Glaucoma and myopia

By 2050, approximately half of the world’s population will exhibit myopic eyes, with an estimated 10% classified as highly myopic.[1] The surge is particularly pronounced in East Asian countries, where the prevalence of myopia among young adults has sharply increased.[2] This exponential increase in myopia presents a unique challenge in ophthalmology, given the unprecedented speed and severity of its rise. Myopia is not just a visual condition; it triggers myopic macular degeneration, retinal detachment, glaucoma, and cataract. Consequently, the visual impairment and blindness associated with myopia will become great social and healthcare challenges in the near future.

Glaucoma stands as a leading global cause of blindness, and myopia is recognized as a risk factor for its development.[3] Structural alterations in the optic nerve head and peripapillary tissue in myopic eyes pose challenges for glaucoma diagnosis. Meta-analyses have demonstrated a dose-response relationship between the severity of myopia and the development of glaucoma.[4] Hence, early glaucoma diagnosis in myopic eyes assumes paramount importance, as well as understanding the factors associated with glaucoma progression, especially in highly myopic eyes.

Glaucoma diagnosis and monitoring in high myopia is challenging, primarily due to difficulty in distinguishing between glaucomatous changes and myopic alterations. Structural and functional glaucomatous changes sometimes coincide with myopic changes of the optic nerve head and eyeball. Disc tilt, parapapillary atrophy, chorioretinal atrophy, and eyeball elongation further complicate the identification of glaucomatous structural changes. Highly myopic open-angle glaucoma often exhibits a large, elongated disc with shallow cupping and enlarged parapapillary atrophy. Notably, the retinal nerve fiber layer (RNFL) defect appears less frequently and tends to manifest as more diffuse rather than localized damage.[5]

Certain indicators aid in diagnosing glaucoma in myopic patients. Disc hemorrhage, for instance, exhibits a more frequent lamina cribrosa-type proximal location in myopic glaucomatous eyes compared to non-myopic ones.[6] While myopic eyes may present more diffuse RNFL defects than localized ones in glaucoma, the identification of superotemporal or inferotemporal RNFL defects in fundus or red-free RNFL photography can be indicative of glaucoma. Studies utilizing RNFL photography have highlighted that highly myopic eyes with early glaucoma are more prone to papillomacular bundle defects compared to non-highly myopic eyes.[7] It has been demonstrated that parapapillary atrophy-to-disc-area ratio, lamina cribrosa defect, and central visual field defect are associated with the papillomacular bundle defect in highly myopic glaucoma eyes.[8]

RNFL measurements by optical coherence tomography in highly myopic eyes may exhibit variations owing to disc tilting, large parapapillary atrophy, and segmentation error. The convergence of RNFL bundles temporally represents a common cause of artifacts associated with axial elongation, potentially inducing pseudodefects in RNFL maps when using non-myopic normative databases, a phenomenon that occurs both in Asian and European eyes.[9,10] To overcome these pseudodefects, a customized myopic normative database can be used.[11,12] However, practically, it may be difficult to use the customized database in a busy clinic. The other way would be to look at the RNFL thickness curve and to know whether the defect is due to the shifting of the RNFL peaks or if it is a real defect caused by the actual thinning of the RNFL. Another way is to look at the GCIPL thickness map at the macular region.[13] Like the glaucoma hemifield test in Humphrey visual field, analyzing GCIPL thickness asymmetry across the horizontal raphe (temporal raphe sign) in the GCIPL thickness map can be an excellent tool to distinguish between the pseudodefect and the true glaucomatous defect in highly myopic eyes because the test is independent of the normative database.[14,15]

Another approach to distinguishing between glaucomatous and myopic change involves observing the patient’s progression without medication. Myopic changes typically coincide with axial elongation during adolescence, whereas glaucomatous changes typically manifest after axial elongation. The myopic change usually accompanies axial elongation at adolescence, but the glaucomatous change occurs after the axial elongation. Consequently, adult myopic eyes suspected of glaucoma, without other risk factors, may necessitate follow-up without immediate treatment to monitor the potential progression of optic nerve damage for accurate glaucoma diagnosis.

Various studies have reported risk factors associated with the progression of myopic glaucoma. In mild-to-moderate myopic glaucoma, worse baseline visual field mean deviation and thinner baseline RNFL thickness have been identified as risk factors for visual field and RNFL progression, respectively.[16] Age and baseline intraocular pressure (IOP) have been found to be associated with myopic glaucoma progression in other investigations.[17] In addition, increased IOP fluctuation has been linked to significant glaucoma progression in myopic normal tension glaucoma eyes, emphasizing the role of IOP.[18] Recently, after an average 12-year follow-up of highly myopic glaucoma eyes with medication, it was demonstrated that lowering IOP significantly slowed down the progression of glaucoma, while disc hemorrhage emerged as a significant risk factor for progression.[19]

To prevent glaucomatous vision loss in this era marked by a myopic epidemic, early detection of glaucoma and risk assessment are imperative. Consequently, the role of glaucoma specialists will assume increasing significance in the coming decades.

About the author

Ki Ho Park

Ki Ho Park is a professor of ophthalmology at Seoul National University and the President of the Glaucoma Research Society (GRS), President of the Korean Myopia Society (KMS), Vice-President of the Asia Pacific Ocular Imaging Society (APOIS), and Board Member of the International Council of Ophthalmology (ICO). He is Associate Editor at the Journal of Glaucoma and International Glaucoma Review (IGR); Section Editor at the British Journal of Ophthalmology, Japanese Journal of Ophthalmology, and Asia Pacific Journal of Ophthalmology; and an Editorial board member of IOVS, Scientific Reports, and Korean Journal of Ophthalmology. He has served as the immediate past president of the Asia Pacific Glaucoma Society (APGS) and the Korean Ophthalmological Society (KOS) and was on the Board of Governors of the World Glaucoma Association (WGA). He has published more than 400 papers in SCI journals. He was awarded the AAO Senior Achievement Award and the APAO Senior Achievement Award.