Abstract
OBJECTIVE: Anterior cervical discectomy and fusion (ACDF) is a well-established surgical intervention for cervical disc herniation; however, the biological mechanisms underlying its superior pain relief compared to conservative treatment remain incompletely understood. This study aims to evaluate the efficacy of ACDF in treating neurogenic pain and its impact on inflammatory factors and substance P (SP). METHODS: We retrospectively analyzed 110 patients (2016-2023) with neurogenic pain, divided into an ACDF group (n = 51) and a conservative treatment group (n = 59). We assessed serum levels of inflammatory factors [interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), monocyte chemotactic protein 1 (MCP-1)], pain mediators [substance P (SP), β-endorphin (β-EP), nitric oxide (NO), prostaglandin E2 (PGE2)], electromyography F-wave parameters, and clinical scores [Visual Analog Scale (VAS) score, Present Pain Intensity (PPI) score, Japanese Orthopedic Association (JOA), Oswestry Dysfunction Index (ODI)] before and 3 months after treatment, with statistical analysis performed using t-tests, χ(2) tests, and rank-sum tests as appropriate. RESULTS: Baseline characteristics and complication rates were comparable (p > 0.05). The ACDF group achieved a higher excellent-good rate (72.55% vs. 54.24%, p < 0.05). After treatment, both groups showed improvements in all biomarkers and clinical scores, but the ACDF group demonstrated significantly greater reductions in IL-6, TNF-α, MCP-1, SP, NO, and PGE2, and a greater increase in β-EP (all p < 0.05). F-wave latency shortened and frequency increased more markedly in the ACDF group (p < 0.05). Clinical scores (VAS, PPI, ODI, JOA) also improved more significantly in the ACDF group (all p < 0.05). CONCLUSION: ACDF is superior to conservative treatment in alleviating neurogenic pain and improving neurological function, and it is also safe. This study provides biochemical and electrophysiological evidence for the superior efficacy of ACDF by elucidating its modulatory effects on the neuro-inflammatory cascade, offering new insights into its mechanism of action. The significant modulation of inflammatory factors and pain mediators suggests their potential role as objective indicators for pain assessment.