The Missing Piece in Glaucoma?

Abstract

Glaucoma is defined as an optic disc neuropathy meaning the nerve fibers are being atrophied similar to the fate occurring in non-glaucomatous optic atrophies. Furthermore, the nerve fibers are always being destroyed randomly in all the non-glaucomatous optic atrophies. In contrast, the nerve fibers in glaucoma are invariably destroyed in an orderly tandem fashion, from peripheral to central, never randomly. Is glaucoma really an optic disc neuropathy in light of orderly destruction of nerve fibers in glaucoma? The current prevailing theories in glaucoma such as posterior bowing of the lamina cribrosa or cupping can’t explain the orderly destruction of nerve fibers occurring in glaucoma. In fact, there is no biological mechanism acting directly on the nerve fibers or their RGCs which could lead to their orderly destruction. Therefore, there should be some mechanical way, which could result in the orderly destruction of nerve fibers even though this mechanical scenario may have resulted from the direct biological effect of raised IOP on some important component of the optic disc. It is proposed that the border tissue of Elschnig (BT) atrophies due to chronic ischemia caused by raised IOP, and as a result, the lamina cribrosa (LC) begins sinking in the scleral canal—a mechanical problem. Due to sinking of the LC, the nerve fibers get stretched and broken starting with the most peripheral nerve fibers being closest to the edge of the scleral opening and ending with the most central nerve fibers in an orderly tandem fashion. Therefore, in view of the orderly destruction of nerve fibers, glaucoma may not be an optic disc neuropathy but an optic disc axotomy.