摘要视盘玻璃疣（ODD）是无细胞性沉积物，位于视盘的筛板前部。大多数患者无明显临床症状，通常被忽视，也容易与全身高危疾病导致的视盘水肿相混淆。目前主流观点认为，视神经纤维轴突代谢紊乱，导致细胞内线粒体钙化，轴突慢性崩解后钙化的线粒体不断释放到细胞外，导致细胞外钙浓度远较细胞内高，钙质不断积聚从而产生微小的钙化体，多个钙化体逐渐融合形成ODD。增强深度成像OCT能敏感地检测ODD，其影像特征是被强反射边缘完整或部分包绕的弱反射核心。ODD是造成视盘拥挤的重要原因，在青春期，埋藏型玻璃疣逐渐发生钙化，向视盘浅表迁移，转变为浅表型ODD，因而部分ODD患者在青春期突然进展，成年期趋于稳定，可以伴发视野缺损、前部缺血性视神经病变等血管并发症。

abstractsOptic disc drusen (ODD) is an acellular deposit located in front of the cribriform of the optic disc. ODD has been much underdiagnosed due to few obvious clinical symptoms. These clinical symptoms are easily confused with optic disc edema caused by systemic high-risk diseases. The current mainstream view is that optic nerve fiber axon metabolism is disordered, leading to intracellular mitochondrial calcification. After axon chronic disintegration, calcified mitochondria continuously release outside the cell, resulting in a much higher concentration of extracellular calcium than inside the cell. The continuous deposit and accumulation of extracellular calcification fuse to small calcified corpuscles, which lead to ODD formation. OCT enhanced deep imaging can detect ODD sensitively, and its image feature is a weak reflection core completely or partially surrounded by a strong reflection edge. ODD is one of the common causes for optic disc crowding. During adolescence, the accumulating calcified bodies buried in the deep optic disc gradually extrude and migrate to the superficial optic disc, which turn into superficial ODD. As a consequence, part of these ODD patients rapidly progress during adolescence and generally become stable in adulthood with anterior ischemic optic neuropathy, or other vascular complications.