Interaction of Myopic Optic Neuropathy (MON) and Glaucomatous Optic Neuropathy (GON): Pathophysiology and Clinical Implications.

Objective

To clarify the pathophysiology of myopic optic neuropathy (MON) and its relationship to glaucomatous optic neuropathy (GON).

Background

MON is presumed to be associated with posterior pole ectasia and deformation of the lamina cribrosa (LC) and parapapillary region. Its dependance on intraocular pressure is expected to be weaker than that of GON; however, the characteristics and clinical behavior of MON remain incompletely understood.

Methods

A PubMed search using the keywords myopia, glaucoma, retinal nerve fiber, optic disc, and axonal transport identified 234 relevant publications, which were analyzed in this narrative review.

Results

In myopic eyes, a large optic disc, thin or defective LC, and parapapillary microvasculature dropout (pMvD) are considered signs of increased vulnerability to glaucomatous injury. Despite these structural risk factors, visual field (VF) progression in myopic patients with glaucoma is often slow. The involvement of MON, which likely develops in young adulthood and stabilizes with aging, may explain this discrepancy. MON may substantially contribute to the development of central VF defects in myopic glaucoma, which are associated with elongation of papillomacular bundle, pMvD, and normal tension glaucoma. Experimental studies demonstrating impaired axonal transport at the optic disc margin provide important insights into the pathogenesis of MON. Additionally, optic disc deformations in myopia including disc tilting, rotation, and focal thinning or defects of the LC may contribute to atypical VF defects and altered susceptibility to glaucomatous damage.

Conclusions

Interaction between MON and GON may explain atypical VF defects and the relatively slow VF progression observed in myopic patients with glaucoma-like VF defects.