Department of Ophthalmology, Samsung Medical Center, Sungkyunkwan University, School of Medicine, 81 Irwon-ro, Gangnam-gu, Seoul 06351, South Korea.
Department of Ophthalmology, Samsung Medical Center, Sungkyunkwan University, School of Medicine, 81 Irwon-ro, Gangnam-gu, Seoul 06351, South Korea.
Prog Retin Eye Res. 2017 Sep;60:20-43. doi: 10.1016/j.preteyeres.2017.08.002. Epub 2017 Aug 30.
Disc hemorrhage is known to be associated with glaucoma development and progression. Several hypotheses have been proposed to explain the pathogenesis of disc hemorrhage in glaucoma, including mechanical and ischemic theories. However, no theory has yet provided a clear explanation of cellular-level events and related histologic findings. Moreover, research has yet to elucidate why glaucomatous disc hemorrhage occurs around the optic disc and at the margin of the retinal nerve fiber layer defect. Understanding the pathogenic mechanism of disc hemorrhage will facilitate interpretation of its clinical importance, and provide better insight into clinical practice. In this review, we sought to provide a plausible hypothesis for the development of glaucomatous disc hemorrhage that could explain the aforementioned characteristic features. We suggest a new and detailed mechanism for disc hemorrhage. Critical microscopic events are also discussed in relation to reactive gliosis in glaucoma. With proliferative reactive gliosis, fibrous glial scar forms, and we suggest that the traction force induced by glial scar formation might disrupt capillary at the border between the healthy and damaged retinal nerve fiber layer, and develop splinter-shaped peripapillary hemorrhage. In addition to glial scar formation, remodeling and deformation of lamina cribrosa beams would insult the capillary surrounding the pore of the lamina cribrosa, and lead to development of round blotch-shaped cup hemorrhage. Histopathologic confirmation of these findings should be explored in future investigations.
盘状出血已知与青光眼的发生和进展有关。已经提出了几种假说来解释青光眼盘状出血的发病机制，包括机械和缺血理论。然而，没有一种理论能够清楚地解释细胞水平的事件和相关的组织学发现。此外，研究尚未阐明为什么青光眼盘状出血发生在视盘周围和视网膜神经纤维层缺损的边缘。了解盘状出血的发病机制将有助于解释其临床重要性，并为临床实践提供更好的见解。在这篇综述中，我们试图为青光眼盘状出血的发生提出一个合理的假说，该假说可以解释上述特征。我们提出了一个新的、详细的盘状出血机制。还讨论了与青光眼反应性神经胶质增生相关的关键微观事件。随着增生性反应性神经胶质增生，纤维状神经胶质瘢痕形成，我们推测神经胶质瘢痕形成引起的牵引力可能会破坏健康和受损的视网膜神经纤维层交界处的毛细血管，并发展为碎片状的视盘周围出血。除了神经胶质瘢痕形成外，筛板梁的重塑和变形也会损伤筛板孔周围的毛细血管，导致出现圆形斑点状杯状出血。在未来的研究中应探讨对这些发现的组织病理学证实。
