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Summary In order to better differentiate ante-mortem lesions from post-mortem retinal autolysis, the temporal sequence of post-mortem changes was studied in a well-controlled mouse model. Mice were of the same strain, age and sex, and were held at a constant ambient temperature. Eyes were collected at various times up to 72 h after death and immersion-fixed in either Davidson's fixative or 10% neutral buffered formalin, paraffin-embedded and sections cut and stained with haematoxylin and eosin. The most prominent, and early, autolytic change was retinal detachment, and subsequent folding, which occurred immediately after death in formalin-fixed eyes, but not until 2 h post mortem with Davidson's fixative. Retinal separation was complete at 16 h, or almost complete by 2 h, in formalin, but in Davidson's fixative, was only partial and segmental, the latter not becoming total until much later. Retinal detachment was attended by progressively more severe disruption and dissolution of photoreceptors and, particularly in Davidson's-fixed retinas, the rod outer segment often showed marked homogenization from 30 min to 4 h after death. The other major early change was nuclear pyknosis in the inner nuclear layer. Ganglion cells initially had cytoplasmic swelling, followed by shrinkage and basophilia (at 4 h with formalin and 16 h with Davidson's), with nuclear pyknosis becoming increasingly common over time. While the three retinal neuronal layers eventually became more attenuated and depleted of cells, the thickness of these layers was augmented by severe swelling. These findings show that the post-mortem interval at which histological interpretation of retinal changes becomes potentially compromised is dependent on the duration of this interval and the fixative used.

Summary Stem cell transplantation shows enormous potential for treatment of incurable retinal degeneration (RD). To determine if and how grafts connect with the neural circuits of the advanced degenerative retina (ADR) and improve vision, we perform calcium imaging of GCaMP5-positive grafts in retinal slices. The organoid-derived C-Kit+/SSEA1− (C-Kit+) retinal progenitor cells (RPCs) become synaptically organized and build spontaneously active synaptic networks in three major layers of ADR. Light stimulation of the host photoreceptors elicits distinct neuronal responses throughout the graft RPCs. The graft RPCs and their differentiated offspring cells in inner nuclear layer synchronize their activities with the host cells and exhibit presynaptic calcium flux patterns that resemble intact retinal neurons. Once graft-to-host network is established, progressive vision loss is stabilized while control eyes continually lose vision. Therefore, transplantation of organoid-derived C-Kit+ RPCs can form functional synaptic networks within ADR and it holds promising avenue for advanced RD treatment., Highlights •C-Kit+ RPCs migrate and integrate in 3 major layers of advanced degenerative retina • Host inputs evoked by light activates graft neural response • 2-photon imaging visually defines graft-to-host synaptic Ca2+ transients in retina • Grafts connecting with the host retinal circuits preserves vision, In this article Liu, Yin, and colleagues show C-Kit+ retinal progenitor cells can migrate and integrate in three major layers of advanced degenerative retina, form functional synapses with the hosts, and connect with the neural circuits. They provide state-of-the-art techniques to visually demonstrate exceptional synaptic repair and vision restoration, opening up a feasible avenue for advanced RD treatment.

The standard model system for studies of inherited retinal pathologies consists of C3H mice, which have a mutation in the Pde6b gene. These animals show impairment to the functioning of rod phosphodiesterase, leading to photoreceptor death and complete loss of vision by day 4 of life. C3H mice obtained from Charles River Laboratories – strain C3H/Crl – were found to have an additional mutation in the Gpr179 gene, which leads to impairment to the operation of the transduction cascade of retinal ON bipolar cells. Despite the wide use of C3H/Crl mice as a study system, detailed investigation of the characteristics of the photoreceptor degeneration process has yet to be carried out. The aim of the present work was to study the time dynamics of morphological and functional changes occurring at early age in the retinas of C3H/Crl mice. The control group consisted of wild-type mice, i.e., strain C57Bl/6J. The functional state of the retina was assessed using in vivo electroretinography, with morphological analysis of histological preparations of eye tissues. Retinal responses to light stimulation in C3H/Crl mice were found not to involve any contribution from rods or ON bipolar cells throughout the measurement period, starting from day 18 of life, while cone responses disappeared by day 25. The numbers of photoreceptors and neurons in the inner nuclear layer of the retina in C3H/Crl mice were decreased by day 16 of life and photoreceptors almost completely degenerated by day 25. At the same time, response amplitude and retinal sensitivity in wild-type mice underwent no significant changes at early age. These data suggest a picture of the development of retinal pathology in C3H/Crl mice.

Purpose The purpose of this study is to investigate anatomic and morphologic features of inner and outer retinal layers in patients recovered from COVID-19 with Spectral Domain Optical Coherence Tomography (SD-OCT), whether correlate with any symptoms during disease process. Methods 32 patients recovered from COVID-19 and age- and gender-matched 36 healthy controls were included in this cross-sectional study. Ganglion cell-inner plexiform layer, macular and peripapiller retinal nerve fiber layer (RNFL), inner nuclear layer (INL), outer nuclear layer (ONL), outer plexiform layer (OPL) and the outer retinal hyperreflective bands including external limiting membrane (ELM), ellipsoid zone (EZ) and interdigitation zone (IZ) were examined with SD-OCT. The differences of each retinal layers thickness among subgroup analysis of ocular pain and headache were also compared. Results Macular RNFL of inner and outer nasal and outer inferior quadrants were thinner in COVID-19 patients compared to healthy control group (p = 0.046, p = 0.014 and p = 0.016, respectively). Thinning in outer superior quadrant of GCIPL and INL quadrants were detected in patients with headache (p = 0.026 and p = 0.01). Superonasal and inferotemporal sectors of pRNFL were thinner in patients with ocular pain compared to patients without ocular pain (p = 0.024 and p = 0.015). Integrity of EZ, ELM and IZ was evaluated as continuous line and protected on each OCT scans. Conclusion The study demonstrated convincing evidence that SARS-CoV-2 can affect the inner and outer retinal layers, with subclinical localized alterations, particularly in patients with headache and ocular pain symptoms during COVID-19 period. Supplementary Information The online version contains supplementary material available at 10.1007/s10792-021-01952-5.

Introduction: Over the past few years, the incidence of retinal ischemic disorders has been increasing, due to a rising prevalence of such socially burdensome diseases as diabetes and hypertension, which ultimately lead to ocular vascular pathology. The identification of new treatment options that would prevent retinal neuron death is a crucial task of modern pharmacology. Materials and methods: The research was carried out on male Wistar rats. Retinopathy was modeled by inducing a 30-min ischemic episode, with a 72-hour period of reperfusion and subsequent administration of Retinalamin and Emoxypine for 10 days. The effectiveness of the drugs was evaluated by electroretinographic, ophthalmoscopic and morphological assessments. Results and discussion: On Day 14 of the experiment, a dose-dependent preservation of the electroretinogram b-wave/a-wave amplitude ratio was observed in the animals treated with Retinalamin depending on a dose (1.39±0.06, 1.46±0.03 and 1.49±0.04 in low (0.214 mg/kg), medium (0.428 mg/kg) and high (0.857 mg/kg) Retinalamin dose groups, respectively). The ophthalmoscopic picture of the fundus oculi also improved following the treatment with Retinalamin (1.42, 1.69 and 1.90 times lower ophthalmoscopic scores compared to placebo-treated animals in low, medium and high dose groups, respectively). The morphologic “coefficient of change” applied to ganglion cell layer was 2.2, 1.7 and 1.6 points in low, medium and high dose Retinalamin groups, respectively. These results are significantly different from both intact and placebo group (p

CLINICAL RELEVANCE: The SARS-COV 2 virus, which is responsible for the COVID-19 pandemic, acts on the angiotensin converting enzyme 2 (ACE-2) receptor in the host cell. Ocular effects may occur because of the ACE-2 receptor in the retina. BACKGROUND: To investigate the impact of COVID-19 on the retinal layers and optic disc parameters in previously confirmed COVID-19 patients using spectral domain optical coherence tomography (SD-OCT). METHODS: This study included 60 eyes of 60 subjects; 35 of them were in the COVID-19 group and the remaining 25 were in the control group. Patients with the diagnosis of COVID-19 that had a negative result after treatment were included in the study. Macular and peripapillary retinal nerve fiber layer (RNFL) thickness measurements, each retinal layer thickness of all participants were done 14-30 days after COVID-19 symptom onset, following the negative result of real time reverse transcriptase-polymerase chain reaction test using SD-OCT. RESULTS: The mean value of central macular thickness was significantly higher in the COVID-19 group than the control group (p = 0.02). The mean values of the ganglion cell layer and inner nuclear layer thickness in the COVID-19 group were signii¬cantly thinner than control group (p = 0.04 and p = 0.04, respectively). Even though mean RNFL thickness measurements in all sections in the COVID-19 group was thinner than controls, there were no significant differences between groups (p > 0.05 for all). CONCLUSION: In the early recovery phase, changes in the macula, ganglion cell layer and inner nuclear layer could be seen. These patients should be followed up closely for the recognition of new pathologies that could be seen in the late recovery phase.

PURPOSE To evaluate microstructural changes in cystoid macular edema in retinitis pigmentosa after intravitreal dexamethasone implant injection. METHODS In an extended cohort of a randomized trial of intravitreal dexamethasone implant for the management of retinitis pigmentosa-associated cystoid macular edema, microstructural changes during six months after the treatment were evaluated using spectral-domain optical coherence tomography. RESULTS Forty-two eyes were included, and all had cystoid space in the inner nuclear layer (INL) at baseline. No eyes showed subretinal fluid, and 28.6% showed hyperreflective foci. Among 38 eyes with cystoid space both in the INL and outer nuclear layer/Henle's layer, 13 (34.2%) showed complete resolution and 12 (31.6%) showed cystoid space only in the INL at 2 months after injection, whereas others showed persistent cystoid space in both layers. After complete resolution, cystoid space recurrence was earlier in the INL than in the outer nuclear layer/Henle's layer. Multivariable analysis showed that greater cystoid space area in the INL and outer nuclear layer/Henle's layer, presence of macular leakage, and longer intact external limiting membrane at baseline were associated with greater cystoid space area decrease after the treatment. CONCLUSION Resolution and recurrence pattern of retinitis pigmentosa-associated cystoid macular edema after dexamethasone treatment showed that the INL is the primary layer of cystic change, and this suggests its pathogenesis is most likely caused by Muller cell dysfunction.

This retrospective study was performed to classify diabetic macular edema (DME) based on the localization and area of the fluid and to investigate the relationship of the classification with visual acuity (VA). The fluid was visualized using en face optical coherence tomography (OCT) images constructed using swept-source OCT. A total of 128 eyes with DME were included. The retina was segmented into: Segment 1, mainly comprising the inner nuclear layer and outer plexiform layer, including Henle’s fiber layer; and Segment 2, mainly comprising the outer nuclear layer. DME was classified as: foveal cystoid space at Segment 1 and no fluid at Segment 2 (n = 24), parafoveal cystoid space at Segment 1 and no fluid at Segment 2 (n = 25), parafoveal cystoid space at Segment 1 and diffuse fluid at Segment 2 (n = 16), diffuse fluid at both segments (n = 37), and diffuse fluid at both segments with subretinal fluid (n = 26). Eyes with diffuse fluid at Segment 2 showed significantly poorer VA, higher ellipsoid zone disruption rates, and greater central subfield thickness than did those without fluid at Segment 2 (P

Objectives: To examine the relationship between keratoconus (KC) stage and the thickness of the retinal layers. Materials and Methods: Retinal layer thicknesses were compared between 85 eyes of 85 KC patients and 40 eyes of 40 controls similar in age, sex, and axial length. KC patients were staged as stage 1, 2, or 3 according to the Amsler-Krumeich staging system, and segmentation of the retinal layers was performed with spectral domain optical coherence tomography automatic segmentation program. The thickness of the retinal nerve fiber layer (RNFL), ganglion cell layer (GCL), inner plexiform layer (IPL), inner nuclear layer (INL), outer plexiform layer (OPL), outer nuclear layer (ONL), and retinal pigment epithelium (RPE) in the central 1 mm Early Treatment Diabetic Retinopathy Study subfield was analyzed. Results: There was no significant difference between the control and KC groups in the segmentation of the RNFL, GCL, IPL, or OPL (p=0.306; p=0.661; p=0.893, p=0.664, respectively). The INL differed significantly between control and stage 2 KC, control and stage 3 KC, stage 1 and 2 KC, and stage 2 and 3 KC, increasing in thickness with higher stage (p=0.004; p=0.005: p=0.001; p=0.002, respectively). The RPE also differed significantly between control and stage 2 KC, control and stage 3 KC, stage 1 and 2 KC, and stage 2 and 3 KC, showing decreased thickness with higher stage (p=0.03; p=0.001; p=0.001; p

Background The arginine-glutamic acid dipeptide repeats gene (RERE) encodes a nuclear receptor coregulator that modulates gene expression through its interaction with transcriptional machinery. In humans, RERE deficiency causes neurodevelopmental disorder with or without structural defects of the brain, eye, heart, and kidney (NEDBEH). Ophthalmological defects are seen in approximately one third of individuals with NEDBEH and in RERE-deficient mice which can serve as a useful animal model. Results In mice, RERE is expressed in a subset of retinal ganglion cells (RGC), the lens epithelium, and the ciliary body during the embryonic period. RERE expression expands into the outer nuclear layer and the inner nuclear layer during the postnatal period. RERE-deficient mice have retinal and optic nerve atrophy. We show that RERE deficiency causes progressive loss of retinal cells and apoptosis of retinal cells in the ganglion cell layer as early as E17.5. The number of RGCs is also reduced in RERE-deficient embryos and mice. Conclusions We conclude that RERE is required to control the apoptosis of retinal cells in the developing retina, and that RERE deficiency results in the retina atrophy through degeneration of the retinal cells and optic nerve atrophy through the loss of RGCs.

Osmoregulation is critical for cell and tissue survival yet there are relatively few methods available to determine osmotic gradients from water and elemental concentration either in single cells or across multiple cellular layers of tissue. X-ray microanalysis of frozen-hydrated preparations in a scanning electron microscope is one such powerful, sensitive, nondestructive technique. Here we use x-ray microanalysis to quantitatively analyse intracellular element concentrations and oxygen concentrations, as a proxy for water concentrations, in selected individual cells of the posterior eye. Using frozen-hydrated preparations of the retinal complex of chicken eyes, it is shown that structural preservation is sufficient to identify cell layers and individual cells. The quantitative analysis of selected areas in the photoreceptor layer, inner nuclear layer and ganglion cell layer, where specific cell types were known to be present, provided measurements of intracellular element concentrations comparable with the analysis of individual cells. It is also shown that in the cells of the retinal pigment epithelium and outer photoreceptor segments elemental analyses were reasonably consistent at the cellular level in different depth levels of the same sample. Comparison of oxygen concentrations, as a proxy for water concentration, at two accelerating voltages (15 and 5 kV) indicated that at 15 kV oxygen concentration was largely derived from intracellular water. Water concentrations could be calculated and concentrations of diffusible elements (Na, K) could be defined in mmol/L. From the latter it is possible to calculate osmotic concentrations of individual cells and osmotic gradients across the tissue. LAY DESCRIPTION: Understanding many cellular processes, in both healthy and diseased states, depends on knowing how the water content of cells and their surrounding fluids is controlled. The transport of water is generally down its concentration gradient or against the osmotic concentration gradient defined by solutes such as sodium, potassium and chloride dissolved in the water. We have refined a microanalytical method, that detects the x-rays emitted from specific elements when they are bombarded by electrons in a scanning electron microscope, to apply it to the analysis of the retina of the eye. The method facilitates the measurement of the elemental composition, water and osmotic concentration gradients of cells and tissues in the eye, that may be involved in the development of myopia, or short sightedness, a condition that afflicts many people including some 80 - 90% of children in Asia.

Introduction To examine the compatibility of intravitreally injected epidermal growth factor (EGF) and amphiregulin as EGF family member. Methods Four rabbits (age: 4 months; body weight: 2.5 kg) received three intravitreal injections of EGF (100 ng) uniocularly in monthly intervals and underwent ocular photography, tonometry, biometry, and optical coherence tomography. After sacrificing the rabbits, the globes were histomorphometrically examined. In a second study part, eyes of 22 guinea pigs (age: 2–3 weeks) received two intravitreal administrations of amphiregulin (10 ng) or phosphate buffered solution (PBS) in 10-day interval, or were left untouched. Ten days after the second injection, the guinea pigs were sacrificed, the enucleated eyes underwent histological and immune-histological examinations. Results The rabbit eyes with EGF injections versus the contralateral untouched eyes did not show significant differences in intraocular pressure (7.5 ± 2.4 mmHg vs. 6.8 ± 2.2 mmHg; P = 0.66), retinal thickness (158 ± 5 µm vs. 158 ± 3 µm; P = 1.0), cell counts in the retinal ganglion cell layer (3.3 ± 1.7 cells/150 µm vs. 3.0 ± 1.4 cells/150 µm; P = 0.83), inner nuclear layer (46.4 ± 23.2 cells/150 µm vs. 39.6 ± 6.4 cells/150 µm; P = 0.61), and outer nuclear layer (215 ± 108 cells/150 µm vs. 202 ± 47 cells/150 µm; P = 0.83), or any apoptotic retinal cells. The guinea pig eyes injected with amphiregulin versus eyes with PBS injections did not differ (P = 0.72) in the degree of microglial activation, and both groups did not differ from untouched eyes in number of apoptotic retinal cells and retinal gliosis. Conclusions Intravitreal applications of EGF (100 ng) in rabbits nor intravitreal applications of amphiregulin (10 ng) in guinea pigs led to intraocular specific inflammation or any observed intraocular destructive effect. The findings support the notion of a compatibility of intraocular applied EGF and amphiregulin.

Chromium galvanic production have leaded to biosphere pollution. Therefore advisable to study of role in the neurodegenerative development in retinal diseases under experimental conditions. The aim is to study the Enterosgel effect on morphological changes in rats retina with Cr(VI) – induced retinopathy. Materials and methods. An experimental study had carried out on 72 outbred white male rats. The rats had divided into 3 groups: I – control group of intact rats (n = 24). Control rats were received drinking water, II group – rats (n = 24), were received drinking water with Cr (VI) (K2Cr2O7) – 0.02 mol/L, III group – animals (n = 24) were received drinking water with K2Cr2O7– 0.02 mol/L and hydrogel methylsilicic acid (Enterosgel) at a dose of 0.8 mg/kg per day as a corrector. The animals had been decapitated under ether anesthesia. The retina had been studied on days 20, 40 and 60 of the experiment. Morphologically and morphometrically they had analyzed. Results. According to histological studies, it has proved that Cr (VI) causes dystrophic and degenerative changes in all rats retina layers. They increase as the duration of the experiment. The use of Enterosgel as a corrective therapy showed positive results in restoring the morphological structure of rats retina. After Enterosgel 20 days using as a corrector of Cr (VI) exposure, there is a barely noticeable swelling of the outer and inner nuclear layers. Other layers of the retina, morphologically, look undamaged. Forty days Enterosgel treatment have outer and inner nuclear layer edema of retina of animals persists but does not increase. It is easy noticeable swelling of the outer and inner layers of mesh, but no signs of damage processes of cell populations nuclear layers. State ganglionic layer and nerve fiber layer entirely satisfactory. These pathological changes are not critical. After 60 days from the beginning of loading of Cr (VI) and application of Enterosgel in the retina of rats there are initial degenerative changes in the photosensory layer. Cystic dilated outer segments of rods and cones were visible throughout, and areas of their fragmentation were observed. Ganglion neurons are not damaged, but their axons appear somewhat thickened and fluffy. But in general, the typical structure of the retina is preserved. Conclusions. Chromium-induced toxicity in rats is characterized by pronounced histological and morphometric changes and retinal thickness, which appear after 20 days, increase by 40 days and acquire maximum transformations after 60 days of the experiment. The use of Enterosgel improves picture morphological structures of the retina in rats under the influence of Cr (VI). The changes were expressed on days 20 and 40, which indicates the presence of protective properties for the retina

To determine the factors significantly associated with anterior protrusion of the macula in eyes with a macula-off rhegmatogenous retinal detachment (RRD) and to determine the relationship between the intraretinal cystoid cavities (ICCs) and the anterior protrusion and function of the fovea. Retrospective cross-sectional study. Sixty-nine eyes of 69 patients with successfully reattached macula-off RRD were retrospectively analyzed. Six radial spectral-domain optical coherence tomographic (OCT) images were used to evaluate the effects of the ICCs on detached macula and to measure the angle of the retina at the macula as a parameter to evaluate the anterior protrusion of the detached retina. The findings were compared to other parameters. The mean angle of the retina at the macula was 143.1 ± 15.9° with a range of 108 to 172°. Preoperatively, 51 eyes (74%) had ICCs in the inner nuclear layer and/or the outer plexiform layer and Henle fiber layer complex, but none was present after surgery. Multivariate regression analyses revealed that the angle of the retina was significantly associated with the presence of ICCs (β = -0.637, P

Muller cells (MC) are considered dormant retinal progenitor cells in mammals. Previous studies demonstrated ephrin-As act as negative regulators of neural progenitor cells in the retina and brain. It remains unclear whether the lack of ephrin-A2/A3 is sufficient to promote the neurogenic potential of MC. Here we investigated whether the MC is the primary retinal cell type expressing ephrin-A2/A3 and their role on the neurogenic potential of Muller cells. In this study, we showed that ephrin-A2/A3 and their receptor EphA4 were expressed in retina and especially enriched in MC. The level of ephrinAs/EphA4 expression increased as the retina matured that is correlated with the reduced proliferative and progenitor cell potential of MC. Next, we investigated the proliferation in primary MC cultures isolated from wild-type and A2-/- A3-/- mice by 5-ethynyl-2'-deoxyuridine (EdU) incorporation. We detected a significant increase of EdU+ cells in MC derived from A2-/- A3-/- mice. Next, we investigated the role of ephrin-A2/A3 in mice undergoing photoreceptor degeneration such as Rhodopsin knockout (Rho-/-) mice. To further evaluate the role of ephrin-A2/A3 in MC proliferation in vivo, EdU was injected intraperitoneally to adult wild-type, A2-/- A3-/- , Rho-/- and Rho-/- A2-/- A3-/- mice and the numbers of EdU+ cells distributed among different layers of the retina. EphrinAs/EphA4 expression was upregulated in the retina of Rho-/- mice compared to the wild-type mice. In addition, cultured MC derived from ephrin-A2-/- A3-/- mice also expressed higher levels of progenitor cell markers and exhibited higher proliferation potential than those from wild-type mice. Interestingly, we detected a significant increase of EdU+ cells in the retinas of adult ephrin-A2-/- A3-/- mice mainly in the inner nuclear layer; and these EdU+ cells were co-localized with MC marker, cellular retinaldehyde-binding protein, suggesting some proliferating cells are from MC. In Rhodopsin knockout mice (Rho-/- A2-/- A3-/- mice), a significantly greater amount of EdU+ cells were located in the ciliary body, retina and RPE than that of Rho-/- mice. Comparing between 6 and 12 weeks old Rho-/- A2-/- A3-/- mice, we recorded more EdU+ cells in the outer nuclear layer in the 12-week-old mice undergoing severe retinal degeneration. Taken together, Ephrin-A2/A3 are negative regulators of the proliferative and neurogenic potentials of MC. Absence of ephrin-A2/A3 promotes the migration of proliferating cells into the outer nuclear layer and may lead to retinal cell regeneration. All experimental procedures were approved by the Animal Care and Use Committee at Schepens Eye Research Institute, USA (approval No. S-353-0715) on October 24, 2012.

We aimed to develop an outer retinal degeneration pig model induced by temporary intravitreal loading of N-methyl-N-nitrosourea (MNU) during vitrectomy. In a preliminary experiment involving 5 mini-pig cases to determine the appropriate concentration of MNU, the vitreous cavity of each eye was filled with 4, 8, 10, 12, or 16 mg/mL MNU for 10 min, which was then replaced with a balanced salt solution. Multimodal examinations including spectral-domain optical coherence tomography (OCT) images and full-field electroretinography (ffERG) were obtained at baseline and week 2, week 6, and week 12. The retinal degeneration was classified according to the amplitudes of a dark adaptive (DA) 10.0 a-wave amplitude. The degree of moderate retinal degeneration was defined as DA 10.0 a-wave amplitude ≥ 10% and

Purpose To evaluate the differences in individual segmental retinal layer thickness in adult patients with high myopia. Methods This study compared the retinal layers of patients with high myopia (axial length of ≥26.0 mm) with those of normal controls using spectral-domain optical coherence tomography. The thicknesses of the retinal layers were compared using nine Early Treatment Diabetic Retinopathy Study subfields. Choroidal thickness was also measured in the subfoveal area. Results We included 37 eyes with high myopia and 37 eyes of healthy subjects. The mean age was 42.95 and 47.73 years (p = 0.114), and the mean axial length was 27.28 and 24.47 mm (p l 0.001), respectively. The parafoveal areas (outer ring segment) of the ganglion cell layer and inner plexiform layer, all segmental areas except the subfoveal region of the inner nuclear layer, most segmental areas (inner superior, inner inferior, outer superior, outer temporal, and outer nasal) of outer plexiform layer, and most segmental areas (subfovea, inner temporal, inner inferior, inner nasal, outer temporal, and outer inferior) of outer nuclear layer were thinner in eyes with high myopia than in normal eyes (all p l 0.05). There were no statistically significant differences between the levels of photoreceptor layer, retinal pigment epithelium, and nerve fiber layer. The mean choroidal thickness was 153.81 ± 64.80 and 239.54 ± 44.28 μm in the high myopia and control groups, respectively, which were significantly different (p l 0.001). Conclusions In high myopia without pathologic changes, there was a meaningful thinning of the retina and choroid, especially in most Early Treatment Diabetic Retinopathy Study subfield areas of the deep vascular complex, perifoveal area of the superficial vascular complex, and most areas of the outer nuclear layer in the outer retinal layer, which are associated with myopic axial elongation.

Paracentral acute middle maculopathy (PAMM) is a relatively new optical coherence tomography finding, defined by hyperreflectivity in the inner nuclear layer. In this article, we present a case of a 73-year-old woman who presented with transient vision loss followed by the sudden onset of complete vision loss to counting fingers at 1 foot for one day in the left eye. Dilated examination showed a right cotton wool spot, left pallid optic disc edema, and retinal edema in the distribution of the cilioretinal artery. OCT demonstrated hyperreflective band at the level of the inner nuclear layer, compatible with PAMM. Clinical and laboratory findings were consistent with GCA, for which she was prescribed high-dose oral prednisone, with confirmation of GCA on a subsequent temporal artery biopsy. PAMM may be seen in the context of GCA, and OCT of the macula serves as an important adjunct to define the retinal manifestations of this condition.

To establish with negative electroretinogram (ERG) the clinical entity of eight patients with unilateral severe photophobia, essentially normal fundus, good visual acuity, and severe cone and rod dysfunction. Multicenter retrospective observation case series. Comprehensive ophthalmologic examinations were performed, including best-corrected visual acuity (BCVA), full-field ERGs and multifocal ERGs (mfERGs), fundus photographs, and OCT. Systemic and genetic examinations were performed. The mean (± SD) age at the onset was 60.0 ± 8.4 years, and the six patients noticed severe photophobia in the affected eye in spite of almost normal fundus appearance and good BCVA. The dark-adapted bright flash ERGs in the affected eye had relatively well-preserved a-waves and depressed b-waves, i.e., a negative ERG. Cone ERGs and both b- and d-waves of the photopic long-duration ERGs were almost undetectable. Rod ERGs were severely reduced; however, only two patients complained of night blindness. In five patients, the mfERGs were extinguished in the periphery but preserved in the central retina, resulting in good BCVA. Electrophysiological findings indicated a severe diffuse dysfunction of the inner retina affecting bipolar cells of both ON- and OFF-pathways, and in five patients there was a reduction in the thickness of the inner nuclear layer. In seven patients the retinal arteries were attenuated. Anti-retinal antibodies were detected in the serum of two patients. No genetic causes were found. The common features in the eight patients with unilateral negative ERGs suggest a new disease entity of unilateral acute inner retinal layer dysfunction. In most patients, the only subjective complain was photophobia.

Central retina imaging is important for early Parkinson’s disease (PD) recognition. We aimed to investigate central retina changes using spectral domain-optical coherence tomography (SD-OCT) in PD patients. We systematically searched PubMed and EMBASE to identify studies comparing the whole or individual layer thickness of central retina between PD patients and health controls using SD-OCT from inception to April 25, 2020. Data were extracted at eye level. We pooled the mean difference with random effects model. Subgroup analysis and mete-regression were done to detect possible source of heterogeneity. We included 27 studies (28 sets of data) enrolling 1470 PD patients (2288 eyes) and 1552 health controls (2524 eyes) in our meta-analysis. Compared with control eyes, the whole thickness of central retina decreased significantly at fovea center by mean difference − 2.70 μm (95% CI [− 4.87, − 0.53], p = 0.01) and in all quadrants in PD eyes. The combination of ganglion cell layer and inner plexiform layer thinned by an average mean difference of − 3.17 μm (95% CI [− 5.07, − 1.26], p = 0.001). The nerve fiber layer thinned by an average mean difference − 0.66 μm (95% CI [− 1.09 to − 0.23], p = 0.003). There was no significant difference in the thickness of inner nuclear layer, outer plexiform layer and outer nuclear layer between eyes of PD and controls. The results of subgroup analysis and mete-regression were consistent. The whole thickness, the thickness of the combination of ganglion cell layer and inner plexiform layer, and nerve fiber layer of central retina decreased significantly in PD patients.

Pigs are considered one of the relevant animal models for ocular research as they share several histological and anatomical similarities with the human eye. With the increasing interest in juvenile animal models, this study aimed to describe the postnatal development of ocular structures in 16 Göttingen minipigs and 25 F2 domestic pigs, between birth and 6 months of age, using histopathology and immunohistochemistry against Ki-67, caspase-3, calbindin, glial fibrillary acidic protein, rhodopsin, and synaptophysin. All ocular structures in both pig breeds were incompletely developed at birth and for variable periods postnatally. Noteworthy histological features of immaturity included vascularization in the corneal stroma in neonatal Göttingen minipigs, increased cellularity in different substructures, remnants of the hyaloid vasculature, short and poorly ramified ciliary body processes, and a poorly developed cone inner segment. Increased cellular proliferation, highlighted by abundant Ki-67 immunolabeling, was observed in almost all developing structures of the pig eye for variable periods postnatally. Apoptosis, highlighted with caspase-3 immunolabeling, was observed in the retinal inner nuclear layer at birth and in the regressing hyaloid vasculature remnants. Immunohistochemistry against rhodopsin, synaptophysin, and calbindin demonstrated the short size of the developing photoreceptors and the immature cone inner segment morphology. Calbindin labeling revealed significant differences in the amount of positively labeled cone nuclei between the retinal area centralis and the non–area centralis regions. The elongation of Müller cell processes in the developing retina was shown with glial fibrillary acidic protein. In both pig breeds, the eyes reached histomorphological and immunohistochemical maturity at 6 months of age.

OBJECTIVE: To examine structural changes in retinal layers over time in patients with non-arteritic anterior ischaemic optic neuropathy (NAION) and determine the layers that predict visual outcomes. METHODS: The optical coherence tomography parameters in NAION eyes at