Primary angle-closure glaucoma (PACG) is a common cause of blindness. Angle closure is a fundamental pathologic process in PAGC. With the development of imaging devices for the anterior segment of the eye, a better understanding of the pathogenesis of angle closure has been reached. Aside from pupillary block and plateau iris, multiple-mechanisms are more common contributors for closure of the angle such as choroidal thickness and uveal expansion, which may be responsible for the presenting features of PACG. Recent Genome Wide Association Studies identified several new PACG loci and genes, which may shed light on the molecular mechanisms of PACG. The current classification systems of PACG remain controversial. Focusing the anterior chamber angle is a principal management strategy for PACG. Treatments to open the angle or halt the angle closure process such as laser peripheral iridotomy and/or iridoplasty, as well as cataract extraction, are proving their effectiveness. PACG may be preventable in the early stages if future research can identify which kind of angles and/or persons are more likely to benefit from prophylactic treatment. New treatment strategies like adjusting the psychological status and balancing the sympathetic-parasympathetic nerve activity, and innovative medicines are needed to improve the prognosis of PACG. In this review, we intend to describe current understanding and unknown aspects of PACG, and to share the clinical experience and viewpoints of the authors.

Purpose.: To examine the morphologic features of parapapillary atrophy by using enhanced depth imaging optical coherence tomography (EDI-OCT) and color fundus photographs. Methods.: The clinical observational comparative study included 80 normal eyes of 46 subjects and 80 eyes of 46 patients with primary open-angle glaucoma. Both groups did not vary significantly in axial length (P = 0.62) and refractive error (P = 0.30). Color fundus photographs and cross-sectional B-scan images obtained by EDI-OCT were examined. On the EDI-OCT images, we measured a gamma zone defined as the region between the temporal disc margin to the beginning of Bruch's membrane, and a beta zone defined as Bruch's membrane without retinal pigment epithelium. Results.: The gamma zone (mean area: 1.13 ± 2.04 mm²) was significantly associated with longer axial length (P < 0.001; standardized coefficient beta: 0.48), longer vertical disc diameter (P < 0.001; beta: 0.43), older age (P = 0.008; beta: 0.22), and the absence of glaucoma (P = 0.03; beta: −0.19). The beta zone (mean area: 0.85 ± 0.60 mm²) was associated with longer axial length (P < 0.001; beta: 0.39) and the presence of glaucoma (P < 0.001; beta: 0.48). Conclusions.: In addition to associations with older age, increasing myopia, and larger disc size, the EDI-OCT–defined gamma zone of parapapillary atrophy was associated with the absence of glaucoma, whereas the EDI-OCT–defined beta zone was associated with the presence of glaucoma. Differentiation between the beta zone and the gamma zone may be clinically useful.

Purpose: This study aimed to determine whether patients with dry eye syndrome [DES] have more symptoms of anxiety and depression than controls without DES. Methods: In this case-control study, the sample consisted of 89 DES subjects (13 diagnosed with Sjögren’s syndrome [SS]) and 73 control subjects. Each subject was diagnosed as having DES or was chosen as a control subject by an ophthalmologist. The Zung Self Rating Anxiety Scales (SAS), Zung Self Rating Depression Scales (SDS), and Ocular Surface Disease Index (OSDI) were administered to all subjects. Scores of SAS and SDS, measuring level of anxiety and depression symptoms, were compared between the DES group and the control group. Correlations with other health status measures were conducted. Results: The SAS and SDS scores of the DES group were significantly higher than the control group (P < 0.001, P < 0.001). The prevalence of DES subjects with anxiety or depression symptoms was significantly higher than in the control group (P = 0.003, P < 0.001). In the DES group, SAS scores were found to be correlated with OSDI and educational level. SDS scores were found to be correlated with OSDI. Neither SAS nor SDS scores were correlated with age, sex, household income, tear break up time (BUT), Schirmer Test 1 (S1T), corneal fluorescein staining (FL), or visual acuity. Conclusion: Anxiety and depression are correlated with DES, demonstrating that DES is an important public health problem that merits increased attention and research.

Objectives The aim of this study was to evaluate the peripapillary and parafoveal perfusion of young, healthy myopic subjects with spectral domain optical coherence tomography (OCT) angiography. Design A prospective comparative study was conducted from December 2014 to January 2015. Setting Participants recruited from a population-based study performed by the Eye, Ear, Nose and Throat Hospital of Fudan University in Shanghai. Participants A total of 78 Chinese normal subjects (78 eyes) with different refraction were included. Myopia was divided into 4 groups on the basis of the refractive status: 20 eyes with emmetropia (mean spherical equivalent (MSE) 0.50D to −0.50D), 20 eyes with mild myopia (MSE −0.75D to −2.75D), 20 eyes with moderate myopia (MSE −3.00D to −5.75D), and 18 eyes with high myopia (MSE≤−6.00D). Main outcome measures Peripapillary and parafoveal retinal and choroidal perfusion parameters and their relationships with axial length (AL) and retinal nerve fibre layer (RNFL) thickness were analysed. Results Significant differences were found for the retinal flow index and vessel density in the peripapillary area among the 4 groups, but not in the parafoveal area. The high myopia group had the lowest peripapillary retinal flow index and vessel density. In addition, there was a negative correlation (β=−0.002, p=0.047) between the AL and peripapillary retinal flow index and a positive correlation between RNFL thickness and the peripapillary retinal perfusion parameters (flow index: β=0.001, p=0.006; vessel density: β=0.350, p=0.002) even after adjustment for other variables. Conclusions Highly myopic eyes have a decreased peripapillary retinal perfusion compared with emmetropic eyes. Such vascular features might increase the susceptibility to vascular-related eye diseases.

Background: Glaucoma, the leading cause of irreversible blindness worldwide, is a type of retinal disease characterized by the selective death of retinal ganglion cells (RGCs). However, the pathogenesis of glaucoma has not been fully elucidated. Transient receptor potential vanilloid 4 (TRPV4) is a pressure-sensitive and calcium-permeable cation channel. TRPV4 is widely distributed in the retina and its sustained activation leads to RGC death; indicating that TRPV4 may be a possible target for glaucoma treatment. Here, we investigated the effects of TRPV4 on RGC apoptosis in a rat model of chronic ocular hypertension (COH), then examined the mechanism underlying these effects. Methods: The COH model was established by injection of micro-magnetic beads into the anterior chamber of adult male rats. The expression levels of TRPV4, glial fibrillary acidic protein, and inflammatory factors were assessed by immunohistochemistry and immunoblotting. RGC apoptosis and visual dysfunction were evaluated by TUNEL assay and photopic negative response. Functional expression of TRPV4 was examined by electrophysiology and calcium imaging. Real-time polymerase chain reaction and immunoblotting were employed to investigate the molecular mechanism underlying the effects of TRPV4 on tumor necrosis factor-α (TNF-α) release. Results: We found that TRPV4 played an essential role in glaucoma, such that high levels of TRPV4 expression were associated with elevated intraocular pressure. Furthermore, TRPV4 activation was involved in glaucoma-induced RGC apoptosis and RGC-related reductions in visual function. Mechanistic investigation demonstrated that TRPV4 activation led to enhanced Müller cell gliosis and TNF-α release via the JAK2/STAT3/NF-kB pathway, while TRPV4 inhibition could reverse these effects. Finally, TRPV4 activation could lead to elevated expression of TNF receptor 1 in RGCs, while inhibition of TNF-α could reduce TRPV4-mediated RGC apoptosis. Conclusions: TRPV4 activation induces Müller cell gliosis and TNF-α elevation via the JAK2/STAT3/NF-κB pathway, which may exacerbate RGC apoptosis in glaucoma; these results suggest that TRPV4 can serve as a therapeutic target in glaucoma treatment.