Purpose: Complex regional pain syndrome (CRPS) is a rare but refractory pain disorder. Recent advanced information retrieval studies using text-mining and network analysis have suggested nuclear factor kappa B (NFkB) as a possible central mediator of CRPS. The brain is also known to play important roles in CRPS. The aim of this study was to evaluate changes in cerebral NFkB in rats with CRPS. Materials and methods: The chronic post-ischemia perfusion (CPIP) model was used as the CRPS animal model. O-rings were applied to the left hind paws of the rats. The rats were categorized into three groups according to the results of behavioral tests: the CPIP-positive (A) group, the CPIP-negative (B) group, and the control (C) group. Three weeks after the CPIP procedure, the right cerebrums of the animals were harvested to measure NFkB levels using an ELISA. Results: Animals in group A had significantly decreased mechanical pain thresholds (P<0.01) and significantly increased cerebral NFkB when compared to those in groups B and C (P=0.024). Conclusion: This finding indicates that peripheral injury increases cerebral NFkB levels and implies that minor peripheral injury can lead to the activation of pain-related cerebral processes in CRPS.
- Complex regional pain syndrome
- Enzyme-linked immune-sorbent assay
- Nuclear factor kappa B