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Purpose: To report a rare case of severe ocular hypertension following intravenous methylprednisolone treatment in a child with bilateral optic neuritis.Case summary: A 6-year-old girl presented with bilateral severe visual loss and disc swelling. Magnetic resonance imaging revealed optic nerve enhancement, and she received high-dose intravenous methylprednisolone for 3 days and oral prednisolone 30 mg/day for 2 weeks. Two weeks after initiating treatment, ophthalmologic examination revealed an intraocular pressure (IOP) of 46 mmHg in the right eye and 42 mmHg in the left eye. The best-corrected visual acuity was 1.0 in the right eye and 0.6 in the left eye. Relative afferent pupillary defect was noted in the left eye. Fundus examination showed normal cup-to-disc ratio (0.4) in both eyes. The iridocorneal angle was open in all directions. The treatment plan included the cessation of oral prednisolone and initiation of latanoprost and dorzolamide-timolol fixed combination agent. After 12 hours, the IOP decreased to 18 mmHg in the right eye and 14 mmHg in the left eye. Six months later, her visual acuity was 1.0 in both eyes, and IOP was maintained at 11 and 13 mmHg in the right and left eye, respectively. Optic disc examination showed no sign of glaucomatous change with normal cup-to disc ratio in both eyes.Conclusions: Since steroid medication may cause asymptomatic IOP elevation, regular intraocular pressure measurements are required during steroid treatment for pediatric optic neuritis. The administration of IOP-lowering eyedrops returned IOP to the normal range without damaging the optic nerve.

Purpose: To report the effect of removal of a central descemet membrane on the endothelial function, morphology, and clinical symptoms of eyes with Fuch’s endothelial dystrophy.Methods: From August 2019 to January 2021, patients with Fuch’s endothelial dystrophy, i.e., with confluent, central corneal guttae and cataracts that required surgery, underwent phacoemulsification, intraocular lens implantation, and central descemet membrane stripping. To evaluate the effect of descemet stripping only (DSO), visual acuity and intraocular pressure were measured, and corneal pachymetry, slit-lamp and specular microscopy, and anterior segment optical coherence tomography performed, before surgery and at 1, 7, and 30 days and 3 and 6 months after surgery.Results: Seven patients (10 eyes) were included. Visual acuity improved from 1.01 ± 0.40 logarithm of the minimum angle of resolution (logMAR) preoperatively to 0.33 ± 0.22 logMAR 6 months after surgery (p = 0.008). The mean central corneal thickness decreased from 578.50 ± 36.88 μm preoperatively to 568.50 ± 48.61 μm 6 months after surgery; the difference was not significant (p = 0.507). The endothelial cell count increased significantly from 663.80 ± 356.40/mm2 preoperatively to 1,082.00 ± 274.46/mm2 6 months after surgery (p = 0.043).Conclusions: DSO can serve as a useful alternative when corneal transplantation is not possible in patients with Fuch’s endothelial dystrophy, but treatment efficacy and safety require further evaluation.

Chronic activation of microglial cells endangers neuronal survival through the release of various proinflammatory and neurotoxic factors. Paeoniflorin (PF), a water-soluble monoterpene glycoside found in the root of Paeonia lactiflora Pall, has a wide range of pharmacological functions, such as anti-oxidant, anti-inflammatory, and anti-cancer effects. Neuroprotective potential of PF has also been demonstrated in animal models of neuropathologies. Here, we have examined the efficacy of PF in the repression of inflammation-induced neurotoxicity and microglial inflammatory response. In organotypic hippocampal slice cultures, PF significantly blocked lipopolysaccharide (LPS)-induced hippocampal cell death and productions of nitric oxide (NO) and interleukin (IL)-1β. PF also inhibited the LPS-stimulated productions of NO, tumor necrosis factor-α, and IL-1β from primary microglial cells. These results suggest that PF possesses neuroprotective activity by reducing the production of proinflammatory factors from activated microglial cells.