I leave standing one of the opening
quotations of the previous Nederlong, indeed a "quotation" that is
mostly taken from Catch-22, that sums up what I consider to be stark
raving moral and medical incompetence if not medical sadism on the part
of a subset of psychiatrists who seem to have taken over the APA and
the DSM-5, for which see
This serves as a fitting introduction to
the good news, for patients with ME, which is that
there is a new 2011-version of the 2003 so called CCC-criterions
for ME, now internationalized.
2. New CC-criteria: ME: The IC-criteria
3. Some comment on ME: The IC-criteria
Not to have to repeat myself too much, I
will suppose that my readers know what I am talking about and why, and
will repeat some links that give good and full explanations
The first item was compiled by me in
October last year, and consists of links to quite a lot of relevant
material, with my explanations and introductions, or also, if you'd
rather do without them, in a version without them (at the end). It contains
links to the next two:
Criterions were produced by a large group of medical
specialists in 2003, and form the best description of ME by medical
persons in one file that I have seen, and propose a set of criterions
to diagnose ME.
The third item, viz. the Canadian
Criterions Overview, was produced by two
authors of the second item, so as to have a version of it that is
addressed to people who have not studied medicine, and is the best
introduction to ME in one file that I have seen.
Furthermore, the vast majority of
patients with ME that have been able to take the time and trouble to
try to find out about ME using the internet agree that the Canadian
Criterions describe their disease best, and many insist also
that either they have been diagnosed on its basis or else fit the
criterions but haven't been able to find a medical doctor to diagnose
them on its basis.
Since there are millions of patients with
ME, it is worthwhile to remark that there is, to my knowledge, no a
single real patient with ME who testified credibly that he or she has
been helped by psychiatrists, whereas there are many who have testified
that GET and/or CBT, which are the recommended therapies by
psychiatrists and clinical psychologists for what these folks insist
should be called "CFS" or "chronic fatigue", what they insist are forms of neurasthenia =
somatoform disorder = functional somatic syndromes, has
worsened their condition, sometimes a lot. Indeed, psychiatric interventions and
medical, bureaucratic, moral and human incompetence may kill
patients with ME. (*)
2. New CC-criteria:
About the same day that the little
expensive book of horrors, scams and fraudulence called
appeared that I briefly reviewed in More about the DSM-5 and psychiatry
there was accepted for publication in the Journal of Internal
Medicine - not a psychiatric journal, but a journal for
medical doctors who studied real science -
This is the title, and it has no less
than 26 authors, from no less than 13 different
countries, who were 100% agreed on the published paper.
The last link I provided is to a
html-version on the site of the English ME Association, that I will
also partially reproduce below. The next two links are to a pdf-version
and a Phoenix-Rising Forums thread on the subject:
Note that in fact there are TWO name changes:
A: The Canada Consensus
Criteria were reviewed and renamed the
B: The CFS name was reviewed and was
excluded as a diagnosis
for people with ME.
Both changes are quite important in
principle, both medically and morally and legally:
Ad A: Twenty-six authors
from thirteen countries agreed that the revised criteria should
be considered to apply everywhere to patients with the symptoms of ME,
and implicitly oppose thereby all the defamatory and false attributions
by psychiatrists to persons with ME.
This means that patients and patients'
organizations now have a means to oppose being diagnosed as
"somatoformers" by incompetent psychiatrists and health bureaucrats.
One's diagnosis as a patient with ME is in the ICC - and whoever disagrees is probably
incompetent, and certainly needs to do research to make it probable the
patient with ME has none of the marks of ME, before attributing "CFS"
to him or her.
Ad B: What the ICC also implies is that attributing CFS
to a patient who satisfies or may satisfy the ICC
for ME is a medical mistake, a false diagnosis, a sign of
medical negligence or incompetence, that may, and indeed should in many
cases, be sufficient grounds to start court cases for damages and
I have put that in bold because I fear
this will be necessary, preferably in the US, where one can insist on
considerable damages, that I would also like to see imposed on the APA
and the CDC, since these are large institutions with lots of money, who
have been misbehaving around ME/CFS for decades now, causing much pain,
misery and poverty to hundreds of thousands, and giving many cause for
suicide because of the pain, poverty and discrimination instigated by
Now for the text.
I have given links to two full versions of the
International Consensus Criteria for Myalgic Encephalomyelitits, and
now reproduce the text, minus the 26 authors - to whom goes
my heartfelt thanks - from thirteen countries, and minus the
123 notes, though I have left the notes' numbers, but with Table 1
inserted at the place it was meant to be, that both versions I
linked do not.
Of course, my reason to delete the authors and
notes and declarations of interest is to save space in this text.
Also, I have inserted a number of notes by me with the format "
[M1] " etc. that when underlined are links to the sections
with my comments that follows this excerpt from
the full text:
Myalgic Encephalomyelitis: International
Consensus Criteria [M1]
Journal of Internal Medicine, 20 July 2011
The label “chronic fatigue syndrome” (CFS) has
persisted for many years because of lack of knowledge of the
etiological agents and of the disease process. In view of more
recent research and clinical experience that strongly point to
widespread inflammation and multisystemic neuropathology, it is more
appropriate and correct to use the term “myalgic
encephalomyelitis”(ME) because it indicates an underlying
pathophysiology. It is also consistent with the neurological
classification of ME in the World Health Organization’s
International Classification of Diseases (ICD G93.3).
Consequently, an International Consensus Panel consisting of
clinicians, researchers, teaching faculty and an independent patient
advocate was formed with the purpose of developing criteria based on
current knowledge. Thirteen countries and a wide range of
specialties were represented. Collectively, members have
approximately 400 years of both clinical and teaching experience,
authored hundreds of peer reviewed publications, diagnosed or
treated approximately 50,000 ME patients, and several members
coauthored previous criteria. [M4] The expertise and
experience of the panel members as well as PubMed and other medical
sources were utilized in a progression of
suggestions/drafts/reviews/revisions. The authors, free of any
sponsoring organization, achieved 100% consensus through a Delphi
type process. [M5]
The scope of this paper is limited to criteria of ME and
their application. Accordingly, the criteria reflect the complex
symptomatology. Operational notes enhance clarity and specificity by
providing guidance in the expression and interpretation of symptoms.
Clinical and research application guidelines promote optimal
recognition of ME by primary physicians and other health care
providers, improve consistency of diagnoses in adult and paediatric
patients internationally, and facilitate clearer identification of
patients for research studies. [M6]
Myalgic encephalomyelitis (ME), also referred to
in the literature as chronic fatigue syndrome (CFS), is a complex
disease involving profound dysregulation of the central nervous
system (CNS) [1-3] and immune system [4-8], dysfunction of cellular
energy metabolism and ion transport [9-11], and cardiovascular
abnormalities [12-14]. [M7] The underlying
pathophysiology produces measurable abnormalities in physical and
cognitive function and provides a basis for understanding the
symptomology. [M8] Thus, the development of International
Consensus Criteria that incorporate current knowledge should advance
the understanding of ME by health practitioners, and benefit both
the physician and patient in the clinical setting as well as
The problem with broadly inclusive criteria [15,
16] is that they do not select homogeneous sets of patients. The
Centers for Disease Control prevalence estimates increased tenfold
from 0.24% using the Fukuda criteria  to 2.54% using the Reeves
empirical criteria . [M9] Jason et al.  suggest
there are flaws in Reeves’ methodology because it is possible to
meet the empirical criteria for ME without having any physical
symptoms and it does not discriminate ME/CFS patients from those
with Major Depressive Disorder. [M10] Patient sets that
include people who do not have the disease lead to biased research
findings, inappropriate treatments, and waste scarce research funds
Some symptoms of the Fukuda criteria overlap with
depression whereas the Canadian Consensus Criteria  differentiate
ME patients from those who are depressed and identify patients who are
more physically debilitated and have greater physical and cognitive
functional impairments .
International Consensus Criteria
The Canadian Consensus Criteria were used as a
starting point, but significant changes were made. The six-month
waiting period before diagnosis is no longer required. No other
disease criteria require that diagnoses be withheld until after the
patient has suffered with the affliction for six months.
Notwithstanding periods of clinical investigation will vary
and may be prolonged, diagnosis should be made when the clinician is
satisfied that the patient has ME rather than having the diagnosis
restricted by a specified time factor. Early diagnoses may elicit
new insights into the early stages of pathogenesis; prompt treatment
may lessen the severity and impact.
Using “fatigue” as a name of a disease gives it
exclusive emphasis and has been the most confusing and misused
criterion. No other fatiguing disease has “chronic fatigue” attached
to its name – e.g. cancer/chronic fatigue, multiple
sclerosis/chronic fatigue – except ME/CFS.
in other conditions is usually proportional to effort or duration
with a quick recovery, and will recur to the same extent with the
same effort or duration that same or next day. The pathological low
threshold of fatigability of ME described in the following criteria
often occurs with minimal physical or mental exertion, and with
reduced ability to undertake the same activity within the same or
several days. [M15]
The International Consensus Criteria (Table 1) identify
the unique and distinctive characteristic patterns of symptom clusters
of ME. The broad spectrum of symptoms alerts medical practitioners to
areas of pathology and may identify critical symptoms more accurately
[18-20]. Operational notes following each criterion provide guidance in
symptom expression and contextual interpretation. This will assist the
primary clinician in identifying and treating ME patients in the
primary care setting.
(Please insert Table 1 here.)
Table 1 MYALGIC ENCEPHALOMYELITIS:
INTERNATIONAL CONSENSUS CRITERIA Adult and Pediatric ● Clinical
Myalgic encephalomyelitis is an acquired
neurological disease with complex global dysfunctions. [M17]
Pathological dysregulation of the nervous, immune and
endocrine systems, with impaired cellular energy metabolism and
ion transport are prominent features. Although signs and symptoms
are dynamically interactive and causally connected, the criteria
are grouped by regions of pathophysiology to provide general
A patient will meet the criteria for
post-exertional neuroimmune exhaustion (A), at least one symptom
from three neurological impairment categories (B), at least one
symptom from three immune/gastro-intestinal/genitourinary
impairment categories (C), and at least one symptom from energy
metabolism/transport impairments (D).
A. Post-Exertional Neuroimmune Exhaustion (PENE
pen׳-e) Compulsory This cardinal feature is a pathological
inability to produce sufficient energy on demand with prominent
symptoms primarily in the neuroimmune regions. Characteristics
are: 1. Marked, rapid physical and/or cognitive fatigability in
response to exertion, which may be minimal such as activities of
daily living or simple mental tasks, can be debilitating and cause
a relapse. 2. Post-exertional symptom exacerbation: e.g. acute
flu-like symptoms, pain and worsening of other symptoms
3. Post-exertional exhaustion may occur
immediately after activity or be delayed by hours or days.
Recovery period is prolonged, usually taking 24 hours or longer. A
relapse can last days, weeks or longer. 5. Low threshold of
physical and mental fatigability (lack of stamina) results in a
substantial reduction in pre-illness activity level.
Operational Notes: For a diagnosis of ME,
symptom severity must result in a significant reduction of
a patient’s premorbid activity level. Mild (an approximate 50%
reduction in pre-illness activity level), moderate (mostly
housebound), severe (mostly bedridden), or very severe (totally
bedridden and need help with basic functions).
There may be marked fluctuation of symptom severity and hierarchy
from day to day or hour to hour. Consider activity, context and
interactive effects. Recovery time: e.g. Regardless of a patient’s
recovery time from reading for 1⁄2 hour, it will take much longer
to recover from grocery shopping for 1⁄2 hour and even longer if
repeated the next day – if able.
[M21] Those who
rest before an activity or have adjusted their activity level to
their limited energy may have shorter recovery periods than those
who do not pace their activities adequately. Impact: e.g. An
outstanding athlete could have a 50% reduction in his/her
pre-illness activity level and is still more active than
a sedentary person.
B. Neurological Impairments At least One Symptom
from three of the following four symptom categories 1.
Neurocognitive Impairments a. Difficulty processing information:
slowed thought, impaired concentration e.g.
confusion, disorientation, cognitive overload, difficulty with
making decisions, slowed speech, acquired or exertional dyslexia
b. Short-term memory loss: e.g. difficulty remembering what one
wanted to say, what one was saying, retrieving words, recalling
information, poor working memory
a. Headaches: e.g. chronic, generalized
headaches often involve aching of the eyes, behind the eyes or
back of the head that may be associated with cervical muscle
tension; migraine; tension headaches
b. Significant pain can be experienced in
muscles, muscle-tendon junctions, joints, abdomen or chest. It is
non-inflammatory in nature and often migrates. e.g. generalized
hyperalgesia, widespread pain (may meet fibromyalgia criteria),
myofascial or radiating pain [M23]
3. Sleep Disturbance a. Disturbed sleep
patterns: e.g. insomnia, prolonged sleep including naps, sleeping
most of the day and being awake most of the night, frequent
awakenings, awaking much earlier than before illness onset, vivid
dreams/nightmares b. Unrefreshed sleep: e.g. awaken feeling
exhausted regardless of duration of sleep, day-time sleepiness
4. Neurosensory, Perceptual and Motor
Disturbances a. Neurosensory and perceptual: e.g. inability to
focus vision, sensitivity to light, noise, vibration, odour, taste
and touch; impaired depth perception b. Motor: e.g. muscle
weakness, twitching, poor coordination, feeling unsteady on feet,
Notes: Neurocognitive impairments, reported or
observed, become more pronounced with fatigue.
Overload phenomena may be evident when two tasks
are performed simultaneously. Abnormal reaction to light –
fluctuation or reduced accommodation responses of the pupils with
retention of reaction. Sleep disturbances are typically expressed
by prolonged sleep, sometimes extreme,
the acute phase and often evolve into marked sleep reversal in the
chronic stage. Motor disturbances may not be evident in mild or
moderate cases but abnormal tandem gait and positive Romberg
test may be observed in severe cases.
C. Immune, Gastro-intestinal & Genitourinary
Impairments At least One Symptom from three of the following five
1. Flu-like symptoms may be recurrent or chronic
and typically activate or worsen with exertion.
e.g. sore throat, sinusitis, cervical and/or
axillary lymph nodes may enlarge or be tender on palpitation
2. Susceptibility to viral infections with
prolonged recovery periods
3. Gastro-intestinal tract: e.g. nausea,
abdominal pain, bloating, irritable bowel syndrome
4. Genitourinary:e.g.urinary urgency or
Notes: Sore throat, tender lymph nodes, and
flu-like symptoms obviously are not specific to ME but their
activation in reaction to exertion is abnormal. The throat may
feel sore, dry and scratchy. Faucial injection and crimson
crescents may be seen in the tonsillar fossae, which are an
indication of immuneactivation.
D. Energy Production/Transportation Impairments:
At least One Symptom
1. Cardiovascular: e.g. inability to tolerate an
upright position – orthostatic intolerance, neurally mediated
hypotension, postural orthostatic tachycardia syndrome,
palpitations with or without cardiac arrhythmias,
2. Respiratory: e.g. air hunger, laboured
breathing, fatigue of chest wall muscles 3. Loss of thermostatic
stability: e.g. subnormal body temperature, marked diurnal
fluctuations; sweating episodes, recurrent feelings of
feverishness with or without low grade fever, cold extremities
4. Intolerance of extremes of temperature
Notes: Orthostatic intolerance may be delayed by
several minutes. Patients who have orthostatic intolerance may
exhibit mottling of extremities, extreme pallor or Raynaud’s
Phenomenon. In the chronic phase, moons of finger nails may
Symptoms may progress more slowly in children
than in teenagers or adults. In addition to post- exertional
neuroimmune exhaustion, the most prominent symptoms tend to be
neurological: headaches, cognitive impairments, and sleep
disturbances. 1. Headaches: Severe or chronic headaches are often
debilitating. Migraine may be accompanied by a rapid drop in
temperature, shaking, vomiting, diarrhoea and severe weakness.
[M34] 2. Neurocognitive Impairments:
focusing eyes and reading are common. Children may become
dyslexic, which may only be evident when fatigued.
processing of information makes it difficult to follow auditory
instructions or take notes. All cognitive impairments worsen with
physical or mental exertion. [M36] Young people will not
be able to maintain a full school program. 3. Pain may seem
erratic and migrate quickly. Joint hyper-mobility is common.
Notes: Fluctuation and severity hierarchy of
numerous prominent symptoms tend to vary more rapidly and
dramatically than in adults.
Classification ____ Myalgic Encephalomyelitis
____ Atypical Myalgic Encephalomyelitis: meets criteria for
post-exertional neuroimmune exhaustion but has two or less than
required of the remaining criterial symptoms. Pain or sleep
disturbance may be absent in rare cases.
Exclusions: As in all diagnoses, exclusion of
alternate explanatory diagnoses is achieved by the patient’s
history, physical examination, and laboratory/biomarker testing as
indicated. It is possible to have more than one disease but it is
important that each one is identified and treated.
Primary psychiatric disorders, somatoform disorder and substance
abuse are excluded.
Paediatric: ‘primary’ school phobia.
Co-morbid Entities: Fibromyalgia, Myofascial
Pain Syndrome, Temporomandibular Joint Syndrome, Irritable Bowel
Syndrome, Interstitial Cystitis, Raynaud’s Phenomenon, Prolapsed
Mitral Valve, Migraines, Allergies, Multiple Chemical
Sensitivities, Hashimoto’s Thyroiditis, Sicca Syndrome, Reactive
Depression. Migraine and irritable bowel syndrome may precede ME
but then become associated with it. Fibromyalgia overlaps.
Criteria Are Supported by Research
Criterial symptoms are supported by a study of more than
2,500 patients that determined which symptoms had the greatest efficacy
to identify ME patients . Investigations of gene expression [23-27]
and structure further support the criteria at a molecular level
including anomalies of increased oxidative stress [4, 28], altered
immune and adrenergic signalling [29, 30], and altered oestrogen
receptor expression . In addition, evidence supporting a genetic
predisposition to ME points to modifications in serotonin transporter
genes [32, 33], the glucocorticoid receptor gene , as well as HLA
class II involvement . The potential combinatorial effects of these
modifications have received limited attention [36, 37]. Some early
broad based studies show a lack of objective findings such as no
association with HLA genotype . A study of patients from a twin
registry suggested that environmental factors may outweigh any genetic
predisposition in broad based patient populations .
Underlying problems of inconsistent findings in
research studies have been identified [40, 41] and include a need
for studies to be based on larger sample sizes with a more clearly
defined phenotype; in particular one that recognizes the likely
existence of significant subgroups within the patient population.
a study of the Reeves empirical criteria , Jason et al 
reported that thirty-eight percent (38%) of patients diagnosed with
Major Depressive Disorder were misclassified as having CFS and only
ten percent (10%) of patients identified as having CFS actually had
ME. [M40] Accordingly, the primary goal of this consensus
report is to establish a more selective set of clinical criteria
that would identify patients who have neuroimmune exhaustion with a
pathological low-threshold of fatigability and symptom flare in
response to exertion. This will enable like patients to be diagnosed
and enrolled in research studies internationally under a case
definition that is acceptable to physicians and researchers around
A. Post-Exertional Neuroimmune Exhaustion (PENE
“Malaise – a vague feeling of discomfort or
fatigue”  is an inaccurate and inadequate word for the
pathological low-threshold fatigability and post-exertional symptom
flare. Pain and fatigue are crucial bioalarm signals that instruct
patients to modify what they are doing in order to protect the body
and prevent further damage. [M41] Post-exertional
neuroimmune exhaustion is part of the body’s global protection
response and is associated with dysfunction in the regulatory
balance within and between the nervous, immune and endocrine
systems, and cellular metabolism and ion transport [43-47]. The
normal activity/rest cycle, which involves performing an activity,
becoming fatigued, and taking a rest whereby energy is restored,
Numerous papers document abnormal biological
responses to exertion, such as loss of the invigorating effects of
exercise , decreased pain threshold [48-50], decreased cerebral
oxygen and blood volume/flow [51-54], decreased maximum heart rate
, impaired oxygen delivery to muscles , elevated levels of
nitric oxide metabolites , and worsening of other symptoms .
Patients reach the anaerobic threshold and maximal exercise at a
much lower oxygen consumption level . Reported prolonged effects
of exertion include elevated sensory signalling to the brain 
that is interpreted as pain and fatigue , elevated cytokine
activity , delay in symptom activation  and a recovery
period of at least 48 hours . When an exercise test was given on
two consecutive days, some patients experienced up to a 50% drop in
their ability to produce energy on the second evaluation .
[M42] Both submaximal and self-paced physiologically limited
exercise resulted in post-exertional malaise .
B. Neurological Impairments
Some viruses and bacteria can infect immune and neural
cells and cause chronic inflammation. Structural and functional
pathological abnormalities  within the brain and spinal cord suggest
dysregulation of the CNS control system and communication network ,
which play crucial roles in cognitive impairment and neurological
symptoms . Neuroinflammation of the dorsal root ganglia,
gatekeepers of peripheral sensory information traveling to the brain,
has been observed in spinal autopsies. (Chaudhuri A. Royal Society of
Medicine Meeting 2009) Identified cerebrospinal fluid proteomes
distinguish patients from healthy controls and post-treatment Lyme
Neuroimaging studies report irreversible punctuate
lesions , an approximate 10% reduction in gray matter volume [67,
68], hypoperfusion [69-74] and brain stem hypometabolism .
levels of lateral ventricular lactate are consistent with
decreased cortical bloodflow, mitochondrial dysfunction and oxidativestress.
Research suggests that dysregulation of the CNS and autonomic
nervous system alters processing of pain and sensory input [48, 61,
76, 77]. Patients’ perception that simple mental tasks require
substantial effort is supported by brain scan studies that indicate
greater source activity and more regions of the brain are utilized
when processing auditory and spatial cognitive information [78-80].
[M44] Poor attentional capacity and working memory are
prominent disabling symptoms [20, 78, 81].
C. Immune Impairments
Most patients have an acute infectious onset with
flu-like and/or respiratory symptoms.
[M46] A wide range
of infectious agents have been reported in subsets of patients
including Xenotropic murine leukemia virus-related virus (XMRV) 
and other murine leukemia virus (MLV)-related viruses ,
enterovirus [84-86], Epstein Barr virus , human herpes virus 6
and 7 [88-90], Chlamydia , cytomegalovirus , parvovirus B19
 and Coxiella burnetti . Chronic enterovirus infection of
the stomach and altered levels of D Lactic acid producing bacteria
in the gastrointestinal tract have been investigated [85, 94].
Possibly the initial infection damages part of the CNS and immune
system causing profound deregulation and abnormal responses to
infections . Publications describe decreased natural killer cell
signalling and function, abnormal growth factor profiles, decreased
neutrophil respiratory bursts and Th1, with a shift towards a Th2
profile [4-8, 95, 96]. Chronic immune activation , increases in
inflammatory cytokines, pro-inflammatory alleles [4-8, 97-99],
chemokines and T lymphocytes, and dysregulation of the antiviral
riboneuclease L (RNase L) pathway [64, 100-103] may play a role in
causing flu-like symptoms, which aberrantly flare in response to
exertion [5, 95].
D. Energy Production/Transport Impairments
The consistent clinical picture of profound energy
impairment suggests dysregulation of the mitochondria and cellular
energy metabolism and ion transport, and channelopathy [9- 11, 103,
104]. [M47] A biochemical positive feedback cycle called
the ‘NO/ONOO- cycle’ may play a role in maintaining the chronic
nature of ME, the presence of oxidative stress [105-107],
inflammatory cytokine elevation [97-99] and mitochondrial
dysfunction [108-111], and result in reduced blood flow and
vasculopathy [109, 110].
Findings of “small heart” with small left
ventricular chamber and poor cardiac performance in patient subsets
[112, 113] support previous reports of cardiac and left ventricular
dysfunction [114-116], which predispose to orthostatic intolerance
[14, 117]. [M48] Low blood pressure and exaggerated
diurnal variation may be due to abnormal blood pressure regulation
. [M49] Altered control and reduced cortisol
production during and following exercise may be involved.
Orthostatic intolerance is associated with functional impairment and
symptom severity . Measurable vascular abnormalities suggest
that the brain is not receiving sufficient circulating blood volume
in an upright position [12, 117], which is intensified when standing
in one place such as a grocery store check-out line.
Significant reduction in heart rate variability during
sleep is associated with poor sleep quality and suggests a pervasive
state of nocturnal sympathetic hypervigilance .
Application of Criteria
Diagnostic criteria serve two necessary but divergent
functions – the first is diagnosing individuals in a clinical setting
and the second is identifying patient sets for research studies.
A. Clinical Application 1. General
a. Determine whether symptom cluster patterns are
congruent with those expected from dysfunction of an underlying causal
b. Symptoms interact dynamically within a stable cluster
because they share the same deep causal roots. Patients’ contextual
observations are essential in determining the expression of interaction
of symptom patterns and severity of their impact.
c. Symptom severity impact must result in a 50% or
greater reduction of a patient’s premorbid activity level for a
diagnosis of ME. Mild: approximately 50% reduction in activity,
moderate: mostly housebound, severe: mostly bedbound, and very severe:
bedbound and dependent on help for physical functions. [M54]
d. Symptom severity hierarchy should be determined
periodically to help orient and monitor treatment.
e. Criterial subgroups: Post-exertional
neuroimmune exhaustion is the hallmark feature.
may be helpful to subgroup according to which of the other
diagnostic criterial patterns best represent a patient’s cluster of
most severe symptoms: neurological, immune, energy
metabolism/transport, or eclectic (symptoms widely distributed among
f. Separate primary symptoms from secondary symptoms and
aggravators. Distinguish primary symptom complexes formed by a disease
process from secondary effects of coping with the disease, such as
anxiety about finances. Determine the effects and burden of aggravators
and stress enhancers such as fast paced environments and exposure to
g. Determine total illness burden by assessing
symptom severity, interaction and overall impact. Consider all
aspects of the patient’s life – physical, occupational, educational,
social and personal activities of daily living.
Patients who prioritize their activities may be able to do one
important activity by eliminating or severely reducing activities in
other aspects of their life. [M59]
h. The International Symptom Scale should not be part of
the initial clinical interview because it may disturb the weighting and
significance of results obtained for an individual patient. When used
periodically, it can help position the patient within the group, orient
the treatment program and monitor its effectiveness.
2. Paediatric Considerations
a. If possible, interview a young person with both
parents because each may remember different symptoms or
interactive events that may help determine onset and when the illness
began to interfere with daily function.
b. Children cannot be expected to judge pre-illness
function with current function. Assess impact by comparing hobbies,
educational, social and sport activities the child participated in
before illness with present activity level.
c. Children may appear irritable when they are asked to
do something when they feel exhausted. On the other hand, they are
often able to accommodate fatigue by resting, which may be
inappropriately interpreted as being lazy.
d. School Phobia: Young patients spend most of their
out-of-school hours resting whereas children with school phobia will be
socializing and participating in activities. However, it is possible
that school phobia may become a secondary symptom because of bullying
or academic difficulties due to having ME.
e. Natural Course: Children can be very severely
afflicted but those whose symptoms are of mild to moderate severity
generally are more likely to have them go into remission than adults.
Prognosis cannot be predicted with certainty.
B. Research Application
A clinical diagnosis must be confirmed before a patient
can provide useful general knowledge about the disease. The data
obtained from patients allows controlled and meaningful observations
and suggests hypotheses to be tested and confirmed or refuted.
1. General Considerations a. Patients should meet the
full criteria for epidemiological studies. If specific subgroups or atypical ME
are included in a research study, that should be clearly indicated.
b. Specificity: Because critical symptoms are compulsory, it ensures
proper selection of patients. Key operational guidelines enhance
clarity and specificity. Ranking the hierarchy of the most
troublesome symptoms may be helpful in some studies. c.
Symptoms must not be viewed as a nominal checklist. The
International Consensus Criteria focus on symptom patterns, which
increase reliability. [M62] The International Symptom
Scale ensures consistency in the way questions are asked and further
increases reliability of data collected in different locations.
Patients should complete the International Symptom Scale prior to
entering a research study.
2. Optional Considerations
Classifying patients by subgroups to enable comparison
of patients within the diagnosis of ME may be helpful in some studies.
a. Onset: acute infectious or gradual
b. Onset severity may be a good predictor of severity in
the chronic phase. [M63]
c. Symptom severity: mild, moderate, severe, very severe
d. Criterial subgroups: neurological, immune, energy
metabolism/transport, or eclectic
(See clinical application for symptom severity and
The International Consensus Criteria provide a
framework for the diagnosis of ME that is consistent with the
patterns of pathophysiological dysfunction emerging from published
research findings and clinical experience.
patterns interact dynamically because they are causally connected.
This has been formally addressed by some investigators who have used
well-established multivariate statistical techniques, such as common
factor or principal component analyses to identify symptom
constructs [121, 122]. [M65] Others have extended the use
of such methods to guide the analysis of gene expression profiles
 and to delineate patient sub-groups . Consistent with this
approach, the panel is developing an International Consensus Symptom
Scale (ICSS) that will build on these underlying interactions.
However a necessary first step in establishing a quantitative score
for any diagnostic instrument is the specification of measurable
factors that are most relevant to the illness. Establishing such
criteria was the primary objective of this work and we believe the
International Consensus Criteria will help clarify the unique
signature of ME. [M66]
It is important to note that the current emphasis
must primarily remain a clinical assessment, with selection of
research subjects coming later. For this reason the panel is
developing Physicians’ Guidelines, which will include diagnostic
protocol based on the International Consensus Criteria and treatment
guidelines that reflect current knowledge.
Individuals meeting the International Consensus Criteria have
myalgic encephalomyelitis and should be removed from the Reeves
empirical criteria and the National Institute for Clinical
Excellence (NICE) criteria for chronic fatigue syndrome.
These guidelines are designed specifically for use by the
primary care physician in the hope of improving rapid diagnosis and
treatment by first-line medical care providers.
This may result in the development of an additional short form
version that would build on the relationships linking symptoms to
formulate an abbreviated screening protocol. For the first time
clinical, paediatric and research applications are provided, which
will advance the understanding of myalgic encephalomyelitis and
enhance consistency of diagnoses internationally. The compulsory
critical criteria allow comparable data to be collected in various
locations and may assist in developing consistent biomarkers and
further insights into the mechanism and etiology of myalgic
3. Some comment on ME: The IC-criteria
My first comment is that I am very glad to
see this, given the horrible rot - I'm sorry: I am also a moral
human being and a philosopher of science, and that is what it seems
to me - produced by the APA and the DSM-5.
This is a very welcome rejoinder to them,
also since it is explicitly directed at first line medical doctors -
GPs and such - by first line medical doctors with great expertise in
And my second comment is that, since I sowed 70
notes to be made, these will be in the next issue of Nederlog, where
I will also explain why I make them, and link back to this text,
that then will be updated to link to that.
(*) See the website
Sophia and me, about
Sophia Mirza, made by her mother, who is a very brave and
intelligent person, and also a (former) nurse and midwife. Here is
a continuous quotation from her front page:
I believe it is now time that not only the
public in general, but doctors, psychiatrists, the legal
profession and M.P.s should read Sophia's documents. They need
to see them so that they can understand how the doctors,
psychiatrists, social workers and others in high places coldly
ignored the truly terrible physical suffering she endured; how
her right to make a valid choice was brushed aside and her human
rights totally abused. It is clear to me that grave injustices
were done to her, not only in her life, but in what I see as a
'cover up' in her death. This same criteria is still being used
against many thousands of others with M.E. in a similar way.
Officially, Sophia had M.E. since 1999. She
was offered 'treatment' in an M.E. clinic. She asked me to
research it. I spoke to some ex-patients, too frightened to have
their names used, who said it was run on the lines of mental
health. On phoning the clinic I spoke to their Senior
Occupational Therapist who had visited Sophia and had done the
assessment on her. She eventually told me that those with severe
M.E. regressed to their original state of ill-health. Given such
a negative prognosis, Sophia refused this option; for this
reasonable decision she was sectioned in a mental hospital in
The extensive post mortem showed up no cause
of death. We requested an independent neuropathologist to
research Sophia's spine. The findings confirmed that it
contained massive infection. At the inquest the Coroner
confirmed that "She died as a result of
acute renal failure arising from the effects of chronic fatigue
syndrome (CFS)"/ M.E.
See also - amongst a lot more worth seeing and
pondering - the
section Legal on Criona Wilson's site.