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CO-CURE Medical & Research Posts Only Digest - 21 Aug 2006 to 28 Aug 2006 (#2006-40)

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Date:    Tue, 22 Aug 2006 15:15:22 -0400
From:    "Bernice A. Melsky" <bernicemelsky@xxxxx.xxx>
Subject: RES: Peripheral benzodiazepine receptors on platelets of fibromyalgic patients

Peripheral benzodiazepine receptors on platelets of fibromyalgic patients.

Clin Biochem. 2006 Jul 13; [Epub ahead of print]

Bazzichi L, Giannaccini G, Betti L, Italiani P, Fabbrini L, Defeo F,
Giacomelli C, Giuliano T, Rossi A, Uccelli A, Giusti L, Mascia G,
Lucacchini A, Bombardieri S.

Department of Internal Medicine, U.O of Rheumatology, University of Pisa,

PMID: 16919618

OBJECTIVE: The aim of the present study was to analyze if alterations of
peripheral-type benzodiazepine receptor (PBR) characteristics occurred in
platelet membranes of patients affected by primary fibromyalgia (FM).

DESIGN AND METHODS: Platelets were obtained from 30 patients with FM.
Evaluation of kinetic parameters of PBR was performed using [(3)H] PK11195
as specific radioligand compared with 16 healthy volunteers.

RESULTS: The results showed a significant increase of PBR binding sites
value in platelet membranes from FM patients (B(max) was 5366+/-188 fmol/mg
vs. controls, 4193+/-341 fmol/mg, mean+/-SEM) (**p<0.01) but not for
affinity value (K(d) was 4.90+/-0.39 nM vs. controls, 4.74+/-0.39 nM,
mean+/-SEM) (p>0.05). Symptom severity scores (pain and tiredness) were
positively correlated with B(max).

CONCLUSIONS: Our results showed an up-regulation of PBR in platelets of FM
patients, and this seems to be related to the severity of fibromyalgic symptoms.

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Date:    Wed, 23 Aug 2006 06:25:02 -0400
From:    "Bernice A. Melsky" <bernicemelsky@xxxxx.xxx>
Subject: RES: Natural health product use in Canada: analysis of the  national population health survey

Natural health product use in Canada: analysis of the national population
health survey.

Can J Clin Pharmacol. 2006 Summer;13(2):e240-50. Epub 2006 Aug 21.

Singh SR, Levine MA.

PMID: 16921199

Background: The use of natural health products (NHPs) in Western countries
has increased dramatically over the past two decades. Although prevalence
estimates have been published in the U.S. and elsewhere, little is known
about the characteristics of persons who use NHPs.

Objectives: To measure the prevalence of NHP use among adults in Canada,
identify the most commonly used agents, and determine the socioeconomic,
demographic, and health-related correlates of use.

Methods: NHP use by adults was assessed using the 2000-2001 National
Population Health Survey (NPHS), a biennial general health survey conducted
by Statistics Canada. A total of 11,424 adults completed the survey in
2000-2001. NHPs were defined as botanical and naturally-derived
non-botanical products, excluding essential vitamins and minerals.
Prevalence of use estimates were calculated nationally, and by age, gender,
socioeconomic status, disease states, and health care practices.
Multivariate logistic regression modeling was used to simultaneously assess
the correlations of these variables with NHP use.

Results: The prevalence of past 2-day NHP use in Canada was 9.3% in
2000-2001. Fifty-seven percent of users also reported taking a conventional
medicine in the same period. Glucosamine, echinacea, and garlic were the
most frequently used products. Women reported NHP use more frequently than
men (11.5% vs. 7.1%). As compared to young adults, NHP use was about 50%
higher in middle-aged and older Canadians. There were no associations with
either income or education level. Several disease states were associated
with a high prevalence of NHP use: respondents with fibromyalgia (23.3%),
inflammatory bowel disease (17.4%), and urinary incontinence (16.8%) were
most likely to be NHP users. However, in the multivariate analysis, age and
the use of vitamins or minerals were most predictive of NHP use, while
health status variables were of less importance.

Conclusions: NHP use is an important health phenomenon in Canada. Although
respondents in poor health were more likely to use NHPs, a significant
proportion of healthy Canadians also reported NHP use. The use of NHPs also
cut across different socioeconomic groups. Concurrent use of conventional
medications was common and suggests a need for health professionals to
monitor for potential interactions.

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Date:    Wed, 23 Aug 2006 06:28:11 -0400
From:    "Bernice A. Melsky" <bernicemelsky@xxxxx.xxx>
Subject: RES: Long-term follow up of a physical therapy programme for  patients with fibromyalgia syndrome

Long-term follow up of a physical therapy programme for patients with
fibromyalgia syndrome.

Scand J Caring Sci. 2006 Sep;20(3):315-22.

Havermark AM, Langius-Eklof A.

Halsopoolens Rehabklinik, Stockholm, Sweden.

PMID: 16922986

The purpose of this study was to evaluate, in a long-term perspective, the
impact of a physical therapy-based educational programme on patients with
fibromyalgia syndrome (FMS). The programme includes information about the
syndrome, information about pain and muscle physiology, training in warm
water, stretching, body awareness therapy and relaxation in groups of 15
patients twice weekly, 2 hours during 10 weeks.

A total of 240 patients with FMS participated in the study before and
immediately after the programme and at a follow up with a mean of 35 months
after the programme. Health status as measured with the Fibromyalgia Impact
Questionnaire was answered by the patients at all three measurement points.
Questionnaires concerning self-care, self-motivation and sense of coherence
(SOC) were distributed at the follow up.

The results showed a significant improvement on several symptoms when
comparing before and after the programme, and at the time of follow up the
patients' rated well-being was still improved. The results also showed that
the patients' pretreatment perception of symptoms, well-being and SOC are
predictors to the perception of general health at the follow up of a
physical therapy programme.

The conclusion is that a physical therapy programme for patients with FMS
may have a positive impact on patients' general well-being but not on other

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Date:    Wed, 23 Aug 2006 09:57:54 -0400
From:    "Steven Du Pre <isaiah40@xxxxx.xxx> [via Co-Cure Moderators" 
Subject: ACT, RES: Evidence for brain SPECT scan as diagnostic for Myalgic Encephalomyelitis/CFS

The CDC statement against using MRI scans in the diagnosis of CFS
is inaccurate, as shown by the many studies referred to below.
It is also dangerous for physicians to be misguided in this way
by the CDC.

"Magnetic resonance imaging scan: single-photon emission
computed tomography: Some CFS researchers have observed apparent
differences in the cranial blood flow between CFS patients and controls.
These studies remain unconfirmed, and imaging tests should not be
performed as a diagnostic technique for CFS."  (From CDC web site

Below are scientific references, a short summary of Dr. Hyde's
diagnostic use of SPECT scans, and information on the early work
of Dr. Ismael Mena:

References to show Neuroimaging is definitely diagnostic for ME/CFS:

Neurological Dysfunction in Chronic Fatigue Syndrome, Journal of Chronic
Fatigue Syndrome (The Haworth Medical Press, an imprint of The Haworth
Press, Inc.) Vol. 6, No. 3/4, 2000, pp. 51-68. Abhijit Chaudhuri, DM, MD,
MRCP; Peter 0. Behan, DSc, MD, FACP, FRCP

"SPECT Imaging of the Brain: Comparison of Findings in Patients with Chronic
Fatigue Syndrome, AIDS Dementia Complex, and Major Unipolar
Depression," Richard B. Schwartz, Anthony L. Komaroff, Basem M. Garada,
Marcy Gleit, Teresa H. Doolittle, David W. Bates, Russell G. Vasily,
B. Leonard Holman; American Journal of Roentgenology, Vol 162, 943-951,
Copyright  1994 by American Roentgen Ray Society.
Summary: "This study shows that CFS (ME) shares some similarities on
SPECT imaging with AIDS Dementia Complex         acute changes in
radionuclide uptake in the younger population may be caused by inflammatory
processes at the cellular or micro vascular level .... the findings in
are consistent with the hypothesis that CFS (ME) ... results from a
viral infection
of neurons, glia or vasculature .....viral infection can provoke
dysfunction by interfering with intra-cellular mechanisms or membrane
systems .... or by cerebral hypo perfusion due to vasculitis".

Gordon R et al. Cortical motor potential alterations in chronic fatigue
Int J Molec Med. 1999; 4: 493-99.

Proton magnetic resonance spectroscopy of basal ganglia in chronic
fatigue syndrome. Chaudhuri A, Condon BR, Gow JW, Brennan D,
Hadley DM. Neuroreport.  2003 Feb 10;14(2):225-8.

Costa DC, Brostoff J, Douli V, Eli PJ.  Brainstem hypoperfusion in
patients with Myalgic Encephalomyelitis-Chronic Fatigue
Syndrome.  Eur J Nucl Med 1992 19:733.

Brainstem perfusion is impaired in chronic fatigue syndrome.  DC Costa,
C Tannock  and J Brostoff.  Quarterly Journal of Medicine December

Relationship of brain MRI abnormalities and physical functional
status in chronic fatigue syndrome Cook DB, Natelson BH.
Int J Neurosci 2000:107:(1-2):1-6

Brain positron emission tomography (PET) in chronic fatigue
syndrome: preliminary data Tirelli U et al. Am J Med 1998:105:

Brain MRI abnormalities exist in a subset of patients with
chronic fatigue syndrome. Lange G, DeLuca J, Maldjian JA,
Lee H, Tiersky LA, Natelson BH. J Neurol Sci.
1999 Dec 1;171(1):3-7.

 Chronic fatigue syndrome--aetiological aspects. Dickinson CJ.
Eur J Clin Invest.  1997 Apr;27(4):257-67

Brain MR in chronic fatigue syndrome. Greco A, Tannock C,
Brostoff J, Costa DC. AJNR Am J Neuroradiol.  1997 Aug;18(7):

 Relationship of brain MRI abnormalities and physical functional
status in chronic fatigue syndrome. Cook DB, Lange G, DeLuca J,
Natelson BH. Int J Neurosci.  2001 Mar;107(1-2):1-6.

Quantitative assessment of cerebral ventricular volumes in
chronic fatigue syndrome. Lange G, Holodny AI, DeLuca J,
Lee HJ, Yan XH, Steffener J, Natelson BH.  Appl Neuropsychol.

Dr. Byron Hyde, a Canadian specialist in Myalgic Encephalomyelitis
offers this definition of Myalgic Encephalomyelitis: "Myalgic
Encephalomyelitis is a measurable, diffuse post-encephalitic illness.
The illness is characterized by (1) its acute onset,
(2) the diffuse, non-focal persisting nature of the encephalopathy,
and (3) the chronicity of the resulting symptoms.  These symptoms
consist of the rapid exhaustion or loss of stamina of motor, sensory,
intellectual, and cognitive abilities. M.E. is of infectious/autoimmune
origin and less commonly, a toxic/autoimmune origin.

M.E. occurs in epidemics and sporadic cases."

[Note by Rich Van Konynenburg, Ph.D, who reported on Dr.
Hyde's lecture at the recent Wisconsin conference of medical practitioners
specializing in Myalgic Encephalomyelitis: "Basically, what he's saying
here is that Myalgic Encephalomyelitis starts with an inflammation of
the brain that occurs rather suddenly.  This initial inflammation usually
results from an infectious/autoimmune process, but it can also be
caused by a toxic/autoimmune process.  This sudden, short-term
inflammation is followed by a disorder of the brain that continues
over time.  This chronic disorder of the brain is not localized to a
small part of the brain, but is spread out over large regions of the
brain, and it leads to chronic symptoms that can involve essentially
all the normal functions of the brain.  Myalgic Encephalomyelitis
occurs both in epidemic-type clusters of cases as well as cases
that are occasional and isolated."] Dr.  Hyde said that though the
primary injury in Myalgic Encephalomyelitis is the diffuse CNS
encephalopathy, the illness may cause or be associated with
measurable dysfunction in end organs and various body systems.
The most commonly injured end organs and systems are (1) the
thyroid gland, (2) the cardiovascular system and (3) the immune system.
The CNS dysfunctions are caused by widespread, measurable, diffuse
micro-vasculitis affecting normal cell operation and maintenance.

"The evidence would suggest that Myalgic Encephalomyelitis is
caused primarily by a diverse group of viral infections that have
neurotropic characteristics and that appear to exert their influence
primarily on the CNS arterial bed.  The available brain technology
limits the viral site of action to the capillaries and microarterial CNS
bed.  This diffuse vascular site of injury rather than a neurological
cellular site of injury explains the natural history of Myalgic
Encephalomyelitis-type illness." [Note--What he is saying here is that
there is evidence that the causes of Myalgic Encephalomyelitis are
any of a group of viruses that are able to infect the brain.  By means of
high-resolution SPECT scanning, he can tell that they mainly affect the
small arteries and capillaries in the brain.] "It is also noted that many
Myalgic Encephalomyelitis patients also have generalized arterial
pathophysiology [Note --In other words, there are problems with
the arteries all over their bodies.], causing various vascular problems
that include in numerous patients: (1) insufficient blood pressure increase
on exertion, (2) hyperelasticity and hyper-contractibility of arterial blood
vessels, (3) various forms of arterial mediated vascular orthostatic
pathophysiology [Note --In other words, they have difficulty standing up
because of problems with their arteries] as demonstrated by Drs.  David
Streeten, David Bell, and Peter Rowe, and (4) cholinesterase dysfunction
in the arterial wall, causing arterial elasticity dysfunction as
by Dr. Vance Spence at Dundee University, Scotland."

Brain Blood Flow
This article appeared in The Medical Post, January 19, 1993

Patients suffering from chronic fatigue syndrome (CFS) do so
because of cerebral function abnormalities as a result of diminution
of brain blood flow, says a California nuclear medicine specialist.
Dr Ismael Mena of the Harbor-UCLA Center in Los Angeles said:
"All adult patients with chronic fatigue have abnormal diminution of
blood flow to different areas of the brain - mostly in the frontal lobes."
He told a meeting on CFS recently that this diminished blood flow
could reflect damage to those areas, but might also be the result of
damage to another area of the brain that is expressed in the frontal
lobes. He said the primary damage may be in the limbic system,
particularly in the hippocampus. "This is the one that projects
directly in the frontal lobes where most of the damage is seen in
patients with chronic fatigue."

The diminution of blood flow to the temporal lobes could also
explain why patients with chronic fatigue complain of cognitive
impairment as that is where the memory resides. Using brain
Single Photon Emission Computer Tomography (SPECT), Dr
Mena studied the brain flow patterns of 19 normal people with
an average age of 66; 33 CFS patients with an average age of 55;
and 26 patients with depression and a mean age of 62.

Great Precision
Although computed tomography (CT) and magnetic resonance
imaging (MRI) can denote with great precision the structures of
the brain, with brain SPECT the functions of the brain can be
examined. Dr Mena said he examined the brain blood flow
because it is directly related to brain function. Two sets of
measurements were taken - one using 133Xe rCBF to measure
the amount of blood flow in the brain tissue, the other,
99mTc-HMPAO, to provide images of brain blood flow.

Dr Mena said in a normal person the blood flow, when
measured using 133Xe rCBF, fluctuates between 50 and
67 mL/min/100g of brain tissue. However, patients with CFS
don't exhibit a uniformity in blood flow. For example, in one patient,
aged 42, blood flow was 37 mL/min/100g in the right frontal lobe.
"For a person of this age it should be 55,  5", he said. In another
example, a 48 year-old woman, there was extensive hypoperfusion
in the frontal lobes. "But more extensively in the dorsal frontal lobes
with blood flow between 38 mL and 47 mL", he said. The
99mTc-HMPAO data also showed patients had both frontal
perfusion and temporal
hypoperfusion, but to provide a more precise analysis of the data,
Dr Mena said regions of interest were set and a computer
was used to calculate the amount of blood flowing in them.
Approximately 100 measurements were taken per patient.

Dr Mena said when this type of analysis was done, the distribution
of 133Xe rCBF in a normal elderly person is close to
45 mL/min/100g. Again, this data showed in patients with CFS
there was a diminution of blood flow in the right hemisphere. With
the 99m Tc-HMPAO data, Dr Mena said there was significant
hypoperfusion throughout the frontal lobes as well as the right
temporal lobe.

Dr Mena also examined the effect of exercise on patients with CFS.
Patients were given the standard cardiac stress test. While a normal
person usually gets his wind back within five minutes after doing the
test, those with CFS had to wait at least one hour before their levels
of carbon dioxide returned to their pre-exercise levels. "There's a
marked worsening of blood flow in both hemispheres, but mostly in
the right hemisphere, and these abnormalities persist up to 24 hours",
he said. After 24 hours, sometimes even 48 hours, patients' brain
blood flow returned to where it was at normal activity level.

Acknowledgment: Reprinted from The Messenger, March 1993,
newsletter of The M.E. Association of Canada.

Reprinted from Emerge, September 1993.

"America's Biggest Cover-Up by Neenyah Ostrom" Chapter Twenty: CFS
Patients Have A
Brain Defect Similar To That Found In AIDS Dementia "It has been known
for some time
that CFS patients have abnormal
blood flow in their brains; that is, some areas of the brain are not
getting as much blood as they should. Very recently, however, studies
of patients with AIDS dementia have shown that they, too, have
abnormal brain blood flow, raising the question of whether a similar
disease process is taking place in both sets of patients.

It has only been possible to measure blood flow in the brain with the
development, over the last few years, of very specialized types of brain
scan technologies. One type of brain scan that can detect blood flow
abnormalities is called SPECT (which stands for "single photon emission
computer tomography").

Dr. Ismael Mena has studied CFS patients' brains using SPECT scans
at the University of California-Los Angeles, where he is a professor of
radiology. Over several years' investigation, Dr. Mena has consistently
reported that 71 percent of CFS patients have a diminished flow of
blood in their brains.

Dr. Mena has also commented, at scientific conferences, that CFS
patients do not have equal blood flow on the two halves of their brains.
That is, when the blood flow on the right and left sides (or hemispheres)
of the brain were compared in individual CFS patients, the flow in the
two halves of the brain can differ by twice as much as they do in
healthy people.

This information suggests that some type of organic brain disease
may be a component of CFS. While it has long been recognized
that AIDS patients can develop very serious mental problems,
sometimes labeled "AIDS dementia," only recently have such
patients been studied using SPECT scans. The similarity between
 "AIDS dementia" patients' SPECT scans and those of CFS
patients are striking.

SPECT scans in AIDS patients were discussed at the 1992
 international AIDS meeting (in Amsterdam) by a research team
from the Houston Immunological Institute. Rather shockingly, they
found that exactly the same percentage of AIDS patients -- 7
1 percent -- as CFS patients had abnormalities in brain blood flow.
The Houston research team also found that more severe cases of
AIDS dementia showed greater abnormalities in brain blood flow,
and they suggested that SPECT scans could provide a very
  important diagnostic tool for physicians treating patients with AIDS."

Steven Du Pre
Poetry website: http://www.angelfire.com/poetry/soareagle/index.html
"By words the mind is winged."  Aristophanes
Website for National Alliance for Myalgic Encephalomyelitis:

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Date:    Wed, 23 Aug 2006 12:13:47 +0200
From:    "Dr. Marc-Alexander Fluks" <fluks@xxx.xx>
Subject: RES,NOT: Anti-Phospholipid Syndrome

'AntiPhospholipid Syndrome (APS) vs. MS' might be important for 'phosfolipid/
omega-3 vs. CFS/schizophrenia'.

Source: The Times
Date:   August 20, 2006
Author: Simon Crompton
URL:    http://www.timesonline.co.uk/article/0,,8123-1741009_1,00.html
Ref:    http://www.hughes-syndrome.org

Old-fashioned detective work

Dr Hughes discovered a disease that affects 150,000 Britons. Now it bears his
name Just across the river from the Houses of Parliament, tucked away in St
Thomas' Hospital, works a man who should be recognised as one of the heroes of
modern medicine. Yet despite being hailed around the world as having made one
of the most important medical discoveries of the past 50 years, no one beyond a
select band in the UK has heard of him or the syndrome he discovered - even
though it has implications for all areas of medicine and affects 150,000 people
in the UK.

About 20 years ago, the rheumatologist Dr Graham Hughes reported in the British
Medical Journal that he had identified a syndrome that resulted in blood
becoming sticky, leading to potentially dangerous blood clots. Since then, his
discovery has been confirmed as the cause of one in five recurrent miscarriages,
one in five strokes in younger people, and one in five DVTs (deep vein clots).
Sticky blood is also strongly linked with migraine, Alzheimer's disease, and
infertility, and the numbers believed to be affected are larger than those with
high-profile conditions such as Parkinson's disease.

Internationally, hundreds flock to Dr Hughes's lectures and fellow scientists
have hailed his discovery by naming this strange condition Hughes syndrome. The
dean of medicine at Barcelona University has said that there are just two new
diseases of the late 20th century - Hughes syndrome and Aids.

Yet here? Here we're hardly making the most of a great British achievement. Dr
Hughes reckons that only a handful of GPs are alert to the condition and this
lack of knowledge causes thousands of people to suffer needlessly - and
thousands of unnecessary miscarriages. 'Bit by bit, obstetricians and
neurologists are picking up on it but GPs aren't,' says Dr Hughes, who runs
the Lupus Research Unit at St Thomas's. 'It's not easy to pick up because
sticky blood can affect every organ in the body. The commonest problems people
have are migraine, headaches and memory loss. Some cases are picked up in
infertility clinics and there is now a simple blood test provided to some women
who have had two or more miscarriages. But it's not routinely available.
It's inexpensive and should be standard for all pregnant women.'

Perhaps one of the reasons why Hughes syndrome hasn't hit the headlines is
that its discovery was the result of good old-fashioned clinical detective work
- not massive research funding. Dr Hughes made his discovery through carefully
observing and talking to thousands of patients - something, as he is only too
aware, that most doctors nowadays have precious little time to do. He is
obviously a master of the art, in conversation he is polite and enthusiastic -
the kind of doctor you would really want to describe all your symptoms to in

It started in the early 1970s, when he set up Europe's first clinic for lupus
(a type of arthritis) in Hammersmith Hospital. On his ward rounds, he was
struck by the number of people who seemed to have a collection of symptoms -
memory loss, balance problems, recurrent miscarriage, fluctuating blood
pressure and recurrent thrombosis - who then went on to have strokes and heart
attack. Testing their blood, he found that all had high levels of a kind of
antibody that destroys phospholipid - a fat found in cells.

It was clear that these were not simply lupus symptoms. 'Right from the start,
we knew we were on to something,' says Dr Hughes. So he went to other hospital
departments and asked if specialists had seen similar problems. Sure enough,
liver clinics revealed people with liver blood clots who also displayed memory
loss, fluctuating blood pressure and so on. The same pattern appeared in
epilepsy, multiple sclerosis and pregnancy clinics. And all the patients with
these groups of symptoms also revealed high levels of antiphospholipid

Since 1983, a host of research papers has been published, tracing the
antiphospholipid antibody as a key factor in a range of diseases. Dr Hughes
believes he now understands the mechanism behind Hughes syndrome, or
antiphospholipid syndrome as it is also known.

In people with a genetic predisposition to the syndrome, a virus seems to
trigger the release of antiphospholipid antibodies into the blood. These attack
the slippery coating of blood cells, so they become sticky, jam together and
cause clots. Since clotting can affect every sphere of medicine, the syndrome
can be at the root of many conditions. In pregnancy, clots block the placenta
causing it and the foetus to wither and die. In neurological conditions, such
as memory loss, the clots impair blood flow to the brain.

And now research by Dr Hughes and his team at St Thomas' is revealing that
many people with Hughes syndrome are being misdiagnosed as having multiple
sclerosis. 'Thirty per cent of people with Hughes syndrome have that label
hanging over them at some stage,' he says.

Once Hughes syndrome is diagnosed through a blood test, then it is easily
controlled. Taking aspirin, or anticoagulants such as heparin and warfarin,
produces a dramatic reduction in symptoms in 80 per cent of patients. 'We had
one lady who had been wrongly told she had 'mad cow' disease, and she's
well now,' he says. Another was in a wheelchair, paralysed from the waist down
- luckily, she was seen by a neurologist who referred her to us and she can
walk now.'

It must be like being a miracle worker. But you also sense his realism. Sadly,
until doctors throughout the UK become aware of sticky blood, the full
implications of his discovery are unlikely to be realised. 'I'm proud that
the community decided to call it Hughes syndrome,' he says. 'But I think
they only did so because my name is easier to spell than antiphospholipid.'

Have you got it?

If you have had one or more of the following, you may have the sticky blood
condition discovered by Dr Hughes:
* Memory loss; recurring migraine and headaches; a deep vein thrombosis;
  recurrent miscarriage; mini-stroke, or stroke in a young person.
* A testing kit for Hughes Syndrome, 28, pounds is available from TDL
  Pathology, http://stickyblood@tdlpathology.com, 020-7307 7373
* Visit http://www.hughes-syndrome.org, or call 020-7188 8217

What's in a name?

There have never been any strict criteria for a syndrome or disease to be named
after its discoverer - it's usually a matter of medical colleagues deciding
that they deserve it. There's invariably a more technical name for a condition,
too. Here are some stories behind the eponyms.
* Down's syndrome: English physician John Langdon Down published a paper in
  1887 describing the condition now known to be caused by a genetic defect. The
  term was not officially adopted by the World Health Organisation until 1965
  - before then, Down's syndrome was still known as Mongolian idiocy.
* Alzheimer's disease: The German neurosurgeon Alois Alzheimer first referred
  publicly to what he described as a 'peculiar disease of the cerebral cortex'
  in November 1906. By 1910 the condition had become known as Alzheimer's
  disease, despite lobbying by Italians, who favoured the name Alzheimer-
  Perusini in honour of another researcher.
* Reiter's syndrome: a combination of genital, eye and joint inflammation,
  was actually documented by Sir Benjamin Collins Brodie in 1818 - almost 100
  years before Reiter documented a single case. However, a 1942 article
  describing the first known American case of the disease credited Hans Conrad
  Julius Reiter alone as having discovered it, and the eponym stuck. In recent
  years Reiter's record as a Nazi war criminal has prompted efforts by members
  of the American College of Rheumatology to have the disease renamed, but
  there is no clear process for doing so and the title has so far stuck.
* Munchausen's syndrome: the continuous fabrication of symptoms or an illness
  by a patient is named not after its discoverer but after the fictional Baron
  Munchausen, famous for his tall tales - such as sailing to the moon in a

(c) 2006 Times Newspapers Ltd.

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Date:    Thu, 24 Aug 2006 15:03:17 -0400
From:    "Bernice A. Melsky" <bernicemelsky@xxxxx.xxx>
Subject: RES: Sleep Quality in Patients with Fibromyalgia Using the  Pittsburgh Sleep Quality Index

Sleep Quality in Patients with Fibromyalgia Using the Pittsburgh Sleep
Quality Index.

J Rheumatol. 2006 Aug 15; [Epub ahead of print]

Osorio CD, Gallinaro AL, Lorenzi-Filho G, Lage LV.

PMID: 16924687

OBJECTIVE: To characterize and quantify the sleep complaints of patients
with fibromyalgia (FM) using the Pittsburgh Sleep Quality Index (PSQI).

METHODS: The PSQI was applied to 30 patients with FM according to American
College of Rheumatology classification criteria and to 30 healthy controls
in individual sessions under similar conditions.

RESULTS: The median global PSQI scores were [median (25-75%)] 12.0 (10-16)
and 3.0 (2.0-5.0) in patients with FM and controls, respectively (p <0.001). 
All PSQI component scores except sleep medications were
significantly higher in patients than controls. Sleep latency, sleep
disturbances, and daytime dysfunction were the most frequent sleep
difficulties experienced by patients with FM.

CONCLUSION: Our results indicate that the PSQI is a useful instrument for
characterizing and quantifying sleep disturbances in patients with FM.

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Date:    Thu, 24 Aug 2006 14:59:26 -0400
From:    "Bernice A. Melsky" <bernicemelsky@xxxxx.xxx>
Subject: RES: Muscle performance in patients with fibromyalgia

Muscle performance in patients with fibromyalgia.

Singapore Med J. 2006 Sep;47(9):752-6.

Okumus M, Gokoglu F, Kocaoglu S, Ceceli E, Yorgancioglu ZR.

First Physical and Medicine Rehabilitation Deparment, Ankara Research and
Education Hospital, Ulucanlar cad. 06010, Ankara, Turkey.

PMID: 16924355

Introduction: Fibromyalgia (FMS) is a syndrome expressed by chronic
widespread body pain which leads to reduced physical function and frequent
use of healthcare services. This study was performed to examine the muscle
performance comprising abdominal and lumbar muscle strength, and
measurement of chest expansion in osteoporotic patients with FMS; to
evaluate the relation between muscle performance, pain severity, clinical
findings and physical activity; and to compare the results with the
osteoporotic control group.

Methods: 44 osteoporotic women with FMS and 46 osteoporotic women who were
physically inactive underwent measurements of three parameters: abdominal
and lumbar muscle strength, and chest expansion. Student's t-test was used
for statistical analysis.

Results: The strength of lumbar muscles and measurement of chest expansion
were significantly decreased in the FMS patients as compared to the
controls (p-value is less than 0.001). However, lumbar and abdominal
muscles strength was low in both patients and controls.

Conclusion: Our results indicate that osteoporotic patients with FMS have
impairment in strength of lumbar and abdominal muscles and in measurement
of chest expansion. Further studies are needed to investigate the mechanism
of reduced muscle performance and the effects of aerobic exercise in this
patient group.

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Date:    Fri, 25 Aug 2006 11:12:28 -0400
From:    "Bernice A. Melsky" <bernicemelsky@xxxxx.xxx>
Subject: RES: Fibromyalgia: aetiology, diagnosis, symptoms and  management

Fibromyalgia: aetiology, diagnosis, symptoms and management.

Br J Nurs. 2006 Jul 13-27;15(13):729-33.

Longley K.

Freelance Health Writer and Molecular and Cellular Biologist specializing
in fibromyalgia, Bath, Somerset.

PMID: 16926725

Fibromyalgia is believed to affect about 2% of the UK population,
predominantly women, and is characterized by the symptoms of widespread
musculoskeletal pain, persistent fatigue, non-refreshing sleep and
generalized stiffness. It is also accompanied by a variety of associated
symptoms which can appear baffling to both patient and doctor alike.

Research into this often dismissed syndrome has increased exponentially
over the last two decades and the evidence is growing to support an
underlying pathology involving pain amplification, sleep abnormalities,
hormonal imbalance and autonomic nervous system dysfunction.

This review looks at diagnosis, research and current treatment options and
offers an insight into the patients' experience with the medical and
nursing professions.

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Date:    Fri, 25 Aug 2006 12:05:57 -0400
From:    Co-Cure Moderator <ray@xxxxx.xxx>
Subject: NOT,MED: Caution to Patients Discontinuing SRI Antidepressants

Caution to Patients Discontinuing SRI Antidepressants

A recent AP News report - "Some say ending antidepressants daunting" -
calls attention to the sometimes terrifying difficulties that many people
encounter in discontinuing use of a prescription antidepressant, or
switching from one to another. It seems to be another case of "patient,
inform thyself."

Read the complete article at

[AOL: <a

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Date:    Sat, 26 Aug 2006 21:56:39 -0400
From:    "Bernice A. Melsky" <bernicemelsky@xxxxx.xxx>
Subject: RES: Mechanisms of Disease: pain in fibromyalgia syndrome

Mechanisms of Disease: pain in fibromyalgia syndrome

Nature Clinical Practice Rheumatology (2006) 2, 90-98

Roland Staud* and Miguel E Rodriguez

R Staud is a Professor of Medicine at the Evelyn F and William L McKnight
Brain Institute and the Division of Rheumatology & Clinical Immunology, and
ME Rodriguez is a Postdoctoral Rheumatology Fellow at the Division of
Rheumatology & Clinical Immunology, of the University of Florida,
Gainesville, USA.

Correspondence: *McKnight Brain Institute and Department of Medicine,
University of Florida College of Medicine, Gainesville, FL 32610-0221,
USA  Email staudr@ufl.edu

Received 29 June 2005 | Accepted 20 October 2005

PMID: 16932662

Despite extensive research, the pathogenesis of pain in fibromyalgia
syndrome is incompletely understood. Fibromyalgia pain is consistently felt
in deep tissues including ligaments, joints and muscles.

Increasing evidence points towards these tissues as relevant contributors
of nociceptive input that might either initiate or maintain central
sensitization, or both. Persistent or intense nociception can lead to
transcriptional and translational changes in the spinal cord and brain
resulting in central sensitization and pain. This mechanism represents a
hallmark of fibromyalgia and many other chronic pain syndromes, including
irritable bowel syndrome, temporomandibular disorder, migraine, and low
back pain.

Importantly, after central sensitization has been established, only minimal
nociceptive input is required for the maintenance of the chronic pain
state. Other factors, including pain-related negative affect, have been
shown to significantly contribute to clinical fibromyalgia pain.

An improved understanding of the mechanisms that characterize central
sensitization and clinical pain will provide new approaches for the
prevention and treatment of fibromyalgia and other chronic pain syndromes.

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Date:    Sat, 26 Aug 2006 22:02:59 -0400
From:    "Bernice A. Melsky" <bernicemelsky@xxxxx.xxx>
Subject: RES: Therapy Insight: fibromyalgia-a different type of pain  needing a different type of treatment

Therapy Insight: fibromyalgia-a different type of pain needing a different
type of treatment.

Nature Clinical Practice. Rheumatology. 2006 Jul;2(7):364-372.

Dadabhoy D, Clauw DJ.

D Dadabhoy is a Clinical Lecturer in Rheumatology at the University of
Michigan, MI, USA, where DJ Clauw is a Professor of Medicine, the Director
of the Chronic Pain and Fatigue Research Center and the Center for the
Advancement of Clinical Research, and the Assistant Dean for Clinical and
Translational Research.

PMID: 16932722

In the past decade, we have made tremendous progress in our understanding
of fibromyalgia, which is now recognized as one of many 'central' pain
syndromes that are common in the general population. Specific genes that
might confer an increased risk of developing fibromyalgia syndrome are
beginning to be identified and the environment (in this case exposure to
stressors) might also have a significant effect on triggering the
expression of symptoms.

After developing the syndrome, the hallmark aberration noted in individuals
with fibromyalgia is augmented central pain processing. Insights from
research suggest that fibromyalgia and related syndromes require a
multimodal management program that is different from the standard used to
treat peripheral pain (i.e. acute or inflammatory pain). Instead of the
nonsteroidal anti-inflammatory drugs and opioids commonly used in the
treatment of peripheral pain, the recommended drugs for central pain
conditions are neuroactive compounds that downregulate sensory processing.
The most efficacious compounds that are currently available include the
tricyclic drugs and mixed reuptake inhibitors that simultaneously increase
serotonin and norepinephrine concentrations in the central nervous system.
Other compounds that increase levels of single monoamines (serotonin,
norepinephrine or dopamine), and anticonvulsants also show efficacy in this

In addition to these pharmacologic therapies, which are useful in improving
symptoms, nonpharmacologic therapies such as exercise and cognitive
behavioral therapy are useful treatments for restoring function to an
individual with fibromyalgia.

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Date:    Sun, 27 Aug 2006 09:53:51 -0400
From:    "Bernice A. Melsky" <bernicemelsky@xxxxx.xxx>
Subject: RES: Cognitive behavioral therapy for fibromyalgia

Cognitive behavioral therapy for fibromyalgia.

Nat Clin Pract Rheumatol. 2006 Aug;2(8):416-424.

Bennett R, Nelson D.

R Bennett is Professor of Medicine at Oregon Health & Science University,
Portland, OR, USA, where D Nelson is an Adjunct Associate Professor in the
Department of Anesthesiology and Perioperative Medicine, as well as
Associate Professor of Psychology and Associate Director of Clinical
Training in the Department of Psychology & Philosophy, Sam Houston State
University, Huntsville, TX, USA.

PMID: 16932733

Cognitive behavioral therapy (CBT) techniques offer short-term,
goal-oriented psychotherapy. In this respect, it differs from classical
psychoanalysis in emphasizing changes in thought patterns and behaviors
rather than providing 'deep insight'. Importantly, the beneficial effects
of CBT can be achieved in 10-20 sessions, compared with the many years
required for classical psychoanalysis.

Although CBT is often done on a one-to-one basis, it also lends itself to a
group therapeutic setting. CBT was initially used in the treatment of mood
disorders, but its use has subsequently been expanded to include various
other medical conditions, including chronic pain states. Over the past 18
years, several chronic pain treatment programs have used CBT techniques in
the management of fibromyalgia.

In this review, the results from 13 programs using CBT, alone or in
combination with other treatment modalities, are analyzed. In most studies,
CBT provided worthwhile improvements in pain-related behavior,
self-efficacy, coping strategies and overall physical function. Sustained
improvements in pain were most evident when individualized CBT was used to
treat patients with juvenile fibromyalgia.

The current data indicate that CBT, as a single treatment modality, does
not offer any distinct advantage over well-planned group programs of
education or exercise, or both. Its role in the management of fibromyalgia
patients needs further research.

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Date:    Mon, 28 Aug 2006 11:00:37 -0400
From:    "Bernice A. Melsky" <bernicemelsky@xxxxx.xxx>
Subject: RES: (99m)Tc-ECD brain perfusion SPECT in hyperalgesic  fibromyalgia

(99m)Tc-ECD brain perfusion SPECT in hyperalgesic fibromyalgia.

Eur J Nucl Med Mol Imaging. 2006 Aug 25; [Epub ahead of print]

Guedj E, Taieb D, Cammilleri S, Lussato D, de Laforte C, Niboyet J, Mundler O.

Service Central de Biophysique et de Medecine Nucleaire, Assistance
Publique des Hopitaux de Marseille, Centre Hospitalo-Universitaire de la
Timone, 264 rue
Saint Pierre, 13385, Marseille Cedex 05, France, eric.guedj@ap-hm.fr.

PMID: 16933135

PURPOSE: Neuro-imaging studies with (99m)Tc-HMPAO SPECT in fibromyalgia
(FM) patients have reported only limited subcortical hypoperfusion.
(99m)Tc-ECD SPECT is known to provide better evaluation of areas of high
cerebral blood flow and regional metabolic rate. We evaluated a homogeneous
group of hyperalgesic patients with FM using (99m)Tc-ECD SPECT. The aim of
this study was to investigate brain processing associated with spontaneous
pain in FM patients.

METHODS: Eighteen hyperalgesic FM women (mean age 49 years, range 25-63
years; American College of Rheumatology criteria) and ten healthy women
matched for age were enrolled in the study. A voxel-by-voxel group analysis
was performed using SPM2 (p<0.05, corrected for multiple comparisons).
Visual Analogue Scale score for pain was 82+/-4 at the time of the SPECT

RESULTS: Compared with control subjects, we observed individual brain SPECT
abnormalities in FM patients, confirmed by SPM2 analysis, with
hyperperfusion of the somatosensory cortex and hypoperfusion of the
frontal, cingulate, medial temporal and cerebellar cortices.

CONCLUSION: In the present study, performed without noxious stimuli in
hyperalgesic FM patients, we found significant hyperperfusion in regions of
the brain known to be involved in the sensory dimension of pain processing
and significant hypoperfusion in areas assumed to be associated with the
affective-attentional dimension. As current pharmacological and
non-pharmacological therapies act differently on the two components of
pain, we hypothesise that SPECT could be a valuable and readily available
tool to guide individual therapeutic strategy and provide objective
follow-up of pain processing recovery under treatment.

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End CO-CURE Medical & Research Posts Only Digest - 21 Aug 2006 to 28 Aug 2006 (#2006-40)

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