From Mediators of Inflammation, 26 February 2015 (Full text available).
Research Article
Cytokines in the Cerebrospinal Fluids of Patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis
D. Peterson(1), E. W. Brenu(2), G. Gottschalk(1), S. Ramos(2), T. Nguyen(2), D. Staines(2) and S. Marshall-Gradisnik(2)
1) Simmaron Research, 948 Incline Way, Incline Village, NV 89451, USA
2) Griffith Health Institute, School of Medial Sciences, National Centre for Neuroimmunology and Emerging Diseases, Griffith University, Parklands, QLD 4222, Australia
Abstract
OBJECTIVES
Previous research has provided evidence for dysregulation in peripheral cytokines in patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME). To date only one study has examined cytokines in cerebrospinal fluid (CSF) samples of CFS/ME patients. The purpose of this pilot study was to examine the role of cytokines in CSF of CFS/ME patients.
METHODS
CSF was collected from 18 CFS/ME patients and 5 healthy controls. The CSF samples were examined for the expression of 27 cytokines (interleukin- (IL-) 1β, IL-1ra, IL-2, IL-4, IL-6, IL-7, IL-8, IL-9, IL-10, IL-12p70, IL-13, IL-15, IL-17, basic FGF, eotaxin, G-CSF, GM-CSF, IFN-γ, IP-10, MCP-1 (MCAF), MIP-1α, MIP-1β, PDGF-BB, RANTES, TNF-α, and VEGF) using the Bio-Plex Human Cytokine 27-plex Assay.
RESULTS
Of the 27 cytokines examined, only IL-10 was significantly reduced in the CFS/ME patients in comparison to the controls.
CONCLUSIONS
This preliminary investigation suggests that perturbations in inflammatory cytokines in the CSF of CFS/ME patients may contribute to the neurological discrepancies observed in CFS/ME.
From Pain. 5 February 2015. [Epub ahead of print].
Evidence for Sensitized Fatigue Pathways in Patients with Chronic Fatigue Syndrome.
Staud R, Mokthech M, Price DD, Robinson ME.
Departments of Medicine, Oral and Maxillofacial Surgery and Clinical & Health Psychology, University of Florida, Gainesville, Florida 32610.
Abstract
Patients with Chronic Fatigue Syndrome (CFS) frequently demonstrate intolerance to physical exertion that is often reported as increased and long-lasting fatigue.
As no specific metabolic alterations have been identified in CFS patients, we hypothesized that sensitized fatigue pathways become activated during exercise corresponding with increased fatigue.
After exhausting handgrip-exercise, muscle-metabolites were trapped in the forearm tissues of 39 CFS patients and 29 NC by sudden occlusion for up to 5 min. A non-occlusive condition of similar duration was used as control.
Repeated fatigue and pain ratings were obtained before and after exercise. Mechanical and heat hyperalgesia were assessed by quantitative sensory testing (QST).
All subjects fulfilled the 1994 Fukuda-Criteria for CFS. NC and CFS subjects exercised for 6.6 (2.4) and 7.0 (2.7) min (p>.05).
Forearm occlusion lasted for 4.7 (1.3) and 4.9 (1.8) min in NC and CFS subjects, respectively (p>.05). Whereas fatigue ratings of CFS subjects increased from 4.8 (2.0) to 5.6 (2.1) VAS units during forearm occlusion, they decreased from 5.0 (1.8) to 4.8 (2.0) VAS units during the control condition without occlusion (p=.04).
A similar time course of fatigue ratings was observed in NC (p>.05) although their ratings were significantly lower than those of CFS subjects (p<.001). QST-testing demonstrated heat and mechanical hyperalgesia in CFS subjects.Our findings provide indirect evidence for significant contributions of peripheral tissues to the increased exercise related fatigue in CFS patients consistent with sensitization of fatigue pathways. Future interventions that reduce sensitization of fatigue pathways in CFS patients may be of therapeutic benefit.