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.
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