Massage News - February 2017
Massage News - February 2017
Evidence of both systemic inflammation and neuroinflammation in fibromyalgia patients
Researchers have expected that chronic inflammation probably plays a role in the pathophysiology of fibromyalgia (FM). In addition, neuroinflammatory mechanisms are considered to be central to the pathophysiology of many chronic pain conditions. However proving this hypothesis appear to be challenging. Researchers usually analyzed inflammation-related proteins in different body fluids. Previous studies on fibromyalgia on human plasma/serum and/or cerebrospinal fluid (CSF) cytokine only looked at a few cytokine candidates and the results are inconclusive.
Instead of analyzing only a few substances at a time, a new research from Sweden analysed 92 inflammation-related proteins simultaneously. The research was published in Journal of Pain Research.
The researchers investigated the CSF and plasma inflammatory profiles of 40 FM patients compared with CSF from healthy controls (n=10) and plasma from blood donor controls (n=46).
Using statistical data analysis, the authors found evidence of both neuroinflammation (as assessed in CSF) and chronic systemic inflammation (as assessed in plasma). Two groups of proteins (one for CSF and one for plasma) highly discriminating between patients and controls are presented. Notably, they found high levels of CSF chemokine CX3CL1 (also known as fractalkine). In addition, previous findings concerning IL-8 in FM were replicated, in both CSF and plasma. This study provides an evidence for an extensive inflammatory profile in FM patients. Hence, FM seems to be characterized by objective biochemical alterations, and the lingering characterization of its mechanisms as essentially idiopathic or even psychogenic should be seen as definitively outdated.
The authors also clearly stated the limitation of this study (FM patients were all female and the control is limited).
The authors further hypothesize possible mechanism, include (1) central sensitization due to neuroinflammation? (2) an inflammatory risk factor that was present prior to the development of chronic pain (eg, a genetic susceptibility) (3) consequence of the chronic pain condition, eg, pain-related stress, inactivity , depression, etc?
