Background Radiation retinopathy is a dose- and time-dependent neurovascular complication of ocular radiotherapy. Radiation maculopathy denotes macular involvement and may present with early retinal thickening or edema, progressive nonperfusion, or late atrophy. Its biology is not a single linear sequence: endothelial, inflammatory, permeability, ischemic, and neuronal changes overlap. Objective To critically review terminology, classification, plaque-related dosimetry, multimodal imaging biomarkers, and preventive and therapeutic evidence for radiation maculopathy after plaque brachytherapy for uveal melanoma. Methods PubMed/MEDLINE was searched from January 2000 through 24 September 2026 using combinations of uveal melanoma, radiation retinopathy, radiation maculopathy, plaque brachytherapy, iodine-125, ruthenium-106, palladium-103, cesium-131, OCT, OCT angiography, fluorescein angiography, laser speckle flowgraphy, anti-VEGF, bevacizumab, ranibizumab, aflibercept, corticosteroid, and laser. Seminal pre-2000 studies and additional records identified from reference lists were retained when they defined classification, natural history, or treatment. Original clinical studies were prioritized for efficacy and imaging claims; reviews were used for context and evidence synthesis. Results Structural OCT can reveal macular edema before ophthalmoscopic radiation retinopathy, but thickness changes also reflect neuronal swelling and late atrophy. OCTA detects capillary-density loss and foveal avascular zone change, yet measurements depend on signal quality and segmentation and are especially vulnerable to cystoid edema. Fluorescein angiography remains important for leakage and wide-field ischemic burden, while laser speckle flowgraphy is an investigational perfusion measure. Anti-VEGF therapy is the best-supported treatment for established radiation-related macular edema and generally requires sustained dosing. Prophylactic anti-VEGF cohorts show lower rates of edema and some radiation complications, but long-term visual superiority is not consistently demonstrated and randomized plaque-specific evidence is lacking. Corticosteroids and laser have selective roles. Conclusions Surveillance should be multimodal and individualized according to tumor location, patient-specific dosimetry, visual potential, and serial structural and perfusion findings. OCTA complements rather than replaces structural OCT and angiography. No validated OCTA threshold currently justifies treatment in an otherwise unaffected eye; prospective studies must define reproducible biomarkers and treatment triggers.
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González-Cortés et al. (2026) studied this question.
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