Ultrasound biomicroscopy (UBM) is an important tool in the diagnosis, evaluation and follow up of glaucoma patients. Even if we are dealing with a primary angle closure glaucoma (PACG) or a primary open angle glaucoma (POAG) patient, the mechanism of angle closure can be revealed by performing an UBM. The device can help differentiate between the two types of glaucoma even in patients with opaque corneas when gonioscopy cannot be performed. Knowing the type of glaucoma is vital, especially regarding an individualized treatment, since each patient is unique and needs to be treated accordingly, in order to prevent glaucomatous optic neuropathy and visual field loss.

Glaucoma is a main cause of irreversible blindness worldwide, with a high impact on productivity and quality of life. The mechanical and ischemic theories are currently the most recognized pathophysiological pathways that explain the neurodegeneration of retinal nerve fibers in glaucoma. In this narrative review, aspects of ischemia in glaucoma are discussed, including vascular dysregulation, retinal ischemia signaling pathways, roles of vascular endothelial growth factors, and future research and therapeutic directions. In conclusion, a better understanding of the ischemic processes in glaucoma may lead to innovative treatment options and improved management and follow-up of our patients.

Glaucoma is a widespread ophthalmological disease, with a high impact and frequent visual morbidity. While the physiopathology of the two types of primary glaucoma (open angle and angle closure) has been studied, there seems to be little relationship between the two. In this study, we gather clinical and preclinical data to support the idea that the two primary glaucomas are “mirrored” in terms of morphological parameters and disease physiopathology. In short, primary angle closure glaucoma (PACG) is associated with hyperopia and low axial length, and primary open angle glaucoma (POAG) is associated with myopia and high axial length. Moreover, in PACG and in primary angle closure or primary angle closure suspect cases, while there is extensive iridotrabecular contact, the intraocular pressure (IOP) is still maintained in the lower half of the normal range throughout the evolution of the disease, which suggests a baseline trabecular hyperfiltration in PACG. In the opposite case, myopic eyes with open angles and a higher risk of developing POAG often have a baseline IOP in the upper half of the normal range, suggesting a baseline trabecular hypofiltration. As we explore clinical, genetic and animal model data regarding these opposing aspects, we hypothesize the existence of a mirroring relationship between PACG and POAG. Defining the relationship between the two potentially blinding diseases, with a high prevalence worldwide, may aid in understanding the mechanisms better and refining diagnosis and treatment. Thus, our theory has been named the Mirror Theory of Primary Glaucomas.

Background and Objectives: Hyperopia is a refractive error which affects cognitive and social development if uncorrected and raises the risk of primary angle-closure glaucoma (PACG). Materials and Methods: The study included only the right eye—40 hyperopic eyes in the study group (spherical equivalent (SE) under pharmacological cycloplegia over 0.50 D), 34 emmetropic eyes in the control group (SE between −0.50 D and +0.50 D). A complete ophthalmological evaluation was performed, including autorefractometry to measure SE, and additionally we performed Ocular Response Analyser: Corneal Hysteresis (CH), Corneal Resistance Factor (CRF); specular microscopy: Endothelial cell density (CD), Cell variability (CV), Hexagonality (Hex), Aladdin biometry: Anterior Chamber Depth (ACD), Axial Length (AL), Central Corneal Thickness (CCT). IBM SPSS 26 was used for statistical analysis. Results: The mean age of the entire cohort was 22.93 years (SD ± 12.069), 66.22% being female and 33.78% male. The hyperopic eyes had significantly lower AL, ACD, higher SE, CH, CRF. In the hyperopia group, there are significant, negative correlations between CH and AL (r −0.335), CRF and AL (r −0.334), SE–AL (r −0.593), ACD and CV (r −0.528), CV and CRF (r −0.438), CH (r −0.379), and positive correlations between CCT and CH (r 0.393) or CRF (r 0.435), CD and ACD (r 0.509) or CH (0.384). Age is significantly, negatively correlated with ACD (r −0.447), CH (r −0.544), CRF (r −0.539), CD (r −0.546) and positively with CV (r 0.470). Conclusions: Our study suggests a particular biomechanical behavior of the cornea in hyperopia, in relation with morphological and endothelial parameters. Moreover, the negative correlation between age and ACD suggests a shallower anterior chamber as patients age, increasing the risk for PACG.

Background: Glaucoma is a progressive optic neuropathy, characterised by a complex pathophysiology, with mitochondrial dysfunction playing a significant role in the cellular damage and apoptosis of ganglion cells. Niacin is a precursor to several molecules acting as coenzymes in the mitochondrial production of ATP, in DNA repair and in the reduction of reactive oxygen species. The objective of this systematic review is to assess the impact of daily niacin intake on glaucoma. Methods: Case–control and cohort studies regarding niacin and glaucoma, indexed in PubMed, Web of Science, Cochrane and Scopus, were included. Other study methodologies, studies regarding niacin in other ocular disease or other nutrients in glaucoma were excluded. Bias was assessed using the Newcastle–Ottawa Scale. The study protocol was registered in the PROSPERO database (no. CRD42024578889). Results: Five case–control studies were included. In the pooled analysis, a significantly higher proportion of patients with high niacin consumption was found in the group without glaucoma compared to those with glaucoma as defined by ISGEO criteria (p-value < 0.00001; OR = 0.66, 95% CI 0.55–0.79) or as defined by retinal imaging (p-value = 0.02; OR = 0.63, 95% CI 0.43–0.94). Conclusions: Daily dietary intake of niacin is significantly lower in patients with glaucoma compared to the general population. Given different average daily intakes of niacin in these populations, different glaucoma definitions and several confounding variables which weaken the associations, large sample, standardised randomised controlled trials are needed to confirm the potential benefits of niacin in glaucoma.

Childhood glaucoma encompasses a group of rare but severe ocular disorders characterized by increased intraocular pressure (IOP), posing significant risks to vision and quality of life. Primary congenital glaucoma has a prevalence of one in 10,000–68,000 people in Western countries. More worryingly, it is responsible for 5–18% of all childhood blindness cases. According to the Childhood Glaucoma Research Network (CGRN), this spectrum of disease is classified into primary glaucoma (primary congenital glaucoma and juvenile open-angle glaucoma) and secondary glaucomas (associated with non-acquired ocular anomalies, non-acquired systemic disease, acquired conditions, and glaucoma after cataract surgery). They present very specific ocular characteristics, such as buphthalmos or progressive myopic shift, corneal modifications such as Haab striae, corneal edema or increased corneal diameter, and also glaucoma findings including high intraocular pressure, specific visual fields abnormalities, and optic nerve damage such as increased cup-disc ratio, cup-disc ratio asymmetry of at least 0.2 and focal rim thinning. Surgical intervention remains the cornerstone of treatment, and initial surgical options include angle surgeries such as goniotomy and trabeculotomy, aimed at improving aqueous outflow. For refractory cases, trabeculectomy and glaucoma drainage devices (GDDs) serve as second-line therapies. Advanced cases may require cyclodestructive procedures, including transscleral cyclophotocoagulation, reserved for eyes with limited visual potential. All in all, with appropriate management, the prognosis of PCG may be quite favorable: stationary disease has been reported in 90.3% of cases after one year, with a median visual acuity in the better eye of 20/30. Immediate recognition of the specific signs and symptoms by caregivers, primary care providers, and ophthalmologists, followed by prompt diagnosis, comprehensive surgical planning, and involving the caregivers in the follow-up schedule remain critical for optimizing outcomes in childhood glaucoma management.