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Background Epiretinal membrane (ERM) is a disease that affects the vitreoretinal interface and causes metamorphopsia, anorthopia, and decreased visual acuity. In this study, ERM patients who underwent internal limiting membrane (ILM) peeling were classified as those with glaucoma (Group G) and a control group (Group C). Changes in ganglion cell complex (GCC) thickness were compared between these groups to investigate whether such changes had an effect on progression of glaucoma from structural change. Methods This was a retrospective, observational study that included 27 eyes of 27 patients. Group C included 22 eyes, and Group G included 5 eyes. Patients underwent ILM peeling, and cataract surgery was combined with vitrectomy for 16 phakic eyes; 2 phakic eyes and 9 aphakic eyes were treated only with vitrectomy. GCC thickness was measured preoperatively and at 2 weeks and 1, 3, and 6 months postoperatively, and these values and the rates of thinning were compared between the two groups. Results The mean age of patients was 66.7±12.8 years (range 30-84 years). There was no significant difference between groups in the thickness of the GCC or its rate of thinning after ILM peeling. Conclusions The present results suggest that this procedure does not cause structural exacerbation of glaucoma in glaucoma patients. Although further studies of the functional effects of ILM peeling are required, the present results suggest that there is no significant difference between the two groups.

We describe the case of a primary open-angle glaucoma patient with re-elevated nocturnal sitting intraocular pressure (IOP) after restarting medical therapy due to a failing bleb. IOP was markedly higher than diurnal IOP during multiple-drug therapy in both eyes, but it did not increase in the left eye with a functional bleb without medical therapy after trabeculectomy with adjuvant mitomycin. However, nocturnal sitting IOP was re-elevated after restarting multiple-drug therapy due to a failing bleb, while diurnal IOP was maintained at a low level.

Background The purpose of this study was to examine changes in the ocular surface before and after phacoemulsification with small incisions and to examine the changes in tear osmolarity. Methods This was a prospective, observational study involving 55 eyes of 39 patients (19 male, 20 female patients; average age 72.0±7.3 years) who had cataract surgery at a Nippon Medical School Hospital between December 2013 and June 2018. Compromised tear dynamics were determined by the Schirmer test or the tear break-up time (BUT). An abnormal ocular surface was identified by positive vital staining with fluorescein or lissamine green. Moreover, tear osmolarity (Tosm) and corneal sensitivity were measured. All assessments were done preoperatively and 1 and 4 weeks (P1W and P4W) after the surgery. Results None of the operations had any complications. Operating time was 17.8±9.3 minutes. BUT was significantly decreased at P1W, and it recovered at P4W. The Schirmer test did not change significantly. The fluorescein staining score (FSS) increased significantly at P1W and recovered at P4W. The Lissamine green score (LSS) did not change significantly. Tear osmolarity increased significantly at P1W and did not recover at P4W. Corneal sensitivity decreased significantly at P1W and recovered at P4W. Conclusion In the present study, there were temporary changes in dry eye-related examinations including tear osmolarity after cataract surgery. In particular, tear osmolarity increased significantly 4 weeks after surgery compared to before surgery, and it showed long-term changes, unlike other factors. After cataract surgery, tear osmolarity, BUT, and FSS increase, resulting in dry eye symptoms. Therefore, it is necessary to pay attention to discomfortable eye symptoms of patients after cataract surgery.

Decreased vision and cystoid macular edema (CME) developed in phakic eyes of a patient who underwent laser iridotomy after changing the glaucoma eye drops from carteolol 2% long-acting ophthalmic solution to omidenepag isopropyl 0.002%. CME completely disappeared at approximately 2 months after discontinuation of omidenepag isopropyl in conjunction with the use of bromfenac sodium 0.1%.

The GUCY2D (guanylate cyclase 2D) gene encodes a photoreceptor guanylate cyclase (GC-E), that is predominantly expressed in the cone outer segments. Mutations in the GUCY2D lead to severe retinal disorders such as autosomal dominant cone-rod dystrophy (adCRD) and autosomal recessive Leber congenital amaurosis type 1. The purpose of this study was to identify the phenotype of a Japanese patient with a probably pathogenic GUCY2D variant.Detailed ophthalmic examinations were performed, and whole exome sequencing was performed on DNA obtained from the patient. The variants identified by exome sequencing and targeted analysis were further confirmed by direct sequencing.A 47-year-old man had atrophic and pigmentary changes in the macula of both eyes. Amplitudes and implicit times on full-field electroretinograms (ERGs) were within normal limits; however, the densities of multifocal ERGs in the central area were reduced in both eyes. Whole exome sequencing identified heterozygous variant c.2527GC, p.Glu843Gln in the GUCY2D gene within the mutation hot spot for adCRD. The allelic frequencies of this variant are extremely low and, according to American College of Medical Genetics and Genomics standards and guidelines, the variants are classified as likely pathogenic.This is the first report of a heterozygous variant, c.2527GC, p.Glu843Gln, in the GUCY2D, in a patient presenting with mild macular dystrophy without a general reduction in cone function. Our findings expand the spectrum of the clinical phenotypes of GUCY2D-adCRD and help clarify the morphological and functional changes caused by defects of dimerization of GC-E in the phototransduction cascade.

Background Brain-derived neurotrophic factor (BDNF) may be involved in the pathogenesis of glaucoma. BDNF concentrations reported in previous studies have varied widely, and the concentration of BDNF in aqueous humor is unknown. In this study, BDNF concentrations in the aqueous humor of glaucoma patients and control patients were measured with ELISA kits. Methods This prospective, observational study examined BDNF levels in aqueous humor in 62 eyes of 43 patients who underwent cataract surgery or trabeculectomy (11 glaucoma patients and 32 non-glaucoma cataract patients as controls). BDNF concentrations were examined by 4 different enzyme-linked immunosorbent assay (ELISA) techniques. Results The mean ± SD patient age was 72.0 ± 10.1 (range 35 to 87) years. Two of the techniques detected no BDNF in aqueous humor in any samples (n=3 and n=9, respectively); the average value was less than zero. An ultrasensitive ELISA kit did not yield reliable measurements. Finally, in an even more sensitive ELISA (Simoa-HD1), performed by an outside contractor, 25 (54.3%) eyes were below the detection limit, including 20 (55.6%) control and 5 (50%) glaucoma cases. For eyes with detectable BDNF, the overall BDNF concentration was 0.158 pg/mL (n=21): 0.196 pg/mL (n=16) in controls and 0.034 pg/mL (n=5) in glaucoma cases. Conclusions BDNF level in aqueous humor varies widely.

Background The adeno-associated virus (AAV) vector is a promising vector for ocular gene therapy. Surgical internal limiting membrane peeling before AAV vector administration is useful for efficient retinal transduction. However, no report has investigated localization of AAV vectors after administration into a post-vitrectomy eye. This study investigated the effects of vitrectomy surgery on intravitreal-injected AAV vector-mediated gene expression in the anterior segment and examined the presence of neutralizing antibodies (NAbs) in serum before and after AAV vector administration. Methods Of six eyes from three female cynomolgus monkeys, four were vitrectomized (Group VIT) and two were non-vitrectomized (Group IV). All eyes were injected with 50 μL of triple-mutated self-complementary AAV2 vector (1.9 × 1013 v.g./mL) encoding green fluorescent protein (GFP). NAbs in the serum were examined before administration and at 2 and 6 weeks after administration. GFP expression was analyzed at 19 weeks after administration. Results Immunohistological analysis showed no GFP expression in the trabecular meshwork in any eye. The GFP genome copy in two slices of the anterior segment was 2.417 (vector genome copies/diploid genome) in Group VIT and 4.316 (vector genome copies/diploid genome) in group IV. The NAb titer was 1:15.9 (geometric mean) before administration, 1:310.7 at 2 weeks after administration, and 1:669.4 at 6 weeks after administration. Conclusion Previous vitrectomy surgery did not affect gene expression in the anterior segment after intravitreal injection of AAV vectors.

Cilioretinal artery occlusion (CLRAO) is a rare disease. Here, we report the case of a 70-year-old man with nonarteritic cilioretinal artery occlusion alone. The patient was allergic to fluorescein. Therefore, we followed the retinal circulation with optical coherence tomography angiography (OCTA). OCTA at 40 days postonset showed partial improvement in the retinal circulation.

Purpose The aim of this study was to measure the serum levels of brain-derived neurotrophic factor (BDNF) in primary open angle glaucoma (POAG) and normal tension glaucoma (NTG) patients in Japan. Methods This was a prospective, observational study that examined serum BDNF levels in 78 patients who underwent cataract surgery or trabeculectomy (27 glaucoma patients and 51 non-glaucoma cataract patients as controls). The patients' age was 68.8 ± 11.1 years (mean ± standard deviation; range 35-86 years). The number of patients with POAG and NTG was 16 and 11, respectively. The diagnosis of POAG was done by intraocular pressure measurement, gonioscopy, optic nerve head change, and the presence of a visual field defect. Results The serum BDNF concentration was significantly lower in the glaucoma group, including both POAG and NTG, than in the control group (7.2 ± 3.6 ng/mL vs. 12.2 ± 9.3 ng/mL, p=0.004). The serum BDNF concentration was lower in the early phase than in the moderate phases of glaucoma. There was no correlation between the serum BDNF concentration and age. When the NTG and POAG patient groups were compared, the serum BDNF concentration was lower in NTG patients than in POAG patients. No significant correlations were found between glaucoma parameters, including optical coherence tomography and visual field defects, and the serum BDNF concentration. Conclusion This is the first study to have investigated serum BDNF concentrations in glaucoma patients in Japan. Further investigations are needed to evaluate the role of BDNF as a potential biomarker of glaucoma.