Pathogenesis of Postherpetic Neuralgia: A Complex Puzzle of Interwoven Multifactors

带状疱疹后神经痛(PHN)的发病机制复杂，其中神经炎症作为核心驱动因素，通过胶质细胞-神经元交互作用加剧疼痛的慢性化。本文聚焦于神经炎症在PHN中的关键作用，系统阐述病毒诱导的外周炎症如何通过细胞因子级联反应激活中枢胶质细胞，促进脊髓及脑区疼痛通路的敏化与重塑。结合最新研究探讨胶质细胞活化、促炎因子释放及靶向治疗的潜在价值，为PHN的精准干预提供理论依据。The pathogenesis of postherpetic neuralgia (PHN) is complex. Neuroinflammation, as a core driving factor, exacerbates the chronicity of pain through the interaction between glial cells and neurons. This article focuses on the key role of neuroinflammation in PHN, and systematically expounds how virus-induced peripheral inflammation activates central glial cells through the cytokine cascade reaction, promoting the sensitization and remodeling of pain pathways in the spinal cord and brain regions. Combined with the latest research, it explores the potential value of glial cell activation, the release of pro-inflammatory factors, and targeted therapy, providing a theoretical basis for the precise intervention of PHN.