Very long and technical article. 22 patients and 30 healthy controls were tested for certain cells that are part of the immune system. They found an unaffected B-cell compartment, a biased NK-cell phenotype and a poorly responsive T-cell compartment as the main immune features of ME/CFS affected individuals. The striking down modulation of T cell mediated immunity may help to understand intercurrent viral infections in CFS.
The cytokine (IFN-γ, IL-6, IL-8, IL-10, MIP-1β , MCP-1, and MIP1-α ) responses to mitogenic activators of PBMC isolated from patients with FM were significantly lower than those of healthy individuals, implying that cell-mediated immunity is impaired in FM patients. This research resulted in a diagnostic test for fibromyalgia.
Researchers found that both CFS/fibromyalgia patients have low Coenzyme Q10 levels and low ATP levels, and increased levels of lipid peroxidation (which is an indicator for damage caused by oxidative stress).
In addition fibromyalgia patients had low levels of two mitochondrial enzymes and a mitochondrial protein, and reduced levels of mitochondrial DNA content, while all of those were normal in CFS patients. Therefor mitochondrial dysfunction-dependent events could be a biomarker to distinguish between FM and CFS.
Positive autoimmune reactions against serotonin were significantly higher in CFIDS patients than controls.
Patients with serotonin( 5-HT ) autoimmune activity displayed higher TNFα, IL-1 and neopterin and increased IgA responses against LPS of commensal bacteria than those without 5-HT autoimmune activity. Anti-5-HT antibody positivity was significantly associated with increased scores on hyperalgesia, fatigue, neurocognitive and autonomic symptoms, sadness and a flu-like malaise.
Researchers found evidence of altered sympathetic-neural and sympathetic adrenomedulla reactivity in CFS.
Exercise stress revealed a subtle catecholaminergic hyporeactivity in CFS patients.
Researchers were able to differentiate patients with FM from those with osteoarthritis (OA) and rheumatoid arthritis (RA), and to identify molecular species associated with the spectral patterns.
They demonstrated the ability of IRMS to achieve reliable resolution of unique spectral patterns specific to FM.
Metabolomic analysis revealed that RA and OA groups were metabolically similar, whereas biochemical differences were identified in the FM that were quite distinctive from those found in the other two groups.
Because it is not possible to differentiate completely between adverse neural tension and strain in muscles, fascia, and other soft tissues, we use the more general term “neuromuscular strain.”
Neuromuscular restrictions are common in CFS, and many symptoms of CFS can be reproduced by selectively adding neuromuscular strain during the examination.
In this paper we submit that neuromuscular strain is a previously unappreciated peripheral source of sensitizing input to the nervous system, and that it contributes to the pathogenesis of CFS symptoms, including cognitive dysfunction.
– braine whitespots/lesions. increased T2-signal lesions.
– spinal tap, elevated proteins for 30%
– some researchers would label ALL patients with somatization, but in reality there are physiological processes responsible for symptoms.
– patients without any co-morbid psychiatric/psychological disorders had high % or physiological abnormalities
– orthostatic intolerance , also in relation to hyperventilation
Mentions Infection hypothesis, Oxidative Stress hypothesis, Free Radicals Hypothesis. (see also Possible causes
20 people (10, really – so it’s a really small study). 5 CFIDS with primary EBV, 5 CFIDS with non-EBV, 10 non-CFIDS who had recovered from EBV.
EBV, HHV and CMV detected with PCR.
Levels of all 3 virusses were similar in controls and they concluded that their data did not support the hypothesis of ongoing or reactivated EBV, HHV-6, or CMV infection in the pathogenesis of CFS.