Abstract
Glaucomatous optic neuropathy (GON) is the pathohistological feature of glaucoma in the optic nerve. The pathogenesis of GON has been hypothesized, to either originate from compromised mechanical conditions at the lamina cribrosa or as associated with pathological vascular involvement. From a historical perspective, glaucoma is the degeneration of retinal ganglion cells (RGC) due to the elevation of intraocular pressure (IOP). The consensus of glaucoma treatment is generally accepted as sufficient IOP reduction. Is there an additional option to treat GON from the perspective of the vascular theory? In this section, two distinguished leaders in glaucoma research advance their views and discuss the current opinions surrounding the two theories regarding the causes of GON in primary open angle glaucoma (POAG) and normal tension glaucoma (NTG).
| Original language | English |
|---|---|
| Pages (from-to) | 243-249 |
| Number of pages | 7 |
| Journal | Japanese Journal of Ophthalmology |
| Volume | 64 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 2020 May 1 |
Keywords
- Axonal transport
- Biomechanical theory
- Glaucomatous optic neuropathy
- Lamina cribrosa
- Mechanical theory
- Vascular theory