Glaucomatous Optic Nerve Research Articles

Quantitative Microstructural Analysis of Cellular and Tissue Remodeling in Human Glaucoma Optic Nerve Head.

PurposeTo measure quantitatively changes in lamina cribrosa (LC) cell and connective tissue structure in human glaucoma eyes.MethodsWe studied 27 glaucoma and 19 age-matched non-glaucoma postmortem eyes. In 25 eyes, LC cross-sections were examined by confocal and multiphoton microscopy to quantify structures identified by anti-glial fibrillary acidic protein (GFAP), phalloidin-labeled F-actin, nuclear 4′,6-diamidino-2-phenylindole (DAPI), and by second harmonic generation imaging of LC beams. Additional light and transmission electron microscopy were performed in 21 eyes to confirm features of LC remodeling, including immunolabeling by anti-SOX9 and anti-collagen IV. All glaucoma eyes had detailed clinical histories of open-angle glaucoma status, and degree of axon loss was quantified in retrolaminar optic nerve cross-sections.ResultsWithin LC pores, the proportionate area of both GFAP and F-actin processes was significantly lower in glaucoma eyes than in controls (P = 0.01). Nuclei were rounder (lower median aspect ratio) in glaucoma specimens (P = 0.02). In models assessing degree of glaucoma damage, F-actin process width was significantly wider in glaucoma eyes with more damage (P = 0.024), average LC beam width decreased with worse glaucoma damage (P = 0.042), and nuclear count per square millimeter rose with worse damage (P = 0.019). The greater cell count in LC pores represented 92.3% astrocytes by SOX9 labeling. The results are consistent with replacement of axons in LC pores by basement membrane labeled by anti-collagen IV and in-migrating astrocytes.ConclusionsAlteration in LC structure in glaucoma involves migration of astrocytes into axonal bundles, change in astrocyte orientation and processes, production of basement membrane material, and thinning of connective tissue beams.

The Topographic Relationship Between Choroidal Microvascular Dropout and Glaucomatous Damage in Primary Angle-Closure Glaucoma.

PurposeTo study the topographic relationship between parapapillary choroidal microvasculature dropout (MvD) and parapapillary retinal nerve fiber layer (RNFL) defect in primary angle-closure glaucoma (PACG) eyes.MethodsThis cross-sectional study was carried out in a glaucoma clinic. Patients with PACG and healthy controls were consecutively enrolled. Each subject underwent optical coherence tomography angiography (OCTA) and OCT testing; additionally, visual field (VF) tests were also conducted in the patients with PACG. MvD was determined when choroidal layer images in OCTA showed a complete loss of the microvasculature. The study included 55 patients with PACG and 30 healthy controls.ResultsFifty-five eyes in 55 patients with PACG and 30 eyes in 30 healthy controls were recruited. MvD was found in 26 PACG eyes (47.3%), but no MvD was found in the healthy eyes. Compared with PACG eyes without MvD, eyes with MvD had thinner average RNFL (P < 0.001), worse VF mean deviation (P = 0.006), and lower peripapillary vessel density (P < 0.001). Between MvD and RNFL defects, there was good topographic consistency in angular circumference (Bland–Altman 95% confidence interval [CI], −24.9° to 21.0°) and position (Bland-Altman 95% CI, −18.6° to 20.6°). There was a significant correlation between the MvD angular circumference and the average peripapillary vessel density (r = −0.505; P = 0.014), average RNFL thickness (r = −0.742; P < 0.001), and VF mean deviation (r = −0.572; P = 0.004).ConclusionsIn patients with PACG, the MvD angular circumference and position were highly topographic consistent with those of the peripapillary RNFL defect area. This study suggests that there is a significant correlation between MvD and glaucoma optic nerve injury.Translational RelevanceGiven the vascular etiology for glaucoma, the current research suggests that the MvD angular circumference may serve as a potential supplementary clue of glaucoma disease severity.

Resistance Training with Blood Flow Restriction and Ocular Health: A Brief Review.

Despite the many health benefits of resistance training, it has been suggested that high-intensity resistance exercise is associated with acute increases in intraocular pressure which is a significant risk factor for the development of glaucomatous optic nerve damage. Therefore, resistance training using a variety of forms (e.g., resistance bands, free weights, weight machines, and bodyweight) may be harmful to patients with or at risk of glaucoma. An appropriate solution for such people may involve the combination of resistance training and blood flow restriction (BFR). During the last decade, the BFR (a.k.a. occlusion or KAATSU training) method has drawn great interest among health and sports professionals because of the possibility for individuals to improve various areas of fitness and performance at lower exercise intensities. In comparison to studies evaluating the efficiency of BFR in terms of physical performance and body composition changes, there is still a paucity of empirical studies concerning safety, especially regarding ocular health. Although the use of BFR during resistance training seems feasible for glaucoma patients or those at risk of glaucoma, some issues must be investigated and resolved. Therefore, this review provides an overview of the available scientific data describing the influence of resistance training combined with BFR on ocular physiology and points to further directions of research.

Elevated intraocular pressure and microvascular retinal injury identified by overhead mounted optical coherence tomography in two infants with glaucoma

OCT imaging (tabletop and handheld/overhead-mounted methodology) aids in evaluating the optic nerve and retina in children. Glaucomatous optic nerve damage can be described on OCT as an isolated loss of ganglion cells in the macula. Using supine imaging with overhead-mounted OCT, we examined the macula in children with glaucoma, hoping to characterize the pattern of glaucomatous nerve damage.

Prospective 12-month outcomes of combined iStent inject implantation and phacoemulsification in Asian eyes with normal tension glaucoma

BackgroundGlaucoma is the leading cause of irreversible blindness. Normal tension glaucoma (NTG) is a subset of open-angle glaucoma, demonstrating glaucomatous optic nerve damage in the absence of raised intraocular pressure (IOP). NTG is more prevalent in Asian populations. While generally slow-progressing, NTG may be associated with significant central visual field loss. In recent years, minimally invasive glaucoma surgery has been added to the armamentarium of glaucoma surgery. This prospective study aims to evaluate 12-month surgical outcomes of combined iStent inject (Glaukos Corporation, Laguna Hills, CA) implantation and phacoemulsification in Asian eyes with NTG.MethodsThis is a prospective, single-centre case series of 30 eyes followed up until 12 months after surgery. Outcome measures included IOP, number of glaucoma medications, best-corrected visual acuity (BCVA) and intra and postoperative complications.ResultsMean age of subjects was 73.1 ± 6.3 years. Majority were ethnic Chinese (n = 27, 90%). Baseline medicated mean IOP was 13.8 ± 2.4 mmHg and mean number of glaucoma medications was 1.3 ± 0.7. Mean Humphrey visual field mean deviation was − 13.7 ± 7.6. The mean IOP reduction at all timepoints from postoperative month (POM) 3 onwards was statistically significant (all P < 0.05), with mean reduction of 1.2 mmHg (95% CI: 0.1–2.2, P = 0.037) by POM12. There was statistically significant reduction in mean number of medications from postoperative day (POD) 1 onwards (all P < 0.05), with mean decrease of 1.0 medication (95% CI: 0.9–1.1, P < 0.001) by POM12. By POM12, 25 (83.3%) eyes were medication-free. Three (10%) eyes had stent occlusion by iris requiring laser iridoplasty. One eye had gross hyphema which resolved on conservative management before POM1. Mean BCVA improved from the baseline 0.3 ± 0.3 logMAR to 0.1 ± 0.1 logMAR postoperatively (P < 0.001). There were no major adverse or sight-threatening events. No eyes required further glaucoma surgery during the 12-month follow-up period.ConclusionAsian eyes with NTG which underwent combined iStent inject implantation and phacoemulsification demonstrated a significant and sustained reduction in IOP and glaucoma medications, up to 12 months postoperatively.

Differential effects of obstructive sleep apnea on the corneal subbasal nerve plexus and retinal nerve fiber layer.

PurposeObstructive sleep apnea (OSA) is an established independent risk factor for peripheral neuropathy. Macro and microvascular changes have been documented in OSA, including high levels of potent vasoconstrictors. In diabetes, vasoconstriction has been identified as an underlying risk factor for corneal neuropathy. This study sought to establish a potential relationship between OSA and corneal nerve morphology and sensitivity, and to determine whether changes in corneal nerves may be reflective of OSA severity.DesignSingle center cross-sectional study.MethodsSixty-seven patients were stratified into two groups: those with OSA and healthy controls. Groups were matched for age, sex, race, smoking, and dry eye status. Outcome measures included serologies, a dilated fundus exam, dry eye testing, anthropometric parameters, corneal sensitivity, subbasal nerve plexus morphology, retinal nerve fiber layer (RNFL) thickness, and the use of questionnaires to assess symptoms of dry eye disease, risk of OSA, and continuous positive airway pressure (CPAP) compliance.ResultsNo significant differences were observed in corneal nerve morphology, sensitivity, or the number of dendritic cells. In the OSA test group, RNFL thinning was noted in the superior and inferior regions of the optic disc and peripapillary region. A greater proportion of participants in the OSA group required a subsequent evaluation for glaucoma than in the control. In those with OSA, an increase in the apnea hypopnea index was associated with an increase in optic nerve cupping.ConclusionsOSA does not exert a robust effect on corneal nerves. OSA is however, associated with thinning of the RNFL. Participants with glaucomatous optic nerve changes and risk factors for OSA should be examined as uncontrolled OSA may exacerbate glaucoma progression.

The Piezo1 ion channel in glaucoma: a new perspective on mechanical stress.

Glaucomatous optic nerve damage caused by pathological intraocular pressure elevation is irreversible, and its course is often difficult to control. This group of eye diseases is closely related to biomechanics, and the correlation between glaucoma pathogenesis and mechanical stimulation has been studied in recent decades. The nonselective cation channel Piezo1, the most important known mechanical stress sensor, is a transmembrane protein widely expressed in various cell types. Piezo1 has been detected throughout the eye, and the close relationship between Piezo1 and glaucoma is being confirmed. Pathological changes in glaucoma occur in both the anterior and posterior segments of the eye, and it is of great interest for researchers to determine whether Piezo1 plays a role in these changes and how it functions. The elucidation of the mechanisms of Piezo1 action in nonocular tissues and the reported roles of similar mechanically activated ion channels in glaucoma will provide an appropriate basis for further investigation. From a new perspective, this review provides a detailed description of the current progress in elucidating the role of Piezo1 in glaucoma, including relevant questions and assumptions, the remaining challenging research directions and mechanism-related therapeutic potential.

Ultrasound Targeted Microbubble Destruction Promotes the Therapeutic Effect of HUMSC Transplantation on Glaucoma-Caused Optic Nerve Injury in Rabbits.

PurposeThe purpose of this study was to explore the therapeutic effect of human umbilical cord mesenchymal stem cell (HUMSC) transplantation alone or assisted with ultrasound targeted microbubble destruction (UTMD) on optic neuropathy in a novel and practical model of experimental glaucoma in rabbits.MethodsEight New Zealand white healthy rabbits were used as the control group (group A). Twenty-four experimental glaucomatous rabbits were established as described previously and randomly divided into three groups: (1) received no treatment (group B); (2) received intravitreal transplantation of HUMSCs (group C); and (3) received UTMD-assisted intravitreal transplantation of HUMSCs (group D). After 4 weeks of treatment, the distribution of HUMSCs, retinal thickness, layer structure, retinal ganglion cells (RGCs), and their axons were examined.ResultsAfter 4 weeks of treatment, HUMSCs were successfully scattered under the retina. HUMSC transplantation significantly increased the regeneration of RGCs and their axons, and restored the retinal structure in glaucomatous rabbits. Moreover, the application of UTMD enhances HUMSC distribution and achieved more significant therapeutic effect.ConclusionsIntravitreal transplantation of HUMSCs effectively repaired glaucomatous optic nerve injury, and UTMD enhanced the successful delivery of HUMSCs into injured retina, promoting its therapeutic effects remarkably.Translational RelevanceThis study demonstrated that HUMSC transplantation repaired the glaucoma-caused nerve injury significantly and the combination of UTMD can augment the therapeutic effect further, which has important clinical guiding significance for the development of therapeutic strategies of glaucoma.

Influence of implantation of diffractive trifocal intraocular lenses on standard automated perimetry

BackgroundThis prospective comparative study aimed to investigate the influence of diffractive trifocal intraocular lenses (IOLs) implantation on standard automated perimetry.MethodsPatients with no diseases affecting the visual field had undergone cataract surgery following the implantation of trifocal or monofocal IOLs from July 2019 to August 2020 were recruited. The normality of the anterior and posterior segments and absence of glaucomatous optic nerve cupping were confirmed preoperatively by slit-lamp examination. Standard automated perimetry was performed using Humphrey Visual Field 10–2 testing, 2–3 months after cataract surgery in only one eye per patient. The mean deviation (MD) and foveal sensitivity were compared between IOLs in eyes with acceptable reliability indices and best-corrected visual acuity of 20/25 or better.ResultsAmong the 83 eyes of the 83 patients included, 39 and 29 eyes eligible for perimetry analysis had trifocal and monofocal IOLs, respectively. The mean MD and foveal sensitivity in eyes with trifocal IOLs were significantly lower than those in eyes with monofocal IOLs (P < 0.021), with mean differences of 0.77 and 1.01 dB, respectively.ConclusionThe comparison in nonglaucomatous eyes demonstrated that the influence of trifocal IOLs on standard automated perimetry was greater than that of monofocal IOLs.

The Retinal Renin-Angiotensin-Aldosterone System: Implications for Glaucoma.

Aldosterone is one of the main effectors of the renin-angiotensin-aldosterone system (RAAS) along with having roles in hypertension, and cardiovascular and renal diseases. Recent evidence has also shown the presence of an active local RAAS within the human eye. It has been shown that at 12 h after a retinal ischemia-reperfusion injury, there is an upregulation of the protein levels of angiotensin II type 1 receptor (AT1-R) in the retina. Furthermore, at 12 h after reperfusion, there is an increase in reactive oxygen species (ROS) production in the retina that is mediated via an NADPH oxidase pathway. This ischemia-reperfusion injury-induced increase of retinal ROS levels and NADPH oxidase expression can be prevented by the administration of an AT1-R antagonist. This suggests that one of the main retinal ischemic injury pathways is via the local RAAS. It has also been reported that progressive retinal ganglion cell loss and glaucomatous optic nerve degeneration without elevated intraocular pressure occur after administration of local or systemic aldosterone. Elucidation of glaucoma pathogenesis, especially normal-tension glaucoma (NTG) subtype by our current animal model can be used for identifying potential therapeutic targets. Based on these results, we are further evaluating NTG prevalence among primary aldosteronism patients.

Alternate Causes for Pathogenesis of Exfoliation Glaucoma, a Multifactorial Elastotic Disorder: A Literature Review.

Exfoliation glaucoma (XFG) is the most recognizable form of secondary open-angle glaucoma associated with a high risk of blindness. This disease is characterized by white flaky granular deposits in the anterior chamber that leads to the elevation of intraocular pressure (IOP) and subsequent glaucomatous optic nerve damage. Conventionally, XFG is known to respond poorly to medical therapy, and surgical intervention is the only management option in most cases. Various genetic and nongenetic factors are known to be linked to the development of XFG. Despite decades of research on the genetic factors in exfoliation syndrome (XFS) by study groups and global consortia involving different ethnic populations, the pathogenesis of XFS and the mechanism of onset of glaucoma still remains an unsolved mystery. The key lies in understanding how the function of a gene (or set of genes) is altered by environmental triggers, along with other molecular events that underlie the key disease attributes, namely, oxidative stress and the disruption of the blood–aqueous barrier (BAB). It remains a challenge to evolve a theory encompassing all factions of molecular events occurring independently or parallelly that determine the disease manifestation (phenotype) or the stage of the disease in the eye (or in any tissue) in exfoliation. Our enhanced understanding of the underlying molecular pathophysiology of XFG, beyond the known genes or polymorphisms involved in the disease, will lead to improved diagnosis and management and the ability to recognize how the environment influences these key events that lead to the disease phenotype or disease progression. This review summarizes the recent observations and discoveries of four key factors that may hold the answers to the non-lysyl oxidase-like 1 (LOXL1) mechanisms behind XFG pathogenesis, namely, the epigenetic factor miRNA, disordered autophagy along with the potential involvement of mitochondrial mutations, and a compromised aqueous–blood barrier.

TrkB Receptor Agonist 7,8 Dihydroxyflavone is Protective Against the Inner Retinal Deficits Induced by Experimental Glaucoma

Glaucoma is an age-related neurodegenerative disorder characterized by retinal ganglion cell (RGC) degeneration and excavation of the optic nerve head (ONH). It is associated with an increase in intraocular pressure (IOP) and progressive decline in the visual field. Reduction in the retrograde axonal transport of neurotrophic factors such as brain-derived neurotrophic factor (BDNF) from the brain to the neuronal cell bodies in retina, has been suggested as one of the key mechanisms underlying selective degeneration of ganglion cells and optic nerve in glaucoma. Multiple studies have indicated that BDNF and its high affinity receptor Tropomyosin receptor kinase B (TrkB) play crucial roles in survival of RGCs and that upregulating BDNF/TrkB signalling using gene therapy can protect the ganglion cells against degeneration. This study corroborates previous findings and demonstrates that glaucoma is associated with downregulation of TrkB downstream signalling and enhanced levels of amyloid β (Aβ 1–42) accumulation in the retina. 7,8 dihydroxyflavone (7,8 DHF) is a TrkB agonist and regular administration of this compound imparted significant protection against loss of GCL density and preserved inner retinal function in experimental glaucoma models. 7,8 DHF treatment stimulated activation of TrkB intracellular signalling as well as ameliorated the increase in the levels of soluble Aβ (1–42) in the retinas of rats and mice exposed to high IOP. The protective effects of 7,8 DHF were also evident in BDNF+/− mice indicating that TrkB agonist mediated activation of TrkB signalling was not altered upon BDNF allelic impairment. These data support BDNF/TrkB axis as a promising therapeutic target in glaucoma and highlight that the detrimental effects of high IOP exposure can be compensated by the exogenous administration of a TrkB agonist.

Minimum Rim Width and Lamina Cribrosa Depth in Non-Glaucomatous and Glaucomatous U.S. Veterans

Purpose: Assess the utility of the MRW and lamina cribrosa depth measurements for detecting differences between non-glaucomatous and glaucomatous U.S. Veterans. Compare inter-eye differences of individuals with glaucoma. Method: 38 subjects were recruited per group: Group 1 included one eye of non-glaucomatous participants, and Group 2 included each qualifying eye of participants with glaucoma. Analysis compared Group 1 with the more affected eye only of Group 2 participants, and separately between the more and less affected eyes of group 2 participants. MRW measurements were obtained with Heidelberg Eye Explorer© (HEYEX). Average lamina cribrosa depths were measured manually utilizing HEYEX. Results: 26 subjects from Group 1 and 33 subjects from Group 2 were included. A significantly thinner MRW was found in glaucomatous eyes vs. non-glaucomatous eyes (210 µm vs. 309 µm; P &lt; .001). The normative database in HEYEX had an 85% sensitivity and 92% specificity to detect glaucomatous nerves. Among the 27 participants in Group 2 who had both eyes tested, eyes with more advanced visual field loss showed significantly thinner global MRW compared to fellow eyes (203 µm vs. 224 µm P = .03). Lamina cribrosa depths were non-significantly deeper in glaucomatous vs. non-glaucomatous eyes (476 µm vs. 429 µm P = .17). Conclusions: The MRW parameter differentiates between glaucomatous and non-glaucomatous optic nerves. Lamina cribrosa depths were non-significantly deeper in glaucomatous vs. non-glaucomatous participants. Post-hoc inter-eye data analysis suggested that inter-eye differences in gMRW values of glaucomatous eyes reflect asymmetric damage as correlated with the visual field

Prevalence of pre-perimetric primary open angle glaucoma in hypertensives of North India.

Systemic hypertension is alleged to increase the risk of glaucoma. As clinically Primary Open angle Glaucoma (POAG) is diagnosed only after approximately 40% of ganglion cell loss has occurred, therefore this study was commenced with an aim to determine the prevalence of pre-perimetric glaucomatous damage and its association with systemic hypertension using optical coherence tomography (OCT). A total of 680 study participants were enrolled in this cross-sectional study. Among them 340 patients were of systemic hypertension (Group 1) and 340 patients without hypertension (Group 2). All patients underwent detailed history, ocular and systemic examination including slit lamp examination, fundus examination by +90 D lens, Humphrey field analyser for field charting and OCT for nerve fiber analysis. For glaucomatous nerve damage. Group 1 and Group 2 had Male: Female ratio of 1:8 and 1:9, respectively (P = 0.809). Maximum participants 48.8% and 54.4% in Group 1 and Group 2, respectively, were in age group 50-59 years. Statistically significant difference was seen in the percentage of pre-perimetric glaucomatous patients between the two groups (P < 0.001). On OCT analysis between pre-perimetric glaucomatous eyes and healthy eyes significant difference in thickness was seen in temporal inner macula, inferior outer macula, temporal outer macula, superior outer macula and nasal outer macula. Significant difference in volume was seen for inferior temporal and nasal outer macula (P < 0.001). In hypertensives, glaucomatous optic nerve damage starts much earlier before the obvious clinical signs of POAG appear, as compared to normotensive individuals.

Veränderungen der Lebensqualität von Glaukompatienten über einen Zeitraum von 8 Jahren

The quality of life (QoL) of glaucoma patients is affected by many factors. In particular, patient activity is compromised by the chronicity of the disease. In this study, we evaluated the change in QoL and its impact on activities over aperiod of 8 years. A total of 43 patients with glaucomatous optic nerve damage were enrolled in this retrospective longitudinal observational study. Changes in intraocular pressure (IOP), best-corrected visual acuity (BCVA) and visual field (VF) parameters, number of IOP-lowering eye drops and IOP-lowering surgery were assessed over aperiod of 8 years. Assessment of QoL was obtained by patient-reported visual functioning using the Rasch-calibrated glaucoma activity limitation9 (GAL-9) questionnaire at baseline and after 8 years. The BCVA of the better eye changed from 0.16 ± 0.22 to 0.21 ± 0.14 logMAR, whereas there was achange from 0.27 ± 0.25 to 1.39 ± 1.1 logMAR in the worse eye. The VF parameter mean deviation (MD) of the better eye changed from -2.39 ± 4.55 dB to -4.83 ± 5.09 dB, while it altered significantly from -8.86 ± 5.86 dB to -12.05 ± 8.07 dB in the worse eye. Values of GAL‑9 changed from -2.39 ± 2.14 to -1.38 ± 2.78 (in the Rasch analysis, more negative values account for abetter QoL), according to asum score change from 79.17 ± 19.63 to 69.22 ± 27.95. This change showed ahighly significant correlation with the MD at follow-up, especially with the worse eye (r = 0.43). The impact of the MD at follow-up on QoL could also be well predicted in aregression model. The QoL of glaucoma patients decreased significantly over time. Changes in the VF, particularly of the worse eye, have agreat impact on reported functioning. Careful treatment, especially of the eye with greater glaucomatous damage, is mandatory.

Neuro-Ophthalmological Optic Nerve Cupping: An Overview

Optic nerve cupping or enlargement of the cup-to-disc ratio is widely recognized as a feature of glaucoma, however it may also occur in non-glaucomatous optic neuropathies. The most well-recognized non-glaucomatous optic neuropathies that cause cupping include compressive optic neuropathies, arteritic anterior ischemic optic neuropathies, hereditary optic neuropathies, and optic neuritis. Cupping is thought to consist of two main components: prelaminar and laminar thinning. The former is a shallow form of cupping and related to loss of retinal ganglion cells, whereas the latter involves damage to the lamina cribrosa and peripapillary scleral connective tissue. Differentiating glaucomatous and non-glaucomatous optic nerve cupping remains challenging even for experienced observers. Classically, the optic nerve in non-glaucomatous causes has pallor of the neuroretinal rim, but the optic nerve should not be examined in isolation. The patient’s medical history, history of presenting illness, visual function (visual acuity, color vision and visual field testing) and ocular examination also need to be considered. Ancillary testing such as optical coherence tomography of the retinal nerve fiber layer and ganglion cell layer-inner plexiform layer may also be helpful in localizing the disease. In this review, we review the non-glaucomatous causes of cupping and provide an approach to evaluating a patient that presents with an enlarged cup-to-disc ratio.

Retinal Nerve Fibre Layer Analysis in Non-Glaucomatous Pseudoexfoliation Syndrome Patients

Abstract Background Pseudoexfoliation syndrome (PXS) is a disorder characterized by the progressive accumulation of fibrillary extracellular deposits in several ocular tissues. It is an independent risk factor for glaucomatous optic nerve damage. Retinal nerve fiber layer (RNFL) thickness analysis using optical coherence tomography is a documented investigative tool to detect glaucoma at an early stage. Objective The aim was to evaluate and compare RNFL thickness in PXS patients without glaucoma with their age- and sex-matched healthy controls and detect the possibility of early glaucomatous damage in patients with RNFL thinning. Study Design This was a cross sectional case–control study. Materials and Methods A total of 100 patients were included, of which 50 were cases (Group A) and 50 were controls (Group B). RNFL thickness of cases and controls were compared using Zeiss Cirrus HD-OCT 500 (ZEISS Medical Technology, United States). Results There were no significant differences between the two groups with respect to mean RFNL thickness in nasal (p = 0.129) and temporal quadrants (p = 0.832). The mean inferior RNFL thickness values were 112.9 ± 21.72 μm in Group A and 120.6 ± 10.35 μm in Group B (p = 0.002). The mean thickness of the retinal nerve fiber layer in superior quadrant in Group A was 101.6 ± 23.16 μm, whereas it was 113.5 ± 13.47 μm in group B (p &lt; 0.001). The average RFNL thickness in Group A was 85.1 ± 13.99 μm and it was 88.9 ± 7.01 μm in Group B (p = 0.017). Conclusion There was statistically significant difference in RNFL thickness between cases and controls in inferior and superior quadrants and in global average thickness.

Bruch's membrane opening - minimum rim width measurement after acute primary angle-closure.

To evaluate Bruch's membrane opening - minimum rim width (BMO-MRW) and peripapillary retinal nerve fiber layer thickness (RNFLT) following an acute primary angle-closure attack (APAC). Nine consecutive patients with unilateral APAC were included. Patients with a bilateral attack, with signs of glaucomatous optic nerve damage or evidence of a previous APAC in either eye were excluded. Three months after the attack, all eyes underwent BMO-MRW and RNFLT measurements with SDOCT. APAC eyes were compared to the contralateral eyes. Three months after the attack, mean BMO-MRWs were 281.22 ± 56.88 μm and 313.78 ± 43.48 μm (P = 0.009) and mean RNFLTs were 78 ± 15.36 μm vs 95.78 ± 10.81 μm (P = 0.008) in the APAC and contralateral eyes, respectively. RNFLT and BMO-MRW measurements had a strong positive correlation (R = 0.7436, P = 0.013). APAC eyes had a shorter axial length (21.85 ± 1.21 vs 22 ± 1.07, P = 0.042) and shallower anterior chamber depth (2.29 ± 0.21 vs 2.41 ± 0.12, P = 0.039) than contralateral eyes. IOP at presentation showed a strong negative correlation with both BMO-MRW (R = -0.7669, P = 0.009) and RNFLT measurements (R = -0.7723, P = 0.008). BMO-MRW and RNFLT measurements are significantly reduced 3 months after an APAC when compared to the contralateral eye. IOP at presentation may have an impact on the reduction of these parameters.

Lens coloboma secondary to neglected buphthalmos

A 36-year-old male presented with progressive diminution of vision OS for 3 months. He was a known case of bilateral congenital glaucoma who underwent trabeculectomy at 6 months and 5 years of age OD and OS respectively. Best corrected visual acuity was 6/24 OD and 1/60 OS. Slit lamp examination revealed bilateral Haab striae (Figure 1a) with lens subluxation OS evident by the scalloped border of the lens with broken zonules in the superonasal quadrant and lens coloboma in the inferonasal quadrant with the absence of zonules (Figure 1b,c,d). A posterior subcapsular cataract was also noted OS. Advanced glaucomatous optic nerve cupping was noted OU. An intraocular pressure of 10 mm Hg OD and 16 mm Hg OS was noted. Biometry documented an axial length of 26.30 mm OD and 28.75 mm OS with a keratometry of 42.50D/46.50D @20˚/110˚OD and 37.75D/40.00D @ 45˚/135˚OS. Ultrasound bio-microscopy depicted increased sphericity of the lens with broken zonules OS (Figure 1e).

COMPARATIVE ANALYSIS OF TONOMETRY METHODS

The principles of glaucoma diagnostics are based on the triad of symptoms -the excess of IOP over the tolerant level, changes in the visual field, primarily in the Bjerrum zone, and also on glaucomatous excavation of the optic nerve head. It should be recognized that the IOP level is the only proven risk factor for the progression of glaucomatous optic nerve atrophy and, at the same time, the only factor that we can influence. That is why the determination of IOP is of great importance in diagnosis and is the basis for evaluating the effectiveness of glaucoma treatment.Keywords: IOP (intraocular pressure), tonometry, glaucoma, primary open-angle glaucoma, glaucomatous optic neuropathy, tonometer, pneumotonometer