.
Clinical
Features
The clinical
features of Myalgic Encephalomyelitis are consistent with the
following characteristics that can easily be documented by the
physician.
1. M.E.
is an acute onset biphasic epidemic or endemic infectious disease:
Both
Epidemic and Non-Epidemic cases are often preceded by a series of
repeated minor infections in a previously well patient that would
suggest either a vulnerable immune system, or an immune system
subject to overwhelming stressors.... [see details about the types
of immune stressors in the complete version of
The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)]
2.
Primary Infection Phase: The first phase is an epidemic or
endemic (sporadic) infectious disease generally with an incubation
period of 4 to 7 days; in most, but not all cases, an infection or
infectious process is evident.
3.
Secondary Chronic Phase: The second and chronic phase follows
closely on the first phase, usually within two to seven days; it
is characterized by a measurable diffuse change in the function of
the Central Nervous System. This second phase is the persisting
disease that most characterizes M.E.
4. The
Presence or Absence of Various Pain Syndromes is highly variable:
The pain syndromes associated with the acute and chronic phases of
M.E. may be described as Early and Late findings. Early Findings:
(a) severe headaches of a type never previously experienced; (b)
these are often associated with neck rigidity and occipital pain;
(c) retro-orbital eye pain; (d) migratory muscle and arthralgia
pain; (e) cutaneous hypersensitivity. Late Findings: Any of the
early finding plus (f) fibromyalgia-like pain syndromes. This is
only a partial list of the multiple pain syndromes. Many
of the pain features tend to decrease over time but can be
activated or increased by a wide range of external and chemical
stressors.
Testable &
Non-testable Criteria
The
technological tests listed below can be used to (a) confirm the
clinical diagnosis of Myalgic Encephalomyelitis and (b) to some
degree gauge its severity and probability of persistence. The
second and chronic phase that clearly defines M.E. is
characterized by various measurable and clinical dysfunctions of
the cortical and/or sub-cortical brain structures.
5.
Diffuse Brain Injury Observed on Brain SPECT: [see
details about the types and degrees of brain injury in the
complete version of
The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)]
6.
Testable Neuropsychological Changes: There are
neuropsychological changes that are measurable and demonstrate
short-term memory loss, cognitive dysfunctions, increased
irritability, confusion, and perceptual difficulties. There is
usually rapid decrease in these functions after any physical or
mental activity. [see details about the types of
neuropsychological changes in the complete version of
The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)]
7.
Testable Major Sleep Dysfunction: This can include all forms
of sleep dysfunction. [see details about specific types of sleep
dysfunction in the complete version of
The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)]
8.
Testable Muscle Dysfunction: This feature may be due to
vascular dysfunction or peripheral nervous or spinal dysfunction
and includes both pain and rapid loss of strength of muscle
function after moderate physical or mental activity. This feature
tends to improve over a period of years but many patients
frequently remain permanently vulnerable to new disease episodes.
Unfortunately only a few major medical centres are equipped to
study this type of dysfunction.
9.
Testable Vascular Dysfunction: This is the most obvious set of
dysfunctions when looked for and is probably the cause behind a
significant number of the above complaints. All moderate to severe
M.E. patients have one or more and at times multiple of the
following vascular dysfunctions. As noted, the primary
vascular change is seen in abnormal SPECT scans and clinically
most evident in patients with:
a. POTS:
severe postural orthostatic tachycardia syndrome. [More
details]
b. Cardiac Irregularity: on minor positional changes or
after minor physical activity, including inability of the heart to
increase or decrease in speed and pump volume in response to
increase or decrease in physical activity. [More
details]
c. Raynaud’s Phenomenon [More
details]
d. Circulating Blood Volume Decrease: this is a nuclear
medicine test in which the circulating red blood cell levels in
some M.E. patients can
fall to below 50%, preventing adequate oxygenation to the brain,
gut and muscles. This is undoubtedly a subcortical dysregulation.
It is associated with serum and total blood volume measurements.
This is a concept that many physicians have difficulty
understanding.[More
details]
e. Bowel Dysfunction: vascular dysfunction may be the most
significant causal basis of the multiple bowel dysfunctions
occurring in M.E. (See d. above.)
f. Ehlers-Danlos Syndromes Group
[More
details]
g. Persantine Effect in M.E. Patients
[More
details]
h. M.E. Associated Clotting Defects
[More
details]
i. Anti-smooth muscle Antibodies [More
details]
j. Cardiac Dysfunction: There are a large number
of cardiac dysfunctions that can regularly appear in an M.E.
patient. Without a clear understanding of these
significant problem areas it is simply
indefensible and potentially dangerous to place and unsuspecting
patient in a graduated exercise program. [More
details]
[More
in-depth details about the testable vascular dysfunction in #9
above can be found
in the complete version of
The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)]
10.
Testable Endocrine Dysfunction: These features are common and
tend to be of late appearance. It is most obvious in:
a.
Pituitary-Thyroid Axis [More
details]
The following changes, while uncommon, may also be related to
an M.E.disease process:
b. Pituitary-Adrenal Axis Changes:
where changes and findings
are infrequent.
c. Pituitary-Ovarian Axis Changes
d. Bladder Dysfunction Changes
[More
details]
[More details about testable endocrine dysfunction
in #10 can be
found in the complete version of
The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)]
[Further
discussion on the foundations and implementation of this
definition, as well as updated additions follow this list of
criteria in the complete version of
The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)
Treatment recommendations are also addressed in the Discussion
section. References included.]
As with all
definitions, the Nightingale Research Foundation’s Definition of
Myalgic Encephalomyelitis will have to be looked at by many
clinicians and researchers and increasingly knowledgeable patients over the years, disagreed about,
changed and improved upon. But what this definition does today is
(a) separate clearly M.E. from CFS and (b) demonstrate that M.E.
is an early diagnosable and provable disease - as are all true
diseases, and (c) assist in the early treatment and cure of M.E.
patients.
This
Nightingale Research Foundation’s Definition will be available
with any updates or corrections, on the Nightingale Research
Foundation’s Website,
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 -
January 29, 2007
Excerpts
from:
Are Myalgic Encephalomyelitis and Chronic Fatigue Syndrome
Synonymous Terms?
by Dr.
Byron Hyde
On
differentiating ME and CFS: "At the 1998 M.E. /CFS
conference in Australia, both Myalgic Encephalomyelitis and
Chronic Fatigue Syndrome were used to describe a chronic illness.
This paper is a discussion on the similarities and differences in
these two terms that may lead to scientific difficulties. The
author suggests that the definitional criteria and epidemic
history of Myalgic Encephalomyelitis (M.E.) and the inclusion
criteria are significantly different from the
CDC definitions and
history. The three typical phases of M.E. are discussed. A
brief review of some of the known deaths in phase 2 of M.E. are
also mentioned."
On ME/CFS deaths: [Found in the
section of this essay on phases of the illness, described as #1: prodromal
phase; #2: Principal Illness, and #3: chronic phase]. Of
note in phase 2, "Very infrequent deaths have been known to occur
in this phase and usually are represented by two different pathophysiologies. Dr. John Richardson of Newcastle upon
Tyne, U.K. has noted deaths in professional athletes who return to
active professional sports, 'to work off the flu'. Cause of death
has been attributed to orthostatic cardiac irregularity. It is
also during this phase that CNS deaths occurred in the Cumberland
Epidemic, in the Akureyri epidemic, and in one of the
Mediterranean epidemics." [Editor's note: Although this
paper was written in 1998, current research and two recently
publicized ME/CFS deaths in 2005 in the US and UK support these
historic observations. The
young U.S. man's autopsy showed extensive inflammation and
viral damage to his heart; the
young U.K. woman's
autopsy showed extensive inflammation to her spinal cord.
See the News page to read brief reports
of these deaths and link to more information.]
More on the similarities and differences
between ME and CFS: "Where M.E. and CFS overlap, they
undoubtedly represent the same illness, however, due to the
considerable definitional and conceptional differences, CFS and
M.E. should not be considered to be the same illness. In phase #3,
the M.E. patient is always prone to unusual and persisting muscle
and CNS fatigability after relatively normal physical or
intellectual exertion. The patients are not chronically fatigued.
When unstressed physically, intellectually or emotionally, the
M.E. patient appears totally normal and often has no difficulty
doing very short-term tasks. The problem is above all, one of
endurance and once exhausted, the increasingly lengthy time to
recover to a reasonable degree of activity."
Dr. Hyde also analyzes historic M.E.
epidemics: "There appears to be a high prevalence of
epidemics or clusters in schools, hospitals and institutions
involving hospital staff. Teachers, residential students or
students engaged in team sports or orchestras traveling in groups
appear more affected. British and previous Australian researchers
have been historically more interested in the enterovirus
association. Enterovirus infections have an incubation period
identical to incubation periods noted in most of the M.E.
epidemics, that is, of 4-6 days. Documented deaths have occurred
in several M.E. epidemics, but are best documented in the
Cumberland epidemic and were well known in the Akureyri epidemic.
All of these deaths involved CNS injury. The Akureyri
epidemic involved at least 7 prepubertal children in Friedrikshavn
who developed M.E. followed by Parkinson-like illness and died.
Documented deaths in sporadic cases of M.E. are known, but it is
my experience that treating physicians often become vitriolic when
the deaths are attributed to M.E by the families of the deceased.
M.E. and CFS may be the only illnesses in history from which some
physicians believe the patient is invulnerable to death."
"Important
Differences That Distinguish M.E. from CFS"
"This M.E.
definition is important in that unlike the CDC definitions of
Chronic Fatigue Syndrome, the Wallace and Ramsay definitions of
M.E. observes the importance the initial acute variable infectious
type illness associated with subnormal temperatures. They then
note the important secondary and resulting chronic illness
characterized by CNS and the autonomic nervous system features and
intellectual and muscle dysfunctions and their chronic
persistence. Enlarged cervical lymph nodes and pharyngitis are
almost never observed in the chronic phases of M.E. and yet by
definition, they form part of the characteristic findings in CFS.
M.E. is also distinguished from CFS in that multiple organ
involvement, seizure activity, death, and autonomic nervous system
dysfunction occur in M.E. and by definition, these simply do not
occur in CFS. Perhaps the most important difference is that
chronic fatigue, by definition occurs in 100% of CFS patients. In
M.E. chronic fatigue is not an essential factor, but rapid CNS and
muscular fatigability with a pathologically slow recovery or loss
of stamina is an essential finding. In M.E., the illness, the
disease process, its investigation and pathology starts on the day
the patient ceases to be well. In CFS, the Atlanta based CDC has
decreed that the disease process starts only on the first day of
the sixth month.
Having stated this, after having examined more than 2,000 chronic
CFS patients, I have almost never found, (1) enlarged cervical
glands, (2) obvious pharyngitis, or (3) elevated temperature. Why
is this? It is my belief that the initial CDC definition, was
created by a group of well meaning researchers and physicians who,
with two or three exceptions, had for all purposes never routinely
seen or examined CFS patients. Further, it is my opinion, that
this group of well meaning individuals, were initially so
complicit in believing that EBV was the cause of CFS, that they
simply incorporated diagnostic features of infectious
mononucleosis (glandular fever) into the CDC, CFS definition. It
is a telling fact, that with the exception of two, perhaps three,
of the original sixteen authors of the CDC definition, the
majority have never again published on CFS or ever routinely seen
and examined any CFS patients. It is also important to note that
three of the physicians, who had the longest experience with M.E./CFS patients, withdrew from the initial CDC definitional
committee."
"Conclusions: Definitions are not diseases, they are often
simply the best descriptions that physicians and researchers can
offer, with their always imperfect knowledge, to describe a
disease. Good definitions are good because they correspond closely
to the disease state being described. It is thus important that
those that attempt to define any disease or illness to have long
term clinical experience with patients with this illness.
There is simply no place for the bureaucrat in defining illness.
All definition of epidemic or infectious illness must be based
upon persistent clinical examination of the afflicted patient, an
understanding and exploration of the environmental factors
producing that illness, and pathophysiological examination of
tissue from those patients. For similar reasons, I believe that
the inclusion of psychiatrists in the defining of an epidemic and
obviously disease of infectious origin, simply muddies the water
for any serious understanding of that disease. The UK
definition of CFS was developed by a panel of physicians who were
primarily psychiatrists, with few if any clinicians who had ever
looked at an epidemic of CFS. A serious attempt must be made to
look at epidemic disease as and where that disease starts. This
has not been done by those who have defined CFS in the USA nor in
the United Kingdom and this factor alone is probably the single
greatest reason why we know so little about CFS today that we did
not know in 1984."
[Note: The
bold in this text has been added for emphasis by the editors.]
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 Syndrome
Invest in ME prepared this abridged version of Dr. Hyde's
"little red booklet" he presented at the 2006 IiME Conference.
An excellent brief summary for both doctors and patients.
Of note to
Americans, in
Dr. Hyde's textbook is a compilation of M.E.
epidemics
(Chapter 16). Included in this chapter are some of the
mid-1980s through early-1990s epidemics in the U.S.: Incline
Village, NV; Chapel Hill, NC; Truckee, CA; Lyndonville, NY;
Yerington, NV; Placerville, CA; Sonora, CA; Roseville, CA; Elkgrove, CA. Given Dr. Hyde's clear distinction between M.E.
and CFS, the illness seen in these epidemics clearly was M.E., not
the newly-devised "CFS" of that time.
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