Cytokine imbalance/activity as a unifying hypothesis for the pathogenesis and pathophysiology of Complex Regional Pain Syndrome?

摘要

Certain features characteristic of Complex Regional Pain Syndrome (CRPS), such as vasodilatation, swelling, and edema can perhaps best be explained by an exaggerated localized inflammatory process as hypothesized long ago by Sudeck [6] and later Goris and van der Laan [8]. Progressive accumulation of immuno-globulin in the affected extremity of acute CRPS, an increase in inflammatory proteins in joint fluid and synovial biopsies, synovial hypervascularity, neutrophil infiltration, and increased free radicals are features that support inflammation as being at least partially etiologic and/or perpetuating in CRPS. Cytokines are perhaps emerging as a unifying pathophysiologic hypothesis of CRPS [l],and a shift towards a pro-inflammatory cytokine profile in patients with CRPS suggests a potential pathogenic contribution of these compounds in CRPS [7]. In blister fluid obtained in the region of CRPS pain, significantly higher levels of IL-6 and TNFalpha were observed in the involved extremity relative to the uninvolved extremity [10].