Abstract

PurposeTo investigate whether the position of the central vascular trunk, as a surrogate of lamina cribrosa (LC) shift, is associated with the initial hemisphere of visual field defect in myopic high-tension glaucoma (HTG) eyes.MethodsThe deviation of the central vascular trunk was measured from the center of the Bruch’s membrane opening (BMO), which was delineated by OCT imaging. The angular deviation was measured with the horizontal nasal midline as 0° and the superior location as a positive value. The initial hemisphere developing visual field defect was defined as three connected abnormal points (having a P value with less than 0.5% probability of being normal) appearing in only one hemisphere in pattern deviation plots. If those points were observed in both hemispheres initially, the eye was classified as bi-hemispheric visual field defect.ResultsInitially, 36 eyes (44%) had superior visual field defects, 27 (33%) inferior visual field defects, and 18 (22%) bi-hemispheric visual field defects. After a mean follow-up of 5 years, the number of bi-hemispheric visual field defects had increased to 34 (42%). A logistic regression analysis revealed that inferior deviation of vascular trunk was the only factor associated with initial inferior visual field defect (P = 0.001), while initial bi-hemispheric visual field defects were associated with worse mean deviation at initial visits (P<0.001). A conditional inference tree analysis showed that both the angular deviation (P<0.001) and initial mean deviation (P = 0.025) determined the initial hemispheres developing visual field defect.ConclusionsAlthough both hemispheres were involved as glaucoma progression, the axons on the side counter to the vascular trunk deviation were damaged earlier in HTG. This finding implies the LC shift could add additional stress to axons exposed to high intraocular pressure.

Highlights

  • Glaucoma is a progressive optic neuropathy that is characterized by selective loss of retinal ganglion cells [1,2,3]

  • lamina cribrosa (LC) shift in high-tension glaucoma. Both hemispheres were involved as glaucoma progression, the axons on the side counter to the vascular trunk deviation were damaged earlier in HTG

  • This finding implies the LC shift could add additional stress to axons exposed to high intraocular pressure

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Summary

Introduction

Glaucoma is a progressive optic neuropathy that is characterized by selective loss of retinal ganglion cells [1,2,3]. In the recent Boramae Myopia Cohort Study, we found that the inner retinal structure of the posterior polar area including the Bruch’s membrane opening (BMO) was relatively preserved during axial elongation, while the outer load-bearing sclera expanded [8,9,10]. This expansion resulted in the shift of the sclera and LC, which may be suggestive of another source of tensile stress exerted on the LC in myopic eyes. Once the vulnerable pores in the direction opposite to LC shift have been severely damaged, glaucoma might not progress, since the pores in the other area would be relatively spared from the LC-shiftassociated tensile stress [11]

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