Introduction
Apart from historical landmark information
and the occasional quotation about ME/CFS from a medical journal
published in more medically enlightened times, the following
illustrations are mainly taken from the “grey” literature on
ME/CFS. Grey literature includes international research
conference proceedings, presentations and papers written by
researchers and/or clinicians that have not been published in
peer-reviewed journals. These include, for example, articles
written for patients’ support group magazines such as The CFIDS
Chronicle during the 1980s and 1990s (when the Chronic Fatigue &
Immune Dysfunction Syndrome [CFIDS, a US term for ME/CFS]
Association of America produced excellent Chronicles including
“A CFIDS Primer” and “Physicians’ Forum” written by leading
clinicians and researchers) and articles or reports (including
case reports and parliamentary reports) that have not been
published by commercial journals.
There is a wealth of important information
about ME/CFS in the grey literature that has been largely
ignored by those intent on denying the existence of ME/CFS as an
organic disorder. Indeed, the UK NHS Policy Plus Guidance
“Occupational Aspects of the Management of Chronic Fatigue
Syndrome: a National Guideline” (2006/273539 / DH Publications)
with which the three Principal Investigators of the PACE Trial
(Professors Peter White, Michael Sharpe and Trudie Chalder) were
involved states that the grey literature on “CFS” was not
comprehensively searched in the preparation of that national
guideline.
The early CFIDS Chronicles described CFIDS
(i.e.. ME/CFS) as a complex illness with a constellation of
symptoms that can resemble many disorders, including multiple
sclerosis, AIDS-related complex (ARC), Lyme disease,
fibromyalgia, post-polio syndrome and autoimmune diseases such
as lupus. Listed symptoms included profound fatigue especially
after exercise; low grade fever; chills and night sweats;
sensitivity to heat and cold; sore throat; swollen glands;
muscle weakness; muscle twitching; myalgia (often a vice-like
pain in muscles); sleep disturbance; headaches of a new type;
chest pains; irregular heartbeat; shortness of breath; dizziness
and balance problems; light-headedness; seizures; numbness or
burning of the face or extremities; dryness of the mouth;
rashes; allergies and sensitivities to odours, chemicals and
medication; abdominal pain; diarrhoea; bladder problems;
migratory arthralgia without joint swelling or redness;
transient visual scotomata (spots before the eyes); blurring of
vision; eye pain; photophobia; frequent prescription changes in
spectacles needed (because of difficulty in maintaining
accommodation); hair loss; hyperacusis; forgetfulness;
irritability; confusion; difficulty thinking; inability to
concentrate; spatial disorientation; dyslogia; intolerance of
alcohol; panic attacks and emotional lability.
In the Summer 2008 issue of The
CFIDS Chronicle, Anthony Komaroff, Professor of Medicine at
Harvard, editor-in-chief of Harvard Health Publications and
senior physician at Brigham and Womens’ Hospital, Boston (who
has published more than 230 research papers on ME/CFS) wrote an
article listing the top ten biomedical research findings in
ME/CFS.
These are summarised at
http://www.prohealth.com/library/showarticle.cfm?libid=14063
and include evidence that (1) many patients with ME/CFS have no
diagnosable psychiatric disorder and that ME/CFS is not a form
of depression; (2) there is a state of chronic, low-grade immune
activation, with evidence of activated T cells and evidence of
genes reflecting immune activation, as well as evidence of
increased levels of cytokines; (3) there is substantial evidence
of poorly-functioning NK cells (white blood cells that are
important in fighting viral infections); (4) there is evidence
of white and grey matter abnormalities in the brain; (5) there
is evidence of abnormalities in brain metabolism (and evidence
of dysfunction of energy metabolism in the mitochondria); (6)
there is evidence of abnormalities in the neuroendocrine system,
particularly in the HPA axis but also in the
hypothalamic-prolactin axis and in the hypothalamic-growth
hormone axis; (7) there is evidence of cognitive difficulties,
especially with information processing, memory and/or attention;
(8) there is evidence of abnormalities in the autonomic nervous
system (including a failure to maintain blood pressure, abnormal
responses of the heart rate, and unusual pooling of blood in the
legs, as well as low levels of blood volume); (9) there is
evidence of disordered gene expression, especially in those
genes that are important in energy metabolism and in genes
connected to HPA axis activity, to the sympathetic nervous
system and to the immune system; (10) there is evidence of
frequent infection with viruses, especially herpesvirus and
enteroviruses.
The overwhelming degree of exhaustion in
ME/CFS is unmistakable and can never be confused with chronic
tiredness or “fatigue”, nor can the objective signs that are
invariably present in ME/CFS be mistaken for chronic “fatigue”;
such signs include:
·
labile blood pressure (this is a
cardinal sign in ME/CFS)
·
nystagmus and vestibular
disturbance (vestibular dysfunction seen in 90% of patients with
ME/CFS)
·
sluggish visual accommodation
·
fasciculation
·
hand tremor
·
neuromuscular incoordination
·
cogwheel movement of the leg on
testing
·
muscular weakness
·
marked facial pallor
·
postural orthostatic tachycardia
syndrome (POTS)
·
positive Romberg
·
abnormal tandem or augmented tandem
stance
·
abnormal gait
·
evidence of Raynaud’s syndrome and
vasculitis (vascular signs cross dermatomes)
·
mouth ulcers
·
hair loss
·
singular reduction in lung function
(shortened breath-holding capacity seen in 60%)
·
enlarged liver (not usually looked
for by psychiatrists)
Laboratory abnormalities in ME/CFS include
abnormal SIgA; weakly positive IgG3 (linked to gastrointestinal
tract disorders); positive IgM; increased T4:T8 ratio (which
always corresponds with disease severity); very low numbers of
NK cells, with decreased cytolytic activity; low levels of
circulating immune complexes (two-thirds of ME patients have
insoluble circulating immune complexes); autoantibodies
(especially antinuclear and smooth muscle); a particular HLA
antigen expression; PCR evidence of abnormalities in muscle; a
positive water loading test with erratic arginine-vasopressin
release; a significant prolactin release in response to a single
buspirone challenge; positive SPECT scans (which show reduced
blood flow through the brain stem in a particular pattern not
found in any other illness or disease process apart from ME/CFS
– QJMed 1995:88:767-773); abnormal fMRI scans; abnormal EEG (80%
of ME patients show prolonged jitter); a positive VP1 test;
positive mast cells; low pancreatic exocrine function; low
copper response test; anomalies in trace element metabolism,
especially low red blood cell levels of magnesium, zinc and
chromium; low potassium levels; low peripheral oxygenation
levels, with poor perfusion and pulsatilities, and increased
hsCRP. According to Peter Behan, Professor of Neurological
Sciences at the University of Glasgow, as these abnormalities
have been shown to occur with such regularity, if they are
present and if the clinical picture is right, then a firm
diagnosis of ME can be made. In 2001, evidence was presented by
SCM Richards et al (including Anthony Cleare who co-authors
papers on ME/CFS with Simon Wessely) at the British Society of
Rheumatologists’ Conference in Edinburgh showing that 53% of
ME/CFS patients were excreting in their urine significant levels
of creatine and other muscle-related metabolites including
choline and glycine, indicating on-going muscle damage, as
creatine has been shown to be a sensitive marker of muscle
inflammation and is objective evidence of muscle pathology.
Given the prevailing editorial bias of many
medical journals on the topic of ME/CFS and the sophistry of the
Wessely School, the important information contained in the grey
literature is in danger of disappearing, but patients,
clinicians and non-medical policy-makers alike need ready access
to such central information in terms that are quickly and easily
understood.
This present document makes no attempt to
provide a comprehensive overview of the grey literature on
ME/CFS or to summarise the proceedings of international clinical
and research conferences since 1988, but hopefully the
illustrations provided will strengthen patients’ correct
perception that they suffer from a serious organic disease that
is neither reversible nor curable by directive psychotherapy as
asserted by those associated with the MRC/DWP PACE Trial.
However, people
with ME/CFS and those who care for them may wish to source for
themselves the presentations made at the following major
conferences on ME/CFS; these include the US NIAID (National
Institute of Allergy and Infectious Diseases) Symposium held at
the University of Pittsburgh in September 1988; the Rhode Island
Symposium in 1988; the Rome Symposium in 1988; the San Francisco
conference in April 1989; the British Post-Graduate Medical
Federation Conference in London in June 1989; the Los Angeles
International Conference in February 1990; the First World
Symposium held in 1990 at Cambridge University, UK; the
Charlotte Research Conference in November 1990; the Canadian
Workshop at the University of British Columbia, Vancouver, in
May 1991; the Dublin International Symposium in May 1994 (held
under the auspices of The World Federation of Neurology); the
First World Congress (also under the auspices of The World
Federation of Neurology) in Brussels in 1995; the Second World
Congress in Brussels in September 1999; the Bloomington
Conference in Minnesota in October 2001, and the International
Clinical and Scientific Meetings presented by the Alison Hunter
Memorial Foundation in Australia, especially the Third
International Meeting in Sydney in December 2001; the
biennial International Research and
Clinical Conferences hosted by the American Association of CFS
(AACFS, now the IACFS / International Association of CFS),
including the Albany, New York, conference in October 1992; the
Fort Lauderdale, Florida, conference in October 1994; the San
Francisco conference in October 1996; the Boston, Massachusetts,
conference in October 1998; the Seattle conference in January
2001; the Chantilly, Virginia (Washington D.C.) conference in
January – February 2003; the Madison, Wisconsin, conference in
October 2004, the Professional Research Conference in Fort
Lauderdale in January 2007, and the numerous Scientific
Workshops such as the one co-sponsored by the US National
Institutes of Health in June 2003 on neuro-immune mechanisms in
ME/CFS and the ME Research UK (MERUK, formerly MERGE) workshops
(including the Royal Society of Edinburgh funded Workshop in
2003, the MERUK Colloquium in July 2006 and the MERUK
International Research Conference on 25th May 2007 at
Edinburgh), the aim of all these conferences being to facilitate
links between research scientists and clinicians working towards
the common goal of understanding the biomedical basis of
ME/CFS.
Given that much of the knowledge and
information about ME/CFS quoted below has been circulating for
over quarter of a century, how is it possible that Wessely
School psychiatrists are even today permitted to ignore and/or
dismiss it?
Professor Michael Sharpe, who it seems has
now left Edinburgh and is back in Oxford, recently responded to
criticism of the PACE Trial
(doi:10.1016/j.jpsychores.2011.03.003) by attempting to justify
the use of the Oxford criteria (of which he was lead author)
stating: “While we excluded people with generally accepted
organic brain diseases…we did not exclude people who described
their symptoms as those of ME”, yet ME is a
WHO-classified neurological disorder, so Sharpe’s argument is
intellectually inconsistent. His position itself is
intellectually inconsistent because he bases it on “CFS/ME”
being “disabling longstanding fatigue” and gives no
credence to the presence of the symptoms that distinguish ME/CFS
from chronic fatigue.
Despite the
proselytising of the Wessely School, the golden rule of ME/CFS
experts is: if a patient improves with exercise, that person
does not have ME.
Moreover, unlike those with
other post-viral states who report that they catch opportunistic
infections, people with classic ME/CFS do not succumb to every
passing common cold because they have incredibly up-regulated
interferon production, which is another distinguishing feature.
Why are the UK patients’ support charities
not vigorously refuting the false reasoning of the Wessely
School about ME/CFS on every possible occasion instead of
colluding with it?
The relentless degree to which the Wessely
School disseminate misinformation about ME/CFS needs to be
equally relentlessly countered with the dissemination of the
biomedical evidence that shows them to be wrong, otherwise they
will continue to suppress and/or disregard it and patients will
continue to suffer iatrogenic harm.
The following
illustrations present a picture of classic ME/CFS that is
nothing like the Wessely School’s “cognitive behavioural” model
of “CFS/ME” which ignores the key symptoms of ME/CFS and is
based on “fatigue” and which many people believe is such a
travesty of both medical science and human rights.
Illustrations
1956:
Dr ED Acheson, later to become Sir Donald Acheson, UK Chief
Medical Officer, coined the term “benign myalgic
encephalomyelitis” (ME).
1964: ME was recognised and
registered as an industrial disease and as grounds for
compensation that has been paid as a weekly pension to a former
Royal Free Hospital nurse since 1964; this was confirmed at a
meeting at the headquarters of the Royal College of Nursing on 2nd
May 1989.
1969: the World Health
Organisation classified ME as a neurological disorder.
1978: The Royal Society of
Medicine accepted ME as a nosological entity.
1981: The Lancet published a
letter from Professor CS Goodwin about necessary criteria for a
diagnosis of ME: “Firstly, symptoms and signs in relation to
muscles, such as recurrent episodes of profound weakness and
exhaustion, easy fatiguability, and marked muscle tenderness.
Secondly, neurological symptoms or signs – pyramidal or
cranial nerve lesions, especially affecting the eyes; or
weakness of peripheral muscles as demonstrated by the voluntary
muscle test; or some loss of peripheral sensation; or
involvement of the autonomic nervous system (orthostatic
tachycardia, abnormal coldness of the extremities, episodes of
sweating or pallor, constipation and bladder disturbances.
Thirdly, biochemical abnormalities, such as raised urinary
creatine, low serum pyruvate, or raised serum myoglobin, or an
abnormal electrophoresis pattern with raised IgM” (Lancet,
3rd January 1981).
1985: Dr RW Gorringe from
New Zealand published “Diagnostic Criteria and Tests for ME” in
October 1985, which provided a comprehensive and useful
diagnostic tool; Gorringe warned that “the commonest
mistake doctors make is failing to take a wide enough view and
cover an adequate systems review”. He noted the classic
symptoms of ME including prominent but intermittent chest pain
(severe enough for hospital admission); sore muscles of the
shoulders, neck and back; muscles that become shaky and
tremulous; frequency of micturition; irritable bowel (colicky
abdominal pain and loose bowels); moist chest; cough;
palpitations; jerkiness of limbs; difficulty in co-ordination;
paraesthesias; shooting pains up nerves; blurred vision; burning
pain behind the eyes; oesophageal spasm; food allergies;
sensitivity to light; intermittent swollen glands and sore
throat; dizziness and nausea. Gorringe noted evidence of
malabsorption and hypoglycaemia (in ME/CFS patients, blood sugar
is known to be under poor control); he pointed out that on TFT
(thyroid function test), TSH was often normal but that T3 may be
low, with subclinical hypothyroidism. He also noted abnormal
immunoglobulins, particularly IgA (often low) and IgM (which
goes up in a relapse but may sometimes be depleted and become
markedly decreased), and abnormal CICs (circulating immune
complexes), with low C3 and C4 (the modified immunoglobulins do
not make proper complexes with allergens taken in, resulting in
(insoluble) circulating immune complexes in the central nervous
system, in the joints and in the kidneys, which can be a very
hazardous state).
1987: in his Medical Address
at the AGM of the ME Association on 25th April 1987,
James Mowbray, Professor of Immunopathology, St Mary’s Hospital
Medical School, London, said: “When we meet a new
infection…the first thing we do is to make IgM antibodies and
then in a matter of a few weeks we switch over and make IgG
antibodies (which) last for a long time and protect us. If
someone has IgM antibodies they have either been recently
infected or they are still infected….We developed a technique
using a specialised antibody…which detects a protein in
enteroviruses which is the same in all 72 enteroviruses (and) we
can use that antibody to look for the virus protein in the
blood. Doing that, we have been able to find a very large
fraction of the ME patients have got an enterovirus
antigen….Just because you find virus proteins in the blood, does
that mean they are infected? Yes, it does….The virus is
present in the intestine. It is also shown to be present in the
muscle….Here is a muscle biopsy where you see the dark brown
infective muscle cells, where the probe has bound to the virus
genes in the muscle cell. (There are) two ways which
demonstrate that in the muscle (in) a patient with ME, there is
an enterovirus….What does it do in the muscle?….(It) does the
thing that viruses usually do, they infect the cell and take
over…saying ‘You must switch off all your genes and read only my
genes’. So (the virus) switches off all the genes that produce
energy to the cells….The virus is being made and is switching
off host genes stopping the cells’ own energy production. If
you now exercise, you rapidly run out of energy in the muscle
and that has been shown by sophisticated techniques….Whilst
(the virus) is there, it severely limits the ability of the
muscle to work….The thing that seems to make it worse is
exhausting the muscle….Sufferers know, they have a kind of
feeling for it, especially as time goes on, about what is going
to be too much….When you have got the disease it is a good
basis for saying do not use up all the muscle energy, do not get
to that stage. It may lead to more virus affecting that
muscle….It is clear that it is not only exhaustion in the muscle
but also in the brain….Either muscle or brain overdoing it
is the same….if you live within the limits of the disease while
you have got the disease, I think you will do much better and we
have now got some good scientific background”.
1987: At the CFS Society,
USA, conference held on 4th-7th November
1987, Infectious Diseases specialist Dr Mark Loveless from the
University of Oregon said the disease was very prevalent, that
the musculoskeletal, neurological and vestibular systems were
involved, and that there are cardiovascular, gastrointestinal
and immunological abnormalities. At the same conference, Dr
Alfred Johnson said that 97% of (ME/CFS) patients have allergies
and that allergic patients have high helper (T4) cells and low
suppressor (T8) cells, causing over-reactivity. Dr Paul
Cheney confirmed that the T4:T8 ratio is elevated in two-thirds
of cases, and that this is considered a more reliable marker of
the illness than other markers. He said there are “impressive
abnormalities” in mitogen stimulus status (an immune
function test) and that symptoms are caused by a hyper-immune
response. He noted that MRI scans showed characteristic brain
lesions in 77% of patients tested (88 of 114 patients) as
determined by two independent neurologists.
1988: Professor James
Mowbray’s team at St Mary’s Hospital, London, began to offer a
test for the detection of enteroviral protein in ME patients.
VP1 stands for Viral Protein 1, described in the ME
Association’s magazine in Autumn 1988 as being: “one of four
proteins forming together the viral capsid which surrounds the
viral genetic material. There is a particular portion of the
VP1 protein which is present in all 72 different enteroviruses”.
The ME Association offered the test to its members for an
administration fee of £3. The following year, at the Clinical
Session of the 1989 AGM of the ME Association, Dr Byron Hyde
from Canada referred to the VP1 test, confirming what Professor
Mowbray himself had said: ME patients with a positive VP1
test become chronic, whilst those with a negative VP1 test
recover. Despite this, the VP1 test was dismissed by
psychiatrist Simon Wessely as “unsuitable for routine
clinical use” [Lancet 1989:1:1028-9] and it is no
longer available in the UK.
1988: An article by Elsie
Brody (Occupational Health, 1988; 446-447) listed key symptoms
of ME, including severe headaches, neck pain, pain in back and
limbs, pins and needles in limbs, vertigo, severe sweating,
impaired memory and difficulty with words, panic attacks (now
known to be due to hyperadrenergic orthostatic intolerance),
tachycardia, extreme fatigue, disturbed sleep, muscle weakness
and tenderness, diplopia, photophobia and chest pain. Mrs Brody
advised that: “As OH professionals, it is our duty to
recognise the disease early (and) educate management on
recognising ME”.
1988: The ME Association’s
magazine “Perspectives” carried an article on “Viruses and “ME”
by consultant microbiologist Dr Betty Dowsett, who wrote: “Many
viruses (including enteroviruses) can enter and alter the
function of the immune cells specially designed to destroy
them. It is important to recognise that these immune
abnormalities are secondary to the virus infection….The
mopping up of free viruses in the bloodstream can be
counter-productive if excess antibody is produced. The
insoluble ‘immune complexes’ that result can be trapped in the
blood vessels and tissues and…maintain infection in the
body….The chemical composition of a virus may mimic that of a
normal body component (such as brain or muscle protein)
whereupon the immune attack is misdirected against the host
while the virus disappears unnoticed. Cardiac and other
complications in ME are an example of such an anomaly”.
1988: At a meeting on ME
held at The Royal Free Hospital on 16th May 1988,
Professor Tim Peters from Northwick Park Hospital said his team
had found abnormalities of Type II muscle fibres (anaerobic) in
ME patients, which were atrophied, with hypertrophy of Type I
muscle fibres; he had measured total RNA in muscle cells and
found it to be significantly reduced in ME patients (if there is
a decline in RNA, there is a decline in the ability to make
muscle protein – infusion of tag-leucine showed overall
metabolism is clearly reduced and the rate at which muscle is
being formed is reduced).
1989: Professor Peters (then
Professor of Clinical Biochemistry and Consultant Chemical
Pathologist at Kings College Hospital, London) wrote on page 24
of the magazine InterAction No: 3 of the charity ME Action, now
AfME: “Exciting studies have recently been reported of
persistent viral RNA in biopsies from patients with ME….Based
on these observations we have started to investigate muscle
protein synthesis; that is, the ability of muscle to repair
itself…in patients with ME. Measurements of muscle RNA, the
machinery for protein synthesis, showed consistently reduced
amounts in their biopsies. Studies of whole body and,
specifically, thigh muscle protein synthesis rate in these
patients show reduced values and thus a pattern
is beginning to emerge of persistent viral infection, and
possibly re-infection, interfering with the machinery for making
tissue protein and thus impairing protein synthesis”.
Discussing the view of those who claim that changes in
mitochondrial function and impaired muscle synthesis are merely
secondary events due to lack of use of the muscles, Professor
Peters continued: “It is hard to see how (this) can explain
the persistence of enteroviral RNA in muscle fibres….immobility
leads to a selective loss of Type I fibres, a feature not seen
in patients with ME”.
The same issue of InterAction reported on
page 22 the neurological abnormalities found by Carolyn Warner
and her team from Buffalo, NY (elevated IgG synthesis, elevated
CSF cell count, prolonged visual evoked response latency,
abnormal EEG and MRI lesions, and neuromuscular abnormalities
including over 20% polyphasic motor units on quantitative EMG,
inflammatory infiltrates and Type II fibre atrophy, these being
reported in Neurology 1989:39:Suppl 1: 420). Commenting on these
abnormalities, Dr Goran Jamal, Consultant in Clinical
Neurophysiology at The Institute of Neurological Sciences,
Glasgow, affirmed that those results are consistent with
disturbed immune function and persistent infection, and that it
proves once again that one can find neurological abnormalities
if one looks.
Still in the same issue of InterAction, Dr
Jamal himself wrote on page 26 about muscle fatigue in ME: “In
recent years a lot of evidence has been accumulating to suggest
that the fatigue in ME is organic in nature….Our findings
clearly showed evidence of disturbance of transmission of
electrical impulses along muscle fibres. This study… provided
one of the first and strongest indications for the organicity of
the syndrome. This work has been reproduced again by
our group and elsewhere. In addition we have looked at other
groups of patients with various psychiatric illnesses using the
same technique of single fibre electromyography, and these
produced absolutely normal findings….Examination of
individual muscle fibres under electron microscopes…showed gross
abnormalities of the structures involved in providing energy for
the muscle fibres….NMR (nuclear magnetic resonance)
showed evidence of disturbed muscle metabolism….Strong
evidence of the presence of viral particles in the muscles of ME
patients has also recently been shown….Any assumptions that the
fatigue in patients with ME is entirely ‘ mental’ or
‘psychogenic’ is not only without any foundation but also
ignores all this solid scientific data”.
1989: Dr Paul Cheney from
the US presented his findings at the San Francisco CFS
Conference on 15th April 1989; 70% of ME/CFS patients
tested had depressed levels of salivary IgA (SIgA), and
ME/CFS patients with low SIgA levels tended to have high levels
of insoluble circulating immune complexes. Microscopic
analysis of tissues showed lymphocytic vasculitis (lymphoid
infiltrates in the blood vessel wall) in 75% of patients tested.
1989: In a talk given on 15th
May 1989, Peter Behan (Professor of Neurological Sciences at the
University of Glasgow) said that ME is a viral infection of the
gut with gross exhaustion and tachycardia accompanied by
malaise. He said the real tragedy of ME is the far-reaching
effects on the medical profession of two not-very-talented
psychiatrists in 1977, one of whom had only just qualified.
Behan stressed the importance of separating psychiatric fatigue
from ME fatigue. He explained that the brain produces
Interleukin 1 (IL-1) as a result of the cell being stimulated by
a virus, and IL-1 will cause the liver to be abnormal; it will
affect muscle and nerve cells, and it is found in extreme
fatigue. He said that in the majority of true ME cases, IL-1
levels are extremely high.
1989: In the summer issue of
the ME Association’s magazine, Dr David Smith wrote about
slow-onset ME: “I am afraid that there is probably less
chance of a spontaneous cure, and in that disease undoubtedly
there is a natural progression of symptomatology….I do believe
that the slow onset type persistent enterovirus infection is
ME”. In “A Letter from our President” in the winter issue
of the ME Associations’ magazine, Dr Melvin Ramsay wrote: “The
onset of the disease may be sudden or gradual….The crucial
difference between ME and other forms of postviral fatigue
syndrome lies in the striking variability of the symptoms, not
only in the course of a day but often within an hour. This
variability and intensity of symptoms is not found in postviral
fatigue states”.
1989: In December 1989
the magazine of the Australia and New Zealand ME Society
(ANZMES Meeting-Place issue 32) reproduced an article by Thomas
English MD, formerly Assistant Clinical Professor of Surgery at
Duke University in the US who had to retire due to ME/CFS.
English wrote: “I issue a challenge to medical sceptics who
suggest that CFIDS (ie. ME/CFS) is only a form of
depression or ‘psychoneurosis’. The challenge is this. Give
yourself a one month course of alpha-interferon. Don’t be
timid; get your serum levels up above 300 where mine have been.
Have the courage of your convictions; experience for 30 days
what patients have endured for years….If our illness is as
trivial as you suggest, each of you should be willing to step
away from your pseudo-intellectual façade of CFIDS scepticism.
After 30 days, tell us what you think. I daresay that no CFIDS
critic should be taken seriously until he has done this”.
1990: On 17th
March 1990 Professor Peter Behan from Glasgow made a
presentation to the Mid-Anglia branch of the ME Association in
Cambridge. He began by giving an over-view of the historical
perspective and went on to discuss the cardinal symptoms of ME,
these being (1) onset precipitated by a viral infection; (2)
local and generalised fatigue arising from the brain as in
multiple sclerosis; (3) post-exercise myalgia, especially in the
shoulder girdle, back, neck and left side of the chest; (4)
mental changes, including poor control of emotions, poor task
performance and cognitive disturbances; (5) sleep disturbance;
(6) cardiac disturbances (a significant number have cardiac
symptoms) and (7) vestibular disturbance, with dysequilibrium
and sometimes true vertigo. He discussed the hypothalamic
dysfunction, noting that 50% of ME patients cannot produce
steroids in response to stimulus. He presented objective
evidence of Type II muscle fibre atrophy on histological section
and evidence of mitochondrial damage, and showed identification
of enteroviral RNA in muscle.
1990: On 10th- 12th
April 1990 the First World Symposium on ME/CFS was held at the
University of Cambridge. Speakers presented evidence on acute,
latent, persistent and reactive virus/host interaction; on
cytopathological studies; on electron microscopy studies; on
immunological abnormalities, genetics and autoimmunity; on
interferons and their role in virus infections; on muscle
studies of abnormal metabolic function; on cardiac disease in
ME/CFS; on lesions in the brain and on paediatric ME/CFS.
The predominant view was of a persistent or chronic viral
infection which either gave rise to, or was the result of, a
continuing abnormal immune response and abnormalities of the
muscle and central nervous system. Evidence was presented of an
infective vasculitis in ME/CFS. The Symposium brought
together leading international researchers to review all aspects
of ME/CFS. The proceedings were subsequently published as the
724 page seminal textbook on ME/CFS (The Clinical and Scientific
Basis of Myalgic Encephalomyelitis Chronic Fatigue Syndrome,
edited by Drs Byron Hyde, Jay Goldstein and Jay Levy; The
Nightingale Research Foundation, Ottawa, 1992). The
conclusion of the Symposium was plain: ME/CFS is a true organic
disease, with abundant evidence of its organicity.
1990: In September 1990 the
CFIDS Association of America produced a special “Research
Breakthrough” issue of its Chronicle. The Special Issue reported
on the press conference on CFIDS (ME/CFS) held on 5th
September 1990 in San Francisco, at which Dr Paul Cheney said: “The
most specific neurological symptom…is dysequilibrium. These
patients have a balance disturbance and on certain simple
neurological tests they fall over. On more sophisticated tests
of vestibular function they’re often grossly abnormal….Other
evidence of central nervous system involvement can be
demonstrated by tests looking directly at the central nervous
system. These are slices of brain created by using magnetic
resonance imaging. These inflammatory and/or demyelinating
plaques can be seen in white matter, in the cerebellum and white
matter tracks throughout the high cerebral convexities and in
the frontal lobes. Over half of CFIDS patients will typically
show lesions within the central nervous system….Switching
from neurology to immunology, I want to show you what I believe
to be the most striking immunologic defect in these patients.
It is most convincing. This is the 2-5 A Synthetase/RNase L
pathway….This system turns on and protects cells from viral
infection and replication….This system is only turned on by a
virus….In terms of severity, this is phenotypically unique to
CFIDS….It’s an absolutely striking observation suggesting
a viral problem in these patients….These cells are infected with
virus”.
Dr Cheney then discussed biopsies from
ME/CFS patients that showed an infiltration of mononuclear cells
around small blood vessels within the deep dermis (causing, for
example, loss of fingerprints). Cheney said “It’s called
perivasculitis, or perivascular cuffing….What’s interesting
about this kind of lesion is that if this lesion occurred within
the brain, in small vessels within the brain, it would produce
many of the lesions we see on MRI scans. So I think that this
pathology is not limited to fingertips. It can be found
anywhere”.
Wishing to make sure that the press corps
understood how serious a disease ME/CFS is, Cheney continued:
“I think it’s really important for members of the press to
recognise that what we’re talking about here is not common
fatigue….What we’re talking about here in this systemic
illness is that the debilitating fatigue is one of the primary
symptoms, as it is in almost all autoimmune diseases and many
other systemic diseases….We need to constantly separate out
people who have common fatigue from people who have this
illness….People who have competent immune systems don’t get bad
diseases like this in any numbers….Retroviruses have the
capacity to impair immune systems in a subtle way”.
In response to a question as to why ME/CFS
is more common in women than in men, Cheney said: “There
are a number of immunologic problems in which women dominate.
Lupus and MS are examples. Immunologic disturbances are seen
more commonly in women….In MS you have a ratio of two to three
women to men”.
At the conclusion of the press conference,
when Drs Paul Cheney and David Bell were asked to comment on how
seriously ill ME/CFS patients are, Dr Cheney said: “These
patients’ …ability to experience life is destroyed. You see
their entire social structures, work interactions and family
units, come crashing down….It’s an unbelievable illness”
and Dr Bell said: “ At the tip of the iceberg there
are some patients who have it in extremely severe form and it
can destroy their lives….So even without the injury caused by
medical mismanagement, there’s a very significant disability
caused by this illness”.
23rd November 1990:
Notes of the ME Study Group Meeting record that, in complete
disregard of all this circulating biomedical evidence,
contributors to a Press Briefing on ME by the Royal Society (one
of the oldest scientific institutions in the world) that was
designed to inform medical correspondents about ME emphasised
the psychiatric approach: muscle abnormalities were stated to be
secondary to inactivity, and reassurance together with graduated
exercise were considered to be the best therapeutic approach.
Psychological factors that pre-disposed, precipitated and
perpetuated “fatigue” syndromes received considerable
prominence, and one contributor attributed ME in children to
school phobia.
(click
here for Part II of this article)
(click
here for Part III of this article)
)