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Co-Cure Weekly Digest of research and medical posts only - 26 Feb 2007 to 5 Mar 2007

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Date:    Tue, 27 Feb 2007 12:40:28 -0500
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: A Nationwide Study of Connective Tissue Disease and Other Rheumatic Conditions Among Danish Women With Long-Term Cosmetic Breast Implantation

A Nationwide Study of Connective Tissue Disease and Other Rheumatic
Conditions Among Danish Women With Long-Term Cosmetic Breast Implantation.

Ann Epidemiol. 2007 Feb 23; [Epub ahead of print]

Fryzek JP, Holmich L, McLaughlin JK, Lipworth L, Tarone RE, Henriksen T,
Kjoller K, Friis S.

 From the International Epidemiology Institute, Rockville, MD, and the
Departments of Medicine (J.P.F., J.K.M., R.E.T.) and Preventive Medicine
(L.L.), Vanderbilt University Medical Center, Vanderbilt-Ingram Cancer
Center, Nashville, TN; and Institute of Cancer Epidemiology, Danish Cancer
Copenhagen, Denmark (L.H., T.H, K.K., S.F.).

PMID: 17321754

PURPOSE: Numerous epidemiologic studies have demonstrated that breast
implants are not associated with connective tissue diseases (CTDs).
However, many CTDs are rare, and continued follow-up of women with breast
implants is warranted.

METHODS: We extended by 5 years the follow-up of our earlier
population-based cohort study of Danish women with cosmetic breast implants
(n = 2761) and comparison groups of women with other types of cosmetic
surgery (n = 8807). All women were followed from January 1977 through
December 2001. Hospitalization and outpatient data for CTD and ill-defined
and other rheumatic conditions in the implant and comparison groups were
compared with those in the general Danish population. Additionally, CTDs
and fibromyalgia were confirmed through medical chart review, and direct
comparisons of the breast implant cohort with the comparison cohort were

RESULTS: When compared with general population rates, CTDs were not
statistically significantly elevated in either the implant or the
comparison cohorts. However, unspecified rheumatism was similarly increased
in the implant (standardized rate ratio = 1.9; 95% confidence interval =
1.6 to 2.2) and comparison (standardized rate ratio = 1.5; 95% confidence
interval = 1.4 to 1.7) cohorts. In analyses of diagnoses validated by chart
review, women with cosmetic breast implants compared with those having
other types of plastic surgery or consultation for plastic surgery had no
statistically significant excess for any specific confirmed CTD or combined
CTDs (hazard ratio = 1.3; 95% CI = 0.9 to 1.9). In addition, there was no
relation between breast implants and confirmed fibromyalgia (hazard ratio =
1.2; 95% CI = 0.6 to 2.1).

CONCLUSIONS: This extension of our earlier cohort study further supports
the consensus of epidemiologic research that breast implants are unrelated
to the development of CTD.

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Date:    Tue, 27 Feb 2007 19:25:45 +0100
From:    "Dr. Marc-Alexander Fluks" <fluks COMBIDOM.COM>
Subject: RES,NOT: Suhadolnik receive $1M grant from NIH for HIV amd CFS research

Source: Temple University
Date:   February 27, 2007
Author: Vicky Thomas <victoria.thomas@temple.edu>
URL:    http://media.www.temple-news.com/media/storage/paper143/news/2007/02/27/News/Doctors.Receive.1m.Grant.For.Hiv.Prevention.Research-2744077.shtml

Doctors receive $1M grant for HIV prevention research
Through the use of gene therapy, researchers are striving to find ways to
stop the spread of HIV.

   Dr. Robert Suhadolnik, in his laboratory, isolates DNA from a carrier.
   Suhadolnik and his research team have worked for 20 years toward
   attaining a treatment alternative for the HIV infection.

Researchers in the School of Medicine are making progress in the
understanding and treatment of two diseases caused by abnormalities in the
human antiviral pathway: HIV and Chronic Fatigue Syndrome.

According to the Centers for Disease Control and Prevention, approximately
40,000 people will be infected with HIV this year in the United States
alone. The virus' rapid mutation rate allows it to resist many drug
therapies, making it impossible for a vaccine to guard the body against the
spread of an infection.

But the research team, headed by Dr. Robert J. Suhadolnik, a professor of
biochemistry in the School of Medicine, is developing a way to immunize
against the spread of HIV through the use of gene therapy.

After 20 years of researching the intracellular immunization approach to
inhibit HIV, Suhadolnik's six-member team was recently awarded a $1 million
research grant by the National Institutes of Health to continue its work.

"We have shown now that we can protect the cell from HIV infection in vitro,
in the laboratory," Suhadolnik said. Gene therapy immunization, as opposed
to vaccines, introduces an antiviral pathway into a patient's genes. The
gene replicates and becomes incorporated into the patient's system. When the
HIV virus is introduced to the body, the gene becomes active and kills the

"The HIV virus has developed ways to counteract the natural antiviral
pathways," said Suhadolnik, adding that this new therapy could stop the
spread of HIV because the delivery of antiviral genes to cells would restore
the antiviral defense pathways. "Gene therapy is extremely interesting
because we're using the body's own immune system to combat the virus without
outside chemicals or agents," said Sean Roberts, a graduate student in the
School of Medicine and a member of the research team. "It's important towards
finding a cure. Our primary goal is to find a cure."

Suhadolnik said the earlier antiviral construct had shortcomings because
there was a chance that the modified cell could contain infectious particles.
"Now we have a self inactivating vector that we can put the antiviral pathway
in by way of gene therapy, and the target cells get activated when the virus
comes along," said Suhadolnik.

He also explained that, like a vaccination, the particles would be inactive
until infection was introduced. "When you get vaccinated, you don't know that
those antibodies are present, but when an infectious particle comes in the
body, then the antibodies are made and the disease is wiped out," Suhadolnik

Gene therapy has also been successful in curing other immune deficiency
diseases, such as Severe Combined Immunodeficiency or "Bubble Boy" disease,
which was once considered a fatal condition.

The study of antiviral pathways has been the center of Suhadolnik's research
program and is also applied to the team's research on CFS, said Nancy
Reichenbach, an associate scientist in the School of Medicine and a member of
the research team.

According to Suhadolnik, the cause of CFS is unknown and can occur suddenly
with flu-like symptoms and debilitating fatigue.

The illness, which was once believed to be a psychological disorder
connected to depression, is common in women. But Suhadolnik and his research
team have found that CFS is not a clinical depression disease, but rather
caused by a defect in the antiviral defense pathway.

While HIV turns off the human antiviral defense mechanism, CFS is a disorder
caused when the antiviral pathway is working too hard, making the patient
exhausted. "Initially we reported that the antiviral pathway was abnormal in
patients diagnosed with Chronic Fatigue Syndrome," Suhadolnik said. "In
subsequent studies, we reported the appearance of an abnormal protein in the
blood cells of the patients diagnosed with CFS. In essence, what we showed
was the appearance of a new protein."

In addition to the grant for their HIV research, Suhadolnik and his team
were also granted a U.S. patent for their research and discovery of diagnosis
for CFS.

(c) 2007 Temple University

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Date:    Thu, 1 Mar 2007 15:06:44 +0100
From:    Jan van Roijen <j.van.roijen CHELLO.NL>
Subject: act,med: The NICE approach to ME is outrageous


Send an Email for free membership
       >>>> Help ME Circle  <<<<
 >>>>   1 March 2007  <<<<
Editorship : j.van.roijen chello.nl
Outgoing mail scanned by Norton AV

From: DEnlander aol.com

Reference: *RiME's Summary of APPG Meeting*
Help ME Circle,  February 28:

The NICE approach to ME is outrageous.

It would be akin to a physician treating polio in the 1940's with
Graded Exercise Therapy. Exercise then was helpful in reducing
atrophy but did little to cure polio.

A polio victim was naturally depressed because of the
debilitating illness, Cognitive behavioral therapy CBT if it was
used then, thank the Lord it was not, may have made the patient
less depressed but would have done little to cure the underlying

Translate polio to ME and we have the ludicrous modern day
equivalent with its waste of scarce research funds and futile
efforts to promote a self serving psycho babble.

Derek Enlander, M.D. M.R.C.S., L.R.C.P.
New York

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Date:    Thu, 1 Mar 2007 13:05:52 -0500
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Stress, depression and fibromyalgia

Stress, depression and fibromyalgia.

Acta Neurol Belg. 2006 Dec;106(4):149-56.

Van Houdenhove B, Luyten P.

Dept of Liaison Psychiatry, University Hospital Gasthuisberg, Leuven,
Belgium. boudewijn.vanhoudenhove uz.kuleuven.ac.be

PMID: 17323832

There is increasing evidence that stress and depression may play a crucial
role in the aetiology and pathophysiology of fibromyalgia (FM). We first
review recent studies on the possible role of life stress, including
childhood trauma, in FM. Subsequently we focus on clinical and
aetio-pathogenetic links between stress, depression and pain.

We put forward the hypothesis that chronic stress/depression may contribute
to a dysregulation of neuro-endocrine, immune and central pain mechanisms
in FM. Finally, we discuss some future directions, including the use of new
conceptual models, research topics and strategies, as well as potential
implications from recent studies in affective disorders for the treatment of FM.

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Date:    Fri, 2 Mar 2007 11:58:05 -0500
From:    "The CFIDS Association of America <cfidslink@cfids.org> via Co-Cure Moderator"
Subject: NOT,MED: March 10 Seminar: kNOw MORE! (Robert Wood Johnson Univ. Hospital in New Brunswick, NJ)

Until there is no more chronic fatigue syndrome (CFS), itís vitally
important for patients, caregivers and clinicians to know more about
this illness. Please plan to join us in New Jersey on Saturday, March
10, 2007, from 11:00 a.m. to 5:15 p.m. for a seminar comprised of three
topical sessions on CFS. The seminar will be held at Robert Wood
Johnson University Hospital at One Robert Wood Johnson Place in New
Brunswick, New Jersey.

The CFIDS Association is collaborating with the New Jersey Chronic
Fatigue Syndrome Association (NJCFSA) on this special joint program
combining the CFIDS Associationís kNOw MORE CFS seminar series and the
spring conference of the NJCFSA.

The conference will start with a session on the national CFS public
awareness campaign sponsored by the Centers for Disease Control and
Prevention and the CFIDS Association of America. Registrants will have
the opportunity to hear a campaign update from CFIDS Association
president and CEO Kimberly McCleary and to see campaign components like
the TV and radio PSAs, print ads, online banner ads, patient brochure,
CFS toolkit for medical professionals, major press coverage and the
acclaimed CFS photo exhibit called "The Faces of Chronic Fatigue
Syndrome." This compelling exhibit features the portraits and
stories of CFS patients, family members and health care professionals.
Two of the participants in the photo exhibit, Jacqueline Niederle and
Brian Bernard, will also speak at this session about the power of
personal advocacy.

Nancy Klimas, MD, of the University of Miami School of Medicine, will
provide an update on the current CFS research landscape, with
particular attention to research presented at the 8th International
Association for CFS Conference in Ft. Lauderdale in January. Dr.
Klimas, an internationally known expert on CFS, will help seminar
participants understand the significance of new research findings.

Alan Pocinki, MD, the speaker for the clinical session, practices in
Washington, DC, where he treats both CFS and FM patients in his general
medical practice. He will discuss how to work with a clinician to
develop individualized treatment programs to accommodate the
considerable variability in CFS symptom expression, in symptom severity
and in the efficacy of specific treatment protocols. He is an Associate
Clinical Professor of Medicine at George Washington University.

A joint question-and-answer forum will follow the presentations,
allowing participants to interact with speakers, ask questions and
learn practical information about CFS and FM and how to manage these
medical conditions.

Tickets for the seminar are $30 if purchased by March 2, $35 if
purchased after this deadline or at the door. Seating is limited so
preregistration is encouraged. (Our most recent kNOw MORE program sold
out with 280 participants!) To receive a brochure with complete details
and a registration form, please send an e-mail to cfids cfids.org with
the subject line "KNOW MORE", call 704-364-0466 or visit
http://capwiz.com/cfids/utr/1/CSSFGUORZU/LZRJGUOUVQ/1082450201=6 to
purchase tickets online.

Hope to see you there!

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Date:    Fri, 2 Mar 2007 13:08:38 -0500
From:    Jim Roache <jfroache SYMPATICO.CA>
Subject: RES: Fibromyalgia - gene scanning - fibromyalgia syndrome - genetics and the CNS

Just taking a flyer here....from Ottawa, Canada:

I don't know if member of the group or one that we can locate (in the
publish or perish brigade) might be interested in an FM Project.

With so many among the world population having it, a drug or other therapy
to dampen the genes or mute the symptoms (pain, fatigue and brain fog, etc)
would make Billions, plus relieve incredible suffering, increasingly
resulting in suicide.

Researchers are identifying genes related to medical problems every day
now. They have isolated those for ME/CFS/CFIDS (Chronic Fatigue Syndrome) -
as I said to one doctor, call it XYZ if you like, so long as we both know
what we mean by the term.

Three big Pharma companies have drugs coming through the system - numbered
only (no names), but I'll bet they are neuropathic....as such, they will
not be effective in FMS. I have tried some off label - and as expected -

There have been great breakthroughs in FMS research in the last 18 months
using gene scanning. It's genetic and effects the CNS (brain and spinal
column), in turn unbalancing the neurotransmitters (confirmed by spinal tap
if necessary), disrupting blood flow to the pain centres of the brain
(fMRIs show it) and causing up to 50+ pseudo symptoms - the body feeling
pain and dysfunction that is NOT there (in the normal sense) - except in
the CNS (HPS Axis), autonomic nervous system and the DNA.

They now have one or two genes targeted - but there are at least five
subsets of the condition. And there are more genes to be isolated (more
gene scanning).

Our family has confirmed cases to the third cousin, multi-generational
level and controls (no FMS). My niece, sister, uncles, aunts and third
cousins have confirmed cases (severe). Others have none.

I think we would be a great collection of lab rats -  5-6 generations
(that's the only way third cousins could have it as well as my niece). And
there are family "controls"....perfect because like many, they think we are
hypochondriacs. We are literally all over North America.

Any gene lab wanting to isolate the additional genes would at least get a
great paper for peer review publication - and then big pharma might come
running if the study were to find a consistent pattern of under and over
active genes....as has happened with CFS.

The Health Sciences Centre at Memorial University in St. John's, NF now has
a Genetics Lab, and they have agreed to at least test my sister and me for
genetic abnormalities (mutations) in common, but we are wait listed.

I have been active with several national organizations in Canada, and we
have an International Consensus Document (as you know) that has become
something of a clinical standard, a new paradigm for Dx and Rx (as opposed
to the older WHO research standard) which  was as helpful to physicians
outside the lab or to patients trying to prove they really did have a
problem illness.

In Canada, as elsewhere, we lobby government and educate the public. I
spend a lot of time peer-counselling and trying to figure out what is
happening in the HPA axis with so many people - 15% of whom are disabled by
a pain amplification syndrome that was until recently a total mystery.

My family (not all) will volunteer to participate in genetics studies to
isolate the genes - the equivalent of turning your stereo top high and
being unable to locate the volume button again, or turning the thermostat
top high and breaking the switch.

  I realize isolating the genes is only the first step, but then I think
big pharma will support development of medications to dampen the genes or
break that closed loop we have in the CNS - as in the stereo or thermostat
i.e. block the signal to the furnace to fun top high or cut the wire to the
streeo or its speakers and stop or reduce the  the pain.

Pain medications to date - NSAIDs, narcotics and neuropathic drugs - act on
the wrong pain receptors - the incoming signal or stimulus. What we need to
do is find something to act on the outgoing signal from the brain to the
HPA axis and the autonomic nervous system - having first targeted the genes
that have been triggered (in one of several ways) to cause the CNS to
respond in the wrong way - the gas peddle is stuck to the floor with the
car in neutral and were have to get the engine off or breal the like -
peddle to carburetor to engine before other damage is done.

I don't think the study has to be large, given what we have come to know in
the last 18 months. If the pattern is consistent in a large family like
ours, it will be identical with most if not all others (at least for slow
onset FMS).

I have not even discussed this with the lab in question, but simply thought
I would look for someone interested in doing or funding (grant money -
trusts) such a research project.

Since we have one interested and willing - in a medical teaching and
research facility  - if the possibility of funding were there, and a
perfect study group (lab rats) is in place (us), I thought I could/should
at least ask.

This can be done though our national organizations, the University/ies, the
Medical School/s, the neurology department/s (specific physician/s) or the
genetics lab/s. I have known for a long time that FMS is a CNS syndrome.
Genetics has just proven it.

Now the next step is a good study - what could be better than one extended
family with it's own controls and people of some knowledge of the condition
plus genetics.

At the end of the day, the pharmacy company producing the medication would
make billions -a huge international market awaits the medication. Royalties
could go back to the national organizations and to further genetic
research. Win-win. Some could even go back to additional related research
while the medication is under patent.

Am I even close here?

Jim Roache, MBA
Ottawa, ON

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Date:    Sat, 3 Mar 2007 13:25:25 -0500
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Incidence, Prognosis, and Risk Factors for Fatigue and Chronic Fatigue Syndrome in Adolescents: A Prospective Community Study

Incidence, Prognosis, and Risk Factors for Fatigue and Chronic Fatigue
Syndrome in Adolescents: A Prospective Community Study

Journal: PEDIATRICS Vol. 119 No. 3 March 2007, pp. E603-E609

Authors: Katharine A. Rimes, DPhil [a], Robert Goodman, PhD [b], Matthew
Hotopf, PhD [a], Simon Wessely, MD [a], Howard Meltzer, PhD [c] and Trudie
Chalder, PhD [a]

Affiliation: King's College London, Institute of Psychiatry
   [a] Section of General Hospital Psychiatry
   [b] Department of Child and Adolescent Psychiatry, London, United Kingdom
   [c] Academic Department of Psychiatry, Brandon Mental Health Unit,
Leicester General Hospital, Leicester, United Kingdom

NLM Citation: PMID: 17332180

OBJECTIVE. The objective of this study was to describe the incidence,
prevalence, risk factors, and prognosis of fatigue, chronic fatigue, and
chronic fatigue syndrome in 11- to 15-year-olds.

METHODS. A random general population sample (n = 842) of British
adolescents and their parents were assessed at baseline and 4 to 6 months
later. The main outcomes were fatigue, chronic fatigue, and chronic fatigue
syndrome, operationally defined.

RESULTS. The incidence over 4 to 6 months was 30.3% for fatigue, 1.1% for
chronic fatigue, and 0.5% for chronic fatigue syndrome. The point
prevalence was 34.1% and 38.1% for fatigue, 0.4% and 1.1% for chronic
fatigue, and 0.1% and 0.5% for chronic fatigue syndrome at time 1 and time
2, respectively. Of participants who were fatigued at time 1, 53% remained
fatigued at time 2. The 3 cases of chronic fatigue and 1 case of chronic
fatigue syndrome at time 1 had recovered by time 2. Higher risk for
development of chronic fatigue at time 2 was associated with time 1 anxiety
or depression, conduct disorder, and maternal distress; in multivariate
analysis, baseline anxiety or depression remained a significant predictor
of chronic fatigue. Increased risk for development of fatigue at time 2 was
associated with time 1 anxiety or depression, conduct disorder, and older
age; in multivariate analyses, these factors and female gender all were
significant predictors of fatigue.

CONCLUSIONS. The incidence rates for chronic fatigue and chronic fatigue
syndrome in this adolescent sample were relatively high, but the prognosis
for these conditions was good. This prospective study provides evidence for
an association between emotional/behavioral problems and subsequent onset
of fatigue/chronic fatigue.

Key Words: chronic fatigue . incidence . prognosis . risk factors . prevalence
Abbreviations: CFS-chronic fatigue syndrome . CF-chronic fatigue .
CDC-Centers for Disease Control and Prevention . GHQ-General Health
Questionnaire . CI-confidence interval

Accepted Oct 16, 2006.

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Date:    Sun, 4 Mar 2007 14:44:23 +0100
From:    "Dr. Marc-Alexander Fluks" <fluks COMBIDOM.COM>
Subject: RES,NOT: Alpha-Delta sleep in CFS

Source: American Journal of the Medical Sciences
        Vol. 333, #2, pp 78-84
Date:   February 2007
URL:    http://www.amjmedsci.com/pt/re/ajms/home.htm



Defining the Occurrence and Influence of Alpha-Delta Sleep in Chronic Fatigue
Elke Van Hoof, PhD; Pascale De Becker, PhD; Charles Lapp, MD; Raymond Cluydts,
PhD; Kenny De Meirleir, PhD

>From the Department of Human Physiology (EVH, PDB, KDM) and the Department
  of Psychology (EVH, RC), Vrije Universiteit, Brussels, Belgium; and from
  the Hunter-Hopkins Center, Charlotte, North Carolina (CL).
Submitted May 11, 2006; accepted in revised form September 11, 2006.
Correspondence: Elke Van Hoof, Vakgroep COBI, Faculty of Psychological and
  Educational Sciences, Pleinlaan 2, 1050 Brussels, Belgium
  (E-mail: Elke.Van.Hoof vub.ac.be).


Patients with chronic fatigue syndrome (CFS) present a disordered sleep
pattern and frequently undergo polysomnography to exclude a primary sleep
disorder. Such studies have shown reduced sleep efficiency, a reduction of
deep sleep, prolonged sleep initiation, and alpha-wave intrusion during
deep sleep. Deregulation of the 2-5A synthetase/RNase L antiviral pathway
and a potential acquired channelopathy are also found in a subset of CFS
patients and could lead to sleep disturbances. This article compiles a
large sleep study database on CFS patients and correlates these data with a
limited number of immune parameters as it has been thought that RNase L
could be associated with these sleep disturbances.

Forty-eight patients who fulfilled 1994 Centers for Disease Control and
Prevention criteria for CFS underwent extensive medical evaluation, routine
laboratory testing, and a structured psychiatric interview. Subjects then
completed a complaint checklist and a two-night polysomnographic
investigation. RNase L analysis was performed by gel electrophoresis using
a radiolabeled 2',5'-oligoadenylate trimer. Basic descriptive statistical
parameters were calculated.

Patients experienced a prolonged sleep latency, showed a low sleep
efficiency index, and had a low percentage of slow wave sleep. The present
alpha-delta intrusion correlated with anxiety; no correlations appeared,
however, between alpha-delta sleep and immunologic parameters, including
RNase L.

The main findings are 1) validation of sleep latency problems and other
sleep disturbances as already suggested by several authors; 2) alpha-delta
intrusion seems associated with anxiety; and 3) elevated RNase L did not
correlate with alpha-delta sleep.

Alpha-delta sleep; Median-split; Anxiety; Specificity; CFS.

Chronic fatigue syndrome (CFS) is a clinically defined syndrome that is
characterized by chronic fatigue and a constellation of other symptoms and
physical findings.1-3 In our sample in Brussels, CFS is diagnosed using a
clinical case definition established by the Centers for Disease Control and
Prevention (CDC) in 19881 that was revised in 1994.4 The major
distinguishing symptom is debilitating fatigue of more than 6 months'
duration associated with a marked decrease in daily activity that cannot be
attributed to any known medical cause. Other nonspecific symptoms including
joint pain, night sweats, visual disturbances, exaggerated allergic
reactions, memory loss, emotional lability, and sleep problems such as
unrefreshing sleep, accompany the fatigue.4

Patients with CFS describe a disordered sleep pattern with difficulty
getting to sleep, frequent awakenings, and, less commonly, early morning
wakening. Sleep is nonrestorative, with most patients more aware of their
symptoms in the mornings and improving slightly as the day progresses.5-7 In
the diagnostic process, patients undergo a polysomnographic investigation to
exclude a primary sleep disorder. The use of electroencephalographic (EEG)
techniques to investigate the sleeping brain reveals a wealth of electrical
activity in a seemingly passive body.8 Sleep is divided into rapid eye move-
ment (REM) sleep and non-REM sleep. In turn, non-REM sleep is divided into
stages 1, 2, 3, and 4, with slow delta waves comprising stages 3 and 4.8,9
In practice, the alpha rhythm normally occurs during quiet wakefulness and
is located over the posterior part of the scalp. The onset of sleep is
characterized by the disappearance of this rhythm and the appearance of
other EEG frequencies such as theta (3-7 Htz), K-complexes, sleep spindles
(12-15 Htz), and later, delta or slow waves (0.5-2.5 Htz) or stages 3 and 4
non-REM sleep.

Polysomnographic studies in CFS have shown reduced sleep efficiency, a
reduction of REM sleep, and a longer sleep initiation.5,7,10-15 CFS patients
have a significantly lower percentage of stage 4 sleep and alpha wave
intrusion in deep sleep or alpha-delta sleep.10,11,13 Alpha-delta sleep is
an abnormal sleep EEG rhythm characterized by alpha activity that is
superimposed on delta waves of slow wave sleep stages 3 and 4.16 This
activity was first reported by Hauri and Hawkins in 1973 in 9 psychiatric
patients with somatic malaise and fatigue.17 Now, alpha sleep has been
broadened to include alpha intrusion into all stages of non-REM sleep.18
However, it seems not to be specific for CFS and has been seen in
fibromyalgia,19,20 rheumatoid arthritis,21 and other conditions associated
with chronic pain.22,23

In sleep architecture, specific reductions in REM sleep have been reported.
Due to this reduction, interferences in daily functioning seem
inevitable.10,15 Also, CFS patients have a reduced percentage of delta sleep
in their non-REM period.14

Chronic fatigue syndrome is associated with several immunologic
abnormalities or discrepancies.24 An intracellular immune deregulation is
also widely reported in patients with CFS. After the discovery by Suhadolnik
and colleagues, the deregulation of the 2-5A synthetase/RNase L antiviral
pathway is frequently found in a subset of CFS patients.5 The
hyperactivation of RNase L has been reported at length in the scientific
literature,5-8 but also the discovery of the abnormal low molecular weight
RNase L (37 kDa) in patients with CFS5 was confirmed by several other
researchers.7-9 It had been thought that RNase L level gives a clear picture
of immune deregulation and that the suggested acquired channelopathy that
occurs as a consequence will lead to central fatigue and sleep

Increased RNase L activity creates interaction of ABC transporters with the
ankyrin fragment of RNase L upon its release by proteolytic cleavage.26
Subsequently, it is thought that improper ion channel function will develop,
leading toward an ac- quired channelopathy of the ABC transporters. This
suggested acquired channelopathy with loss of intracellular potassium will
lead to metabolic and intracellular abnormalities, including central fatigue
and sleep disturbances such as alpha-delta intrusion.25

This article subjects alpha-delta sleep to an indepth study. First of all,
the occurrence of alpha-delta sleep in a randomized study group is examined.
If alpha-delta sleep is present in this study population, a median split
will be used to check whether more alpha-delta sleep is equivalent with more
subjective complaints and more immunologic deviances. Correlation analysis
may reveal associations between the subjective feeling of unrefreshing
sleep, total sleep time, immunologic parameters, and alpha-delta sleep.
After the theory presented by Englebienne and De Meirleir, it has been
thought that RNase L would be associated with alpha-delta intrusion and
other self-reported as well as objective sleep parameters.25,26 If any of
the parameters (RNase L, NK-cells, T-cells, total sleep time, or
unrefreshing sleep) correlated significantly with alpha-delta sleep, then a
regression analysis might reveal the exact associations between the
parameters and alpha-delta in CFS patients.


Recruitment of CFS Patients

Study subjects were recruited from the outpatient fatigue clinic, Vrije
Universiteit Brussels between October and February 2003. Generally, patients
are referred by their general practitioner to the outpatient fatigue clinic.
To fulfill the 1994 CDC criteria for CFS, clinically evaluated, unexplained,
persistent, or relapsing chronic fatigue that is of new or definite onset
should result in a substantial reduction in previous levels of occupational,
educational, social, or personal activities.2 Furthermore, at least 4 of the
following symptoms must have persisted or recurred during 6 or more
consecutive months and must not have predated the fatigue: impairment in
short-term memory or concentration, tender cervical or axillary lymph nodes,
muscle pain, multijoint pain, headaches, unrefreshing sleep, and
postexertional malaise lasting more than 24 hours.2 Any active medical
condition that may explain the presence of chronic fatigue prohibits the
diagnosis of CFS. Hence, all subjects underwent an extensive medical
evaluation, consisting of a standard physical examination, medical history,
exercise capacity test, and routine laboratory tests. The laboratory tests
included a complete blood cell count, determination of the erythrocyte
sedimentation rate, serum electrolyte panel, measures of renal, hepatic and
thyroid function, and rheumatic and viral screens. If the patients' medical
history did not exclude a psychiatric problem at the time of disease onset,
a structured psychiatric interview, based on the Diagnostic Statistical
Manual for Psychiatric Disorders (DSM), was performed. In a number of cases,
further neurologic, gynecologic, endocrine, cardiac, and gastrointestinal
evaluations were performed. The medical records were also reviewed to
determine whether patients suffered from organic or psychiatric illness that
could explain their symptoms. If any of the laboratory or additional
analyses revealed any active medical or psychiatric condition that could
explain the presence of the patient's symptoms, then CFS could not be
diagnosed and those patients were excluded from the study.

During a 2-night polysomnographic investigation, blood samples were taken.
Only CFS patients who completed a 2-night polysomnographic investigation and
had a diagnosis of CFS according to the CDC criteria4 were included in the


Patients spent 2 nights in the sleep unit, with the first night being
considered as a habituation night and followed by an all-night
polysomnography examination on the second night. Subjects were prepared for
the polysomnographic recordings between 10:00 and 11:00 PM and were allowed
to retire when they wished (good night time). They were awakened around 7:30
AM if they did not arise spontaneously (good morning time). Polysomnography
involved an electroencephalogram, which was recorded from C4-A1, C3-A2,
Fpz2-A1, Fpz1-A2, O2-A1, O1-A2 sites, as well as an electrooculogram, a
submental electromyogram, and an anterior tibialis electromyogram. Nasal and
oral airflow, respiratory effort (thoracic and abdominal belt), and arterial
oxygen saturation were recorded during the second night. The sleep
recordings were recorded on Nicolet Ultrasom and visualized on screen and
scored by trained sleep technicians in 30-second epochs according to
standard criteria. The technicians scored during their routine clinical
activities, without knowledge of the aims of the study.

The studied sleep variables were: slow-wave sleep (min) (SWS), REM sleep
(min) (STGE-REM), time awake (min) (awake) from good night time to good
morning time, sleep latency (LAPSTGE2), sleep quality index (SE%),
micro-awakenings (MAI) (n/h), total sleep time (TST) (min), REM latency
(REMLATN) (min), number of shifts between stages (STSHIFTS), percentage time
awake in bed (A%TIB), percentage slow-wave sleep (SWS%TIB), percentage of
non-REM sleep (Nrem%TIB), percentage total sleep time (TST%TIB), and
alpha-intrusion in slowwave sleep (SWS%AI). Patients were excluded if the
TST of 1 night was less than 120 minutes.

Immunological Data (Immunophenotyping)

Anticoagulated blood (EDTA) was collected between 9:00 and 11:00 AM and used
for white blood cell enumeration, differential counts (Celldyn 4000, Abbott
Laboratories, Abbott Park, IL) and flow cytometric studies. Lymphocyte
populations were analysed with dual color direct immunofluorescence on a
EPICS xl flow cytometer (Coulter, Miami, FL), with aid of the System I
computer software. A collection of 100 muL of whole blood was incubated
with the appropriate combination of monoclonal antibodies for 25 minutes at
4&C. Red blood cells were then lysed using lysis buffer (Becton Dickinson)
for 7 minutes, centrifuged, and washed once with 2 mL phosphate buffered
saline. Resuspension was immediately followed by cell analysis. Commercially
available (Becton-Dickinson) phycoerythrin or fluorescein isothiocyanate
labeled monoclonal antibodies were used (Table 1). Estimates of absolute
numbers of lymphocyte subsets were determined by multiplying peripheral
lymphocyte counts by the percentage of each surface marker.

Assessment of peripheral blood mononuclear cells, cell extracts, and serum
and quantification of 37-kDa 2-5A-BP in peripheral blood mononuclear cell
extracts were performed in a similar fashion as the method described by
Demettre et al.26

Subjective Complaints

A complaint checklist was presented to the patients. They were asked to
complete the checklist and rate their complaints on a Likert scale from 0
(absent) to 3 (commonly present). Fatigue, postexertional fatigue,
depressive feelings, anxiety, self-perceived personality changes, emotional
lability, muscle aches, joint aches, sleep problems, and nonrefreshing sleep
were completed. No psychometric parameters are known.

Statistical Analyses

Basic descriptive statistical parameters are reported. A onetailed
Kolmogorov-Smirnov test was performed to check normal distribution. For the
reporting of the location and spread of the distribution of the various
variables in this study, the median is more appropriate, as most of the data
are either ordinal or continous, but skewed. The mean, standard deviation,
and range are also reported as additional information, to make a comparison
with other studies possible. The relationship between the different
variables was quantified using the nonparametric Spearman rank correlation
coefficient for the same distributional reasons as given previously.
Kendall's tau was also computed but was not reported in the paper because
the results were very much in line with the Spearman coefficient. To assess
the significance of the correlations, the P-value for the correlation
coefficients was determined. Because of the many correlations, a Bonferoni
correction was applied to keep the type I error under control. Therefore
correlations are considered to be significant when the P-value is less than
0.002 instead of 0.05.

The above statistical computations were performed using the SPSS statistical
package [SPSS 2000, SPSS Syntax reference 12.0 SPSS Inc. Chicago, Il]



Forty-eight patients were included in this study, of which 19 were male
(40%) and 29 were female (60%). The mean age of the patients was 45 years
(p/m 10.46 years). The mean number of years the pa- tients experienced
symptoms was 8.98 (p/m 7.71 years). The mean scores on the immune parameters
are presented in Table 2. None of the immune variables fell outside their
reference score.

Rnase L

The mean RNase L was 4.47 (p/m 0.71) with a median of 2.80. The deregulation
of the RNase L pathway can be quantified by dividing the amount of 37 kDa
RNase L by 83 kDa RNase L, and multiplying this quotient by 10. The outcome
of this formula, frequently referred to as RNase L ratio, is considered
normal when it remains below 0.5. In any other case, the RNase L ratio is
considered increased, suggestive of deregulation of the 2.5A synthetase
RNase L pathway.27 Thirty-nine patients (86.67%) presented an increased
RNase L ratio.

Subjective Complaints

Sixty percent of the patients reported significant fatigue. The mean score
of fatigue on a scale from 0 to 3 was 2.56 (p/m 0.58). Almost 75% of
patients suffered from post-exertional fatigue, with a mean score of 2.66
(p/m 0.70). Almost 75% reported signifi- cant sleep problems with a mean
score of 2.09 (p/m 1.04) and significant nonrefreshing sleep with a mean
score of 1.94 (p/m 1.17). The other symptoms are summarized in Table 1.

Sleep Continuity

Table 3 describes the group variables for the sleep parameters. The sleep
latency or the time from lights-off until stage 2 was 61.40 minutes (p/m
7.35 minutes). Table 4 shows the results from Fischler et al,13 who also
used a Belgian population. Sleep latency time was lower than in our
population. The sleep efficiency index shows 72.35% (p/m 2.15), which is
lower than the results presented by Fischler et al13 (Table 4). Our
population presented 9.53 (p/m 1.10) micro-awakenings per hour. Again the
results in the study performed by Fischler et al13 were relatively lower
(Table 4).

Sleep Architecture

The patients spent 71.49% (p/m 2.19) of the time in sleep. The patients had
70.19 minutes (p/m 5.02) of slow wave sleep or delta-sleep. On average the
REM sleep time was 261.96 minutes (p/m .31). The total sleep time was 326.21
minutes (p/m 10.46), which is approximately 5.5 hours of sleep. The test
showed a mean number of shifts between stage of 67.29 times (p/m 4.55). The
percentage slow wave sleep was 22.49% (p/m 1.71) with a mean non-REM sleep
percentage of 80.90% (p/m 1.31). The percentage of alpha waves in slow wave
sleep appeared to be 4.32% (p/m 0.80) (Table 3).

Alpha-Delta Intrusion

A median split was performed on the percentage of alpha waves in slow wave
sleep (SWS%AI). A median split was performed to examine whether a high
percentage of alpha-delta intrusion results in more subjective complaints or
alteration in immune parameters. This method could shed more light on the
potential importance of the influence of the alpha-delta intrusion. The
median was 2. The meanage of the group with few alpha-delta intrusion was
44.73 years of age (p/m 2.18) and a mean onset of symptoms with a mean of
8.73 years (p/m 1.56). The group with the most alpha-delta intrusion had a
mean age of 45.32 years of age (p/m 2.11) with a mean onset of 9.27 years
(p/m 1.62). There was no significant difference between the ages of the two
groups (chi^X2=2.8; P=0.196). No significant difference could be identified
for the onset of both groups (U=268.00, Z=0.374, P=0.708). Table 5 shows the
significant differences in subjective complaints and immunologic parameters.
Only "subjectively perceived anxiety" differed significantly between the
group with high alpha-delta intrusion and low alpha-delta intrusion. The
high alpha-delta intrusion group reported the most self-reported anxiety
(Table 4).


Alpha-delta intrusion correlated with anxiety, although this was just a
statistical trend (R=0.317; P=0.03). No other correlations revealed
significant information (data not shown). Because no significant
correlations could be found, no regression analyses were performed to reveal
exact associations.


Sleep architecture variables demonstrated significantly different sleep
onset latency and sleep disturbances in CFS patients (Table 4). Because of
the resemblance between the CFS patients used by Fischler et al13 and Fossey
et al15 and our CFS population, their results may apply to our sample,
although no healthy control group was used. Similar results were already
reported by several other authors, such as Whelton et al10 and Stough and
Withers.14 CFS patients present less sleep continuity. Patients experience
problems falling asleep, represented by the large sleep latency. The low
sleep efficiency index and the high number of micro-awakenings objectify the
subjectively presented complaints of a distorted sleep pattern and a
nonrestorative sleep.5-7 The patients slept about 5.5 hours. They spent
almost 30% of the time awake in bed. Interestingly, a lot of shifts between
stages are apparent. Again, the results of the sleep architecture underscore
the distorted sleep pattern and an unrefreshing sleep.

Alpha-delta intrusion is present although a wide range of the percentage of
this intrusion indicates its nonspecific nature. This sleep anomaly is
thought to be accompanied by indications of vigilance during sleep and the
subjective experience of unrefreshing sleep. The latter seems not solely
associated with alpha-delta intrusion because no differences in feelings of
fatigue and unrefreshing sleep could be found between CFS patients with low
or high alpha-delta intrusion. Our results emphasize the nonspecific nature
of alpha-delta sleep in CFS patients, a suggestion made by several
authors.19-23 For instance, Manu and associates found no correlation between
alpha-delta sleep and CFS, fibromyalgia, major depression, primary sleep
disorders, or Lyme disease but did find that alpha-delta sleep was more
common among chronic fatigue patients without major depressive disorders.23

Although the sample showed high RNase L, no differences were apparent
between patients with low and high alpha-delta intrusion. Furthermore, no
correlations appeared between alpha-delta sleep and immunologic parameters,
including RNase L. So far, it has been thought that a potential acquired
channelopathy, a consequence of immune deregulation through RNase L, leads
to sleep disturbances including alpha-delta sleep.25,26 Our results suggests
that RNase L and the subsequent channelopathy are not associated with
alpha-delta intrusion. Moreover, none of the self-reported sleep problems,
nor the objective sleep parameters, are associated with RNase L. This result
questions at least a part of the suggested hypothesis proposed by
Englebienne and De Meirleir.25 The suggested acquired channelopathy with
loss of intracellular potassium should lead to metabolic and intracellular
abnormalities, including central fatigue and sleep disturbances such as
alpha-delta intrusion. Our results do not support the inclusion of sleep
disturbances including alpha-delta intrusion in the list of potential
consequences of the suggested channelopathy.

The results the deregulation of the 2-5A synthetase/RNase L pathway are
similar to those of previous studies.27,28 It is still unclear, however,
whether the 37 kDa RNase L ratio is representative of the CFS population in
general, and whether the 37 kDa RNase L ratio is characteristic of a
particular stage in the course of the illness or if it fluctuates over time
(as is the case with symptom severity in the majority of CFS patients).
Recent research suggest the ratio could be associated with (the severity) of
the experienced complaints and its associated clinical causes.25 For
instance, the deregulation of the 2-5A synthetase/RNase L pathway appears to
accompany different aspects of immune dysfunction in CFS patients. A reduced
number and activity (cytotoxicity) of NK-cells have been reported in
patients with CFS.29-31 In addition, a negative correlation between the
RNase L ratio and both the number and percentage of NK-cells was observed in
CFS patients. In our study, no deviant NK-cells percentages were found.
Moreover, no correlations were found between the RNase L ratio and the

To be a biological gradient, a correlation between the biological parameter
of interest (i.e., impairment of the RNase L pathway) and the clinical
severity of the disorder of interest (i.e., CFS) is required. No significant
correlations regarding self-reported complaints, objective sleep parameters,
and immune parameters were found in this study. For interpreting a
correlation analysis, however, one should focus on the correlation
coefficient rather than interpreting the P-value. Correlation coefficients
as low as 0.2, regardless of the P-value, suggest no association is present.
Although no significant associations were found, some correlation
coefficients suggested possible relationships. The Bonferroni-corrections
and the small sample size could prevent any significant results. Further
research is necessary to clarify possible associations. Using our present
results, no significant findings appeared, casting into question the
biological gradient of the RNase L ratio regarding the NK-cells and sleep

Anxiety differed between low and high alpha-delta sleep. People suffering
from high alpha-delta intrusion experience more anxiety. Anxiety could be
the result of the higher vigilance in slow wave sleep. The major clinical
importance of this study is that because of alpha wave intrusion in phase 3
and 4 of the non-REM sleep, full benefit is not taken from the recuperative
function of slow wave sleep.

This study had several limitations. First, the study was done
retrospectively and therefore strong causal relations were difficult to
make. Second, a limited number of CFS patients were enrolled and there was
no healthy control group, although the results were similar to those of
Fischler et al13 and Fossey et al,15 who did include a healthy control
group. Therefore, more research is needed, not only with a increased number
of CFS patients that would give more accurate results, but also with the
same polysomnographic protocol and adequate control subjects, including
patients with non-CFS-induced fatigue. The relatively small number of CFS
patients in this study was due to recent changes in polysomnographic
protocols; only 41 CFS patients were found to have completed a similar
2-night polysomnographic protocol. Moreover, 1-night polysomnographic
protocols should be avoided due to the first-night effect.32 In summary, one
obvious limitation of the present study is the lack of power due to a small
sample size. However, the well-documented expense related to laboratory
sleep research,33 as well as the difficulties regularly encountered with
subject attrition in such extensive, demanding, and lengthy investigations
make small sample size an unfortunate but common consequence. Nevertheless,
the comprehensive data collected make an important contribution to CFS
research and should form the basis for future investigations.

Summarizing, the main findings of this study are as follows: 1) The
existence of sleep latency problems and other sleep disturbances are
validated, as already suggested by several authors. 2) Alpha-delta-intrusion
seems associated with anxiety. 3) An elevated RNase L-ratio did not
correlate with alpha-delta sleep. 4) The results from the correlation
analysis questions RNase L as a biological gradient. To our knowledge, this
is the first study in which immune parameters were correlated to
polysomnographic variables in CFS patients. More research is undoubtedly
necessary to state causal relationships, although some interesting
suggestions have been made.


Our Department would like to thank Kim Borremans in collecting the
appropriate data and Nancy Reichenbach for her help in academic writing.


Table 1. Subjective Symptoms Reported by the Patients
Variable                0-Absent   1          2          3-Present   X (SD)
                                                         all the time
Depressive feelings     23%        25%        33%        19%         1.48 (1.05)
Anxiety                 44%        10%        31%        15%         1.17 (1.16)
Self-perceived          46%        17%        27%        10%         1.02 (1.08)
   personality changes
Emotional lability      19%        19%        33%        29%         1.73 (1.09)
Muscle aches            23%         6%        27%        42%         1.89 (1.20)
Joint aches             31%        10%        29%        27%         1.53 (1.21)

Table 2. Group Variables of Immune Parameters
Item           Reference, %   Patients, n  Mean   SD     Median  Range
RNAse L         --            45            4.47  0.71    2.80   21   CFS marker
CD3HLADR        2-9           44            4.55  0.43    4.00   12
CD8            23-41          44           26.73  1.08   26.00   32
CD19 CD5+       1-4           44            2.15  0.25    2.00    8
CD3-CD16CD56+   4-22          44            7.07  0.85    5.50   32
CD4/CD8        0.9-2.6        44            2.22  0.13    2.13    4

Table 3. Group Variables for the Sleep Parameters
Item      Description                      Mean    SD   Median   Range
SWS       Slow wave sleepDelta sleep (min)  70.19  5.02  67.50   134
STGE-REM  REM-sleep (min)                  261.96  7.31 265.50   221
LAPSTGE2  Sleep latency (from lights-off    61.40  7.35  47.00   269
          until stage 2) (min)
SE%       Sleep quality index (%)           72.35  2.15  75.65    56.2
MAI#/u    Micro-awakenings (n/u)             9.53  1.10   8.35    28.6
TST       Total sleep time (min)           326.21 10.46 334.50   387
STSHIFTS  Number of shifts between stages   67.29  4.55  67.50   120
A%TST     % Awake time in bed               46.28  5.54  32.25   160.8
SWS%TST   % Slow wave sleep                 22.49  1.71  20.95    52.7
NREM%TST  % Non-REM sleep                   80.90  1.31  81.05    42
TST%TIB   % Total sleep time                71.49  2.19  75.05    56.2
SWS%AI    % Alpha-waves in slow wave sleep   4.32  0.80   2.00    21

Table 4. Comparison with Data of Fischler et al., 1997 (means)
Item                      Fischler's        Fischler's CFS   Our
                          Controls          Patients         Population
Sleep latency              21.5^a            39^a             61.40
Micro-awakenings            2.8               3.2              9.53
Total sleep time          382a              339a             326.21
REM latency                89.5              96.0               --
Sleep efficiency, %        87.8^a            76.5^a           72.35
Number of shifts           21.9^a            28.7^a           67.29
Stage 1 sleep, %            9.0              13.9               --
Stage 2 sleep, %           45.5^a            38.2^a             --
Stage 3 sleep, %            9.0              11.0               --
Stage 4 sleep, %           14.6               8.8               --
SWS%                       23.6              19.8               --
REM sleep, %               14.1              12.0               --
^a Statistically significant at 0.001

Table 5. Differences in Subjective Complaints and Immunologic Parameters Using
         a Median Split in Alpha-Delta Intrusion
Variable                     Alpha-delta      Alpha-delta      P-Value^a
                             < Median (SD)    > Median(SD)
Immunological parameters
RNase L                      3.62 (0.71)      5.44 (1.28)      0.645
CD4/CD8                      2.15 (0.17)      2.29 (0.21)      0.892
CD3-CD16CD56                 5.91 (0.70)      8.33 (1.59)      0.371
CD3 HLADR                    4.48 (0.60)      4.62 (62)        0.777
CD19 CD5                     1.89 (0.35)      2.43 (0.36)      0.169

Subjective complaints
Fatigue                      2.46 (0.11)      2.68 (0.12)      0.174
Postexertional fatigue       2.60 (0.16)      2.73 (0.12)      0.807
Depressive feelings          1.35 (0.21)      1.64 (0.22)      0.366
Anxiety                      0.77 (0.22)      1.64 (0.22)      0.009
Self-perceived personality   0.88 (0.20)      1.18 (0.24)      0.380
Emotional lability           1.65 (0.21)      1.82 (0.23)      0.597
Muscle aches                 1.80 (0.26)      2.00 (0.24)      0.769
Joint aches                  1.56 (0.27)      1.50 (0.24)      0.762
Sleep problems               2.08 (0.20)      2.09 (0.24)      0.809
Nonrefreshing sleep          2.12 (0.22)      1.73 (0.27)      0.297
^a Statistical significance (Bonferroni-correction): 0.002


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(c) 2007 Southern Society for Clinical Investigation
(c) 2007 Lippincott Williams & Wilkins

[Return to top]


Date:    Mon, 5 Mar 2007 15:40:37 -0500
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Rehabilitation of chronic myofascial pain disorders

[Rehabilitation of chronic myofascial pain disorders.]
[Article in Norwegian]

Tidsskr Nor Laegeforen. 2007 Mar 1;127(5):604-8.

Wigers SH, Finset A.

Opptreningssenteret Jeloy Kurbad Bratengaten 94 1515 Moss.
sigrid.wigers c2i.net

PMID: 17332816

BACKGROUND: Chronic musculoskeletal pain of diffuse origin affects many,
and at a significant cost. Evidence-based guidelines for therapeutic
interventions are presented and exemplified.

MATERIAL AND METHODS: 200 patients with chronic myofascial pain and/or
fibromyalgia who participated in a 4-week multidimensional rehabilitation
programme, were included in the study. The programme included education and
pain management in a cognitive setting, various forms of aerobic exercises,
myofascial pain treatment, relaxation and medication as needed. The
patients filled in questionnaires on arrival, at follow-up after six and
12-months and at discharge. They completed visual analogue scales (pain,
fatigue, sleep problems, depression), the Nottingham Health Profile, the
Fibromyalgia Impact Questionnaire, global subjective improvement, and
during the follow-up period also the physical activity level, changes in
quality of life and occupational workload. Work capacity, a tender point
count and whether patients met the diagnostic criteria for fibromyalgia
were assessed at baseline and at discharge.

RESULTS: Significant improvements were seen in all variables throughout the
follow-up period. 30 % of the fibromyalgia patients no longer met the
diagnostic criteria at discharge. There was a significant increase in
quality of life over time. After one year, more patients had returned to
work and fewer were off sick, but there was also an increased number on
disability pensions. The majority did exercise training on a regular basis.

INTERPRETATION: Our findings confirm the existing evidence-based guidelines
by showing that multidimensional rehabilitation is an effective
intervention for patients with widespread chronic pain. It is a challenge
for health politicians to change today's common practice towards that
described in evidence-based guidelines.

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Date:    Mon, 5 Mar 2007 20:58:34 -0500
From:    "From CF Alliance <cf_alliance yahoo.com> via Co-Cure Moderators"
Subject: NOT,MED: Doctors Urged To Change The Way They Prescribe Pain Relievers For Chronic Pain

Source: American Heart Association
Date: March 4, 2007
   Doctors Urged To Change The Way They Prescribe Pain Relievers For
Chronic Pain


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End of Co-Cure Weekly Digest of research and medical posts only - 26 Feb 2007 to 5 Mar 2007

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