~*Online WACOC News 2006 August 11*~

Women and Children of CFIDS
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*Science is an international enterprise*
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Lord Sainsbury of Turville

[ http://www.dti.gov.uk/ministers/speeches/sainsbury141004.html]


by Douglas Fraser




*...what we really think we are looking at is a very good
example of the brain-body interaction...we are trying to get
them to come to the CDC chronic fatigue syndrome
website... right now the UK National Health Service has
implemented, as the National Health Service, an evaluation
and treatment programme for CFS on a National level, it`s
still symptomatic and Cognitive Behavioural Therapy...*.
Dr William Reeves, Principal investigator of chronic fatigue
syndrome for the Centers for Disease Control and Prevention -
August 9th 2006.


*...this disease cleans you out, it takes everything from
you that was normal...sometimes I don`t get downstairs at
all... when you (overdo and) go backwards, you really
really go backwards fast and disastrously, and it can be
many many years before you get better...we can`t hold
marches on Washington...*. Laura Hillenbrand - August 9th
2006 after 20 years of CFIDS *brain-body interaction*.

http://minnesota.publicradio.org/display/web/2006/08/09/midmorning2/



The CDC website was updated this May and I`ve only just gotten
around to perusing it, having been away a couple of months.

It`s interesting to see that MERGE`s website, now *ME
Research UK*, is actually larger (and far more interesting and
qualitatively rigorous) than the mighty CDC CFS website.

On the CDC CFS website`s Glossary page, it is stated that ME
is synonymous with CFS:

*myalgic encephalomyelitis: A synonym for
chronic fatigue syndrome in common usage
in the United Kingdom and Canada.*

Someone must have made a mistake in letting that go through,
but perhaps it`s a useful hook for writing to the CDC and
enquiring into why the History, of ME a.k.a. CFS as they clearly
state, has gone missing on their website ?

After all one can`t predict the future without understanding and
absorbing the past, in any field of inquiry. No less an authority
than Susan Haack put it another way:

*..any serious inquirer is required to seek out all the potentially
available evidence, and to go where it leads, even if he would
prefer to avoid, ignore, or play down information that pulls
against what he hopes is true.*

[ http://www6.miami.edu/ethics/jpsl/archives/all/haackpaper.html]



I may be wrong, but I can only find 4 inconsequential references
to myalgic encephalomyelitis within some 179 webpages at the
CDC/CFS website.

(Church and Dale of Great Ormond St Hospital suggested in
2004 that the re-emerging horrible condition *encephalitis
lethargica* is probably the fall-out (possibly autoimmune) from a
simple streptococcal infection (sore throat), and that they went
back to early accounts starting in 1918 to check the clinical
picture while there`s still no diagnostic test. *We have recently
seen 20 patients with a similar EL phenotype, 55% of whom had
a preceding pharyngitis. The patients had remarkable similarity
to the historical descriptions of EL*. Prof Basant Puri mentions
this episode analogously in his book *A Natural Way to Treat
ME*)

There appears to be only one single reference (Shelokov &
Henderson) to anything remotely related to historical
descriptions of ME, and even then it`s only a passing reference
within an old surveillance paper by Fukuda, Holmes, Reeves etc
(1994 ), which probably few would look near. *Surveillance for
chronic fatigue syndrome - four US cities, September 1989
through August 1993.

*Outbreaks of similar illnesses were described before the early
1980s (3 ), when interest in endemic CFS was heightened (4 )*

3.- Henderson DA, Shelokov AS. Epidemic
neuromyasthenia-clinical syndrome? N Engl J Med
1959;260:757-64.

(4) - Holmes GP, Kaplan JE, Stewart JA, Hunt B, Pinsky PF,
Schonberger LB. A cluster of patients with a chronic
mononucleosis-like syndrome: is Epstein-Barr virus the cause?
JAMA 1987;257:2297-302.*


Anyone consulting the CDC website, scientists, the public,
politicians, media, could be forgiven for thinking that *CFS* is a
new disease discovered by CDC circa 1983 AD. There can`t be
such a thing as a new disease of course, just Darwinian themes
and variations on what`s always been there, though in America,
as in the UK, possibly half the population might believe
otherwise: think AIDS.

(On their HIV/AIDS website the CDC make available some early
documents including one described as an important *historical
report*.)


However, we have Dr Bill Reeves visiting the MRC, and
Professor Pete White visiting CDC etc. This has been followed
by Dr Reeves recent public approval of CBT and *rehabilitation*,
the *therapies* condemned by so many in the UK, which
continue to drain the Public Purse and Public Research Funds,
while people with ME remain ill regardless, and some, who
believed the hype, are placed in a vulnerable position when it
doesn`t work out curatively (how can it?).
http://www.sayer.abel.co.uk/MES-Nnye.html

And now the CDC's *public awareness* campaign already
raising the spectre of the British Mind-over-Matter *solution*
being shipped lock stock and barrel to the US.

(another recent video news report at
http://wcco.com/topstories/local_story_218211856.html ).



But back to those pioneers.

Donald Henderson ..

Donald Henderson (*Henderson DA* - above), who must be
around 80 years of age now, seems to remain as Dean
Emeritus at St Johns, and was once White House Chief of
Science, amongst other distinguished appointments. He`s a
*Resident Scholar* at the Centre for Biosecurity, and was very
much responsible for wiping out smallpox through the 60`s and
70`s.

I can`t seem to find Professor Sir Ernest Donald Acheson with
Google (?).

However, I do wonder what Prof`s Acheson and Henderson
might think nowadays, if indeed they`re still interested, and how
they would view the virtual disappearance of their contributions.


Dr J Gordon Parish, Patron of the small high quality charity *ME
Research UK* wrote: *Many of the findings described in the
landmark Acheson 1959 paper are very much relevant to our
understanding of ME today*

http://www.meresearch.org.uk/information/publications/achesonreview.html


*The Clinical Syndrome Variously Called Benign Myalgic
Encephalomyelitis, Iceland Disease and Epidemic
Neuromyasthenia E.D. Acheson, D.M., M.R.C.P....

....Sir (Ernest) Donald Acheson, KBE 1986, has just retired after
holding the post of Chief Medical Officer, Departments of Health
and Social Security for Great Britain. It is of notable interest that
this principal early M.E./CFS researcher had risen to become
the chief Medical Officer for Great Britain.

Dr. Donald Henderson, one of the early American M.E./CFS
pioneers whose work is also in this book, went on to become
Dean of Medicine of Johns Hopkins and is presently the White
House Chief of Science for the U.S.A.

After Sir Donald Acheson graduated from Oxford in 1946 he
held numerous senior positions, including Professor of Clinical
Epidemiology, University of Southampton, Chairman of Slow
Virus Group, Visiting Professor, McMaster University, Canada
1977. He has also held numerous important posts in many
universities in the United Kingdom and New Zealand. The
information about Sir Acheson was obtained from the British
Who's Who 1992, Collier Mcmillian Press, Cambridge, Ontario.*

http://www.meresearch.org.uk/information/keypubs/Acheson%20-%20Am%20J%20Med..pdf

Professor Donald Henderson`s current details seem to be here:

[ http://faculty.jhsph.edu/?f=Donald&l=Henderson ]

Donald Henderson Professor - Emeritus
Dean Emeritus

Academic Degrees: MD, University of Rochester, 1954; MPH,
Johns Hopkins School of Hygiene and Public Health, 1960
Departmental Affiliation: Health Policy and Management Joint
Departmental Affiliations: Epidemiology Departmental Address
Email: dahzero @ aol.com Phone: 443-573-3304



Research and Professional Experience

Donald A. Henderson, MD, MPH '60, is presently a Resident
Scholar at the Center for Biosecurity of the University of
Pittsburgh Medical Center. The Center for Biosecurity was
originally founded in 1998 as the Center for Civilian Biodefense
Studies at the Johns Hopkins Medical Institutions. The Center
was established to increase national and international
awareness of the medical and public health threats posed by
biological weapons. Immediately after the 9/11 attack, Dr.
Henderson was appointed as the government's first Director of
the Office of Public Health Emergency Preparedness. He
continues to serve as senior science advisor to Secretary
Thompson of the Department of Health and Human Services
and as Chair of the Secretary's Council on Public Health
Preparedness.

Dr. Henderson is a Johns Hopkins University Distinguished
Service Professor Emeritus and Dean Emeritus of the School,
with a joint appointment in the department of Epidemiology. He
is also Professor of Medicine and Public Health of the University
of Pittsburgh School of Medicine. He rejoined the Hopkins
faculty in June 1995 after five years of federal government
service in which he served initially as Associate Director, Office
of Science and Technology Policy, Executive Office of the
President (1991-1993), and later as deputy assistant secretary
and senior science advisor in the Department of Health and
Human Services.

From 1977 through August 1990, Dr. Henderson was dean of
the Johns Hopkins School of Public Health. He came to Hopkins
after directing the World Health Organization's global smallpox
eradication campaign (1966-1977). Dr. Henderson was
instrumental in initiating WHO's global program of immunization,
which has vaccinated 80 percent of the world's children against
six major diseases and has as a goal the eradication of
poliomyelitis.

Keywords

Surveillance, smallpox, eradication, biodefense, biological
weapons, bioweapons, bioterrorism, anthrax, polio, influenza.

Honors and Awards

Presidential Medal of Freedom (2002); the National Medal of
Science; National Academy of Sciences' Public Welfare Medal;
the Japan Prize; Edward Jenner Medal of the Royal Society of
Medicine; Honorary Fellow of the New York Academy of
Medicine, the Royal College of Physicians of the United
Kingdom, the London School of Hygiene and Tropical Medicine
and the American Academy of Pediatrics; member of the
Institute of Medicine and Fellow of the American Academy of
Arts and Sciences; Honorary degrees from 16 universities and
awards and decorations from 14 nations, the World Health
Organization and the Pan American Health Organization.
Selected Publications etc.....Last Updated: 05/09/2005

No slouch there either !


Another dedicated scientist, Dr Vance Spence recently
remarked : *From 1934-90, there were at least sixty-three
outbreaks of epidemic proportions, all well documented, and
distributed geographically in North America (29 outbreaks), the
UK (16), the rest of Europe (11), Australasia (4), Africa (2), and
Asia (1). One of the most studied, and possibly the most
controversial, of these outbreaks occurred at the Royal Free
Hospital, London, in 1955, during which 292 people were
affected. Indeed, outbreaks may still be occurring, and some of
the patients who currently come under the CDC-1994 CFS
definition have clinical features similar to the classical
description of post-infectious ME patients defined above.

The fact that we are still aware of these details is in no small
measure due to Dr J. Gordon Parish, who is attending this
workshop today. Dr Parish has, over many years, collected
reports of these outbreaks of ME (Parish, 1978; Shelokov &
Parish, 1989), and has a complete archive of the relevant
literature. A complete listing of these references can be found at
the MERGE web site.*

http://www.meresearch.org.uk/information/publications/workshop/spencetalk3.html


In a similar pattern with respect to the Medical Research Council
in the United Kingdom, people in the United States challenge the
CDC (from what I can gather) it seems, `til they`re also blue in
the face.


In view of the reference on the CDC website to the UK, the
claim that Myalgic Encephalomyelitis is synonymous with CDC-
CFS, and given the various emerging connections of
convenience, perhaps it would not be unreasonable for some at
this side of the Pond, the *United Kingdom*, to request some
explanation from the CDC/CFS group about this potentially
misleading aspect of their website, before the CDC invite ever
more American Citizens to visit their website, who will
consequently remain ignorant of the history and nature of M.E.
a.k.a. chronic fatigue syndrome, as this would now appear to be
the avowed intention?

BW
Doug Fraser


``````````

[Here are some very truncated extracts from Professor Rachel
Jenkins Introduction to *Post-Viral Fatigue Syndrome (Myalgic
Encephalomyelitis)* of 1991: Jenkins and Mowbray - Editors,
John Wiley & Sons ]

*...It has been said that nothing can now be learned from
the early epidemics of ME; that they happened too long
ago for us to be sure what really occurred. Nothing, of
course, could be further from the truth. Some of the
epidemics are brilliantly described in careful clinical and
epidemiological terms which we would do well to emulate
today. The men who described them raised questions
which we have yet to answer and, in their thoughtful
discussions, anticipated much of the ensuing debate on
the aetiology of the condition.

It is more than half a century since the first descriptions of
a puzzling new clinical entity began to emerge in the
medical literature, under the names of 'abortive
poliomyelitis' or a 'disease resembling or simulating
poliomyelitis'. The illness generally occurred in both
epidemic and endemic forms, although it was the
epidemics which were easiest to recognise and which
caught most medical attention.




THE EARLY EPIDEMICS

The first recorded epidemic occurred among the doctors and
nurses of several hospitals in Los Angeles, USA in 1934. On 12
June 1935, two orthopaedic surgeons, John Wilson and Pierre
Walker, read a paper before the Joint Meeting of the American
Medical Association and the Canadian Medical Association,
Atlantic City, where they reported an outbreak of supposed
poliomyelitis in Los Angeles which was not only more extensive
but also milder than any previous outbreak of poliomyelitis in
California.

Peculiar features of this epidemic which Wilson and Walker
noted were the unusual communicability of the disease, the
early peak (in June) and the large number of adults infected. In
children the disease followed the usual clinical course of
poliomyelitis, but amongst the adults, an atypical form of the
disease was observed, in which sensory, vasomotor and
arthritic symptoms predominated, and recurrent exacerbation of
acute symptoms occurred over the following 12 months. Out of
100 cases, 35 still had muscle weakness after a year.

Wilson and Walker suggested that the mildness of the attack,
the marked degree of muscle weakness without proportionate
atrophy and without loss of tendon reflexes, and the recurrences,
all suggested that this was, at the very least, atypical
poliomyelitis, rather than the usual form of acute anterior
poliomyelitis. They also considered the possibility that many of
the later symptoms complained of by the adult patients may have
been of 'functional', i.e. of psychological, origin. However, they
argued that the striking uniformity of the clinical picture
presented by the patients, and the prostrating severity of the
symptoms, led most observers to believe that an organic basis
for the complaints was present in virtually every case.

Wilson and Walker carefully described the symptoms of the
illness in 100 of the patients they saw in the orthopaedic
department of the Los Angeles General Hospital.

These symptoms included muscle weakness, involuntary muscle
contractions and twitching, clonic movements and cramps in the
affected muscles, and muscular inco-ordination. However,
sensory symptoms predominated, with pain in the back and
extremities which was often intractable, excruciating and
persistent for weeks or even months, and which only responded
to opiates.


There was also local tenderness of muscles, hyperaesthesia,
paraesthesia, and areas of anaesthesia, sometimes following
the distribution of a nerve trunk and sometimes involving a whole
extremity. Vasomotor and trophic disturbances were almost
constant findings. There was excessive sweating or abnormal
dryness of the skin, coldness, cyanosis and brittle nails. The
authors wrote 'It was the impression of many observers that a
generalised disturbance of vasomotor control occurred in these
patients, which best explained the emotional instability'.

Inflammation of the joints occurred in a third of adult cases, with
a third of these being transitory and the remaining two-thirds
developing permanent arthritic changes in the joints.


The authors acknowledged that their 100 reported cases cannot
serve to give a true cross-sectional picture of the epidemic
because of the selection factors which influence the process of
admission to an orthopaedic ward, and they commented that
many patients are included in the lists of public health reports at
the time who presented the picture of a mild and rapidly
vanishing illness.

The same epidemic was described by A. G. Gilliam in more
detail and covering the whole of the hospital, as it occurred
among the personnel of Los Angeles County General Hospital in
that same year, 1934 (Gilliam, 1938).

Dr Gilliam, writing from the Office of Epidemiological Studies,
US Public Health Service, balanced the epidemiological facts
with the clinical features, and he noted that the timing of the
epidemic in the personnel of the Los Angeles General Hospital
was similar to the time distribution of the epidemic in Los
Angeles City and County combined.

The epidemic in the community in 1934, when compared with
other epidemics of poliomyelitis, was characterised
epidemiologically by a relatively high attack rate and high
communicability, a low case fatality rate and a low paralytic rate,
relative age selection of adults over children, and coincident
institutional epidemics in the personnel of the Los Angeles
County General Hospital, the Children's Hospital, the Ross-Loos
Clinic, the Pasadena Hospital, the Glendale Medical Group and
the Orthopaedic Hospital.

There was also an outbreak among nurses in the Orange County
Hospital. None of these other institutional outbreaks were
reported in detail, and no other institutional outbreak was
reported elsewhere in California in 1934.


Gilliam obtained his clinical data by painstaking personal
interviews of the patients, together with examination of the
hospital case notes. The main features of the illness in hospital
staff as described by Gilliam were:

(a)* Fever characterised by daily fluctuations in temperature
from 97°F to 99°F (36.0-37.2°C) was more characteristic than
an elevation of temperature above 100°F (37-38°C).

(b)* Pain which was described as rheumatoid or influenzal in
character, an ache in the muscles or bones, but often of
sufficient intensity to awaken the patient from sleep, and, in most
instances, it was aggravated by exercise. It was not confined to
any particular part of the body, and characteristically varied from
day to day in its distribution. However, common sites were the
muscles at the back of the neck, between the shoulders, and in
the lumbar region of the back. Pain in the muscles of the limbs
was also common. Abdominal cramps, associated with tender
and painful abdominal muscles, were not infrequent.

(c)* Headaches.

(d)* Muscle tenderness (Gilliam reported that it was the
impression of some clinicians that the muscles found to be
tender early in the illness were those that were later involved in
weakness).

(e)* Muscle twitching, which consisted of fibrillar twitching of
muscle fibres, individual muscles or whole groups; tremors.

(f)* Nausea, and, occasionally, vomiting.
(g)* irritability and drowsiness.
(h)* Stiff neck and back.
(i)* Vertigo.

(j)* Photophobia accompanied by severe ocular pain.

(k)* Sore throat, coryza, or cough and chills and diarrhoea were
usual prodromal symptoms.

(l)* Sensory symptoms included skin hyperaesthesia,
paraesthesia, and anaesthesia, and varied from day to day.
(m)* Easy fatigability.

(n)* Menstrual disturbances (increase or decrease in flow, or
change in cycle).

(o)* Emotional upsets, including irritability and crying spells.
(p)* Memory difficulty, difficulty in concentration.
(q)* Transient personality changes of varying degree of severity.
(r)* Urinary difficulties giving a clinical picture of cystitis.
(s)* insomnia.

(t)* Localised muscle weakness, obtained from records of the
hospital physiotherapists, orthopaedic surgeons and personal
interview of the patients....


``````````

Among all employees of the General Hospital, the groups most
severely attacked were nurses and doctors, with attack rates of
10.7% and 5.4%. The picture was similar in the County Hospital,
11.4% of nurses and 6.2% of doctors being attacked...

Gilliam deduced that the observed distribution of the disease
was similar to that of scarlet fever, spread by direct personal
contact with cases and carriers...

In the late 1930s there were several epidemics in Switzerland
with similar symptoms, in both military and community hospitals,
affecting both patients and staff (Gsell, 1958). The prolonged
convalescent period was noted to be characterised by relapses,
marked fatiguability and autonomic disturbances (Gsell, 1949,
1958). There was also a small epidemic among young nurses at
Harefield Sanatorium in England at the same time in 1939
(Houghton and Jones, 1942). Pyrexia and muscle pains
persisted for up to five months, with accompanying menstrual
disturbances and spontaneous epistaxis. The authors
suggested that the condition was due to an unidentified
myotropic strain of virus...

In the early months of the winter 1948 to 1949, an extensive
epidemic of a disease apparently involving the central nervous
system (CNS) broke out in the town of Akureyri, on the northern
coast of Iceland. This epidemic, which was again at first thought
to be poliomyelitis, presented such peculiar features that the
authors decided it justified a detailed clinical description
(Sigurdsson et al.,1950). ... The cerebrospinal fluid (CSF) was
examined in eight patients, four of whom had slightly raised cell
and protein readings. Viral studies at the time failed to
demonstrate poliomyelitis, Coxsackie or known encephalitic
viruses.

In 1955, 39 patients affected by the 1948 epidemic in Akureyri
were re-examined (Sigurdsson and Gudmundsson, 1956) and it
was found that of those more severely affected in 1948, only
25% had completely recovered... the agent responsible for the
1948 epidemic would appear to be able to inhibit the
pathological effects of poliomyelitis...

A few months after the 1948 Akureyri epidemic in Iceland, an
epidemic of poliomyelitis started in May 1949 in Adelaide,
Australia. By August, cases of epidemic neuromyasthenia, as it
was then called, had begun to appear and continued to spread
until, by 1951, 800 patients had been admitted to North-field
Infectious Diseases Hospital (Pellew, 1951). ..Material from
each of five cases was inoculated into a pair of monkeys. The
monkeys inoculated from three cases remained well, but the four
monkeys inoculated from two of the cases became ill and one
died of the illness. At post-mortem examination, minute red
spots were observed along the course of the sciatic nerves.
Microscopically, infiltration of nerve roots with lymphocytes and
mono-nuclear cells was seen and some of the nerve fibres
showed patchy damage to the myelin sheaths and axon
swellings...

In the late summer and early autumn of 1950, a widespread
epidemic of poliomyelitis occurred in New York State. Most
cases were diagnosed as acute anterior poliomyelitis, abortive
poliomyelitis or 'poliomyelitis suspect'. However, two
physicians, White and Burtch (1954), noted that certain definite
distinctive features distinguished many of the cases from
poliomyelitis, and they became increasingly convinced that the
disease they were seeing was not poliomyelitis...

Many subsequent epidemics occurred in the ensuing decade in
Denmark (Fog, 1953; Pederson, 1956), Rockville USA
(Shelokov et al, 1957) and elsewhere (Parish, 1978). Detailed
descriptions of outbreaks in this country also exist for this
period. ..In 1953, 'towards the end of a busy poliomyelitis
season', 13 nurses in a Coventry hospital became ill with
symptoms involving the CNS, and were described by the
medical superintendent J. F. Galpine at Whitley Hospital,
Coventry and the bacteriologist of the Virus Reference
Laboratory at Colindale (Macrae and Galpine, 1954)....

In 1954 Acheson published an account of an outbreak of an
infection of the CNS accompanied by intense myalgia in 14
nurses resident at the Middlesex Hospital, describing its unusual
features and its resemblance to other atypical epidemics such
as those in Iceland, Adelaide and New York (Acheson, 1954)....

Acheson concluded that either the characteristics of
poliomyelitis were changing due to a milder strain of the virus or
that these cases were caused by an unidentified virus similar to
that causing the epidemic in Iceland, Adelaide, Coventry and
New York...

During the summer of 1955, the Royal Free Hospital Teaching
Group, with a total staff of about 3500, experienced an epidemic
of encephalomyelitis simulating poliomyelitis which affected
more than 300 people. By late November, 255 cases had been
admitted to the Royal Free Hospital, while the remainder were
either nursed at home or admitted elsewhere. The epidemic was
described by the consultant physician, Melvin Ramsay, and E.
O'Sullivan, the senior registrar at the time (Ramsay and
O'Sullivan, 1956), and subsequently by Richardson (1956),
Medical Staff of the Royal Free Hospital (1957), and Crowley et
al. (1957)...

It became clear early on in the outbreak that there was organic
involvement of the CNS, but there were also abnormal signs
outside, particularly lymphadenopathy and mild fever,
accompanied by severe malaise. Nearly half the cases had
cranial nerve palsies affecting mostly the oculomotor, facial and
vestibular nerves. Occasional pupillary changes occurred, but
the fundi and visual fields remained normal. Bulbar palsy
occurred in 7% of cases...

As Crowley et al. (1957) argued, the failure to isolate the
infectious agent does not mean it was not an infectious disease.
The course of the illness was wholly consistent with changing
phases of a host-parasite relationship which are reflected in the
clinical picture. ..

Acheson (1959) reviewed 14 outbreaks, including those
described in this chapter

Firstly, he drew attention to the difficulties inherent in defining a
disorder from which no deaths have occurred, and for which no
causative infective or toxic agent has been discovered. He
stated 'recognition has to depend on the clinical and
epidemiological pattern. These features must be sufficiently
characteristic to separate the disorder from other conditions'. He
drew two helpful parallels, one with the diagnosis of encephalitis
lethargica which is made on the basis of the clinical triad of
fever, stupor and ophthalmoplegia in the absence of specific
pathology or specific diagnostic testing; and the other with
Bornholm disease (epidemic myalgia or epidemic pleurodynia)
where the disease became established as a clinical entity on
clinical grounds long before the discovery of the Coxsackie
viruses.

Clinically, all the outbreaks he reviewed displayed the following
characteristics of (1) headache, (2) myalgia, (3) paresis, (4)
symptoms or signs other than paresis suggestive of damage to
the brain, spinal cord or peripheral nerves, (5) mental symptoms,
(6) low or absent fever, and (7) no mortality. In addition, (1) a
higher frequency in women, (2) a predominantly normal CSF,
and (3) relapses, have occurred in almost all outbreaks. In 11 of
the 14 epidemics which he reviewed, symptoms which suggest
activity and chronicity of the disease have persisted for months
or even years in a few cases. In eight instances, there was an
apparent predilection for the nursing or medical profession. The
case for a clinical entity depends on the distinctiveness of these
findings...

Secondly, he thoroughly reviewed the common epidemiological
and clinical features. ...

Thirdly, he confronted the issue that it might be argued that at
least some of the apparent clinical similarities are due to
unconscious bias or undue emphasis on the part of observers
familiar with the features of previous epidemics....

Fourthly, Acheson carefully examined the question of hysteria as
a cause of illness. ...Epidemic hysteria has been recognised for
many centuries as a particular hazard in institutions containing
women or female adolescents. However, as Acheson points out,
no-one can seriously contend that every patient in all the
outbreaks has been hysterical...

Acheson's final points against mass hysteria as a major factor in
the syndrome were the consistency of the course of illness, and
the similarities in the symptoms described, in spite of a wide
variation in the types of community affected, from hospital staffs
on the one hand to semi-rural and urban populations on the
other...

A further description of an outbreak, which, like Acheson's
review, is well worth reading in the original and which was not
known to Acheson at the time he wrote his review, is a general
practitioner's careful analytical description of the
epidemiological and clinical features of an epidemic in his
practice in Dalston, Cumbria in 1955 (Wallis, 1957)....

Wallis, like the other early observers of this condition, made the
diagnosis on clinical grounds in the absence of any specific test
and without the isolation of a causative organism. His clinical
criteria were dizziness; headache and extreme lassitude;
drowsiness and lethargy by day and restlessness by night;
blurred vision, diplopia on upward and lateral gaze, and a mild
conjunctival reaction; spontaneous severe pain in the back of the
neck and the lower limbs, and frequently also in the back and
upper limbs; muscle tenderness and some loss of muscle
power; paraesthesia and some degree of sensory impairment;
tender enlargement of lymph glands in the neck, inguinal region
and axillae, splenic and hepatic tenderness and subcostal pain;
depression, with feelings of foreboding and a labile emotional
state; and low-grade fever or subnormal temperature with mild
tachycardia....

During these same years, endemic cases also appeared but
received less publicity for obvious reasons. Innes, writing from
the Neurological Unit in Edinburgh in 1970, reported four cases
which presented at intervals of some months, did not arise in a
closed community, and were all males; there was no
poliomyelitis 'scare' at the time. His case histories resembled
the descriptions of benign ME but seemed to follow an initial
enteroviral infection... Innes warns that cases such as these are
in some danger of being dismissed as 'functional'. ...

Lewis-Price (1961) reported the cases of two patients, who had
no contact with any known case of myalgic encephalitis or with
any other well-defined virus illness, who developed symptoms of
benign ME. ..

Kendall (1967) described two endemic cases of epidemic ME
with severe psychological sequelae persisting over many years..

They both developed such severe and longstanding changes in
mood and behaviour afterwards that Kendall argued that
damage to cerebral mechanisms underlying the control of mood
and behaviour must underlie such severe and prolonged
disturbances....

In 1978, a symposium was held at the Royal Society of Medicine
(RSM) to discuss the disease and plan research. There was
clear agreement that ME is a distinct nosological entity...

From the patient's point of view, the adjective 'benign' is also
misleading, because the illness may be devastating even though
it is not fatal. A British Medical Journal leader at the time
concluded that the organic basis of the illness was now clear
from the finding that the putative agent can be transferred to
monkeys (Fellow and Miles, 1955), the detection of an
increased output of creatine (White and Burtch, 1954; Albrecht
et al, 1964), the persistent finding of abnormal lymphocytes in
peripheral blood (Wallis, 1957), the presence of lymphocytes
and an increased protein concentration in some patients
(Acheson, 1959) and the neurological findings. At the RSM
symposium, more new evidence was produced to support the
organic nature of the disease. Increased serum concentrations
of lactic dehydrogenases and transaminases have been found in
several patients in the acute phase. Immunological studies in the
outbreak at Great Ormond Street Hospital showed a high
incidence of anti-complementary activity and the presence of
ill-defined aggregates on electron microscopy of acute phase. A
perplexing finding, suggesting the possibility of a persistent virus
infection, was the ability of lymphocytes from patients to
proliferate and survive in vitro for up to 19 weeks (Editorial,
1978)....

Compston concluded: Those of the medical staff of the Royal
Free Hospital who witnessed the epidemic in 1955 are firmly of
the conclusion that they were dealing with an organic disease
complicated by encephalomyelitis in which myalgia was a
dominant feature. Objective evidence of brain stem and spinal
cord involvement was observed...


~~~~~~~~


Research holds all our answers
Praying for world peace
How does a human heart hurt so deeply and still survive is beyond ME
CFIDS FM...

Enjoy the sunsets and sunrises,

Diana Saba
Retired Nurse
FM ME/CFIDS
Related Neurological Disorders
CDC's Wm Reeves Must Go
Bring Back the GAO
Where did over 4 Million $'s of misappropriated funds go to?
CDC website linked NCF to Porn for over one year ~ Why?

Grassroots Action for Myalgic Encephalomyelitis / Chronic Fatigue
Syndrome
http://www.co-cure.org/Congressional_Action.htm

Please Support NCF's Research Plans
http://www.ncf-net.org/
http://www.ncf-net.org/Discoveries.htm

Please Sign Petitions
http://www.petitiononline.com/MEitis/petition.html
http://www.petitiononline.com.cfs2004/

May 12th Awareness Day
http://www.geocities.com/capitolhill/4277/

The One Campaign
http://www.one.org/

The HHV-6 Site
http://hhv6.freeservers.com/

Betrayal By the Brain:
The neurological basis of chronic fatigue syndrome, fibromyalgia
syndrome and related neural network disorders.
by Dr. Jay A Goldstein
http://home.vicnet.net.au/~mecfs/general/goldstein_summary.html

CFSAC Meeting Presentation ~ June 21, 2004
http://listserv.nodak.edu/scripts/wa.exe?A2=ind0407a&L=co-cure&F=&S=&P=541

~*I truly hope the January 2006 CFSAC meeting will be addressing our
continued efforts and concerns about our nations blood supply and FM
ME/CFIDS and all related neurological disorders*~

The January 10, 2006 CFSAC meeting did not take place
http://www.hhs.gov/advcomcfs

FM ME CFIDS Information Forum
Co-Cure Archives
http://listserv.nodak.edu/archives/co-cure.html

TCJRME
http://www.geocities.com/tcjrme/

Reading, Researching, Posting to AMF
1997-2006
http://hometown.aol.com/dgsaba/myhomepage/index.html

Type AMF Abusers into the google search engine box.
http://groups.google.com/group/alt.med.fibromyalgia/search?q=AMF+Abus...

Be safe...Be aware...Be alert...

"What lies behind us and what lies before us, are tiny matters,
compared to what lies within us" ~ Ralph Waldo Emerson

.