Although their etiologies differ, myopia and glaucoma involve structural and functional optic nerve head (ONH) changes. Here, I discuss these changes, their similarities, when myopia-induced changes lead to glaucoma, and the clinical implications of this information.
Myopia-induced Changes
Excessive axial elongation eventually leads to:
- Tilted or obliquely inserted optic discs;
- Horizontal elongation due to disc tilt;
- Temporal crescent formation due to peripapillary atrophy;
- Thinned retinal nerve fiber layer (RNFL), more diffuse and often temporal;
- Lamina cribrosa elongation, making the ONH vulnerable to mechanical stress;
- Nonspecific VF defect pattern that may mimic glaucomatous defects; and
- Progression of ONH changes even after stabilization of axial elongation.
These changes complicate RNFL thickness and VF defect interpretation during glaucoma assessment due to similarities with glaucoma-caused changes.1
Glaucoma-caused Changes
Glaucoma’s progressive damage to the ONH due to increased IOP or other susceptibility factors, such as vascular insufficiency and biomechanical weakness of the lamina cribrosa, leads to:
- RNFL thinning, predominantly in the inferior and superior regions;
- Vertical elongation of the cup-to-disc ratio (CDR); and
- Specific arcuate or paracentral VF defects.
Similarities
Myopia and glaucoma-related ONH changes share these similarities:
- RNFL thinning
- Cup-to-disc ratio changes
- Peripapillary atrophy
- Early VF defects
- Biochemical stress of the lamina cribrosa
From Myopia to Glaucoma
Axial elongation is a major risk factor for glaucoma due to:
- Scleral stretching and thinning. As the eye elongates axially, the sclera stretches, resulting in thinning, especially at the posterior pole. This thinning compromises the sclera’s structural integrity, making it less capable of supporting the ONH and more susceptible to deformation under IOP.2
- Scleral collagen fiber remodeling. This alters scleral stiffness. Some studies suggest it may become either more compliant or stiff, depending on the extent of the remodeling and the individual’s response. These changes can affect the transmission of IOP-related stress to the ONH.3 More specifically, in the case of increased scleral stiffness, the uneven distribution of the stress could potentially cause localized damage within the ONH. On the other hand, a more compliant (less stiff) sclera, which is commonly present in myopic eyes, deforms more under elevated IOP, transmitting greater stress and strain to the ONH.
- Lamina cribrosa elongation and thinning. This deformation reduces the support for retinal ganglion cell (RGC) axons, which pass through the lamina cribrosa, increasing their vulnerability to mechanical stress and potential damage.4 Additionally, lamina cribrosa thinning can alter the translaminar pressure gradient between the intraocular space and the cerebrospinal fluid, impairing the retrograde transport of essential neurotrophic factors, which leads to RGC axon degeneration.5
- Peripapillary structural changes. Axial elongation is associated with peripapillary border tissue elongation and Bruch’s membrane changes, including gamma and delta zone development. The delta zone increases the risk of glaucomatous optic neuropathy (GON) among myopic patients.6 These alterations can impact the ONH’s biomechanical environment, contributing to an increased susceptibility of glaucomatous damage.7
Clinical Implications
The increasing prevalence of high myopia underscores the importance of differentiating between myopia-induced changes and glaucomatous damage, particularly as excessive axial elongation significantly amplifies glaucoma risk.
Advanced imaging technologies, such as optical coherence tomography (OCT) with myopia-specific normative databases, can enhance glaucoma screening specificity.
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Also, optical biometry in myopia management is essential to incorporating axial length measurements into routine glaucoma risk assessments.
Finally, establishing baseline retinal imaging during the early stages of axial elongation facilitates the differentiation between retinal changes caused by myopia and those indicative of glaucoma. OM
References
1. Jonas JB, Wang YX, Dong L, Panda-Jonas S. High Myopia and Glaucoma-Like Optic Neuropathy.Asia Pac J Ophthalmol (Phila). 2020;9(3):234-238. doi:10.1097/APO.0000000000000288
2. Jonas JB, Bikbov MM, Wang YX, Jonas RA, Panda-Jonas S. Anatomic Peculiarities Associated with Axial Elongation of the Myopic Eye.J Clin Med. 2023;12(4):1317. Published 2023 Feb 7. doi:10.3390/jcm1204131
3. Sayah, D.N., Lesk, M.R. (2021). Ocular Rigidity and Glaucoma. In: Pallikaris, I., Tsilimbaris, M.K., Dastiridou, A.I. (eds) Ocular Rigidity, Biomechanics and Hydrodynamics of the Eye. Springer, Cham. https://doi.org/10.1007/978-3-030-64422-2_18
4. Jonas, J.B., Panda-Jonas, S. (2021). The Optic Nerve Head in High Myopia/Abnormalities of the Intrapapillary and Parapapillary Region. In: Spaide, R.F., Ohno-Matsui, K., Yannuzzi, L.A. (eds) Pathologic Myopia. Springer, Cham. https://doi.org/10.1007/978-3-030-74334-5_12
5. Hopkins AA, Murphy R, Irnaten M, Wallace DM, Quill B, O'Brien C. The role of lamina cribrosa tissue stiffness and fibrosis as fundamental biomechanical drivers of pathological glaucoma cupping.Am J Physiol Cell Physiol. 2020;319(4):C611-C623. doi:10.1152/ajpcell.00054.2020.
6. Jonas JB, Weber P, Nagaoka N, Ohno-Matsui K. Glaucoma in high myopia and parapapillary delta zone. PLoS One. 2017 Apr 5;12(4):e0175120.)
7. Dai Y, Wang L, Hong J, Sun X. Eight Years and Beyond Longitudinal Changes of Peripapillary Structures on OCT in Adult Myopia.Am J Ophthalmol. 2024;264:178-186. doi:10.1016/j.ajo.2024.03.012.