| Jan van Roijen 2005-01-11, 7:07 pm |
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11 January 2005
Editorship : j.van.roijen@chello.nl
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Quote:
The results support two hypotheses:
that some CFS patients have a neurological
abnormality that may contribute to the clinical
picture of the illness
and that immune dysregulation within the central
nervous system may be involved in this process.
~jvr
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From: Maggie Wallace <zen38947@ZEN.CO.UK>
Via: CO-CURE@LISTSERV.NODAK.EDU
Clin. Diagn. Lab. Immunol. 2005; 12(1): p. 52-55
http://cdli.asm.org/cgi/content/abstract/12/1/52
Spinal Fluid Abnormalities
in Patients with Chronic Fatigue Syndrome
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Benjamin H. Natelson,1* Shelley A. Weaver,1 Chin-Lin Tseng,2
and John E. Ottenweller1
CFS Cooperative Research Center,1 Department of
Neurosciences and Department of Preventive Medicine,
University of Medicine and Dentistry of New Jersey-New Jersey
Medical School, Newark, New Jersey2
Received 2 May 2004/ Returned for modification 3 September
2004/ Accepted 6 October 2004
Arguments exist as to the cause of chronic fatigue syndrome
(CFS). Some think that it is an example of symptom
amplification indicative of functional or psychogenic illness, while
our group thinks that some CFS patients may have brain
dysfunction.
To further pursue our encephalopathy hypothesis, we did spinal
taps on 31 women and 13 men fulfilling the 1994 case definition
for CFS and on 8 women and 5 men serving as healthy controls.
Our outcome measures were white blood cell count, protein
concentration in spinal fluid, and cytokines detectable in spinal
fluid.
We found that significantly more CFS patients had elevations in
either protein levels or number of cells than healthy controls (30
versus 0%), and 13 CFS patients had protein levels and cell
numbers that were higher than laboratory norms; patients with
abnormal fluid had a lower rate of having comorbid depression
than those with normal fluid.
In addition, of the 11 cytokines detectable in spinal fluid, (i) levels
of granulocyte-macrophage colony-stimulating factor were lower
in patients than controls, (ii) levels of interleukin-8 (IL-8) were
higher in patients with sudden, influenza-like onset than in
patients with gradual onset or in controls, and (iii) IL-10 levels
were higher in the patients with abnormal spinal fluids than in
those with normal fluid or controls.
The results support two hypotheses:
that some CFS patients have a neurological abnormality that
may contribute to the clinical picture of the illness
and that immune dysregulation within the central nervous system
may be involved in this process.
* Corresponding author. Mailing address: Fatigue Research
Center (129), VA Medical Center, 385 Tremont Ave., East
Orange, NJ 07018. Phone: (973) 395-7737. Fax: (973)
395-7114. E-mail: bhn@njneuromed.org.
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