Background: Radiation maculopathy (RM) is a delayed, sight-threatening complication of ocular radiotherapy. Traditionally regarded as a pure microvascular disease, emerging evidence points to the central role played by retinal neuroinflammation, driven by microglial activation and cytokine dysregulation affecting both the retina and the choroid. Hyperreflective retinal foci, neuroinflammatory in origin (I-HRF), visualized through advanced imaging modalities such as spectral domain optical coherence tomography (OCT), have been identified as early and critical biomarkers of both preclinical and clinical retinal neuroinflammation. Materials and Methods: This review synthesizes findings from experimental and clinical studies to explore the pathophysiology of neuroinflammation and the associated imaging parameters in RM. Results: The integration of experimental and clinical evidence specifically underscores the significance of I-HRF as an early indicator of neuroinflammation in RM. OCT enables the identification and quantification of these biomarkers, which are linked to microglial activation and cytokine dysregulation. Conclusions: The pathophysiology of RM has evolved from a predominantly vascular condition to one strongly secondary to neuroinflammatory mechanisms involving the retina and choroid. In particular, I-HRF, as early biomarkers, offers the potential for preclinical diagnosis and therapeutic intervention, paving the way for improved management of this sight-threatening complication.
背景：放射性黄斑病变（RM）是眼部放疗后一种迟发性、威胁视力的并发症。传统上被视为单纯的微血管疾病，但新近证据表明，由小胶质细胞活化及细胞因子失调驱动的视网膜神经炎症在视网膜和脉络膜中均发挥核心作用。通过频域光学相干断层扫描（OCT）等先进成像技术观察到的、源于神经炎症的高反射视网膜病灶（I-HRF），已被确定为临床前及临床视网膜神经炎症的早期关键生物标志物。材料与方法：本综述综合实验与临床研究结果，探讨RM中神经炎症的病理生理学机制及相关影像学参数。结果：实验与临床证据的整合特别强调了I-HRF作为RM神经炎症早期指标的重要意义。OCT技术能够识别并量化这些与小胶质细胞活化及细胞因子失调相关的生物标志物。结论：RM的病理生理机制已从以血管病变为主，演变为一种主要由涉及视网膜和脉络膜的神经炎症机制继发的疾病。特别是I-HRF作为早期生物标志物，为临床前诊断和治疗干预提供了可能，为改善这一威胁视力的并发症的管理开辟了新途径。
Neuroinflammation in Radiation Maculopathy: A Pathophysiologic and Imaging Perspective
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