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Co-Cure Weekly Digest of research and medical posts only - 9 Jul 2007 to 16 Jul 2007

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Date:    Tue, 10 Jul 2007 14:26:18 -0400
From:    Fred Springfield <fredspringfield1 VERIZON.NET>
Subject: RES: Symptoms of autonomic dysfunction in chronic fatigue syndrome

Symptoms of autonomic dysfunction in chronic fatigue syndrome.

Journal: QJM. 2007 Jul 7; [Epub ahead of print]

Authors: Newton JL, Okonkwo O, Sutcliffe K, Seth A, Shin J, Jones DE.

Affiliation: From the Fatigue Interest group and Liver Research Group,
Institute for Cellular Medicine, University of Newcastle, Newcastle, UK.

NLM Citation: PMID: 17617647

BACKGROUND: Chronic fatigue syndrome (CFS) is common and its cause is unknown.

AIM: To study the prevalence of autonomic dysfunction in CFS, and to
develop diagnostic criteria. DESIGN: Cross-sectional study with independent
derivation and validation phases.

METHODS: Symptoms of autonomic dysfunction were assessed using the
Composite Autonomic Symptom Scale (COMPASS). Fatigue was assessed using the
Fatigue Impact Scale (FIS). Subjects were studied in two groups: phase 1
(derivation phase), 40 CFS patients and 40 age- and sex-matched controls;
phase 2 (validation phase), 30 CFS patients, 37 normal controls and 60
patients with primary biliary cirrhosis.

RESULTS: Symptoms of autonomic dysfunction were strongly and reproducibly
associated with the presence of CFS or primary biliary cirrhosis (PBC), and
correlated with severity of fatigue. Total COMPASS score >32.5 was
identified in phase 1 as a diagnostic criterion for autonomic dysfunction
in CFS patients, and was shown in phase 2 to have a positive predictive
value of 0.96 (95%CI 0.86-0.99) and a negative predictive value of 0.84
(0.70-0.93) for the diagnosis of CFS.

DISCUSSION: Autonomic dysfunction is strongly associated with fatigue in
some, but not all, CFS and PBC patients. We postulate the existence of a
'cross-cutting' aetiological process of dysautonomia-associated fatigue
(DAF). COMPASS >32.5 is a valid diagnostic criterion for autonomic
dysfunction in CFS and PBC, and can be used to identify patients for
targeted intervention studies.

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Date:    Wed, 11 Jul 2007 19:14:54 +0200
From:    Jan van Roijen <j.van.roijen CHELLO.NL>
Subject: act,med: Letters re. NHS Clinics - July 2007 -(RiME)


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Campaigning for Research into ME (RiME)
Letters re. NHS Clinics - July 2007

Ref: 602 Leader of Kent Maidstone Group

Dear Dr Turner,

I am writing to you in your capacity as Chairman of the APPG on

I attended the CBT clinic in Maidstone and do not believe that it
offers anything to those with neurological conditions like ME.
Those members of our Group I have spoken to feel that that
money would be far better spent on biomedical research instead
of psychiatric treatment offered by the Kent clinics.

At the APPG meeting of 22 February 2007, I sent a message
stating that our Group welcomed the fact that the APPG
recognized ME as a neurological illness, as defined by ICD 10
G93.3, and asked if you were aware that the Kent clinic should
by definition exclude patients who meet this criteria.

People with ME in Kent are not concerned about being
excluded, but are worried that the service offered by the clinics is
not about their condition (ie neurological ICD-ME). I enclose
letters from people who are boycotting them for this reason, as
they do not want funding of them to continue.

Is it possible to let parties other than MEA and AfME, despite
their much smaller membership, have their say at future APPG
meetings, and include those who can not attend because of their
condition, to have their say by proxy?

I ask that at the APPG meeting on 12 July 2007, that the Group
discuss biomedical research and not the NHS clinics which offer
the wrong kind of treatment entirely.

May I also request that you read these points out at the meeting?

I look forward to hearing from you.

Ref: 550 Lancs

For the past twelve years there has been a CFS clinic at North
Manchester General Hospital run by four specialists who believe
ME is a biological illness. The clinic has taken referrals from all
over the North West of England.

When the Manchester CNCC on CFS/ME was set up two years
ago a psychiatrist, unknown to me, who also works at North
Manchester General got the job of Clinical Champion. The four
local specialists who believe ME is a biological illness were
never even told that the job of Clinical Champion was available
until AFTER the post was filled. The Manchester Psychiatrist
Clinical Champion is now also chair of the whole English CNCC
on CFS/ME collaborative. At the launch meeting for the
Manchester CNCC he quoted only the psychosocial theory of
ME. I have the lecture slides to prove this. At the lecture he
expressed the psychosocial dogma that doctors who believe
ME is a biological illness are an obstacle to the recovery of ME
sufferers. When I asked him at a committee meeting to confirm if
he truly believed in this dogma he refused to answer.

I have just been told that after twelve years the CFS clinic run by
the specialists who believe ME is a biological illness is to be
closed and the psychiatrist is to get all the money that used to go
to the running of the clinic.

People in Greater Manchester will no longer have access to an
NHS specialist who believes ME is a biological illness. This is
all thanks to the new CNCC on CFS/ME set up. In future we will
only have access to a service controlled by a psychiatrist who
believes ME is a psychosocial illness.

I am horrified that the Chair of the CNCC on CFS/ME
Collaborative for the whole of England is a psychiatrist who
believes ME is a psychosocial illness and is opppsed to doctors
who believe ME is a biological illness.

The Chair of the Collaborative is in charge of training and
education for all the CNCCs on CFS/ME...

Ref: 604 Yorks (Castleford)

Dear Dr Turner,

... father of a young ME Sufferer aged 25 who has suffered from
ME for the past 15 years. During this time she has had to put up
with disbelief from the medical and educational establishments.

Various management theories and treatments have been
suggested and tried all to no avail; some have had short term
benefits but nothing lasting. Even counselling at the Leeds CFS
Clinic, to help her come to terms with her fatigue has not been of
such a great benefit, she still suffers from the physical aspects of
ME, and the pain and depression that goes with the continues
ignoring of the fact that what is really needed

It is with the past in mind that I consider the 8.5 million spent on
such management would have been far better spent on
biomedical research. I would be grateful if you would mention
this at the APPG Meeting on July 12 2007...

Ref: 605 Yorks (Leeds)

Dear Dr Turner,

I am writing to you in your capacity as Chair of the APPG on ME,
and the meeting July 12 which will discuss the issue of the NHS
'CFS/ME' Clinics.

The Leeds CNCC has nothing to offer people with genuine ME. I
haven't attended nor has anyone else I know with ME.

I enclose information about the 2006 Florida Conference. How
much longer can the UK Government ignore the overwhelming
evidence which indicates physical damage in ME patients?
ME needs proper biomedical research not more psychiatric
treatment ie Graded Exercise/CBT programmes.

Since I will be unable to attend July 12 because of the ME, I ask
that you include these points by proxy...

Ref: 607 Derbys

... I was the leader of MEND (North Derbys ME group) from
1992 through the 1990's. It had a membership of 250.

Please note that the title of the Group was Myalgic
Enacephalomyelitis (ME).

The only way forward to help people with ME is proper research
into the physical causes and disease process of the
neurological illness ME, as defined by WHO G.93.3 and the
Canadian Criteria.

Re. the new centres which have been set up: The nearest is the
Sheffield CNCC which offers CBT - P.35 of 'CFS/ME Service
Investment Program Report 2004-6', authored by Prof. Pinching
+ Pat Noons, (enclosed) - I can't relate to it at all.

Not only is this form of treatment inappropriate to ME patients,
but I feel the results will be 'skewed' (imprecise admittance
criteria) and used by the Government as an excuse not to
research the physical causes of ME.

Is it not ironic that this meeting is not about the former - ME
Research - but psychiatric/psychological models of treatment
which are not helpful to people with ME?

Please read this out July 12, if you have the opportunity.

Ref: 609 Leics

Dear Dr Turner,

The East Midlands CNCC is not about neurological ICD-ME and
offers same old, same old...

I think there is a problem in that the APPG gives too much
weight to what the MEA and AfME say on matters such as the

Many who don't subscribe to the above (the vast majority with
ME) would like to be at the APPG meeting July 12 to (1)
challenge the nature of the 'CFS/ME' clinics (2) ask that the
8.5m be diverted into biomedical research.

Since I will be able to attend, would you please read out thses
points on my behalf...

Ref: 612 Bucks

Dear Dr Turner,

I am writing to you in your role as Chair of the All Party
Parliamentary group on ME.

 From 1989-94, as secretary to the Beds/Herts Group, whose
membership averaged 450-500, I met many whose career had
been suspened if not ended and lives ruined by the physical
consequences of ME.

 From (a) listening to the experiences of members of this group
(b) professional experience (NHS physiotherapist) (c) personal
experience of ME, I am convinced of the potentially damaging
effects of exercise and/or psycho-therapeutically based
management of ME.

Re. the centres which are currently being set up, the nearest
seems to be the clinic at Barts in London. I don't deem the types
of treatment which are being practiced there ie Graded Exercise
and CBT as an appropriate way forward for patients with the
neurological illness ME.

There is ample and irrefutable evidence of the physical basis of
ME. Do you think it shameful that the British Govt lags behind
countries such as Chile and Latvia in promoting and supporting
research into the physical causes of ME, so these patients have
a chance to recover and resume a useful position in society?

This, in my opinion, is what the APPG should currently be

Since I am unable to attend the next APPG meeting July 12,
would you please make these points by proxy...

Ref: 615 Cornwall

... The clinics in the West country are ****.

I hope the ME issue, like the property crisis, will lend weight to
the Cornish Independence Movement. We pay tax to the
Treasury at Westminster, and what do we get in return? Clinics
run by psychiatrists and psychologists, and the stupid PACE +
FINE Trials. Just think, if we had a Cornish Parliament we could
have a say in how those taxes are spent; hopefully, a biomedical
ME Research program...

Pleased you are going to Westminster and raising people's
concerns re. the clinics. Aren't there any people in London/South
East who can support you...

Ref: 617 Surrey

Dear Dr Turner,

I sent the enclosed to a number of MPs last June:

.... In May you asked the Secretary of State for Health a question
about the new NHS 'CFS/ME' Centres... The nearest to me is
Sutton. The job description... appeared on AfME's website, last
year (see RiME Newsletter, Spring 2005).

Do you really think that the above will help with the neurological
illness ME, and that it is worth saving? Do you not think that ME
might be being confused with something else? One wonder if
politicians are paying sufficient to the crucial issue of
nomenclature... If you want to help people with ME, I suggest
your next PQ is about why the Govt is not researching the
underlying physical causes of ME...

A year on, there is little I can add to these points.

I sincerely hope the funding for the 'CFS/ME' Clinics does run
out. I would like to see the money diverted into biomedical ME

I won't be able to attend the meeting July 12, so please make
this point in my absence...

Ref: 618 London (Greenwich)

Dear Dr Turner,

I fail to see how CNCCs like the one at Barts will help people
with neurological ICD-ME.

Let's compare what is in its leaflet 'The Chronic Fatigue Service'
to the NICE Draft Guidelines:

Barts Leaflet: GET: GET is about gradually increasing your
physical activity. Usually you see a physiotherapist who helps
you work out a basic activity routine, then together you plan to
gradually increase the amount of physical activity or exercise you

NICE: GET: Adults... should be offered a program that
includes planned increases in duration of physical
activity/exercise followed by increases in intensity leading to
aerobic exercise....

Other clinics eg Kent also prescribe GET. A leaflet entitled West
Kent Chronic fatigue Service refers patients to Trudie Chalder's
book, 'Coping with Chronic Fatigue' (didn't you sign a document
- The Gibson Report - which descbibed her work 'impressive'?)
which says Ch.6, 'Exercise three times a week, half an hour of
exercise. Make sure it is something you enjoy. A brisk walk in
the country is enough... '

Also: Base-Line Activity:

NICE: Managing setbacks: During a setback, when
there is an increase in CFS/ME symptoms or symptoms are
exacerbated, exercise or physical activity should be maintained
if possible to avoid the negative effects of de-conditioning and
withdrawal form activity....

Are you aware that rigid base-lines are being implemented via
the NHS Clinics eg a person who attended the Maidstone Clinic
says, ' .... Our individual baseline was then set at whatever we'd
managed that week, with instructions to maintain it at that level.
This wasn't at all successful as a number of the group then
pushed themselves for the following two weeks, to their

Dr Turner, didn't you condemn the NICE Guidelines, 'no use to
man nor beast' (APPG Meeting Nov. '06) but support the
'CFS/ME' Clinics per se (House of Commons 6/3/06)? In which
case are there not anomalies that need addressing?

I would like to be there July 12 to put these points to you to you
directly but, as I will be unable to, would you please raise them
by proxy, and then address them.

I ask for a reply, also, in writing please...

Ref: 620 Kent (Isle of Grain)

In January 2003 I had an appointment to attend the Maidstone
Clinic (Maidstone is approx 25 miles from where I live). The
Chronic Fatigue Clinic was situated away from the hospital next
to the psychiatric unit. I was interviewed twice to assess whether
I was suitable for CBT. At the time I was not aware of being
assessed for CBT, but found out later. I did not want to go as,
having had ME 11 years, I was pacing and adjusting my life style
to compensate for the ME. However, if I did not go I could never
cite or say what happened.

In January 2004 I was given an appointment at Medway
Maritime Clinic (14 miles from home); I could drive there and
park in the disabled bays. I certainly was not ready for the trek
through Medway hospital to the appointed room; by the time I
reached the room I was in pain, exhausted and a bit out of it.
Undeterred, I stayed; the room started to fill up with other ME
people, filling up the uncomfortable chairs. There must have
been about 15 of us and, at the time, I thought it very strange that
a CBT session should be a group as CBT is personal and
everyone is an individual and will have different problems; some
will be to shy to share; others will dominate the group and the
whole thing will become ineffectual; as people needs are not met
they will not come again and fall through the net, which did

The session started the same as any other group, name
introduction act. There were three leaders: a lady who ran the
session, a physiotherapist and a nurse. I am not sure why they
were there as they did not do much. We were all asked our
goals and aspirations, and what we would like to gain from this
experience. Some of the answers saddened me, as people
would say I would like to get better from having CBT, others just
wanted some relief. Personally, I wanted less pain and
exhaustion. I asked about pain control and was told there was

The monthly sessions entailed forms to be filled in at home on
our pacing methods. If you know anything about ME trying to fill
in forms when you have cognitive fog just does not happen.
When I am ill I cannot write a letter let alone fill in what I am doing
as I have not got the energy to even find a pen.

Each month I would turn up and for over a week after attending I
was ill from pain and exhaustion. However, still undeterred, I
made it for the whole year's sessions leaving out one as I was
too ill to go.

October 2005, they ended the monthly get togethers and told us
we would be emailed re. our next session.

October 2006, we were now down to five persons and were
asked how we felt the CBT had helped. And that this was the last
appointment; the look on the four people with me was one of
astonishment and questions like - is that it, no follow-up? We left
in utter dismay; we had seen no consultants; nothing was ever
done for us medically, just flip charts and forms.

In one of the sessions a man collapsed we were afraid for him
because most of us knew that when a person collapses with ME
he needs to be laid down and cared for; as he fell forward in his
chair, the group leader said leave him, he will be ok; there was
no compassion for this man.

Conclusion: ... The whole exercise was a waste of NHS money
as we were all long term sufferers who had learnt to PACE,
through trial and error. For the people who suffered ME pain
there was no help; we were told that for our pain it would be
better if we steer clear of certain kinds of pain killers that were
likely to help, as they were mainly morphine based and we would
end up having addictive problems.

Extracts from RiME Newsletter, Autumn 2005:

Kathleen McCall, leader of the Winchester and
Eastleigh ME Group:

... What makes me laugh is that to our face they call this the
ME/CFS Clinic when in reality it's the Hants and IOW Chronic
Fatigue Service.... We are meant to be reassured by the fact
that the Southampton Clinic is modelled on the Wareham Clinic
in Dorset. From correspondence I've received from PWME
who've attended the Wareham Clinic, I'm not reassured at all, as
Wareham seems to show a strong psychiatric bias of it's own.
One ME patient at Wareham was told she was having treatment
based on physical strategies for dealing with ME; they then
wrote to her GP saying treatment was focused on 'identifying
and challenging negative thought processes that could have
hindered her recovery... ' What PWME primarily want is proper
research into their condition and, with this mind, we support
RiME's efforts... ''

... Chair of Birmingham Solihull Group, 13/7/05:

The members wish to express their deep concern that the
patients' representatives... are clearly being excluded form any
meaningful dialogue in the development of the new services for
ME/CFS at the Birmingham and West Midlands CNCC and the
S Birmingham LMDT. Assurances were given that, although the
Birmingham + Solihull Mental Health trust was chosen to 'site'
the bid, the new ME/CFS services would operate independently
from the psychiatric service. This is not the case.... Accordingly
Solihull and S Birmingham Support group have advised their
patient representatives to disengage from any further

The latter, 11/2/07:

I see West Midlands CNCC going the same way as many others
- very short of funding and not much on offer in the way of
anything except diagnosis. Our members' view is mostly the
same as your contacts - nothing in it for them and certainly not
what they wanted. We asked the members who had been to the
clinic to rate it out of five and we had a lot of zeros.

<rimexx tiscali.co.uk>


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Date:    Fri, 13 Jul 2007 11:33:48 -0400
From:    "Bernice A. Melsky" <bernice.melsky1 VERIZON.NET>
Subject: RES: Increased Levels of Neurotrophins Are Not Specific for  Chronic Migraine: Evidence from Primary Fibromyalgia Syndrome

Increased Levels of Neurotrophins Are Not Specific for Chronic Migraine:
Evidence from Primary Fibromyalgia Syndrome.

J Pain. 2007 Jul 3; [Epub ahead of print]

Sarchielli P, Mancini ML, Floridi A, Coppola F, Rossi C, Nardi K,
Acciarresi M, Alberto Pini L, Calabresi P.

Neurologic Clinic, Department of Medical and Surgical Specialties and
Public Health, University of Perugia, Perugia, Italy.

PMID: 17611164

All data obtained in experimental animal pain models support the role of
nerve growth factor (NGF) as a putative candidate intervening in the
pathogenesis of chronic pain, including chronic daily headache (CDH).

Few studies have been carried out to establish its role in maintaining pain
states in humans. The present study was aimed at investigating
cerebrospinal fluid (CSF) levels of NGF and brain-derived neurotrophic
factor (BDNF), both measured by sensitive immunoassay, in 20 chronic
migraine (CM) patients and 20 patients affected by primary fibromyalgia
syndrome (PFMS), compared with those of 20 age-matched control subjects.

Significantly higher levels of both neurotrophins and glutamate were found.
A significantly positive correlation emerged between CSF values of BDNF and
those of NGF (r = .61, P < .001; r = .53, P < .01) and glutamate (r = .44,
P < .02; r = .51, P < .01) in CM and PFMS patients, respectively.

These findings suggest the possibility of a NGF-mediated up-regulation of
BDNF involved in the pathophysiological events underlying long-term
neuroplastic changes in persistent chronic painful conditions, such as CM
and fibromyalgia. NGF might indirectly exert its effect through enhancing
glutamatergic transmission via BDNF. The above mechanisms could account for
sustained central sensitization in both chronic pain states.

PERSPECTIVE: This article presents findings of higher NGF and BDNF levels
correlated to increased glutamate levels in the CSF of both chronic
migraine and fibromyalgia patients. This opens new insights into the
pathogenic mechanisms of chronic pain and offers clinicians new therapeutic
perspectives targeting the above mechanisms in both painful disorders.

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Date:    Fri, 13 Jul 2007 19:18:07 +0200
From:    "Dr. Marc-Alexander Fluks" <fluks@COMBIDOM.COM>
Subject: RES,NOT: CDC sponsors CFS photo exhibit

Source: CNHI News Service
Date:   July 13, 2007
Author: Julie Kirkwood
URL:                                        http://www.eagletribune.com/pulife/local_story_194093857?keyword=topstory

Fighting fatigue: Local woman, art show work to battle stigma of chronic
fatigue syndrome

Jean Harrison knows that some of her former colleagues in the art world
think she was a prima donna, or worse, that she was lazy.

Toward the end of her career restoring paintings, she was working at the
Peabody Essex Museum in Salem, Mass., and had days when she couldn't get
herself out of bed before 1 p.m. She often worked at the museum alone
until 11 p.m. or later eating Cheez-It crackers and drinking Diet Coke.
Her work sometimes wasn't finished until the very last minute. Some days,
she slept 16 or 18 hours.

Thinking it might be depression, she saw a doctor. She took kung fu
classes, hoping exercise would help. She even got tested for attention
deficit disorder. "I was eager to find anything that would treat this,"
Harrison said. "I knew there was something wrong." Nothing worked. She got
worse. "I went to the museum one day and said I thought I would probably
be out of work for a while," Harrison said. "I was crawling on the floor -
crawling, literally - to get to the bathroom... I was probably asleep
almost 20 hours a day, easily."

That was in 1994. Harrison, 54, now knows she has chronic fatigue
syndrome, a disease that affects an estimated 1 million Americans, the
majority of whom have never been diagnosed.

It is a disease that many people assume is all in the patient's head, even
though numerous research articles have been published showing otherwise,
said Kim McCleary, president and chief executive officer of a patient
advocacy group called The Chronic Fatigue and Immune Dysfunction Syndrome
Association of America.

That's why The CFIDS Association has put together a photo exhibit, funded
by the federal Centers for Disease Control and Prevention, of people who
have chronic fatigue syndrome. It opens at the Boston Public Library on
Monday, July 16. "We chose people who might, as a group, represent people
you'd see in the mall or the library, people who would remind you of all
the people in your life that could have this," McCleary said.

The purpose is to help the roughly 80 percent of patients who don't know
they have the disease to learn about chronic fatigue syndrome and feel
comfortable seeking help, she said. "This is real and it has a devastating
effect on people's lives," McCleary said. "But there's hope out there.
There's courage and dignity, even though there is still some stigma."

Harrison believes her chronic fatigue symptoms started when she was only 6
years old, and have reoccurred periodically throughout her life. She was
lethargic through most of her childhood, but she got good grades and
breezed through Wellesley College, she said, earning an art history
degree. Then she had a bad episode several years later when she was in
England learning art restoration. She felt ill and her glands were so
swollen, she said her doctor thought she had lymphoma. This was in the
1980s, a few years before the phrase "chronic fatigue syndrome" was coined
and made a big splash in the American media.

What brought it to the public's attention were two cluster outbreaks of
the symptoms, McCleary said, and the scientists looking for the cause
quickly discovered other patients who weren't associated with the
clusters. The stigma followed close behind, as patients - often Caucasian,
upper-middle-class women who could afford to push for answers - went to
their doctors complaining of symptoms that couldn't be confirmed by any
laboratory test.

"The term 'yuppie flu' came into use," McCleary said. "That was a real
misnomer but it stuck. Then it sort of developed into this perception that
these were just whiny, white women - type A personalities - who said 'I
want it all,' then decided they didn't want it all anymore and this was
their way out... Medical providers just sort of wrote these people off
as having a character weakness or something. It really did create a
barrier to medical care."

Harrison was fortunate enough to find a doctor who took her condition
seriously and supported her, even when she wanted to try an experimental
new treatment. Harrison had read studies showing that some chronic fatigue
syndrome patients have low blood volume, so she went to Salem (Mass.)
Hospital to get tested. Sure enough, her blood volume was low.

Her doctor supported her decision to try something experimental: regular
infusions of saline solution directly into her bloodstream. Initially the
infusions were given through her arms, but she now has a Port-A-Cath
surgically implanted in her chest. She gives herself infusions several
times a week.

Though the infusions made her feel much better, she said chronic fatigue
is still something she fights every day. In some ways it's harder now, she
said, because she looks healthy. "I'm not missing an arm," Harrison said.
"I'm not missing a leg. I look fine."

As a result, people don't understand why she avoids even the lightest
physical exertion, which she has learned through experience will make her
exhausted for days.

Even her own family looks at her with skepticism when she suddenly has to
lie on the floor because her blood pressure has dropped, even though
"orthostatic instability" (instability when standing) is a well-documented
side effect of chronic fatigue syndrome.

When Harrison stands up, her blood pressure drops, her pulse races, she
feels dizzy and her brain goes haywire. If she stands up in the middle of
a telephone conversation, she said, she loses her train of thought. "I'm
not stupid," she said. "It's just there's something neurologically wrong."

Harrison said she hesitated about telling her story because some people
still don't take the disease seriously. She said she knows other people
living North of Boston who have chronic fatigue syndrome but don't tell
anybody because they don't want to lose credibility. Instead, she said,
they say they have a back problem, or make up some other excuse to lie

What made her decide to tell her story is the same thing that McCleary
believes motivated patients to have their portrait taken for the chronic
fatigue photo exhibit.

"It's so important that the message get out, how devastating this can be,"
Harrison said.

If you go

* What: "The Faces of Chronic Fatigue Syndrome" photo exhibit, part of a
  $6 million public awareness campaign funded by the U.S. Centers for
  Disease Control and Prevention
* Where: Boston Public Library, 700 Boylston St., Boston
* When: Monday, July 16, through Monday, July 23
* How: Admission is free. For more, call 800-442-3437 or check out http://www.cfids.org.

(c) 2007 Community Newspaper Holdings, Inc.

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Date:    Fri, 13 Jul 2007 20:54:33 -0400
From:    "LK Woodruff <lkw777 charter.net> [via Co-Cure Moderators]
Subject: MED: ME - Tests which can aid diagnosis


ME: Tests which can aid diagnosis include:

 SPECT and xenon SPECT scans of the brain

 SPECT scans have demonstrated decreased cerebral blood flow most
frequently in the frontal, parietal, temporal, occipital and brain stem
areas of the brain. This decrease in cerebral blood flow has also found
to be worsened further still 24 - 48 hours post-exertion. These
abnormalities have also been shown to correlate with clinical status.
(Carruthers et al. 2003)

Dr  Byron Hyde MD adds that, 'I do not describe a patient as having
M.E. unless there is an abnormal SPECT. If the SPECT is normal,
I often repeat it along with xenon SPECT. If the brain scans remain
normal, I conclude that it is unlikely to be M.E.' (Hyde, 2003)

 MRI scans of the brain

 MRI scans have shown the presence of small white matter lesions
 predominantly in the frontal lobes. Punctate, subcortical areas of high
 signal intensity consistent with edema or demyelination were identified
by  MRI in 78% of M.E. patients (similar to those seen in MS). The
abnormalities in M.E. patients most closely resemble those seen in
AIDS encephalopathy.

 Research has shown that an estimated 80% of M.E. patients will have
abnormal MRI scans. (Hyde, 2003) (Carruthers et al. 2003) M.E.
patients with abnormalities on MRI have been reported as being more
severely impaired than those without such abnormalities. In a comparison
of intracranial abnormalities in M.E. patients by MRI and SPECT, the
SPECT scan abnormalities appeared to correlate with clinical status
while the MRI changes were irreversible. (Carruthers et al. 2003)

 MRI scans are also not recommended however for those patients which
relapse when exposed to loud noises (a common symptom of M.E.); an
MRI scan can cause severe and extended relapse in such patients.

Dr Byron Hyde MD also explains that a normal MRI does not conclusively
prove that a person has no CNS dysfunction as the MRI demonstrates
only abnormal anatomy and so a normal MRI should never be used to
prove that a person does not have CNS dysfunction or is not ill. (2003)

 PET scans of the brain

 PET scans have shown decreased metabolism of glucose in the right
 mediofrontal cortex. PET scans have also shown generalised hypoperfusion
of  the brain with a particular pattern of decreased neuronal metabolism in
the  brain stem. (Carruthers et al. 2003)

(CT scans however are not appropriate or useful for diagnosing M.E. or
for  investigating M.E. pathology. Most M.E. patients will have a normal
CT scan.)

 Neuropsychological testing

 Of the CNS dysfunctions that make up M.E., cognitive dysfunction is easily
 one of the most disabling characteristics of the illness. The cognitive
 dysfunction in M.E. can be extremely severe. (Hyde, 1992)

Neuropsychological testing can be used to identify cognitive dysfunction
and/or to confirm a M.E. diagnosis. It should focus on the abnormalities
known to differentiate M.E. from other causes of organic brain dysfunctions.
(Carruthers et al. 2003)

Dr Sheila Bastien PhD. is easily the expert in this field with over 20
 years experience in neuropsychological testing and more than 6 years
 experience in applying these tests to M.E. patients. She explains that:

 Deterioration of IQ levels, as well as cognitive and motor dysfunction in
 these patients, suggest a pathological process in the brain. The pattern of
 focal and lateral impairments is consistent with patients who have this
 particular neurologic dysfunction. The impairment pattern is consistent
 across the study group [of M.E. patients] although impairment levels vary.
 This pattern is not seen in other diseases or injuries, such as Alzheimers,
 stroke, head injuries, multiple sclerosis, systemic lupus erythematosis,
 personality disorders, depression, psychosis, malingering, anxiety or panic
 disorders, somatisation or situational stress disorders. The pattern of
 impairment is one of focal and lateral deficits, consistent with a
 multi-focal organic brain syndrome. Tests suggest that the most impaired
 focal areas are the left temporal, right paretal, and left temporal lobes;
 although there are lesser bilateral impairments in the opposite lobes as
 well. (1992, pp. 453 - 454)

Dr Byron Hyde MD adds that: 'This is a complex type of testing, and a
 physician should attempt to locate an experienced neuropsychologist without
 ties to the insurance industry. Most neuropsychologists today are employed
 by the insurance industry, and if they find too much pathology, I suspect
 that they are no longer engaged. Do not be fooled by a negative
 insurance-paid neuropsychological report; psychologists whose primary
 training is not neuropsychology prepare many of these reports.' (2003)

 One of the most useful texts on neuropsychological testing in M.E. is
 chapter 51 of the book 'The Clinical and Scientific Basis of ME' written by
 Dr Sheila Bastien Ph.D. Several other chapters of this book also describe
 the various cognitive effects of M.E. in detail. (Details of this book are
 given below.) See also The Ultra-comprehensive Myalgic Encephalomyelitis
 Symptom List for more information about the specific cognitive deficits
 commonly seen in M.E.

 EEG brain maps and QEEG brain maps

 95% of M.E. patients have been found to have abnormal cognitive-evoked
EEG brain maps (Hooper, 2001 [Online]). But Dr Byron Hyde MD argues
that QEEG brain maps are even more accurate:

 An EEG only records activity on the outer millimeter of the brain. A QEEG
 simply an EEG attached to a computer that contains appropriate software. A
 QEEG will immediately demonstrate tumors and brain activity or lack of it
 related to specific stimuli that are simply not possible to detect on a
 non-computer-driven EEG. Using QEEG technology operated by an expert
 physician, we have been able to demonstrate not only lack of normal
 in ME patients but migration of the normal activity centers from injured
 areas to different parts of the brain. (Hyde, 2003)

 Romberg or tandem Romberg test

 The test involves standing with eyes open and then with eyes closed with
 feet together or one behind the other. A positive Romberg is when the
 position is maintained with eyes open but not when they are closed. It is a
 useful test of brain stem function. Professor Malcolm Hooper explains that,
 'In his 1995 Australian Workshop, M.E. expert Dr Paul Cheney said that
more than 90% of patients have an abnormal Romberg versus 0% of controls.'
 (Hooper et al. 2001 [Online.])

 Neurological examination

 Most M.E. patients have abnormal neurological examination.
(Hooper et al.  2001 [Online.])

 Tests of the immune system

 The immune system abnormalities in M.E. patients mimic the immune pattern
 seen in viral infections. Specific findings include (but are not limited

Increased numbers of activated cytotoxic T cells (most patients have
 evidence of T-cell activation)
Low natural killer cell numbers/percentage and function (cytotoxicity)
Elevated immune complexes
Atypical lymphocyte count
Significantly reduced CD8 suppressor cell population and increased
 activation marker (CD38, HLA-DR) on CD8 cells
Abnormal CD4/CD8 ratio
Elevations of circulating cytokines
Immunoglobulin deficiencies (most often IgG 1 and IgG 3)

 (McLaughlin, 2004 [Online]) (Carruthers et al. 2003) (Hooper et al. 2001

 One doctor commented (in a presentation on the immunological markers in
 M.E.) that:

 The NK (natural killer) cell is a very critical cell in [M.E. equivalent]
 CFS because it is clearly negatively impacted. The most compelling finding
 was that the NK cell cytotoxicity in CFS was as low as we have ever seen it
 in any disease. This is very, very significant data. [In CFS] the actual
 function was very, very low -- 9% cytotoxicity: the mean for the controls
 was 25, In early HIV and even well into ARC (AIDS related complex, which
 often precedes the fully developed condition), NK cytotoxicity might be
 around 13 or 14 percent. (ME)CFS patients represent the lowest cytotoxicity
 of all populations we've studied. (Klimas, 1990)

Professor Malcolm Hooper adds that: 'There is mounting international
 evidence that M.E. is an autoimmune disorder, with similarities to systemic
 lupus erythematosus. Evidence of antilamin antibodies has been found in the
 blood of M.E. patients: antibodies against this protein are proof of
 autoimmunity and of damage to brain cells.' (2001 [Online.])

 RNase L

 A more specific immune system abnormality has been discovered in
ICD-CFS of  increased activity and dysfunction of the 2-5A RNase-L
antiviral pathway in lymphocytes. The dysregulation of the RNase-L
pathway strongly supports the hypothesis that viral infection plays a
role in the pathogenesis of the illness. Between 80 - 94.7% of M.E.
patients have evidence of an up-regulated 2-5A antiviral pathway; are
so positive for this marker. The degree of elevation of 37 kDa Rnase L
has also been shown to correlate with symptom severity. This test is as
yet not widely available but may be one of the most useful tests in helping
to diagnose ICD-CFS in the future.
(See Red Labs for more information.) (Carruthers et al. 2003)

 Erythrocyte Sedimentation Rate (ESR)

An unusually low sedimentation rate of less than 5mm/hr is common in
M.E. (although there may also be brief periods where there is an elevated
rate >20mm/hr). (Hooper et al. 2001 [Online.]) ESR rates as low as 0
have been documented in M.E. patients.

 Insulin Levels and Glucose Tolerance Tests

 Derangement of insulin response and insulin levels is a frequent finding in
 M.E. patients. Glucose tolerance curves are often abnormal.
(Hooper et al. 2001 [Online.])

 24 Hour Holter Monitor

A 24 hour Holter monitor (a type of heart monitor) may show repetitively
 oscillating T-wave inversions and/or a flat T-wave may be found.
(A standard 12 lead ECG is usually normal however.)
(Hooper et al. 2001 [Online.])

 Holter monitors may also show heart rates as high as (or higher than) 150
 beats per minute as an immediate or delayed response to the patient
 maintaining an upright posture, or at rest. (Carruthers et al. 2003) Heart
 rates as low as 40 beats per minute may also be observed (during sleep).
 (Hyde, 2003)

 Dr Byron Hyde MD explains that:

 I routinely use a Holter monitor on all patients. The cardiologist often
 reports these as normal. Do not trust this report. What the cardiologist or
 computer is basing the report on is the number of ischemic events [which is
 not relevant to the heart problems caused by M.E.]. However, read the
lowest heart rate at night, and note that it sometimes falls to the low
 Though this may be normal in an athlete, it is not in a sedentary M.E.
 patient. For a patient who is not active all day long and has an average
 heart rate that flirts with 100 beats per minute or more, you know that
 is not normal. These abnormal tests, however, are often reported as
 (Hyde, 2003)

Dr Byron Hyde MD and the Canadian Guidelines both recommend that
patients or doctors must always specifically request to be informed of these
specific patterns as they may not be reported (or may be subsumed under
non-specific T-wave changes) by the interpreter.
(Hyde, 2003) (Carruthers et al. 2003)

 Tilt Table Examination

 The Canadian Guidelines explain that:

 Investigation by tilt test is indicated if there is a fall in blood
 and/or excessive rapidity of heart beat upon standing, which improves when
 sitting or lying down. Patients often report that they experience
 feeling light-headed or 'woozy' upon standing, or feeling faint when they
 stand up or are standing motionless such as in a store checkout line.
 Patients may exhibit pallor and mottling of the extremities. These
 historical symptoms and signs are sufficient for the initial diagnosis. As
 [M.E.] patients often have a delayed form of orthostatic intolerance,
 the blood pressure after standing may not be effective in diagnosis. Rather
 than having the patient stand for a period of time where there is a risk of
 him/her falling, we recommend using the tilt test where the patient is
 strapped down. The tilt test involves the patient lying horizontally on a
 table and then tilting the table upright to a 60-70 angle for
45 minutes during which time blood pressure and heart rate are
 monitored.' (2003)

 Orthostatic intolerance is very common in M.E. patients and may manifest
as one of, or a combination of the following:

 Neurally mediated hypotension (NMH): Involves disturbances in the autonomic
 regulation of blood pressure and pulse. There is a precipitous drop that
 would be greater than 20-25 mm of mercury of systolic blood pressure upon
 standing, or standing motionless, with significant accompanying symptoms.
 The patient feels an urgency to lie down.

 Postural orthostatic tachycardia syndrome (POTS): Excessive rapidity in the
 action of the heart (either an increase of over 30 beats per minute or
 greater than 120 beats per minute during 10 minutes of standing); and a
 in blood pressure occurring upon standing. Syncope can but usually does not

 Delayed postural hypotension: As above except the drop in blood pressure
 occurs many minutes (usually ten or more) after the patient stands rather
 than upon standing. (Carruthers et al. 2003) (Bassett 2005, [Online])



 Dr Byron Hyde MD warns about tilt table testing in M.E. patients however

 I frequently find gross abnormalities in M.E. patients with this test.
 a circulating blood volume and a complete cardiac investigation should be
 done first. This is not a test to undertake lightly since the patient's
 heart sometimes stops and may have to be restarted. This test should only
 done in major hospital centers in the presence of an appropriate physician
 where such emergency capabilities can be instituted.' (Hyde, 2003)


 Exercise testing and chemical stress tests

 Cardiopulmonary exercise testing (CPX) is widely used for the diagnosis
 functional assessment) of various cardiac and metabolic disorders and can
 also be used in the diagnostic evaluation of M.E. patients. Heart rate and
 blood pressure responses during the exercise test may reveal abnormalities
 specific to ME including: lower cardiovascular and ventilatory values at
 peak exercise (patients only being able to attain half the expected maximal
 workload and oxygen uptake compared to sedentary controls), elevated
 heart rates and an inability to reach maximum age-predicted heart rates
 (suggesting cardiac or peripheral insufficiency and/or reduced blood
 volume). (Carruthers et al. 2003)

 Many more severely affected M.E. patients however will be either too ill to
 complete such tests altogether, or may be able to complete these tests only
 at the cost of a potentially severe and unnecessary relapse (which usually
 peaks 24 - 48 hours post-exercise and will then persist for days, weeks or
 even months afterward depending on the patient's illness level). In
 to the risk of relapse, there have also been reports of sudden deaths in
 M.E. patients following exercise as M.E. expert Dr Elizabeth Dowsett
 explains: 'Some 20% [of M.E. patients] have progressive and frequently
 undiagnosed degeneration of cardiac muscle which has led, in several cases,
 to sudden death following exercise.' (2000 [Online]) As exercise tests are
 not appropriate for many M.E. sufferers, Dr Byron Hyde MD writes:
 Patients with ME frequently cannot do exercise tests, and so I then do
 chemical testing as a second best. Several of our patients have reacted
 severely to the chemical test with excruciating pain. This is not true
 angina, and although the pain sometimes ceases as soon as the chemical is
 stopped and the antidote given, sometimes it persists for weeks after the
 procedure with no sign of coronary artery disease. I do not understand this
 phenomenon, but it is obviously vascular. The cardiologists state that this
 pain does not occur with the same frequency in non-ME patients. (2003)

 Miscellaneous other abnormalities commonly found in M.E. patients:

 Cholesterol (high), cortisol (low), thyroid stimulating hormone (TSH)
 potassium (low), prolactin (high).

 Physical Exam

 There are also abnormalities visible on physical exam in M.E. patients.
 These abnormalities are not usual in healthy patients but they are also
 found in people with other illnesses (so they are not specific to M.E.). In
 cases of severe or acute M.E. there are always definite physical signs
 indicative of physical illness but virtually all patients will have some
 abnormality on physical exam. Not all patients will have all signs and
 with a fluctuating course of the illness from hour to hour and from day to
 day being one of the key characteristics of M.E., signs of the illness may
 also change or fluctuate during the course of a day. As M.E. expert
 Professor Malcolm Hooper explains: 'a patient examined in the morning might
 have nystagmus, which would disappear at midday, recur later, disappear and
 recur the next day; thus a once-only cursory examination could be
 misleading.' (Hooper et al. 2001 [Online.])

 Physical signs of illness commonly observed in M.E. patients include:

Nystagmus; nystagmus is jelly-like and variable (15% of M.E. patients will
 have nystagmus)
Sluggish visual accommodation
Unequal pupils and contrary pupil reaction to light
A labile blood pressure (sometimes as low as 84/48 in an adult at rest)
Shortness of breath (particularly on exertion)
Sometimes marked falling pulse pressure in arterial pressures taken first
 when prone, then sitting, then standing
Rapid heart rate on minor activity such as standing
Subnormal temperature
Patients show significant reduction in all lung function parameters tested
Liver involvement (an enlarged liver or spleen)
Abnormal tandem or augmented tandem stance
Abnormal gait
Hand tremor
Cogwheel movement of the leg on testing
Muscular twitching or fasciculation
Hyper-reflexia without clonus
Facial vasculoid rash
Vascular demarcation which can cross dermatomes with evidence of Raynaud's
 syndrome and / or vasculitis and spontaneous periarticular bleeds in the
Mouth ulcers
Hair loss
Destruction of fingerprints is sometimes seen (atrophy of fingerprints is
 due to perilymphocytic vasculitis and vacuolisation of fibroblasts)
Ghastly pallor of face with frequent lupus-like submaxillary mask
Parkinsonian rigidity of facial expression
Scanning, disjointed speech, or speech reversals
Nasal passage obstruction and inflamed areas around tonsillar pillars
Sicca syndrome of conjunctiva and mucous membranes
Frequent equivocal Babinski/plantar reflex on one side
Unusual sensitivity of cervical vertebrae area
Nodular thyroid
(Hooper et al. 2001 [Online.]) (Hyde, 2003)

 In addition, the diagnosis of M.E. should never be made without the
 post-exertional paralytic muscle weakness which is unique to M.E. being

 M.E. authority Dr Melvin Ramsay explains that this unique symptom:

 'is virtually a sheet-anchor in the diagnosis of Myalgic  Encephalomyelitis
and without it a diagnosis should not be made.' Muscles may function
normally to begin with but there is a continued loss of  post-exertional
muscle power after even a minor degree of physical effort;  three, four
or five days, or longer, elapse before full muscle power is restored.
([Online]) (In sedentary controls full muscle power is restored
after just 200 minutes.) All muscles are affected, including the heart.
(Hooper et al. 2001 [Online.])

Thus a patient may be easily able to lift/push/squeeze something with
close to normal strength several times, or for a short period; but be unable
to complete the same task (or even a trivial task) repeatedly (such as
lifting a soup spoon many times for example). Professor Malcolm Hooper
recommends testing for this by         observing the patient repeatedly
lifting something weighing around 2 pounds for a period of time.

He explains that, 'M.E. patients can often manage a small number of repeats
but performance rapidly falls off and recovery is very slow compared to
healthy controls. More sophisticated treadmill tests will also show the same
effect.' This sudden onset muscle weakness (or paralysis) and very slow
recovery is uniquely characteristic of M.E. patients. (2003).

SOURCE: http://www.ahummingbirdsguide.com:80/testingforme.htm
by Jodi Basset

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Date:    Sat, 14 Jul 2007 13:58:16 +0200
From:    "Dr. Marc-Alexander Fluks" <fluks@COMBIDOM.COM>
Subject: RES,NOT: Brown & Jason study on CFS, FM, and MCS

Source: American Chronicle
Date:   July 13, 2007
Author: Lourdes Salvador
URL:                                        http://www.americanchronicle.com/articles/viewArticle.asp?articleID=31056

The Effect of Illness Accumulation on Quality of Life

It would seem obvious to most people that the more illnesses one has, the
less functional they would be. Scientists, on the other hand, must prove
things via empirical studies.

In a study titled Functioning in individuals with chronic fatigue syndrome:
increased impairment with co-occurring multiple chemical sensitivity and
fibromyalgia, Brown and Jason (2007) set out to "differentiate these
diagnoses by comparing individuals with one or more illnesses on functioning,
psychiatric comorbidity, coping style, and in vivo physical measures".

Brown and Jason were spurred by the proposal that chronic fatigue syndrome
(CFS), multiple chemical sensitivity (MCS), and fibromyalgia (FM) commonly
co-occur and may be manifestations of the same illness.

The researchers surveyed 114 men and women who met the criteria for CFS.
They further diagnosed FM during a physical examination, and MCS using a
questionnaire. The men and women were then divided into four groups based on
  43.9% met criteria for CFS,
  23.7% met criteria for CFS & MCS, 15.8% met criteria for CFS & FM,
  16.7% met criteria for all three.
Demographics varied widely. A total of 46% were referred by physicians,
34% from media advertisements, and 20% from word-of-mouth.

After an initial screening, participants were given a CFS questionnaire to
collect demographics, health status, medication usage, and symptom data.
This was followed by a structured clinical interview for DSM-IV (Diagnostic
and Statistics Manual of Mental Disorders) disorders to determine presence of
any mental disorders. A medical assessment of CFS was performed, including an
in-depth medical and neurological history, and physical exam. A self-report
measure was used for general functioning. The Fatigue Severity Scale was
added to measure fatigue and the Beck Depression Inventory was included to
measure depression.

A Brief Cope and Brief Pain was administered to determine how subjects
reacted to stress and pain respectively. An Actiograph, designed to measure
activity during every minute of a week was worn to record daily activities. A
six minute walking test measured physical functioning and the Rating of
Perceived Exertion was used to measure subjects perception of the intensity
of their activity based on bodily sensations. Sit and reach, hand grip, and
employment status were the final factors examined that concluded this
extensive battery of measures.

As you undoubtedly guessed, the more conditions the subject had, the more
impaired they were. Those with CFS alone were the highest functioning and
those with CFS, FM, and MCS were the lowest functioning, leading Brown and
Jason to conclude that "this study provides evidence that having more than
one illness exacerbates one's disability beyond CFS alone", which we have
already guessed would be the case.

No significant differences were found in varying socio-demographic
categories. A rather large percent of subjects (68%) had a college degree or
higher, suggestive of prior functioning.

A substantial number of CFS patients (56%) had co-occurring MCS and/or FM,
which is consistent with prior study findings that have shown significant
overlap between MCS, CFS, and FM.

Depression was more common in those with MCS, CFS, and FM combined,
suggesting increased prevalence of depression in those who are more severely

Overall, this exhaustive study has shown that increased disability means
decreased functioning. It is important to remember that all participants in
this study suffered from CFS. FM and MCS was not evaluated alone or as a pair
without the presence of CFS.


Brown, MM & and Jason, LA (2007). Functioning in individuals with chronic
fatigue syndrome: increased impairment with co-occurring multiple chemical
sensitivity and fibromyalgia. Dynamic Medicine 2007, 6:6

(c) 2007 American Chronicle

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Date:    Sat, 14 Jul 2007 19:44:32 -0400
From:    "Bernice A. Melsky" <bernice.melsky1 VERIZON.NET>
Subject: RES: Paraoxonase and arylesterase activities in fibromyalgia

Paraoxonase and arylesterase activities in fibromyalgia.

Redox Rep. 2007;12(3):134-8.

Altindag O, Gur A, Calgan N, Soran N, Celik H, Selek S.

Department of Physical Medicine and Rehabilitation, Faculty of Medicine,
Harran University, Sanliurfa, Turkey. ozaltindag yahoo.com

PMID: 17623520

We aimed to evaluate the association of serum paraoxonase and arylesterase
activities and oxidative/antioxidative status in patients with fibromyalgia.

Forty-two patients with fibromyalgia and 53 healthy controls were included
in the study. Serum paraoxonase and arylesterase activities were measured
spectrophotometrically. Oxidative and antioxidative status were evaluated
by measuring serum lipid hydroperoxide (LOOH) levels, total antioxidant
status (TAS) and free sulfhydryl groups (-SH = total thiol). Lipid
parameters were determined by routine laboratory methods.

Serum paraoxonase and arylesterase activities, and TAS were lower in
patients with fibromyalgia than in controls (P < 0.001, for all), and the
-SH level was also lower in the patient group (P = 0.03). LOOH levels were
higher in the patient group than in controls (P = 0.01).

Our results suggest that patients with fibromyalgia were exposed to
oxidative stress, and paraoxonase and arylesterase activities were
decreased in these patients. Patients with fibromyalgia might be prone to
development of atherosclerosis with reduced paraoxonase and arylesterase

[Return to top]


Date:    Sun, 15 Jul 2007 12:30:51 -0400
From:    "Bernice A. Melsky" <bernice.melsky1 VERIZON.NET>
Subject: RES: The pain of fibromyalgia syndrome is due to muscle  hypoperfusion induced by regional vasomotor dysregulation

The pain of fibromyalgia syndrome is due to muscle hypoperfusion induced by
regional vasomotor dysregulation

Medical Hypotheses, Volume 69, Issue 3, 2007, Pages 517-525

David L. Katz [a, b, *], Lindsey Greene [a], Ather Ali [a, b] and Zubaida
Faridi [a]

[a] Yale Prevention Research Center, Yale University School of Medicine,
130 Division Street, Derby, CT 06418, USA
[b] Yale University School of Public Health, Yale University School of
Medicine, 60 College Street, New Haven, CT 06520, USA
[*] Corresponding Author. Present address: Yale Prevention Research Center,
130 Division Street, Derby, CT 06418, USA. Tel.: +1 203 732 1265; fax: +1
203 732 1264.

Received 12 October 2005;
accepted 16 October 2005.
Available online 28 March 2007.


Fibromyalgia syndrome (FMS) is a condition of chronic muscle pain and
fatigue of unknown etiology and pathogenesis.

There is limited support for the various hypotheses espoused to account for
the manifestations of FMS, including immunogenic, endocrine, and
neurological mechanisms. Treatment, partially effective at best, is
directed toward symptomatic relief without the benefit of targeting known,
underlying pathology.

A noteworthy commonality among partially effective therapies is a
vasodilatory effect. This is true both of conventional treatments,
unconventional treatments such as intravenous micronutrient therapy, and
lifestyle treatments, specifically graduated exercise.

The pain of fibromyalgia is described in terms suggestive of the pain in
muscles following extreme exertion and anaerobic metabolism. Taken
together, these characteristics suggest that the pain could be induced by
vasomotor dysregulation, and vasoconstriction in muscle, leading to
low-level ischemia and its metabolic sequelae.

Vasodilatory influences, including physical activity, relieve the pain of
FMS by increasing muscle perfusion. There are some preliminary data
consistent with this hypothesis, and nothing known about FMS that refutes
it. The hypothesis that the downstream cause of FMS symptoms is muscle
hypoperfusion due to regional vasomotor dysregulation has clear
implications for treatment; is testable with current technology; and should
be investigated.

Copyright  2007 Elsevier Ltd All rights reserved.

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Date:    Mon, 16 Jul 2007 11:40:50 -0400
From:    "Bernice A. Melsky" <bernice.melsky1 VERIZON.NET>
Subject: RES: Dysautonomia, fibromyalgia and reflex dystrophy

Dysautonomia, fibromyalgia and reflex dystrophy.

Arthritis Res Ther. 2007 Jul 6;9(4):105 [Epub ahead of print]

Eisinger J.

Unit Infomyalgies, Centre Hospitalier, 83056 Toulon, France.

PMID: 17626612


Autonomic nervous system dysfunction observed in fibromyalgia,
characterized without exception by a sympathetic hyperactivity and
hyporeactivity, has been reported. However, several studies demonstrated
reduced levels of norepinephrine and neuropeptide Y at rest and after tilt
table in some patients, which was improved by beta-stimulating agents.

These findings support heterogeneity in fibromyalgia-associated
dysautonomia. Fibromyalgia could be a generalized sympathetic dystrophy
since both conditions are activated by trauma and partly linked to
sympathetic mechanisms.

Yet they differ on several points: hormonal and neurochemical abnormalities
are observed in fibromyalgia whereas activation by peripheral trauma and
hyperosteolysis are observed in reflex sympathetic dystrophy.

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End of Co-Cure Weekly Digest of research and medical posts only - 9 Jul 2007 to 16 Jul 2007

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