Changes in cerebrospinal fluid levels of pro-inflammatory cytokines in CRPS

TLDR

CRPS I and II are marked by sensory, autonomic, and motor abnormalities, with pain disproportionate to the inciting event, and animal studies link exaggerated pain states to elevated pro‑inflammatory cytokines that can induce or amplify neuropathic and inflammatory pain. The study aimed to compare CSF levels of IL‑1β, IL‑6, and TNF‑α in CRPS patients versus patients with and without painful conditions. High‑sensitivity ELISA was employed to quantify these cytokines in cerebrospinal fluid samples. CSF IL‑1β and IL‑6 were significantly elevated in CRPS patients compared to controls, while TNF‑α was unchanged; cytokine levels in painful versus non‑painful controls did not differ,.

Abstract

Complex Regional Pain Syndrome (CRPS) Types I and II are characterized by various combinations of sensory, autonomic and motor abnormalities. Pain disproportionate to the severity and duration of the inciting event is the most devastating symptom. In animal studies, conditions resulting in exaggerated pain states demonstrate elevated pro-inflammatory cytokines. In addition, pro-inflammatory cytokines have been shown to induce or increase neuropathic and inflammatory pain. Utilizing high sensitivity enzyme linked immunosorbent assay (ELISA), we compared the levels of the pro-inflammatory cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6) and Tumor Necrosis Factor-alpha (TNF-α) in the cerebrospinal fluid (CSF) of patients afflicted with CRPS to CSF levels found in other patients with and without painful conditions. The results from this study demonstrated significant increases in IL-1β and IL-6, but not TNF-α in the CSF of individuals afflicted with CRPS as compared to controls. CSF cytokine levels in controls with painful conditions did not differ from levels in controls without pain. These increases showed no correlation with the patient's gender or weight. These results are consistent with studies that suggest that the pathogenesis of CRPS is due in part to central neuroimmune activation.