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Purpose: To determine the mechanism behind macular bulge height increase in eyes with dome-shaped macula (DSM)., Design: Retrospective, observational case series., Methods: Eyes presenting with DSM followed up for a minimum of 1 year were examined using ocular biometry and spectral-domain optical coherence tomography at baseline and at end of follow-up. Axial length (AL), DSM bulge height, and central and peripheral choroidal thickness (nasal, temporal, superior, and inferior quadrants) were reported. Eyes were categorized into 2 groups for comparison: the "mini-DSM" group (DSM < 100 μm) and the "classic" DSM group (DSM > 100 μm)., Results: Fifty-eight eyes (33 patients) were studied: 32 (55%) were classic DSM and 26 (45%) mini-DSM. During the mean follow-up of 51.76 ± 36.01 months, mean AL increased from 26.99 ± 2.94 mm to 27.12 ± 3.09 mm (P = .010) and mean macular bulge height increased from 235.88 ± 282.47 μm to 262.34 ± 317.15 μm (P < .001). DSM height change was significantly higher than AL change (P < .001). Mean peripheral choroidal thickness significantly decreased nasally (P = .008), temporally (P = .026), and inferiorly (P < .001). Mini-DSM eyes exhibited shorter AL (26.17 vs 27.66 mm; P = .027), greater visual acuity (0.169 vs 0.437 logMAR; P = .002), and fewer macular complications compared to classic DSM eyes., Conclusions: Macular bulge increase in DSM is associated with eye elongation and overall thinning of the peripheral choroid. DSM might result from differential elongation of the eye predominant in the peri-dome region. Mini-DSM (ie, inferior to 100 μm) are characterized by slower evolution, better visual prognosis, and fewer complications compared to "classic" DSM., (Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.)

Purpose: To report immediate and long-term outcomes of acute traumatic maculopathy., Methods: Retrospective case series. Acute traumatic maculopathy was defined as a macular opacification after blunt trauma. Patients were examined at presentation, 1 week, and 6 months. Retinography and time-domain and spectral-domain optical coherence tomographies were performed in all patients. Central macular thickness, the qualitative aspect of the macular profile, and retinal nerve fiber layer thickness were assessed. Multifocal electroretinography was performed at presentation and after 6 months., Results: Twenty patients (20 eyes) were studied. Their mean age was 20.8 years, and the initial visual acuity was 20/100. In all cases, initial optical coherence tomographies revealed an increase in reflectivity of the inner and outer segment junction, with an apposition of the latter to the retinal pigment epithelium. Optical coherence tomography profiles were back to normal at the 1-week visit. Initial multifocal electroretinography performed in six patients showed a decrease in amplitudes in the central area but not in the periphery. There was no delay in latency. Similar electroretinal dysfunction persisted after 6 months., Conclusion: Macular opacification observed in acute traumatic maculopathy is associated with an increase in reflectivity of the inner and outer segment photoreceptor junction on optical coherence tomography. Although visual recovery is excellent, reduction in the electroretinal activity observed 6 months after the trauma suggests that the retina does not fully recover from the initial disorganization of its external layers.

Purpose: To describe an unusual feature in myopic eyes responsible for visual loss, which we call a dome-shaped macula., Design: Retrospective, observational case series., Methods: After observing isolated cases of dome-shaped macula, we analyzed optical coherence tomography (OCT) scans of 140 highly myopic eyes present in our OCT database to find similar cases. Fifteen eyes of 10 patients had a dome-shaped macula. These patients all had undergone fluorescein angiography (FA), indocyanine green angiography (ICGA), and B-scan ultrasonography examinations., Results: The mean refractive error of the affected eyes was -8.25 diopters (D; range, -2 to -15 D). Median visual acuity was 20/50. Recent visual impairment was noted in 11 of the 15 eyes studied, and metamorphopsia was noted in eight eyes. Four eyes were asymptomatic. FA showed atrophic changes in the macular retinal pigment epithelium (RPE) in all eyes, combined with focal points of leakage in seven of the 15 eyes. The dome-shaped appearance of the macula was visible on both B-scan ultrasonography and OCT: a characteristic bulge of the macular retina, RPE, and choroid within the concavity of the moderate posterior staphyloma was present in all eyes. In 10 eyes, OCT also showed a shallow foveal detachment at the top of the dome-shaped macula., Conclusions: A dome-shaped macula within a myopic staphyloma is an unreported type of myopic posterior staphyloma. The dome-shaped macula often is associated with RPE atrophic changes and foveal retinal detachment, which may explain the visual impairment in these eyes.

In 1970s, taurine deficiency was reported to induce photoreceptor degeneration in cats and rats. Recently, we found that taurine deficiency contributes to the retinal toxicity of vigabatrin, an antiepileptic drug. However, in this toxicity, retinal ganglion cells were degenerating in parallel to cone photoreceptors. The aim of this study was to re-assess a classic mouse model of taurine deficiency following a treatment with guanidoethane sulfonate (GES), a taurine transporter inhibitor to determine whether retinal ganglion cells are also affected. GES treatment induced a significant reduction in the taurine plasma levels and a lower weight increase. At the functional level, photopic electroretinograms were reduced indicating a dysfunction in the cone pathway. A change in the autofluorescence appearance of the eye fundus was explained on histological sections by an increased autofluorescence of the retinal pigment epithelium. Although the general morphology of the retina was not affected, cell damages were indicated by the general increase in glial fibrillary acidic protein expression. When cell quantification was achieved on retinal sections, the number of outer/inner segments of cone photoreceptors was reduced (20 %) as the number of retinal ganglion cells (19 %). An abnormal synaptic plasticity of rod bipolar cell dendrites was also observed in GES-treated mice. These results indicate that taurine deficiency can not only lead to photoreceptor degeneration but also to retinal ganglion cell loss. Cone photoreceptors and retinal ganglion cells appear as the most sensitive cells to taurine deficiency. These results may explain the recent therapeutic interest of taurine in retinal degenerative pathologies. [ABSTRACT FROM AUTHOR]

The article highlights medical information regarding myopic foveoschisis (MF) with the hope of helping to improve its medical and surgical management. The reasons behind the prevalence of MF are mentioned. Also described are the optical coherence tomography (OCT) characteristics of MF. The pathophysiology of MF, which seems to involve vitreous traction on the retina, is discussed. The treatment for MF is explained as well.

Purpose: To characterize the evolution of serous retinal detachment (SRD) combined with diabetic macular edema (DME) using optical coherence tomography (OCT). Design: Observational retrospective case series. Methods: In our institution, 64 eyes of 40 diabetic patients who had SRD combined with DME were studied. All patients had fluorescein angiography and several OCT3 examinations during follow-up. Foveolar neuroretinal thickness (NRT) and SRD height were measured. The evolution of OCT macular profiles was qualitatively assessed. Results: Mean follow-up was 11.8 months. DME was focal in 10 eyes (15.6%), diffuse in 17 (26.6%) and both diffuse and focal in 37 (57.8%). Mean initial decimal visual acuity (VA), NRT, and SRD height (± standard deviation) were 0.35 ± 0.21, 346.88 ± 138.61 and 199.48 ± 139.8 μm, respectively. SRD height did not correlate with VA (P = .23) or NRT (P = .31). In 13 eyes (20.3%), NRT above the SRD was normal. In the 19 eyes where DME improved during follow-up, SRD disappeared before the maximal reduction of retinal thickness in seven eyes (36.8%) and after or simultaneously with this reduction, in 12 eyes (63.2%). Among the 45 eyes where DME worsened during follow-up, SRD disappeared from 15 eyes (33.3%). Conclusion: In this series, SRD height did not correlate with retinal thickening. The latter may appear before central neuroretinal thickening and disappear before or after its regression. Consequently, SRD does not seem to be related either to the severity of DME or to its resorption. [Copyright &y& Elsevier]

Abstract: Very early neuroglial changes have been observed to precede major vascular changes in the retina of diabetic patients and animal models. We investigated the sequence of these neuroglial changes further, in mice with alloxan-induced diabetes. Diabetes was induced by a single injection of Alloxan into C57/Bl6 mice, which subsequently received daily insulin injections. Diabetic and control animals were weighed and their blood glucose levels were determined weekly. Electroretinographic recordings and scanner laser ophthalmoscope (SLO) examinations were carried out 15 days, one month and three months after the onset of diabetes. Diabetes induction was confirmed by the presence of glucose in the urine, a tripling of blood glucose level, weight loss and an increase in glycated haemoglobin levels. Three months after diabetes onset, the electroretinogram b/a wave amplitude ratio was decreased at the highest light intensities and oscillatory potentials were delayed. The retinal fundus and vessels remained unchanged. No cell apoptosis was detected in vertical and horizontal sections of the retina by TUNEL or immunocytochemistry for the active caspase 3. No increase in GFAP-immunostaining indicative of a glial reaction was observed in Müller glial cells. By contrast, changes in the morphology of microglial cells were observed, with marked shortening of the dendrites. Thus, the microglial reaction occurs very early in progression to diabetic retinopathy, at about the same time as early electroretinographic modifications. The absence of apoptotic cells, contrasting with previous results in mice with streptozotocin-induced diabetes, is consistent with insulin neuroprotection. [Copyright &y& Elsevier]