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Editors Selection IGR 11-3

Clinical Examination Methods: Morphology and Function in Myopic Eyes with Glaucoma

Shan Lin
Claudio Perez

Comment by Shan Lin & Claudio Perez on:

73167 Multiple Temporal Lamina Cribrosa Defects in Myopic Eyes with Glaucoma and Their Association with Visual Field Defects, Sawada Y; Araie M; Ishikawa M et al., Ophthalmology, 2017; 124: 1600-1611


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The relation between myopia and primary open angle glaucoma (POAG) has been shown in many studies; nevertheless, it is often difficult to differentiate between early stage glaucoma and non-glaucomatous anatomy of the myopic optic disc, and it is also challenging to define progression of glaucomatous changes in myopic eyes.1 Therefore, new diagnostic tools for detecting glaucoma in the myopic population is an important issue. Using the enhanced depth imaging feature of spectral-domain optical coherence tomography (SD-OCT), the cross-sectional study by Sawada et al. compared the number and location of large pores (diameter 60-100 mm) and lamina cribosa (LC) defects (diameter3 100 mm) between eyes with and without open angle glaucoma in a myopic population. They described the novel finding of multiple LC defects at the temporal periphery in myopic eyes with normal tension glaucoma (NTG) and POAG, and showed their association with glaucomatous visual field (VF) loss in both severity and location. The number of temporal LC defects and tilt angle of the optic disc were associated with the presence of paracentral scotomas, whereas the number of inferior and superior LC defects and torsion direction of the optic disc were associated with the presence of superior and inferior VF defects. Myopic eyes without glaucoma exhibited multiple large pores at the temporal periphery of the LC; and the authors suggested that large pores in myopic eyes with more tilted disc may evolve into LC defects, proposing this finding as a unique mechanism that causes VF defects in myopic eyes with glaucoma. This theory may be plausible, because previous studies have shown that LC localized structural changes in glaucoma have been manifested early in the disease process.2 Nevertheless, it is important to note that these interesting findings are in the context of a cross-sectional study. Therefore, it is still inconclusive about whether these LC defects may contribute as risk factors to glaucomatous defects or are the result of glaucomatous damage in myopic eyes.

The authors suggested that large pores in myopic eyes with more tilted disc may evolve into LC defects, proposing this finding as a unique mechanism that causes VF defects in myopic eyes with glaucoma

It should be noted that this study was done in a population of Japanese patients, where NTG is a much more fre-quent disease.3 That aspect may explain the mean untreated IOP of 19.7 mmHg in the glaucoma group and the higher prevalence of paracentral scotoma defects in that glaucoma population (almost 50%). Since the authors used a Humphrey Visual Field 24-2 SITA-standard strategy to detect paracentral scotoma defects, they may have under-diagnosed up to 35% of those types of glaucomatous defects in glaucoma suspects with normal 24-2 VF.4

The study by Sawada et al. shows a more temporal distribution of LC defects in glaucomatous myopic tilted optic discs in comparison with the more superior and inferior distribution in glaucomatous non-myopic eyes.5 Many of the in vivo LC imaging studies have been conducted in Asian glaucoma populations.2 Considering the high prevalence of myopia, tilted disc and other anatomic optic nerve head features more prevalent in (and perhaps relatively specific to) this region, the results may not be extrapolated to other ethnicities including those of Caucasian, Hispanic or African descent. For example, it has been published that young Asian myopic patients with tilted disc can present with non-progressive (presumably, non-glaucomatous) stable visual field defects.6 In the future, it would be interesting to evaluate if a similar group of non-progressive young patients have associated LC defects or not.

In conclusion, the improvements in OCT technology have led to interesting findings in relation to in vivo LC imaging within the optic nerve. These findings may help to improve the diagnosis and management of glaucoma. It would be of special interest for future upcoming prospective studies to evaluate if LC defects precede VF or retinal nerve fiber layer defects, and thus a structural risk factor for early glaucoma diagnosis and for detecting glaucoma progression.

References

  1. Hsu C, Chen R, Lin SC. Myopia and glaucoma: sorting out the differ-ence. Curr Opin Ophthalmol 2015, 26:90-95.
  2. Kim YW, Jeoung JW, Kim YK, et al. Clinical implications of in vivo lamina cribosa imaging in glaucoma. J Glaucoma 2017;26:753-761.
  3. Iwase A, Suzuki Y, Araie M, et al. The prevalence of primary open-angle glaucoma in Japa-nese: the Tajimi Study. Ophthalmology 2004 Sep;111(9):1641-8.
  4. De Moraes GG, Hood DC, Thenappan A, et al. 24-2 Visual fields miss central defects shown on 10-2 tests in glaucoma suspects, ocular hyper-tensives, and early Glaucoma. Ophthalmology 2017 Oct;124(10):1449-1456.
  5. Tatham AJ, Miki A, Weinreb RN, et al. Defects of the lamina cribrosa in eyes with localized retinal nerve fiber layer loss. Ophthalmol-ogy. 2014;121:110-118.
  6. Doshi A, Kreidl K, Lombardi L, et al. Non-progressive glaucomatous cupping and visual field abnormalities in young Chinese males. Ophthalmology 2007;114:472-479.


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