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Previous concepts for the pathogenesis of proliferative vitreoretinopathy (PVR) have focused on the central role of retinal pigment epithelium cells only, potentially contributing to the lack of clinical advances. More recent studies have demonstrated the essential role of retinal glial cells in the PVR healing response but failed to identify a consistent triggering mechanism.We propose a revised concept for the pathogenesis of PVR based on retinal injury and response. A posterior vitreous detachment (PVD) is invariably present in patients with rhegmatogenous retinal detachment and PVR. There is evidence to suggest that the shearing forces of acute PVD can cause mechanical injury to the inner retina and trigger a subsequent intraretinal glial healing response. That response is characterised by subclinical glial cell activation and proliferation that may then be amplified into full-blown PVR by coexisting pathology such as retinal breaks and detachment.Whether a PVD causes interface pathology depends on the plane of separation of the posterior vitreous and areas of increased vitreoretinal adhesions. If the vitreous separates in a plane or location that damages the inner retina then glial cell activation and proliferation are likely to develop. The severity of the subclinical inner retinal damage may then represent one of the missing links in our understanding of the pathogenesis of PVR and would explain many of the findings we encounter in clinical practice. Controlling the process of acute PVD and subsequent intraretinal response may be essential in the prevention and management of PVR., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. No commercial re-use. See rights and permissions. Published by BMJ.)

Competing Interests: The authors declare that they have no conflict of interest.

Mild traumatic brain injury (mTBI) is common with many patients suffering disabling long-term sequelae, with visual symptoms frequently reported. There are no objective biomarkers of mTBI that are routinely used in clinical practice. Optical coherence tomography (OCT) has been used in mTBI research, as it enables visualisation of the neuroretina, allowing measurement of the retinal nerve fibre layer and ganglion cell layer. This systematic review aims to appraise the available literature and assess whether there are significant changes within the retinal nerve fibre layer and ganglion cell layer in subjects after mTBI. A systematic review was carried out in accordance with PRISMA guidelines and registered with PROSPERO (Number: CRD42022360498). Four databases were searched for relevant literature published from inception until 1 September 2022. Abstracts and full texts were screened by three independent reviewers. Initial screening of databases yielded 341 publications, of these, three fulfilled all the criteria for inclusion. All three studies showed thinning of the retinal nerve fibre layer, whereas there were no significant changes in the ganglion cell layer. This systematic review demonstrated that thinning of the retinal nerve fibre layer (but not of the ganglion cell layer) is associated with mTBI. It provides preliminary evidence for the use of the retinal nerve fibre layer as a potential biomarker of damage to the visual system in mTBI. Further prospective longitudinal studies ensuring uniform diagnosis and accurate phenotyping of mTBI are needed to understand the effects on the visual system and potential of OCT as a prognostic biomarker., (© 2024. Crown.)

Purpose: To report a case of a full-thickness macular hole after exposure to an extremely powerful handheld laser pointer., Methods: A 14-year-old boy with a laser-induced full-thickness macular hole was evaluated 1 month after a momentary exposure to a 5,000 mW blue laser pointer. Imaging modalities including fundus color, autofluorescence, and spectral-domain optical coherence tomography, acquired both at our clinic and by the referring physician soon after the injury, are used to describe the clinical evolution of the case., Results: Soon after the injury, an intensely white, circular opacification of the retina approximately 400 μm in diameter was seen in the fovea. Early spectral-domain optical coherence tomography images showed full-thickness hyperreflectivity, likely representing tissue necrosis. One month later, a full-thickness macular hole and eradication of the retinal pigment epithelium at its base were evident in the fundus color, autofluorescence, and spectral-domain optical coherence tomography images., Conclusion: High-power laser pointers have become easily available online. The presenting findings after exposure to such high-power devices are distinct from those reported after exposure to weaker laser pointers. Although long exposure to weaker lasers typically produces extensive, calligraphic figures and yellow placoid lesions involving only the outer retina, in our case, a very brief exposure led to focal full-thickness injury of the fovea.

Purpose: Zebrafish, a small fish model, exhibits a multipotent ability for retinal regeneration after damage throughout its lifetime. Compared with zebrafish, birds and mammals exhibit such a regenerative capacity only during the embryonic period, and this capacity decreases with age. In medaka, another small fish model that has also been used extensively in biological research, the retina's inner nuclear layer (INL) failed to regenerate after injury in the hatchling at eight days postfertilization (dpf). We characterized the regenerative process of the embryonic retina when the retinal injury occurred during the early embryonic period in medaka., Methods: We employed a 10 Gy dose of gamma-ray irradiation to initiate retinal injury in medaka embryos at 3 dpf and performed histopathological analyses up to 21 dpf., Results: One day after irradiation, numerous apoptotic neurons were observed in the INL; however, these neurons were rarely observed in the ciliary marginal zone and the photoreceptor layer. Numerous pyknotic cells were clustered in the irradiated retina until two days after irradiation. These disappeared four days after irradiation, but the abnormal bridging structures between the INL and ganglion cell layer (GCL) were present until 11 days after irradiation, and the neural layers were completely regenerated 18 days after irradiation. After gamma-ray irradiation, the spindle-like Müller glial cells in the INL became rounder but did not lose their ability to express SOX2., Conclusions: Irradiated retina at 3 dpf of medaka embryos could be completely regenerated at 18 days after irradiation (21 dpf), although the abnormal layer structures bridging the INL and GCL were transiently formed in the retinas of all the irradiated embryos. Four days after irradiation, embryonic medaka Müller glia were reduced in number but maintained SOX2 expression as in nonirradiated embryos. This finding contrasts with previous reports that 8 dpf medaka larvae could not fully regenerate damaged retinas because of loss of SOX2 expression.

Non-neuronal cells are key to the complex cellular interplay that follows central nervous system insult. To understand this interplay, we generated a single-cell atlas of immune, glial and retinal pigment epithelial cells from adult mouse retina before and at multiple time points after axonal transection. We identified rare subsets in naive retina, including interferon (IFN)-response glia and border-associated macrophages, and delineated injury-induced changes in cell composition, expression programs and interactions. Computational analysis charted a three-phase multicellular inflammatory cascade after injury. In the early phase, retinal macroglia and microglia were reactivated, providing chemotactic signals concurrent with infiltration of CCR2 + monocytes from the circulation. These cells differentiated into macrophages in the intermediate phase, while an IFN-response program, likely driven by microglia-derived type I IFN, was activated across resident glia. The late phase indicated inflammatory resolution. Our findings provide a framework to decipher cellular circuitry, spatial relationships and molecular interactions following tissue injury., (© 2023. Springer Nature America, Inc.)

Competing Interests: None

Purpose: To compare the anatomical and functional outcomes of silicone oil (SO)-filled foldable capsular vitreous body (FCVB) and SO endotamponade in vitrectomy for patients with no light perception after ocular trauma., Methods: A total of 64 patients (64 eyes) with no light perception caused by severe ocular trauma were divided into FCVB and SO groups based on the surgical treatment. The main outcome measurements were retinal reattachment rate, intraocular pressure, best-corrected visual acuity, and number of operations., Results: Both the FCVB group (29 eyes) and the SO group (35 eyes) showed significant improvement in postoperative best-corrected visual acuity and intraocular pressure. The two groups showed no significant differences in final intraocular pressure and the retinal reattachment rate. The postoperative vision (≥LP) in the FCVB group was significantly worse than in the SO group (FCVB [4/29] vs. SO [18/35], P = 0.003). However, the number of surgeries in the FCVB group was significantly lower than in the SO group (FCVB [1.10] vs. SO [2.23], P < 0.001)., Conclusion: Vitrectomy combined with SO endotamponade shows better short-term improvement in the treatment of no light perception caused by severe ocular trauma. However, SO-filled FCVB can effectively prevent many complications caused by direct SO endotamponade, such as secondary surgeries or SO dependence.

With the widespread popularity of electronic products and the diversification of lighting equipment, ocular photochemical damage caused by light has attracted research attention. Although such equipment mainly cause damage to the retina, the specific pathogenesis has not been systematically elucidated. Thus, the goal of this study was to explore the relationship between mitochondrial dysfunction and the activation of the NOD-like receptor protein 3 (NLRP3) inflammasome in retinal cell death caused by light damage. We used a white light-emitting diode source to establish a mouse model of retinal light damage and observed significant changes of retinal structure and an impairment of visual function. Further experiments revealed that dynamin-related protein 1 (Drp1)-mediated excessive mitochondrial fission induced overproduction of reactive oxygen species in the retinal cells, leading to apoptosis, activation of microglia, and formation of the NLRP3 inflammasome. This, in turn, triggered a series of inflammatory cascade reactions, leading to pyroptosis. We also carried out red light and Drp1 inhibitor treatment and found that retinal damage and the decline in visual function caused by white light could be partially ameliorated. In conclusion, this study clarified the association between mitochondrial dynamics and the NLRP3 inflammasome in retinal light damage and provides opportunities for therapeutic intervention., (© 2021 New York Academy of Sciences.)

Arginase 1 (A1) is the enzyme that hydrolyzes the amino acid, L-arginine, to ornithine and urea. We have previously shown that A1 deletion worsens retinal ischemic injury, suggesting a protective role of A1. In this translational study, we aimed to study the utility of systemic pegylated A1 (PEG-A1, recombinant human arginase linked to polyethylene glycol) treatment in mouse models of acute retinal and brain injury. Cohorts of WT mice were subjected to retinal ischemia-reperfusion (IR) injury, traumatic optic neuropathy (TON) or brain cerebral ischemia via middle cerebral artery occlusion (MCAO) and treated with intraperitoneal injections of PEG-A1 or vehicle (PEG only). Drug penetration into retina and brain tissues was measured by western blotting and immunolabeling for PEG. Neuroprotection was measured in a blinded fashion by quantitation of NeuN (neuronal marker) immunolabeling of retina flat-mounts and brain infarct area using triphenyl tetrazolium chloride (TTC) staining. Furthermore, ex vivo retina explants and in vitro retina neuron cultures were subjected to oxygen-glucose deprivation (OGD) followed by reoxygenation (R) and treated with PEG-A1. PEG-A1 given systemically did not cross the intact blood-retina/brain barriers in sham controls but reached the retina and brain after injury. PEG-A1 provided neuroprotection after retinal IR injury, TON and cerebral ischemia. PEG-A1 treatment was also neuroprotective in retina explants subjected to OGD/R but did not improve survival in retinal neuronal cultures exposed to OGD/R. In summary, systemic PEG-A1 administration is neuroprotective and provides an excellent route to deliver the drug to the retina and the brain after acute injury., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Ghrelin has anti-inflammatory, antioxidant, and antiapoptotic effects, and it may be beneficial for the treatment of many ophthalmic diseases, such as cataract, uveitis, and glaucoma. Our previous work proved that ghrelin pretreatment reduced the apoptosis of lens epithelial cells induced by hydrogen peroxide, reduced the accumulation of reactive oxygen species (ROS), and effectively maintained the transparency of lens tissue. However, no study has yet investigated the effect of ghrelin on retina. In this study, we conducted in vitro and in vivo experiments to explore the effect of ghrelin on high-glucose- (HG-) induced ARPE-19 cell damage and diabetic retinopathy in streptozotocin-induced diabetic rats. ARPE-19 cells were incubated in a normal or an HG (30 mM glucose) medium with or without ghrelin. Cell viability was measured by 3-(4, 5-dimethylthiazol-3-yl)-2,5-diphenyl tetrazolium bromide assay, and apoptosis was detected by the Hoechst-PI staining assay. Intracellular reactive oxygen species (ROS) production levels within cells were measured using 2',7'-dichlorofluorescein diacetate staining, and the contents of superoxide dismutase and malondialdehyde were measured using relevant detection kits. The expression levels of IL-1 β and IL-18 were measured using an enzyme-linked immunosorbent assay, and those of NLRP3, IL-1 β , and IL-18 were measured using Western blotting. The rat diabetes models were induced using a single intraperitoneal injection of streptozotocin (80 mg/kg). The morphological and histopathological changes in the retinal tissues were examined. The results indicated that ghrelin reduced ROS generation, inhibited cell apoptosis and the activation of NLRP3 inflammasome, inhibited the apoptosis of retinal cells in diabetic rats, and protected the retina against HG-induced dysfunction. In conclusion, ghrelin may play a role in the treatment of ocular diseases involving diabetic retinopathy., Competing Interests: The authors declare that they have no competing interests., (Copyright © 2021 Jie Bai et al.)

Mild traumatic brain injury (mTBI) is a major cause of morbidity and mortality with a poorly understood pathophysiology. Animal models have been increasingly utilized to better understand mTBI and recent research has identified visual deficits in these models that correspond to human literature. While visual impairment is being further characterized within TBI, the implications of impaired vision on behavioral tasks commonly utilized in animal models has not been well described thus far. Visual deficits may well confound behavioral tests that are believed to be isolated to cognitive functioning such as learning and memory. We utilized a mouse model of repetitive mTBI (rmTBI) to further characterize visual deficits using an optomotor task, electroretinogram, and visually evoked potential, and located likely areas of damage to the visual pathway. Mice were tested on multiple behavioral metrics, including a touchscreen conditional learning task to better identify the contribution of visual dysfunction to behavioral alterations. We found that rmTBI caused visual dysfunction resulting from damage distal to the retina that likely involves pathology within the optic nerve. Moreover, loss of vision led to poorer performance of rmTBI animals on classic behavioral tests such as the Morris water maze that would otherwise be attributed solely to learning and memory deficits. The touchscreen conditional learning task was able to differentiate rmTBI induced learning and memory dysfunction from visual impairment and is a valuable tool for elucidating subtle changes resulting from TBI.

Aquaporin-4 (AQP4) is the target of the specific immunoglobulin G autoantibody (AQP4-IgG) produced in patients with neuromyelitis optica spectrum disorders (NMOSD). Previous studies demonstrated that AQP4-IgG binding to astrocytic AQP4 leads to cell-destructive lesions. However, the early physiopathological events in Müller cells in the retina are poorly understood. Here, we investigated the consequences of AQP4-IgG binding to AQP4 of Müller cells, previous to the inflammatory response, on two of AQP4's key functions, cell volume regulation response (RVD) and cell proliferation, a process closely associated with changes in cell volume. Experiments were performed in a human retinal Müller cell line (MIO-M1) exposed to complement-inactivated sera from healthy volunteers or AQP4-IgG positive NMOSD patients. We evaluated AQP4 expression (immunofluorescence and western blot), water permeability coefficient, RVD, intracellular calcium levels and membrane potential changes during hypotonic shock (fluorescence videomicroscopy) and cell proliferation (cell count and BrdU incorporation). Our results showed that AQP4-IgG binding to AQP4 induces its partial internalization, leading to the decrease of the plasma membrane water permeability, a reduction of swelling-induced increase of intracellular calcium levels and the impairment of RVD in Müller cells. The loss of AQP4 from the plasma membrane induced by AQP4-IgG positive sera delayed Müller cells' proliferation rate. We propose that Müller cell dysfunction after AQP4 removal from the plasma membrane by AQP4-IgG binding could be a non-inflammatory mechanism of retinal injury in vivo, altering cell volume homeostasis and cell proliferation and consequently, contributing to the physiopathology of NMOSD., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Purpose: To describe "iris shelf" technique for removal of posterior segment intraocular foreign bodies (IOFBs) through a corneal incision combined with phacovitrectomy and to report its outcomes., Methods: Medical records of patients with posterior segment metallic IOFBs who had combined phacovitrectomy were collected and analyzed. In all patients, the IOFB was placed on the iris surface after forming the anterior chamber with viscoelastic to be extracted through a corneal phacoemulsification incision., Results: Thirty-three eyes of 33 male patients with a mean age of 31.6 ± 8.3 years were included in the study. The mechanism of injury was hammering in 24 eyes (72.7%) and gunshot in 9 eyes (27.3%). The mean interval between injury and IOFB removal was 14.76 ± 6 days. The mean IOFB volume was 8.5 ± 5.5 mm3, and its longest dimension was 3.45 mm (range, 1-8 mm). The mean preoperative corrected distance visual acuity changed from 20/1,500 (1.79 logarithm of the minimum angle of resolution) to 20/94 (0.67 logarithm of the minimum angle of resolution), postoperatively (P < 0.001). Postoperative complications included retinal detachment (two eyes), proliferative vitreoretinopathy (one eye), epiretinal membrane (one eye), and posterior synechiae (three eyes)., Conclusion: The "iris shelf" technique with phacovitrectomy is a safe and reproducible approach for posterior segment IOFB extraction through a corneal incision with favorable visual and anatomical outcomes.

Ischemia/reperfusion (I/R) events are involved in the pathophysiology of numerous ocular diseases. The purpose of this study was to test the hypothesis that betulinic acid protects from I/R injury in the mouse retina. Ocular ischemia was induced in mice by increasing intraocular pressure (IOP) to 110 mm Hg for 45 min, while the fellow eye served as a control. One group of mice received betulinic acid (50 mg/kg/day p.o. once daily) and the other group received the vehicle solution only. Eight days after the I/R event, the animals were killed and the retinal wholemounts and optic nerve cross-sections were prepared and stained with cresyl blue or toluidine blue, respectively, to count cells in the ganglion cell layer (GCL) of the retina and axons in the optic nerve. Retinal arteriole responses were measured in isolated retinas by video microscopy. The levels of reactive oxygen species (ROS) were assessed in retinal cryosections and redox gene expression was determined in isolated retinas by quantitative PCR. I/R markedly reduced cell number in the GCL and axon number in the optic nerve of the vehicle-treated mice. In contrast, only a negligible reduction in cell and axon number was observed following I/R in the betulinic acid-treated mice. Endothelial function was markedly reduced and ROS levels were increased in retinal arterioles of vehicle-exposed eyes following I/R, whereas betulinic acid partially prevented vascular endothelial dysfunction and ROS formation. Moreover, betulinic acid boosted mRNA expression for the antioxidant enzymes SOD3 and HO-1 following I/R. Our data provide evidence that betulinic acid protects from I/R injury in the mouse retina. Improvement of vascular endothelial function and the reduction in ROS levels appear to contribute to the neuroprotective effect.

Purpose/Aim : To investigate the risk of laser damage to the unprotected fellow eye of patients undergoing laser retinal photocoagulation with 532 nm diode pumped solid-state laser. Materials and Methods : A mannequin head was fitted with a Vega laser energy meter and PD10 photodiode laser measurement sensor. Lowest measurable energy for this sensor is 2 nJ at 900 nm. Simulated retinal laser treatments were performed on a model eye placed in one of the sockets of the mannequin head, while the laser sensor was placed in the opposite socket. Four simulated sessions of retinal photocoagulation were performed utilizing both slit lamp and indirect laser delivery systems. Each consisted of 10 applications of the laser directly into the model eye and 10 applications near but not directly into the sensor, utilizing various treatment settings. Results : No laser exposure was detected in the model eye during simulated retinal photocoagulation sessions aimed directly into the treatment eye. When the laser application was aimed near the sensor, no laser exposure was detected at the standard setting, however, in all sessions conducted at the higher laser power setting, the mean exposure detected was <6 µJ Conclusions : Laser exposure in the unprotected contralateral eye of patients undergoing retinal laser treatment with the PASCAL laser machine under standard PRP settings was found to be miniscule. However, we still recommend laser safety eyewear for the untreated eye to provide protection in the event of direct accidental laser exposure from surgeon error or laser malfunction, in accordance with the most current laser safety guidelines.

Purpose: To describe the clinical characteristics, surgical outcomes, and management recommendations in patients with traumatic rhegmatogenous retinal detachment (RRD) resulting from self-injurious behavior (SIB)., Design: International, multicenter, retrospective, interventional case series., Participants: Patients with SIB from 23 centers with RRD in at least 1 eye., Methods: Clinical histories, preoperative assessment, surgical details, postoperative management, behavioral intervention, and follow-up examination findings were reviewed., Main Outcome Measures: The rate of single-surgery anatomic success (SSAS) was the primary outcome. Other outcomes included new RRD in formerly attached eyes, final retinal reattachment, and final visual acuity., Results: One hundred seven eyes with RRDs were included from 78 patients. Fifty-four percent of patients had bilateral RRD or phthisis bulbi in the fellow eye at final follow-up. The most common systemic diagnoses were autism spectrum disorder (35.9%) and trisomy 21 (21.8%) and the most common behavior was face hitting (74.4%). The average follow-up time was 3.3 ± 2.8 years, and surgical outcomes for operable eyes were restricted to patients with at least 3 months of follow-up (81 eyes). Primary initial surgeries were vitrectomy alone (33.3%), primary scleral buckle (SB; 26.9%), and vitrectomy with SB (39.7%), and 5 prophylactic SBs were placed. Twenty-three eyes (21.5%) with RRDs were inoperable. The SSAS was 23.1% without tamponade (37.2% if including silicone oil), and final reattachment was attained in 80% (36.3% without silicone oil tamponade). Funnel-configured RRD (P = 0.006) and the presence of grade C proliferative vitreoretinopathy (P = 0.002) correlated with re-detachment. The use of an SB predicted the final attachment rate during the initial surgery (P = 0.005) or at any surgery (P = 0.008. These associations held if restricting to 64 patients with ≥12 months followup. Anatomic reattachment correlated with better visual acuity (P < 0.001)., Conclusions: RRD resulting from SIB poses therapeutic challenges because of limited patient cooperation, bilateral involvement, chronicity, and ongoing trauma in vulnerable and neglected patients. The surgical success rates were some of the lowest in the modern retinal detachment literature. The use of an SB may result in better outcomes, and visual function can be restored in some patients., (Copyright © 2020 American Academy of Ophthalmology. Published by Elsevier Inc. All rights reserved.)

Neuroinflammation has been put forward as a mechanism triggering axonal regrowth in the mammalian central nervous system (CNS), yet little is known about the underlying cellular and molecular players connecting these two processes. In this study, we provide evidence that MMP2 is an essential factor linking inflammation to axonal regeneration by using an in vivo mouse model of inflammation-induced axonal regeneration in the optic nerve. We show that infiltrating myeloid cells abundantly express MMP2 and that MMP2 deficiency results in reduced long-distance axonal regeneration. However, this phenotype can be rescued by restoring MMP2 expression in myeloid cells via a heterologous bone marrow transplantation. Furthermore, while MMP2 deficiency does not affect the number of infiltrating myeloid cells, it does determine the coordinated expression of pro- and anti-inflammatory molecules. Altogether, in addition to its role in axonal regeneration via resolution of the glial scar, here, we reveal a new mechanism via which MMP2 facilitates axonal regeneration, namely orchestrating the expression of pro- and anti-inflammatory molecules by infiltrating innate immune cells.

Purpose: To present a case of visually significant retinal injury due to internal limiting membrane (ILM) peeling using ILM forceps alone., Methods: Case report., Results: A 60-year-old woman who underwent ILM peeling for an epiretinal membrane presented with linear central scotomata. Peeling had been initiated and performed with ILM forceps alone, without the use of other surgical instruments. Fundus examination and spectral domain optical coherence tomography imaging confirmed the presence of several discrete areas of inner and outer retinal injury in the macula, which corresponded to her scotomata., Conclusion: This is a case of visually significant retinal injury due to ILM peeling that was performed with ILM forceps alone. Improper peeling technique can transmit injurious forces to the retina. Surgeons must be mindful of the biomechanical forces involved in ILM peeling to minimize traction on the retina.

Background: Stem cell transplantation has been reported as one of the promising strategies to treat retinal degenerative diseases. But, the application and the role of retina stem cells (RSCs) in the treatment of patients with retinal degenerative diseases have not been fully revealed. This study aimed to investigate the potential role of transplantation of the embryo-derived RSCs into the vitreous cavity in repairing the damaged retina in mice., Methods: RSCs were isolated from Kunming mice E17 embryonic retina and ciliary body tissues, and labeled with 5-bromo-2'-deoxyuridin (BrdU). Retinal optic nerve crush injury was induced in left eyes in male Kunming mice by ring clamping the optic nerve. The 6th -generation of BrdU-labeled RSCs were transplanted into the damaged retina by the intravitreal injection, and saline injected eyes were used as the control. Hematoxylin and eosin histological staining, and BrdU, Nestin and Pax6 immunostaining were performed. Electroretinogram (ERG) was used for assessing the electrical activity of the retina., Results: Embryo-derived RSCs were identified by the positive stains of Pax6 and Nestin. BrdU incorporation was detected in the majority of RSCs. The damaged retina showed cellular nuclear disintegration and fragmentation in the retinal tissue which progressed over the periods of clamping time, and decreased amplitudes of a and b waves in ERG. In the damaged retina with RSCs transplantation, the positive staining for BrdU, Pax6 and Nestin were revealed on the retinal surface. Notably, RSCs migrated into the retinal ganglion cell layer and inner nuclear. Transplanted RSCs significantly elevated the amplitudes of a waves in retina injured eyes., Conclusions: Embryonic RSCs have similar characteristics to neural stem cells. Transplantation of RSCs by intravitreal injection would be able to repair the damaged retina.

Purpose: To report the characteristics and longitudinal visual outcomes of traumatic cataracts and retinal detachments in children with self-inflicted injury., Methods: A retrospective case series of pediatric patients at a tertiary care center who sustained ocular trauma due to self-inflicted injury between 2000 and 2014., Results: A total of 11 children, all with an intellectual disability and a mean age of 10 ± 4.8 years (range, 2.8-16.2), were identified with traumatic cataract secondary to ocular self-inflicted injury over the study period. Five eyes had a concurrent unilateral retinal detachment. Over the course of follow-up, one additional eye developed a cataract and five eyes developed a retinal detachment. Patients underwent an average of 2.5 ± 2.3 procedures and 17.1 ± 10.7 eye examinations over 11.7 ± 4.2 years of follow-up; 36% required general anesthesia for examination. Visual acuity was improved or preserved in 77% of the eyes that underwent surgical interventions, but was worse in the remaining cases due to development of traumatic retinal detachment. The use of protective helmets, eye shields, and immobilizing orthoses were essential in management of active self-inflicted injury., Conclusion: Traumatic cataracts and retinal detachments due to self-inflicted injury may cause severe visual loss. Visual prognosis although poor in children with severe intellectual disabilities may be optimized with risk awareness for early detection and customized interventions.

We performed optical radiation safety evaluations of LED flashlights to determine if they pose potential ocular hazards. Six commercially available flashlight samples were randomly selected from various vendors online. They were evaluated in accordance with specifications provided in the American National Standards Institute/Illuminating Engineering Society of North America (ANSI/IESNA) Standards RP 27.1 and RP 27.3. Four of the flashlights were found to have relatively high blue-light-weighted radiance values with short times (40 to 50 s) to reach the exposure limit specified in RP 27.1. These flashlights are in Risk Group 2 and present a moderate risk for retinal damage. Two of the flashlights are in Risk Group 1 and present a low risk for retinal damage. None of the flashlights present an ultraviolet (UV) radiation hazard or a retinal thermal hazard. Cautionary labeling on the packaging as required by RP 27.3 and on the flashlight handle is recommended for flashlights and on other handheld light sources that are in Risk Group 2 or Risk Group 3.

Objective: To outline the incidence of posterior segment injuries related to soccer-ball blunt trauma in children., Methods: Retrospective search of the computerized hospital medical database between the years 2007 and 2017. All pediatric trauma cases were reviewed and cases with blunt trauma related to direct orbital/ocular hit from a soccer-ball were included. Cases were divided into two groups (non-severe and severe) based on the presence of sight-threatening findings on presentation (e.g. retinal tear, vitreous hemorrhage, retinal detachment, and macular edema)., Results: Out of 343 pediatric patients with relevant diagnoses, 14 (4.1%) were treated for injuries related to soccer-ball trauma. All patients were males at their early-to-mid teens (14.3 ± 2.1 years). The most common funduscopic finding was peripheral commotio retina (13, 93%). There was equal distribution between the two groups (seven each). Retinal injury in the severe group included retinal tear (3), vitreous hemorrhage (4), retinal detachment (1), and macular hole (1). Five patients in this group presented with visual acuity of 20/25 or better. Rate of external signs of injury were similar in both groups., Conclusion: Soccer-ball blunt trauma in children can cause significant posterior segment injuries regardless of the presence of external injury or ocular complaints. A thorough ocular exam is mandatory in all cases for the detection of vision-threatening retinal injuries.

Diverse vascular diseases such as diabetic retinopathy, occlusion of retinal veins or arteries and ocular ischemic syndrome can lead to retinal ischemia. To investigate pathological mechanisms of retinal ischemia, relevant experimental models need to be developed. Anatomically, a main retinal blood supplying vessel is the ophthalmic artery (OpA) and OpA originates from the internal carotid artery of the common carotid artery (CCA). Thus, disruption of CCA could effectively cause retinal ischemia. Here, we established a mouse model of retinal ischemia by transient bilateral common carotid artery occlusion (tBCCAO) to tie the right CCA with 6-0 silk sutures and to occlude the left CCA transiently for 2 seconds via a clamp, and showed that tBCCAO could induce acute retinal ischemia leading to retinal dysfunction. The current method reduces reliance on surgical instruments by only using surgical needles and a clamp, shortens occlusion time to minimize unexpected animal death, which is often seen in mouse models of middle cerebral artery occlusion, and maintains reproducibility of common retinal ischemic findings. The model can be utilized to investigate the pathophysiology of ischemic retinopathies in mice and further can be used for in vivo drug screening.

Retinal regeneration efficiency from Müller glia varies tremendously among vertebrate species, being extremely limited in mammals. Efforts towards the identification of molecular mechanisms underlying Müller cell proliferative and neurogenic potential should help finding strategies to awake them and ensure regeneration in mammals. We provide here an update on the most recent and original progresses made in the field. These include remarkable discoveries regarding (i) unprecedented cross-species comparison of Müller cell transcriptome using single-cell technologies, (ii) the identification of new strategies to promote both the proliferative and the neurogenic potential of mammalian Müller cells, (iii) the role of the epigenome in regulating Müller glia plasticity, (iv) miRNA-based regulatory mechanisms of Müller cell response to injury, and (v) the influence of inflammatory signals on the regenerative process., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Objective: To investigate the effect of high-dose systemic steroids on retinal tissues and the effectiveness of ozone (O 3 ) therapy., Methods: Twenty-four New Zealand white rabbits were divided into three groups of eight. Group 1 was accepted as the control group, Group 2 received intramuscular 20 mg/kg methylprednisolone acetate and Group 3 received 14 sessions of ozone treatment in addition to methylprednisolone acetate. The subjects were sacrificed on the 30 th day. Retinal tissues were removed. Superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), total antioxidant status (TAS) and total oxidant status (TOS) levels were evaluated for tissue biochemistry and serum ischaemic modified albumin (IMA), interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) levels were evaluated with the ELISA method. Haematoxylin-eosin staining and TUNEL evaluation for apoptosis were evaluated as histopathological methods., Results: In the treatment group, antioxidant parameters of TAS, SOD and CAT were higher, oxidative and ischaemic parameters of MDA, TOS and IMA were lower, inflammatory parameters of IL-6 and TNF-α were lower, retinal thickness was better and apoptosis amount was lower., Conclusion: Apoptosis increases in retinal tissues due to high dose systemic steroid administration and the retina becomes thinner. With biochemical examination, oxidation parameters increased while antioxidant parameters decreased. Both histopathological and biochemical parameters improved significantly with ozone treatment.

Retinal ganglion cell degeneration is a characteristic feature of glaucoma, and accordingly, protection of these cells constitutes a major therapeutic objective in the disease. Here, we demonstrate the key influence of caveolin (Cav) in regulating the inner retinal homeostasis in two models of experimentally elevated intraocular pressure (IOP). Two groups of Cav-1 -/- and wild-type mice were used in the study. Animals were subjected to experimentally induced chronic and acutely elevated IOP and any changes in their retinal function were assessed by positive scotopic threshold response recordings. TUNEL and cleaved caspase-3 assays were performed to evaluate apoptotic changes in the retina while Brn3a immunostaining was used as a marker to assess and quantify ganglion cell layer (GCL) changes. H&E staining was carried out on retinal sections to evaluate histological differences in retinal laminar structure. Cav-1 ablation partially protected the inner retinal function in both chronic and acute models of elevated IOP. The protective effects of Cav-1 loss were also evident histologically by reduced loss of GCL density in both models. The phenotypic protection in Cav-1 -/- glaucoma mice paralleled with increased TrkB phosphorylation and reduced endoplasmic reticulum stress markers and apoptotic activation in the inner retinas. This study corroborated previous findings of enhanced Shp2 phosphorylation in a chronic glaucoma model and established a novel role of Cav-1 in mediating activation of this phosphatase in the inner retina in vivo. Collectively, these findings highlight the critical involvement of Cav-1 regulatory mechanisms in ganglion cells in response to increased IOP, implicating Cav-1 as a potential therapeutic target in glaucoma.

The present study was aimed to reveal the function of extracellular RNAs (exRNAs) in retinal ischemia reperfusion (I/R) injury, and evaluate whether RNase administration can effectivelyreduce I/Rinjury. A retinal I/R injury C57BL/6J wild-type mice model was established by elevating intraocular pressure for 1 h. All mice received 3 doses of RNase or the same dose of normal saline at different time points. After 7 days of reperfusion, retinal damage was quantified by counting retinal ganglion cells and measuring retinal layer thickness. The apoptotic retinal cells were detected by the TUNEL experiment, and the expressions of caspase-3, proinflammatory cytokines in retinal tissues, and glial fibrillary acidic protein (GFAP) protein and mRNA were detected to determine the underlying mechanism. It was found that RNase administration (1) reduced the significant loss of retinal morphology caused by I/R injury; (2) down-regulated the expression of NF-κBp65, IL-6 and GFAP relative to the I/R mice; (3) decreased the apoptosis of retinal cells and the levels of caspase-3; (4) attenuated exRNAs levels in retinal tissues on day 7 after retinal I/R. In short, increased exRNAs may contribute to retinal I/R damages in mice, and RNase therapy can effectively attenuate retinal damage by reducing inflammatory response and apoptosis., Competing Interests: Declaration of Competing Interest Without conflict of interest in the submission of our manuscript., (Copyright © 2020. Published by Elsevier B.V.)

Purpose: To quantitatively investigate the reflectivity and structure of the outer retinal layers on spectral-domain optical coherence tomography (SD-OCT) in commotio retinae., Methods: Nineteen patients with acute macular commotio retinae and 19 age-matched normal controls were examined using SD-OCT. Longitudinal reflectance profiles (LRP) were obtained using Image J. The reflectivity of outer retinal layers was measured at the fovea, 1 mm nasal to fovea and 1 mm temporal to fovea. The reflectivity ratios of outer retinal layers divided by the outer nuclear layer (ONL) were calculated for normalization. Photoreceptor outer segment layer thickness was also measured. The results were compared between the patients and controls., Results: The reflectivity ratio of ellipsoid zone/ONL and outer segment/ONL was higher in commotio retinae than in controls only at fovea (12.66 ± 4.73 vs 9.67 ± 3.34, p = 0.041; 7.70 ± 2.20 vs 3.73 ± 1.63, p < 0.001, respectively) but not at 1 mm nasal or temporal to the fovea. Photoreceptor outer segment layer thickness was significantly shorter in commotio retinae compared to controls at all three locations (19.64 ± 3.05 vs 25.16 ± 3.53, 16.95 ± 4.02 vs 20.00 ± 3.00, and 15.42 ± 3.22 vs 20.05 ± 2.48, respectively, all p < 0.05)., Conclusions: Quantitative measurement of SD-OCT images revealed that shortening of photoreceptor outer segment is an additional, and potentially better, biomarker for commotio retinae on top of increased reflectivity.

Glaucoma is a neurodegenerative disease that features the death of retinal ganglion cells (RGCs) in the retina, often as a result of prolonged increases in intraocular pressure. We show that preventing the formation of neuroinflammatory reactive astrocytes prevents the death of RGCs normally seen in a mouse model of glaucoma. Furthermore, we show that these spared RGCs are electrophysiologically functional and thus still have potential value for the function and regeneration of the retina. Finally, we demonstrate that the death of RGCs depends on a combination of both an injury to the neurons and the presence of reactive astrocytes, suggesting a model that may explain why reactive astrocytes are toxic only in some circumstances. Altogether, these findings highlight reactive astrocytes as drivers of RGC death in a chronic neurodegenerative disease of the eye., Competing Interests: Declaration of Interests S.A.L. is an academic founder of AstronauTx Ltd., (Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.)

The light damage (LD) model was mainly used to study some of the main aspects of age related macular degeneration (AMD), such as oxidative stress and photoreceptor death. Several protocols of light-induced retinal degeneration exist. Acute light damage is characterized by a brief exposure (24 hours) to high intensity light (1000 lux) and leads to focal degeneration of the retina which progresses over time. To date there are not experimental data that relate this model to neovascular events. Therefore, the purpose of this study was to characterize the retina after an acute light damage to assess whether the vascularization was affected. Functional, molecular and morphological investigations were carried out. The electroretinographic response was assessed at all recovery times (7, 60, 120 days after LD). Starting from 7 days after light damage there was a significant decrease in the functional response, which remained low up to 120 days of recovery. At 7 days after light exposure, neo-vessels invaded the photoreceptor layer and retinal neovascularization occurred. Remarkably, neoangiogenesis was associated to the up-regulation of VEGF, bFGF and their respective receptors (VEGFR2 and FGFR1) with the progression of degeneration. These important results indicate that a brief exposure to bright light induces the up-regulation of pro-angiogenic pathways with subsequent neovascularization.

Müller glia, the principal glial cell type in the retina, have the potential to reenter the cell cycle after retinal injury. In mammals, proliferation of Müller glia is followed by gliosis, but not regeneration of neurons. Retinal injury is also accompanied by phagocytic removal of degenerated cells. We here investigated the possibility that proliferation and gliosis of Müller glia and phagocytosis of degenerated cells may be regulated by the same molecular pathways. After N-methyl-N-nitrosourea-induced retinal injury, degenerated photoreceptors were eliminated prior to the infiltration of microglia/macrophages into the outer nuclear layer, almost in parallel with cell cycle reentry of Müller glia. Inhibition of microglia/macrophage activation with minocycline did not affect the photoreceptor clearance. Accumulation of lysosomes and rhodopsin-positive photoreceptor debris within the cytoplasm of Müller glia indicated that Müller glia phagocytosed most photoreceptor debris. Pharmacological inhibition of phosphatidylserine and Rac1, key regulators of the phagocytic pathway, prevented cell cycle reentry, migration, upregulation of glial fibrillary acidic protein, and phagocytic activity of Müller glia. These data provide evidence that phosphatidylserine and Rac1 may contribute to the crosstalk between different signaling pathways activated in Müller glia after injury.

Introduction: To establish a rabbit model of posterior penetrating eye injury as a platform to test potential therapeutics., Materials and Methods: Anesthetized rabbits received posterior penetrating eye injury in one eye, whereas contralateral eyes were maintained as uninjured controls. Rabbits were randomized into two experimental groups. Group A was euthanized on Day 14 postinjury to determine retinal fibrosis at an early phase of disease progression. Group B was euthanized on Day 28 postinjury to examine retinal fibrosis at a late phase of disease progression. We examined animals on postinjury Days 7, 14, 21, and 28 with indirect ophthalmoscope and fundus photography. After euthanasia, eyes were processed for histology and immunofluorescence labeling of fibrotic proteins α-smooth muscle actin and collagen I., Results: Early fibrosis was detected by Day 14, as indicated by indirect ophthalmoscopy and fundus imaging. Fibrotic membranes were visible at sites of injury. Immunofluorescence analysis detected α-smooth muscle actin and collagen I within the fibrotic membranes., Conclusions: These data show that ocular fibrosis can be detected within 14 days after initial injury, with more severe fibrosis detected at 28 days postinjury. These results will be used to determine the optimal time points for later studies designed to test treatment strategies., (© Association of Military Surgeons of the United States 2020. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

A 39-year-old man presented to the ophthalmology emergency room complaining of decreased visual acuity and metamorphopsia on his left eye after undergoing Nd:YAG facial hair epilation without wearing proper eye protection. Fluorescein angiography showed a foveal staining initially, with an increase in foveal leakage over late phases. On optical coherence tomography, a subfoveal retinal pigment epithelial detachment with associated subretinal fluid and no signs of choroidal neovascularization or cystoid macular edema was observed. Observation with monthly follow-ups was adopted. By the fourth month, the subretinal fluid had already disappeared and visual acuity had returned to 20/20. Over one-year follow-up, the retinal pigment epithelial detachment experienced a decrease in its size. Conservative management may be a valid option in assessing accidental foveal photocoagulation when choroidal neovascularization or cystoid macular edema is absent. The use of wavelength specific goggles is mandatory for the patient and the aesthetician operating the cosmetic laser, especially when operating on the face or around the eyes. Abbreviations: Nd:YAG = neodymium-doped yttrium aluminium garnet, OCT = optical coherence tomography, PED = pigment epithelial detachment, CME = cystoid macular edema., (©Romanian Society of Ophthalmology.)

Upon retina injury, Müller glia in the zebrafish retina respond by generating multipotent progenitors to repair the retina. However, the complete mechanisms underlying retina regeneration remain elusive. Here we report inflammation-induced mammalian target of rapamycin (mTOR) signaling in the Müller glia is essential for retina regeneration in adult zebrafish. We show after a stab injury, mTOR is rapidly activated in Müller glia and later Müller glia-derived progenitor cells (MGPCs). Importantly, mTOR is required for Müller glia dedifferentiation, as well as the proliferation of Müller glia and MGPCs. Interestingly, transient mTOR inhibition by rapamycin only reversibly suppresses MGPC proliferation, while its longer suppression by knocking down Raptor significantly inhibits the regeneration of retinal neurons. We further show mTOR promotes retina regeneration by regulating the mRNA expression of key reprogramming factors ascl1a and lin-28a, cell cycle-related genes and critical cytokines. Surprisingly, we identify microglia/macrophage-mediated inflammation as an important upstream regulator of mTOR in the Müller glia and it promotes retina regeneration through mTOR. Our study not only demonstrates the important functions of mTOR but also reveals an interesting link between inflammation and the mTOR signaling during retina regeneration., (© 2019 Wiley Periodicals, Inc.)

Background: Foldable capsular vitreous body (FCVB) was designed to treat severe retinal detachment. The aim of this study was to evaluate the efficacy and safety of the implantation of foldable capsular vitreous body in 1-year follow-up., Methods: A retrospective analysis was conducted for 20 patients with severe ocular trauma or silicone oil (SO) dependent eyes underwent vitrectomy and FCVB implantation in a 1-year follow-up. All treated eyes were peformed clinical examinations involved the visual acuity (VA) examination, Goldmann applanation tonometer, noncontact specular microscopy, fundus photography, B-Scan examination and optical coherence tomography (OCT). The groups were compared with t-test and the McNemar - Bowker test., Results: In 1-year follow-up, 20 eyes were evaluated in the study. FCVB well supported the vitreous retina in all treated eyes, and 6 treated eyes achieved retinal reattachment 12 months after FCVB implantation. There were no significant differences in VA before and after FCVB implantation (P = 1.000). In addition, the postoperative IOP markedly elevated from the preoperative IOP of 12.90 ± 7.06 mmHg to 15.15 ± 3.36 mmHg (P = 0.000017). The intraocular pressure (IOP) of 10 eyes maintained at a normal level after surgeries. The other 10 eyes showed slightly lower IOP within the acceptable level. Though two patients developed keratopathy and ocular inflammation respectively, other treated eyes were symmetric with fellow eyes showing satisfactory appearance. Moreover, there was no SO emulsification or leakage happened in the observation., Conclusions: FCVB implantation was an effective and safe treatment in the eyes with severe retinal detachment.

Background: Photoreceptor degeneration is one of the most refractory oculopathy in the world, leading to vision loss in severe cases. Methyprednisolone is one of the most commonly prescribed medications for the treatment of retinal degenerative diseases, either by oral administration or repeated intraocular injections. However, the efficacy was unsatisfactory due to its systemic or local side effects and short retention time within the retina., Methods: Nanoscale zirconium-porphyrin metal-organic framework (NPMOF) was synthesized and characterized. The biotoxicity and imaging capability of NPMOF were evaluated using zebrafish embryos and larvae. NPMOF was then used as a skeleton and loaded with methylprednisolone (MPS) to prepare a novel kind of nanoparticle, MPS-NPMOF. Photoreceptor degeneration was induced by high-intensity light exposure in adult zebrafish. MPS-NPMOF was delivered to the injured retina by intraocular injection. The photoreceptor regeneration and its underlying mechanism were explored by immunohistochemistry, quantitative real-time polymerase chain reaction and behavioral test., Results: NPMOF not only had low biotoxicity but also emitted bright fluorescence. Following a single MPS-NPMOF intraocular injection, the injured retina exhibited the faster photoreceptor regeneration with better visual function by promoting the cell proliferation., Conclusion: NPMOF is an ideal carrier and could be applied in tracking and delivering medications. By intraocular injection, the novel drug delivery system, MPS-NPMOF, accomplishes the sustained release of drug and plays a therapeutic role in photoreceptor degeneration., Competing Interests: The authors report no conflicts of interest in this work., (© 2019 Wang et al.)

Adaptation is a general feature of sensory systems. In rod photoreceptors, light-dependent transducin translocation and Ca 2+ homeostasis are involved in light/dark adaptation and prevention of cell damage by light. However, the underlying regulatory mechanisms remain unclear. Here, we identify mammalian Cul3-Klhl18 ubiquitin ligase as a transducin translocation modulator during light/dark adaptation. Under dark conditions, Klhl18 -/- mice exhibited decreased rod light responses and subcellular localization of the transducin α-subunit (Tα), similar to that observed in light-adapted Klhl18 +/+ mice. Cul3-Klhl18 promoted ubiquitination and degradation of Unc119, a rod Tα-interacting protein. Unc119 overexpression phenocopied Tα mislocalization observed in Klhl18 -/- mice. Klhl18 weakly recognized casein kinase-2-phosphorylated Unc119 protein, which is dephosphorylated by Ca 2+ -dependent phosphatase calcineurin. Calcineurin inhibition increased Unc119 expression and Tα mislocalization in rods. These results suggest that Cul3-Klhl18 modulates rod Tα translocation during light/dark adaptation through Unc119 ubiquitination, which is affected by phosphorylation. Notably, inactivation of the Cul3-Klhl18 ligase and calcineurin inhibitors FK506 and cyclosporine A that are known immunosuppressant drugs repressed light-induced photoreceptor damage, suggesting potential therapeutic targets., (© 2019 The Authors.)

Purpose: To assess whether near infrared autofluorescence (NIR-AF) imaging is a useful imaging modality in the diagnosis of handheld laser retinal injuries., Design: Retrospective observational case series., Methods: Twelve patients identified to have handheld laser retinal injuries were included at 2 academic centers. Patients underwent ophthalmic assessment and retinal imaging including fundus photography, optical coherence tomography (OCT), conventional blue autofluorescence (B-AF), and NIR-AF imaging., Results: In all cases, lesions consistent with retinal laser injury were detected by NIR-AF imaging. The lesions showed a characteristic appearance with central hyperfluorescence and surrounding hypofluorescence, although the number and extent of lesions varied between patients. Findings using other imaging modalities were variable: on color fundus photography these included localized pigmentary changes and on OCT imaging an ellipsoid zone interruption or outer nuclear layer changes. Only subtle changes were evident on B-AF imaging. Other macular conditions, such as poppers retinopathy or solar maculopathy, which may have similar findings on OCT imaging as laser damage, can be differentiated using NIR-AF imaging., Conclusion: An increased incidence of retinal injuries secondary to handheld lasers has been reported in recent years. We show that the diagnosis and full extent of retinal laser injuries is best demonstrated by NIR-AF, as other modalities give variable results. We propose that NIR-AF should be included when investigating patients suspected of macular injury secondary to exposure to handheld lasers., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Purpose: To report a case of a child with strabismus and delayed discovery of a metallic intraocular foreign body with good recovery of visual acuity and stereopsis with 36-month follow-up., Methods: A 4-year-old girl was evaluated due to exotropia of right eye initiated 9 months before with progressive worsening. Visual acuity was 1.00 logMAR (20/200) in the right eye and 0.00 logMAR (20/20) in the left eye. Anterior segment evidenced a small paracentral corneal leukoma, posterior synechia and mild lens opacity in the temporal quadrant only in the right eye. Fundus examination in the right eye identified the presence of an intraocular foreign body, with appearance of metallic components surrounded by retinal pigmented endothelial cells atrophy. Full-field electroretinography (ERG) showed reduced amplitudes and delayed implicit times for both rods and cones in the affected eye. All tests were normal in the fellow eye., Results: Pars plana vitrectomy was promptly performed in the right eye, followed by phacoemulsification with intraocular lens implantation 4 months later due to worsening of the lens opacification. The full-field ERG was repeated after the surgical procedures. The ERG showed mild worsening of all responses in the right eye. After 36 months of follow-up, visual acuity was 0.20 logMAR (20/32) with improvement of the ocular misalignment and with 60 s of arc stereopsis with ERG responses unchanged., Conclusion: In this young girl perforating ocular trauma with metallic material was lately diagnosed with strabismus as a sign of alert. Prompt surgical intervention and proper management were essential to provide reasonable visual function including some degree of stereopsis, even though retinal dysfunction characterized by ERG was persistent.