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C F S
- Information International Neuroendocrine
Immune Dysfunction
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The New Era
Every new piece of scientific
evidence on ME/CFS, and FM, points in the direction of these syndromes
involving a number of organ systems, specifically 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. Abstracts from American Psychosomatic
Society (2007) underlines the interaction between these fields of research, APS.symposium07.txt. Even more so the 2008 CFIDS research grants, grants.CFIDS08.txt. However,
not only ME/CFS have involvement from many organ systems, ‘Neuroendocrine-immune
mechanisms of behavioral comorbidities in patients with cancer’, miller.etal08.txt 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. 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. However,
previously not much hard evidence on the neuroendocrinology of CFS had been
obtained, Cleare, 2003, Cleare, 2003 (pdf). Exploration of neuroendocrine and
immune gene expression in peripheral blood mononuclear cells, nicholson.etal04.txt. Neuroendocrine and immune
network re-modeling in CFS: An exploratory analysis, fuite.etal08.txt. Neuroinflammation – studies on proteomics
New techniques, analysis of minute amounts of
proteins, proteomics, in cerebrospinal fluids seems promising, news.proteomics04.txt, proteomics05.txt. Very interestingly,
this approach has generated a 2008-2009 study at Georgetown university. ‘Analysis
of the fluid flowing from the brain will identify factors that may indicate the
pathology of CFS to direct the creation of new treatments, and serve as
diagnostic biomarkers for future testing’, baraniuk.CFSAC08.txt. ‘Proteomics of
Cerebrospinal Fluid in CFS’. This study is currently recruiting
participants. Verified by Georgetown University, Nov 2008 proteomics.clinical.trial08.txt. Cerebrospinal fluid is interesting with respect to
CRH-content relating to fatigue and pain, mc.lean.etal06.txt.
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 Trauma & Neuroendocrine Dysfunction
Childhood
trauma and risk for CFS: Association with Neuroendocrine Dysfunction, heim.etal08.txt,
heim.etal.08.txt, heim.etal08.pdf. 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 provided
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
‘CFS is accompanied by a
relative resistance of the immune system to regulation by the neuroendocrine
system. Based on these data, we suggest CFS should be viewed as a disease of
deficient neuroendocrine-immune communication’, Kaavelars et al., 2000. ‘CFS
appears to be associated with a disturbed HPA-axis. Moreover, CFS patients
show several immunological changes suggestive of decreased
cellular immunity. It is postulated herein that in CFS patients a decreased
Th1/Th2 balance may be the result of selective effects of GC on the
IL-10/IL-12 regulatory circuit’,
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). 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. |
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