The Effect of Trabecular Aspiration on Intraocular Pressure, Medication and the Need for Further Glaucoma Surgery in Eyes with Pseudoexfoliation Glaucoma.

PURPOSE: To investigate whether trabecular aspiration (TA) has an effective medium-term intraocular pressure (IOP)-lowering and medication-saving effect in patients with pseudoexfoliation glaucoma (PEG). In addition, a subgroup analysis of patients with or without a previous trabeculectomy was performed. METHODS: Records of 290 consecutive eyes with PEG that underwent TA between 2006 and 2012 at the Department of Ophthalmology, Mainz, Germany, were retrospectively analyzed with a follow-up period of 3 years. The main outcomes were IOP and the need for further medical treatment. RESULTS: Of the 290 eyes with PEG that received TA, 167 eyes from 127 patients met the inclusion criteria. Among these eyes, 128 received TA and cataract surgery (Phaco-TA) without having had a trabeculectomy (group I) before, 29 had Phaco-TA after a previous trabeculectomy (group II) and 10 underwent stand-alone TA after a previous trabeculectomy (group III). In the whole cohort, the median IOP decreased immediately after TA and remained significantly lower compared to the baseline throughout the period of 36 months. Likewise, the median number of antiglaucoma drugs was reduced over the whole period. At the same time, in group I, the median IOP and the number of antiglaucoma drugs were reduced over 36 months. In contrast, in the post-trabeculectomy groups (group II and III), the median IOP and the number of antiglaucoma drugs could not be reduced. While most of the patients that received Phaco-TA with or without a previous trabeculectomy (group I and II) did not require further surgical intervention during the follow-up period, almost all patients receiving stand-alone TA after a previous trabeculectomy (group III) needed surgical therapy, most of them between the second and the third year following TA. CONCLUSIONS: Phaco-TA has an effective medium-term pressure-lowering and medication-saving effect, especially in patients without a previous trabeculectomy. In trabeculectomized eyes, the effect of TA is limited but still large enough to delay more invasive surgical interventions in some patients.

Pathological high intraocular pressure induces glial cell reactive proliferation contributing to neuroinflammation of the blood-retinal barrier via the NOX2/ET-1 axis-controlled ERK1/2 pathway.

BACKGROUND: NADPH oxidase (NOX), a primary source of endothelial reactive oxygen species (ROS), is considered a key event in disrupting the integrity of the blood-retinal barrier. Abnormalities in neurovascular-coupled immune signaling herald the loss of ganglion cells in glaucoma. Persistent microglia-driven inflammation and cellular innate immune system dysregulation often lead to deteriorating retinal degeneration. However, the crosstalk between NOX and the retinal immune environment remains unresolved. Here, we investigate the interaction between oxidative stress and neuroinflammation in glaucoma by genetic defects of NOX2 or its regulation via gp91ds-tat. METHODS: Ex vivo cultures of retinal explants from wildtype C57BL/6J and Nox2 -/- mice were subjected to normal and high hydrostatic pressure (Pressure 60 mmHg) for 24 h. In vivo, high intraocular pressure (H-IOP) was induced in C57BL/6J mice for two weeks. Both Pressure 60 mmHg retinas and H-IOP mice were treated with either gp91ds-tat (a NOX2-specific inhibitor). Proteomic analysis was performed on control, H-IOP, and treatment with gp91ds-tat retinas to identify differentially expressed proteins (DEPs). The study also evaluated various glaucoma phenotypes, including IOP, retinal ganglion cell (RGC) functionality, and optic nerve (ON) degeneration. The superoxide (O2-) levels assay, blood-retinal barrier degradation, gliosis, neuroinflammation, enzyme-linked immunosorbent assay (ELISA), western blotting, and quantitative PCR were performed in this study. RESULTS: We found that NOX2-specific deletion or activity inhibition effectively attenuated retinal oxidative stress, immune dysregulation, the internal blood-retinal barrier (iBRB) injury, neurovascular unit (NVU) dysfunction, RGC loss, and ON axonal degeneration following H-IOP. Mechanistically, we unveiled for the first time that NOX2-dependent ROS-driven pro-inflammatory signaling, where NOX2/ROS induces endothelium-derived endothelin-1 (ET-1) overexpression, which activates the ERK1/2 signaling pathway and mediates the shift of microglia activation to a pro-inflammatory M1 phenotype, thereby triggering a neuroinflammatory outburst. CONCLUSIONS: Collectively, we demonstrate for the first time that NOX2 deletion or gp91ds-tat inhibition attenuates iBRB injury and NVU dysfunction to rescue glaucomatous RGC loss and ON axon degeneration, which is associated with inhibition of the ET-1/ERK1/2-transduced shift of microglial cell activation toward a pro-inflammatory M1 phenotype, highlighting NOX2 as a potential target for novel neuroprotective therapies in glaucoma management.

The Impact of Aging on the Function of Retinal Ganglion Cells.

Aging is a major risk factor for retinal neurodegenerative diseases. Aged mammalian retinal ganglion cells (RGCs) lack the ability to regenerate axons after injury. Rodent models suggest that older age increases the vulnerability of RGCs to injury and impairs RGC function as well as their functional recovery. Molecular changes - including decreased circulating levels of brain-derived neurotrophic factor (BDNF) - might contribute to impaired RGC dendritic extension during aging. Moreover, age-related mitochondrial dysfunction plays a major role in aging processes, as it leads to reduced adenosine triphosphate and increased generation of reactive oxygen species. Autophagy activity is necessary for the maintenance of cellular homeostasis and decreases with aging in the central nervous system. During aging, vascular insufficiency may lead to impaired oxygen and nutrient supply to RGCs. Microglial cells undergo morphological changes and functional impairment with aging, which might compromise retinal homeostasis and promote an inflammatory environment. Addressing these age-related changes by means of a low-energy diet, exercise, and neurotrophic factors might prevent age-related functional impairment of RGCs. This review focuses on the current understanding of aging RGCs and key players modulating those underlying mechanisms.

Mid-term real world outcomes of the Hydrus® Microstent in open angle glaucoma.

PURPOSE: To evaluate the mid-term clinical results and the safety aspects of the Hydrus® Microstent (Ivantis, Inc, Irvine, CA) in a real-life setting. DESIGN: Retrospective case series. METHODS: Hydrus® Microstent was implanted in phakic eyes (88 eyes, 87.1%) and in pseudophakic eyes (13 eyes, 12.9%), respectively. Mean follow-up time was 16 ± 9 months with 27 eyes having a follow-up time of more than 24 months. MAIN OUTCOME MEASURES: The primary endpoint was reduction in IOP compared to baseline. Target IOP levels were set at ≤20 mmHg, ≤18 mmHg and ≤15 mmHg. Kaplan-Meier survival was defined as a reduction in IOP of ≥20% compared to baseline. Secondary endpoints were reduction in number of glaucoma medications and safety assessments addressing visual acuity, adverse events, re-surgery rate and identification of factors that made the implantation more difficult. RESULT: 101 eyes underwent Hydrus® implantation. The mean preoperative IOP was 21.60 mmHg (SD 6.6) on 2.18 (SD 1.3) medications. After a mean follow up time of 16 months, the mean IOP was reduced to 14.61 ± 3.7 mmHg on 1.12 (SD 1.1) medication classes (p < 0.001). Mean decrease in IOP was 26.7%. Analysis of the target IOP levels showed that in 29%, 34% and 35% of cases an IOP of ≤15 mmHg, ≤18 mmHg and ≤20 mmHg respectively could be achieved. BCVA improved from 0.56 ± 0.3 at baseline to 0.85 ± 0.3 more than 24 months after surgery (p < 0.001). The rate of re-operation was low at <3%. Adverse events occurred in 4 eyes (<4%). CONCLUSION: This study underlines the effectiveness and the safety of the Hydrus® Microstent in an elective setting, but it also demonstrates certain limits and risk factors of this procedure.

Cytokine Profiling in Aqueous Humor of Glaucoma Patients and in Retinas from an Ex Vivo Glaucoma Animal Model.

BACKGROUND: Although the current role of cytokines and neuroinflammation in glaucoma remains obscure, it represents an expanding field in research. The purpose of this study was to analyze cytokines in the aqueous humor (AH) of glaucoma patients and in retinas from an ex vivo glaucoma animal model, to aid in determining the role of neuroinflammation in glaucoma. METHODS: AH samples were collected from 20 patients during cataract surgeries (controls: n = 10, age = 70.3 ± 9.742; glaucoma: n = 10, age: 66.5 ± 8.073) in Shanghai East Hospital, an affiliate of Tongji University, between September 2018 and March 2019 and analyzed in duplicate by Luminex cytokine polystyrene color bead-based multiplex assay. Retinas from female Sprague-Dawley rats (n = 6) were harvested ex vivo and cultured with or without 60 mmHg of hydrostatic pressure for 24 hours. Retinal ganglion cells (RGCs) were quantified using Brn3a staining. Cytokines in the retina and culture medium were analyzed by rat cytokine array (Abcam). RESULTS: At baseline, patients with primary angle closure glaucoma (PACG) have significantly lower levels of IL-6 and IP-10 and a higher level of PDGF-BB in their AH, compared to the controls. Postoperatively, patients with PACG have significantly higher levels of IL-1ra, IL-13, and MIP-1α and a lower level of IL-6. Elevated hydrostatic pressure led to significant RGC loss in the retina, ex vivo, as well as the upregulation of ciliary neurotrophic factor (CNTF), IL-6, IL-10, IL-4, and TIMP-1 alongside the downregulation of PDGF-AA, MMP-8, TNF-α, and IFN-γ. Furthermore, eight cytokines were detected as being downregulated in the culture medium, including PDGF-AA, MMP-8, and IL-4. CONCLUSIONS: Proinflammatory cytokines showed changes in both AH and ex vivo. Further studies are needed on the role of these cytokines and their corresponding signaling pathways in both neurodegeneration and glaucoma.

European Glaucoma Society research priorities for glaucoma care.

BACKGROUND/AIMS: The goal of health research is to improve patients care and outcomes. Thus, it is essential that research addresses questions that are important to patients and clinicians. The aim of this study was to develop a list of priorities for glaucoma research involving stakeholders from different countries in Europe. METHODS: We used a three-phase method, including a two-round electronic Delphi survey and a workshop. The clinician and patient electronic surveys were conducted in parallel and independently. For phase I, the survey was distributed to patients from 27 European countries in 6 different languages, and to European Glaucoma Society members, ophthalmologists with expertise in glaucoma care, asking to name up to five research priorities. During phase II, participants were asked to rank the questions identified in phase I using a Likert scale. Phase III was a 1 day workshop with patients and clinicians. The purpose was to make decisions about the 10 most important research priorities using the top 20 priorities identified by patients and clinicians. RESULTS: In phase I, 308 patients and 150 clinicians were involved. In phase II, the highest-ranking priority for both patients and clinicians was 'treatments to restore vision'. In phase III, eight patients and four clinicians were involved. The top three priorities were 'treatments to stop sight loss', 'treatments to restore vision' and 'improved detection of worsening glaucoma'. CONCLUSION: We have developed a list of priorities for glaucoma research involving clinicians and patients from different European countries that will help guide research efforts and investment.

The Association between Vascular Abnormalities and Glaucoma-What Comes First?

Glaucoma is a leading cause of irreversible blindness worldwide. While intraocular pressure (IOP) presents a major risk factor, the underlying pathophysiology still remains largely unclear. The correlation between vascular abnormalities and glaucoma has been deliberated for decades. Evidence for a role played by vascular factors in the pathogenesis of glaucomatous neurodegeneration has already been postulated. In addition, the fact that glaucoma causes both structural and functional changes to retinal blood vessels has been described. This review aims to investigate the published evidence concerning the relationship between vascular abnormalities and glaucoma, and to provide an overview of the "chicken or egg" dilemma in glaucoma. In this study, several biomarkers of glaucoma progression from a vascular perspective, including endothelin-1 (ET-1), nitric oxide, vascular endothelial growth factor (VEGF), and matrix metalloproteinases (MMPs), were identified and subsequently assessed for their potential as pharmacological intervention targets.

Efficacy of citicoline as a supplement in glaucoma patients: A systematic review.

PURPOSE: Glaucoma is a leading cause of irreversible blindness worldwide. Retinal ganglion cells (RGC), the neurons that connect the eyes to the brain, specifically die in glaucoma, leading to blindness. Elevated intraocular pressure (IOP) is the only modifiable risk factor, however, many patients progress despite excellent IOP control. Thus, alternative treatment strategies to prevent glaucoma progression are an unmet need. Citicoline has demonstrated neuroprotective properties in central neurodegenerative diseases. However, conclusive evidence of the effect of citicoline on glaucoma progression is missing. This systematic review investigates first-time the therapeutic potential of citicoline in glaucoma patients. METHODS: The present study was conducted according to the PRISMA 2020 statement. PubMed, Web of Science, Google Scholar, and Embase were accessed in July 2023 to identify all clinical studies investigating the efficacy of citicoline on IOP, the mean deviation of the 24-2 visual field testing (MD 24-2), retinal nerve fibre layer (RNFL), and the pattern electroretinogram (PERG) P50-N95 amplitude in glaucoma patients. The risk of bias was assessed using the Review Manager 5.3 software (The Nordic Cochrane Collaboration, Copenhagen) and the Risk of Bias in Non-randomised Studies of Interventions (ROBINS-I) tool. RESULTS: Ten studies were eligible for this systematic review, including 424 patients. The mean length of the follow-up was 12.1 ± 11.6 months. The overall risk of bias was low to moderate. The mean age of the patients was 56.7 years. There were no significant differences in the IOP, MD 24-2, RNFL, or PERG P50-N95 amplitude between patients receiving citicoline and the control group. There was no improvement from baseline to the last follow-up in IOP, MD 24-2, RNFL, or PERG P50-N95 amplitude. CONCLUSION: There is a lack of sufficient evidence to support that citicoline slows the progression of glaucoma.

[Comparison of new and old procedures in glaucoma surgery : Trabeculectomy, Preserflo and XEN]. / Neue und alte Verfahren der Glaukomchirurgie im Vergleich : Trabekulektomie, PreserFlo und XEN.

Glaucoma is one of the most frequent causes of irreversible blindness worldwide. The main risk factor of the disease is an individually too high intraocular pressure and pressure reduction is still the only established treatment. If conservative pressure reduction and adherence are insufficient, and if the patient is unable to tolerate conservative treatment, surgical procedures become necessary. There are nowadays more than a dozen different surgical procedures for lowering the pressure. This article presents and discusses the procedures that have a subconjunctival pre-equatorial drainage in common. These include trabeculectomy, the XEN-gel implant and the Preserflo microshunt.

Long-Term Efficacy and Safety of Modified Canaloplasty Versus Trabeculectomy in Open-Angle Glaucoma.

BACKGROUND: To evaluate the long-term efficacy and safety of modified canaloplasty versus trabeculectomy in open-angle glaucoma. METHODS: In total, 210 subjects with open-angle glaucoma were included. 70 were treated with Mitomycin C-augmented modified canaloplasty with enhanced subconjunctival filtration and 140 with Mitomycin C-augmented trabeculectomy. Cases were matched 1:2 by sex and age. RESULTS: In canaloplasty and trabeculectomy groups, 61.4% and 57.9% of participants were female. Mean age was 60.0 ± 13.9 and 63.0 ± 12.2 years, median follow-up time was 4.6 [IQR 4.3, 5.05] years and 5.8 [IQR 5.4, 6.3]. Strict success was achieved in 20.0% and 56.4%, complete success in 24.3% and 66.4%, and qualified success in 34.3% and 73.6% (each p < 0.001). Kaplan-Meier survival analysis showed a better survival probability for trabeculectomy than for canaloplasty (p < 0.001) and Cox regression analysis revealed an HR of 6.03 (95%-CI 3.66, 9.93, p < 0.001) after canaloplasty. Trabeculectomy showed superiority in terms of IOP decrease (9.2 ± 7.9 mmHg vs. 13.7 ± 10.4 mmHg, p = 0.002), use of AGM (50.0% vs. 10.7%, p < 0.001), and the number of revision surgeries (41.4% vs. 21.4%, p = 0.004). Occurrence of complications was similar in both groups (14.5% vs. 7.5%, p = 0.19). CONCLUSIONS: Trabeculectomy showed superiority in efficacy and equality in safety compared to modified canaloplasty.

The novel role of lymphatic vessels in the pathogenesis of ocular diseases.

Historically, the eye has been considered as an organ free of lymphatic vessels. In recent years, however, it became evident, that lymphatic vessels or lymphatic-like vessels contribute to several ocular pathologies at various peri- and intraocular locations. The aim of this review is to outline the pathogenetic role of ocular lymphatics, the respective molecular mechanisms and to discuss current and future therapeutic options based thereon. We will give an overview on the vascular anatomy of the healthy ocular surface and the molecular mechanisms contributing to corneal (lymph)angiogenic privilege. In addition, we present (i) current insights into the cellular and molecular mechanisms occurring during pathological neovascularization of the cornea triggered e.g. by inflammation or trauma, (ii) the role of lymphatic vessels in different ocular surface pathologies such as dry eye disease, corneal graft rejection, ocular graft versus host disease, allergy, and pterygium, (iii) the involvement of lymphatic vessels in ocular tumors and metastasis, and (iv) the novel role of the lymphatic-like structure of Schlemm's canal in glaucoma. Identification of the underlying molecular mechanisms and of novel modulators of lymphangiogenesis will contribute to the development of new therapeutic targets for the treatment of ocular diseases associated with pathological lymphangiogenesis in the future. The preclinical data presented here outline novel therapeutic concepts for promoting transplant survival, inhibiting metastasis of ocular tumors, reducing inflammation of the ocular surface, and treating glaucoma. Initial data from clinical trials suggest first success of novel treatment strategies to promote transplant survival based on pretransplant corneal lymphangioregression.

Glaucoma as a Neurodegenerative and Inflammatory Disease.

Glaucoma is a neurodegenerative disease that leads to irreversible loss of vision through degeneration of the retinal ganglia cells (RGCs). Glaucoma is one of the most frequent causes of blindness in the world. Intraocular pressure is the main risk factor for the occurrence and development of this disease. Treatment is largely based on reducing internal optical pressure. However, some patients may deteriorate or become blind, despite normal or reduced internal optical pressure. The pathophysiological details are still unclear. Neuroinflammatory processes are also apparently an additional cause. In principle, innate or local responses of the adaptive immune system can be distinguished. The reaction of the innate immune system, particularly the local microglial cells, has long been studied. The macroglia with the astrocytes and Müller cells and their homeostatic effects have also long been known. On the other hand, it has long been thought that the retina with its RGZs was inert to adaptive immunological reactions - due to the function of the blood brain barrier. However, this system may be disturbed by antigen presentation, leading to a reaction of the adaptive immune system, with B cell and T cell responses. In this context, the key proteins are presumably heat shock proteins. We now know that neuroinflammation is important in glaucoma, as in other neurodegenerative diseases. It is important to increase our understanding of these phenomena. In this review article, we present our current knowledge of the role of the micro- and macroglia, the adaptive immune system, and the heat shock proteins.

Intraocular Pressure-Induced Endothelial Dysfunction of Retinal Blood Vessels Is Persistent, but Does Not Trigger Retinal Ganglion Cell Loss.

Research has been conducted into vascular abnormalities in the pathogenesis of glaucoma, but conclusions remain controversial. Our aim was to test the hypothesis that retinal endothelial dysfunction induced by elevated intraocular pressure (IOP) persists after IOP normalization, further triggering retinal ganglion cell (RGC) loss. High intraocular pressure (HP) was induced in mice by episcleral vein occlusion (EVO). Retinal vascular function was measured via video microscopy in vitro. The IOP, RGC and their axons survival, levels of oxidative stress and inflammation as well as vascular pericytes coverage, were determined. EVO caused HP for two weeks, which returned to baseline afterwards. Mice with HP exhibited endothelial dysfunction in retinal arterioles, reduced density of RGC and their axons, and loss of pericytes in retinal arterioles. Notably, these values were similar to those of mice with recovered IOP (RP). Levels of oxidative stress and inflammation were increased in HP mice but went back to normal in the RP mice. Our data demonstrate that HP induces persistent endothelial dysfunction in retinal arterioles, which persists one month after RP. Oxidative stress, inflammation, and loss of pericytes appear to be involved in triggering vascular functional deficits. Our data also suggest that retinal endothelial dysfunction does not affect RGC and their axon survival.

Crystallins Play a Crucial Role in Glaucoma and Promote Neuronal Cell Survival in an In Vitro Model Through Modulating Müller Cell Secretion.

Purpose: The aim of this study was to explore the roles of crystallins in the context of aging in glaucoma and potential mechanisms of neuroprotection in an experimental animal model of glaucoma. Methods: Intraocular pressure (IOP) was significantly elevated for 8 weeks in animals at different ages (10 days, 12 weeks, and 44 weeks) by episcleral vein cauterization. Retinal ganglion cells (RGCs) were quantified by anti-Brn3a immunohistochemical staining (IHC). Proteomics using ESI-LTQ Orbitrap XL-MS was used to analyze the presence and abundance of crystallin isoforms the retinal samples, respectively. Neuroprotective property and localization of three selected crystallins CRYAB, CRYBB2, and CRYGB as most significantly changed in retina and retinal layers were determined by IHC. Their expressions and endocytic uptakes into Müller cells were analyzed by IHC and Western blotting. Müller cell secretion of neurotrophic factors into the supernatant following CRYAB, CRYBB2, and CRYGB supplementation in vitro was measured via microarray. Results: IOP elevation resulted in significant RGC loss in all age groups (P < 0.001). The loss increased with aging. Proteomics analysis revealed in parallel a significant decrease of crystallin abundance - especially CRYAB, CRYBB2, and CRYGB. Significant neuroprotective effects of CRYAB, CRYBB2, and CRYGB after addition to retinal cultures were demonstrated (P < 0.001). Endocytic uptake of CRYAB, CRYBB2, and CRYGB was seen in Müller cells with subsequent increased secretion of various neurotrophic factors into the supernatant, including nerve growth factor, clusterin, and matrix metallopeptidase 9. Conclusions: An age-dependent decrease in CRYAB, CRYBB2, and CRYGB abundance is found going along with increased RGC loss. Addition of CRYAB, CRYBB2, and CRYGB to culture protected RGCs in vitro. CRYAB, CRYBB2, and CRYGB were uptaken into Müller cells. Secretion of neurotrophic factors was increased as a potential mode of action.

Aqueous Humor Cytokine Response in the Contralateral Eye after First-Eye Cataract Surgery in Patients with Primary Angle-Closure Glaucoma, High Myopia or Type 2 Diabetes Mellitus.

BACKGROUND: Bilateral sequential cataract surgery within a short period is becoming more prevalent because of the efficiency and safety of modern cataract surgery. It has been reported that the first surgical eye might affect the contralateral eye. This study investigated the cytokines involved in the immunopathogenesis of pre-existing ocular or systemic conditions, as well as the inflammatory biomarkers in response to topical stimuli, by analyzing the cytokine profile of aqueous humor (AH) from cataract patients without these morbidities as control and with type 2 diabetes mellitus (DM), primary angle-closure glaucoma (PACG) or high myopia (HM) in each eye at the beginning of first (defined as baseline) and second eye cataract surgery. METHODS: Forty patients were recruited in this cohort study (10/group). Bilateral sequential cataract surgeries were conducted at intervals of 12.08 ± 1.2 days. Aqueous humor samples (100-200 µL/eye) were separately collected from 40 first-eyes and 40 second-eyes at the beginning of the cataract surgeries. Twenty-seven selected cytokines were detected with Luminex-multiplex immunoassay. The concentrations of cytokines in the aqueous humor and their association with pre-existing ocular or systemic conditions were analyzed and compared between and within the groups. RESULTS: Before first-eye surgery (baseline), the levels of interleukin (IL)-1ra, IL-13 and tumor necrosis factor (TNF)-alpha were significantly increased in PACG compared with controls. The levels of IL-13 were increased while that of IL-15 were decreased in HM. Compared with controls, 11 cytokines were significantly increased in DM. In the AH of the contralateral eye after first-eye cataract surgery, basic fibroblast growth factor (bFGF) was significantly more abundant in PACG and HM, while the levels of monocyte chemoattractant protein-1 (MCP-1) and interferon gamma-induced protein 10 (IP-10) were decreased in PACG. We also identified 6 significantly upregulated cytokines in DM compared with controls. Compared with baseline, there was an overlap of 5 altered cytokines in the AH of contralateral eyes after first-eye surgery between the four groups. Some were exclusively altered in each subgroup, with 1 in the control group, 4 cytokines in the PACG and HM groups, and none in the DM group. CONCLUSIONS: From the initial profile, it is observed that patients with pre-existing ocular or systemic conditions have some degree of inflammation in their eyes before surgery and in the contralateral eye after the first eye cataract surgery, which could be peculiar of the morbid conditions of the patients. Inflammation was more detectable in patients with type 2 DM before surgery. PACG and HM patients showed stronger intraocular inflammatory reactions to topical stimuli compared with controls and DM patients. Our data suggest that ophthalmologists should pay closer attention to inflammatory responses, especially in cataract patients with pre-existing conditions, although the clinical significance of these changes following surgery remains to be further investigated.

[Regeneration of the optic nerve-Will it one day be reality?] / Regeneration des Sehnerven ­ Wird das einmal Realität?

BACKGROUND: Adult mammalian and human neurons of the central nervous system (CNS) lack the ability to spontaneously regenerate damaged axons. This dilemma of many CNS diseases is still an unsolved problem. OBJECTIVE: The purpose of this article is to examine the question which options have been investigated in more detail in recent years and offer approaches. METHODS: A web-based search of all articles published between 1958 to the present regarding regeneration of retinal ganglion cells was carried out. RESULTS: Over the last three decades it has been shown that axonal regeneration is possible under certain conditions when intrinsic and extrinsic factors are manipulated in retinal ganglion cells and in the optic nerve. Although there is still a long way to go, experimental regenerative approaches are already visible; however, it will take several years or decades before these can be approximately implemented in practice.