Purpose The purpose of this study was to assess the corneal epithelial thickness (CET) of the 9-mm diameter zone in patients treated using topical antiglaucoma medications and to evaluate the factors associated with CET changes. Methods Seventy-five patients treated using topical antiglaucoma medications and 65 healthy subjects were included in this cross-sectional study. Each patient completed the Ocular Surface Disease Index (OSDI) questionnaire and underwent examinations including the Schirmer I test, tear breakup time (TBUT), and fluorescein staining. CET mapping of the 9-mm diameter zone was performed using RTVue XR. The CET of the different analyzed zones was compared between groups. The relationship between CET and confounding factors was investigated. Results The patient group had a significantly shorter TBUT, shorter Schirmer I test, and greater fluorescein staining than those of the control group (all P < 0.05). The mean CET of patients with glaucoma was significantly lower than that of controls in the central, paracentral, mid-peripheral, and peripheral zones (all P < 0.001). Age affected the CET in the paracentral, mid-peripheral, and peripheral zones (all P < 0.01). The number of medications affected the CET in the central, paracentral, and mid-peripheral zones (all P < 0.05). The duration of treatment affected the CET in the central and peripheral zones (all P < 0.05). Conclusions Use of topical IOP-lowering medications leads to epithelial thinning in the 9-mm diameter zone in glaucomatous eyes. Epithelial protection should be considered in older patients and patients treated with multiple medications from the early stages of long-term topical antiglaucoma therapy. Translational Relevance The 9-mm diameter CET mapping by using widefield optical coherence tomography (OCT) can be a valuable and convenient method to assess the ocular surface damage in patients with topical antiglaucoma therapy.

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PURPOSE. Optical treatment can improve visual function in anisometropic amblyopia, but there is no electrophysiological evidence, and the underlying change in visual pathway remains unknown. Our aims were to characterize the functional loss in magnocellular and parvocellular visual pathways in anisometropic amblyopia at baseline and to investigate the effect of optical treatment on the 2 visual pathways. METHODS. Using isolated-check visual-evoked potential, we measured the magnocellularand parvocellular-biased contrast response functions in 15 normal controls (20.13 ± 3.93 years; mean ± standard deviation), 16 patients with anisometropic amblyopia (18.00 ± 6.04 years) who were fully refractive corrected before and 29 (19.41 ± 7.41 years) who had never been corrected. Twelve previously uncorrected amblyopes received optical treatment for more than 2 months and finished the follow-up measurement. RESULTS. Both the magnocellular-and parvocellular-biased contrast response functions in the amblyopic eye exhibited significantly reduced response and weaker contrast gains. We also found that the uncorrected amblyopes showed a more severe response reduction in magnocellular-biased, but not parvocellular-biased condition when compared with those corrected, with a weaker initial contrast gain and lower maximal response. After optical treatment, 12 uncorrected amblyopes demonstrated improved visual acuity of the amblyopic eye and a significant response gain to magnocellular-biased but not parvocellular-biased stimuli. CONCLUSIONS. We demonstrated deficits to both magnocellular-and parvocellular-biased stimuli in subjects with anisometropic amblyopia. Optical treatment could produce neurophysiological changes in visual pathways even in older children and adults, which may be mediated through the magnocellular pathway.

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