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C F S
- Information International Neuroendocrine
Immune Dysfunction
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The New Era
Every new piece of evidence on CFS/ME
and FM points in the direction of these syndromes involving a number of organ
systems including the nervous, the endocrine, and the immune system.
Accordingly, an umbrella term has been proposed for CFS: Neuro-endocrine-immune
Dysfunction Syndrome, FAQ,
NDS, 2002. Two reviews on FM conclude the
existence of a neuroendocrine syndrome,
Adler et al., 2002, and Wigers,
2002. The Gulf
War Syndrome: From environmental toxins to psychoneuroimmunology and
neurodegeneration, Ferguson & Cassaday, 2002. Neuroendocrine and
immune gene expression in peripheral blood mononuclear cells, nicholson.etal04.txt. The need for a new
model: integrating the potential role of stress response systems into a
biopsychosocial model, mclean.etal05.txt. Not much hard evidence on the neuroendocrinology of CFS
had been obtained, Cleare, 2003, Cleare, 2003 (pdf). A 2001-symposium, sponsored by the CDC and the CAA,
resulted in a consensus paper, papanicolaou.etal04.pdf,
and a conclusion that ‘it has become clear that CFS cannot be
understood based on single measurements of immune, endocrine, cardiovascular,
or autonomic nervous system dysfunction. This panel encourages a new emphasis
on multidisciplinary research into CFS’, gerrity.etal04.txt,
gerrity.etal04.pdf. Neuroendocrine and immune network re-modeling in CFS: An exploratory
analysis, fuite.etal08.txt. Neuroinflammation
New techniques, analysis of minute amounts of
proteins, proteomics, in cerebrospinal fluids seems promising, news.proteomics04.txt, proteomics05.txt. Dysautonomia
The concept of dysautonomia in
relation to CFS is discussed,
Goldstein et al., 2002. Anecdotal evidence on gait disturbances (also
a dysautonomic symptom) in CFS after exercise was confirmed in a
2001-study, Paul et al., 2001, Paul et al., 2001(pdf). Cytokines are Neurotransmitters
It is well established that
fatigue and sleep disturbances can be caused by dysfunction of inflammatory transmitters,
cytokines,
Mullington et al., 2001. Also cognitive skills depend on immunologic
factors,
Brimacombe et al., 2002. An interesting paper studies brain blood flow
and cytokines in FM, Gur
et al., 2002. Link between Toxins & Immunity
A lengthy paper on the
influence of toxins on immunity,
Richardson, 2002,
Richardson, 2002 (pdf). Neurologic Dysfunction
A study on neurotologic
manifestations,
Bayazit et al., 2002. A paper asks directly "Is FM a
neurological disease ?" Bradley et al., 2002. Altered central nervous system
signal during motor performance in CFS, siemionow.etal04.txt, sieminonow.etal04.pdf. Studies on nasal secretion in CFS provide documentation
for a neurogenic factor in CFS, baraniuk.etal04.txt,
baraniuk.etal04.pdf and baraniuk.etal05.txt. Definition of non-allergic rhinitis
approaching, staevska.baraniuk05.txt.
The 5-HT3 Receptor
Physiology and pathophysiology of the 5-HT3
receptor. The 5-HT3 receptor is a ligand-gated cation channel located in the
central and peripheral nervous system; and on a variety of other cells.
Clinical efficacy was shown for various forms of emesis like
chemotherapy-induced, radiotherapy-induced, and postoperative emesis,
diarrhoea-predominant irritable bowel syndrome, anxiety, CFS, alcohol abuse,
and in pain syndromes such as FM and migraine, farber.etal04.txt.
5-HT3 receptor antagonists was found clinically effective in
diarrhoea-predominant irritable bowel syndrome, in fibromyalgia and related
pain disorders, haus.etal04.txt. Central pain
processing is altered in patients with FMS. The serotonin metabolism,
especially the 5-HT3 receptor, seems to play an important role, koeppe.etal04.txt. ‘The assessment of
vegetative and functional symptoms in FM patients: the tropisetron
experience’, kohnen.etal04.txt.
‘5-HT3 receptor blockade transiently affects monocyte tissue
infiltration, modulates T-H1 cytokines in clinical responders as well as
MIP-1beta in moderate responders, and transiently affects the ex vivo
response to exogenous TNF-alpha’, schneider.etal04.txt.
‘Local treatment of tendinopathies and myofascial pain syndromes with
the 5-HT3 receptor antagonist tropisetron’, muller.stratz04.txt. ‘Treatment of
fibromyalgia with tropisetron--dose and efficacy correlations’, spath.etal04.txt. ‘Influence of tropisetron
on the serum substance P levels in FM patients’, stratz.etal04.txt. ‘Intravenous treatment
of fibromyalgia with the 5-HT3 receptor antagonist tropisetron in a
rheumatological practice’, tolk.etal04.txt.
More information on the serotonin receptor type 2
(5HT(2)), smith05.txt. Brain Transmitters
FM is a pain syndrome involving
norepinephrine, martinez-lavin.etal02.txt.
Disturbed uptake of acetylcarnitine in CFS, Kuratsune et al., 2002. Latest
on the role of Th1/Th2 balance in stressed chronic pain patients, eisner.etal07.txt The HPA - Immune System - Nervous System
An imbalanced response by the
immune system from the HPA signals,
Kaavelars et al., 2000. A Dutch paper: The disturbed HPA axis is
connected with the immune system,
Visser et al., 2000. A solid review of FM and neuroimmune dysfunction, Buskila & Press, 2001 (pdf). The role of
stress on the HPA axis is studied, Heim
et al., 2000. The interaction between HPA and the
sympathetic nervous system (SNS) is the basis for this interesting
review, Elenkov et al., 2000 and Elenkov et al., 2000 (pdf). Clonidin studies
concluded, that CFS patients may display supersensitive central post-synaptic
alpha-2 adrenoceptor function associated with the release of cortisol and
growth hormone and initial thinking time in planning tasks, Morriss et al., 2002. Greek endocrinologists (diabetes researchers)
published a comprehensive review of the complex interaction of various
hormone systems and stress, suggesting CRH-potentiators as future treatment
options in FM/CFS,
Tsigos & Chrousos, 2002, Tsigos & Chrousos, 2002 (pdf). Cerebrospinal fluid is interesting with respect to
CRH-content relating to fatigue and pain, mc.lean.etal06.txt.
Neurotransmitter Dysfunction
Serotonergic agents reduce the
pain in FM,
Miller & Kubes, 2002. No
effect of galantamine hydrobromide (acetyl cholesterone inhibitor)
treatment in CFS, a randomized controlled trial, blacker.etal04.txt, blacker.etal04.pdf.
An editorial relating to this work, straus04.txt,
and a ‘letter to the editor’, letter.blacker04.txt. The Muscles
The muscle pain symptoms felt
by FM patients for the most part can be explained by neuroendocrine
disturbances, editorial, Bengtsson, 2002. The fatigue felt as
coming from muscles, is also best explained in terms of neural efferent
mechanisms,
Gibson et al., 2001. Many
other studies on nociceptive nerve endings have pointed in the same
direction, mense03.txt, mense03.pdf. Using EMG researchers found diminished
central activation during maximal voluntary contraction in CFS patients, schillings.etal04.txt, schillings.etal04.pdf. One study asks Is
CFS a connective tissue disorder? vanderputte.etal05.txt. |
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