Abstract: Glaucoma is a complex clinical syndrome with common phenotype of “characteristic optic neuropathy", while its underlying pathogenesis is with multiple etiologies. In order to understand this complex condition, a subclassification strategy based on the characteristics of its clinical phenotype, especially its relationship with intraocular pressure (IOP) elevation, pathophysiology of retinal ganglion cells (RGCs) /their axons and non-IOP mechanism, is imperative. Thereafter, fundamental scientific questions could be raised and investigated using basic research methodology. In this perspective, we have categorized glaucoma into two major sub-categories. Type I: Genuinely elevated IOP to a significant level, which is capable of primarily and directly destroying massive number of RGCs and their axons with subsequent glaucomatous optic neuropathy (GON), while secondary neuroimmune inflammation may participate as an accomplice. Type II: IOP is unable or insufficient to destroy massive RGCs and their axons directly, leading to GON. In this scenario, neuroimmune inflammation may play a more critical role in the initiation and propagation of secondary RGCs/axons damages. Subsequently, we have further subcategorized Type I glaucoma into 5 subtypes and Type II glaucoma into 4 subtypes, respectively. (Ophthalmol CHN, 2020, 29: 1-5)

Key words: glaucoma, optic neuropathy, intraocular pressure