The immune system has different ways to cause pain: in rheumatoid arthritis a powerful pro-inflammatory cytokine called IL-1B appears to be associated with decreased paraympathetic (rest and digest) nervous system activity. In FM the IL-8 cytokine that is also associated with inflammation and with oxidative stress and innate (early)) immune activity was associated with pain. A different but similar) kind of autonomic nervous system problem - increased sympathetic nervous system activity (fight or flight) was found in FM.
Many different pathways to producing pain exist it appears...
J Neuroimmunol. 2015 Mar 15;280:49-5
Evidence of different mediators of central inflammation in dysfunctional and inflammatory pain - Interleukin-8 infibromyalgia and interleukin-1 β in rheumatoid arthritis.
Abstract
The purpose of this study was to relate central inflammation to autonomic activity (heart rate variability (HRV)) in patients with rheumatoid arthritis (RA) and fibromyalgia (FM). RA patients had reduced parasympathetic activity and FM patients had increased sympathetic activity compared to healthy controls. Comparisons between RA and FM showed higher cerebrospinal fluid (CSF) interleukin (IL)-1β inversely correlated to parasympathetic activity in RA. The FM patients had higher concentrations of CSF IL-8, IL-1Ra, IL-4 and IL-10, but none of these cytokines correlated with HRV. In conclusion, we found different profiles of central cytokines, i.e., elevated IL-1β in inflammatory pain (RA) and elevated IL-8 in dysfunctional pain (FM).
Many different pathways to producing pain exist it appears...
J Neuroimmunol. 2015 Mar 15;280:49-5
Evidence of different mediators of central inflammation in dysfunctional and inflammatory pain - Interleukin-8 infibromyalgia and interleukin-1 β in rheumatoid arthritis.
Abstract
The purpose of this study was to relate central inflammation to autonomic activity (heart rate variability (HRV)) in patients with rheumatoid arthritis (RA) and fibromyalgia (FM). RA patients had reduced parasympathetic activity and FM patients had increased sympathetic activity compared to healthy controls. Comparisons between RA and FM showed higher cerebrospinal fluid (CSF) interleukin (IL)-1β inversely correlated to parasympathetic activity in RA. The FM patients had higher concentrations of CSF IL-8, IL-1Ra, IL-4 and IL-10, but none of these cytokines correlated with HRV. In conclusion, we found different profiles of central cytokines, i.e., elevated IL-1β in inflammatory pain (RA) and elevated IL-8 in dysfunctional pain (FM).