Visual and anatomical responses after RNB loading dose are significant predictors of both early term and long-term visual acuity improvement after switching to corticosteroids in patients with DME unresponsive to anti-VEGF.

No abstract

The aim of this study was to perform quantitative optical coherence tomography angiography (OCTA) assessment of arteritic and non-arteritic anterior ischemic optic neuropathies (AION; NAION). The study was designed as an observational, cross-sectional case series. All patients underwent complete ophthalmologic evaluation including LogMAR best-corrected visual acuity (BCVA), structural optical coherence tomography (OCT) and OCTA images, and dye-based angiography. Retinal nerve fiber layer (RNFL) thickness was obtained from structural OCT, and vessel density (VD) and vessel tortuosity (VT) were measured for each optic nerve head vascular plexus. After selecting the quadrants showing visual field defects, measured by Humphrey 30.2 perimetry (Zeiss Meditec, Dublin, CA, USA), we assessed the correlation between the localization of visual field defects and the quadrants showing impairments of RNFL, VD, and VT. Thirty naïve AION patients (15 arteritic AION (AAION) and 15 non-arteritic AION (NAION)) were included. LogMAR BCVA was 0.6 ± 0.2 for AAION and 0.3 ± 0.3 for NAION (p < 0.01). AAION and NAION eyes showed significant differences in terms of visual field involvement as well as VD and VT values, with remarkably worse alterations affecting AAION eyes. VD values perfectly matched with the quadrants showing RNFL and visual field defects. On the contrary, VT resulted remarkably decreased in all the quadrants, with even worse values in the quadrants showing RNFL and visual field alterations. The present study showed that AAION eyes are more injured than NAION ones. VD represents a good parameter for the detection of the main site on vascular impairment. Remarkably, VT resulted in a more sensitive parameter for the quantitative detection of blood flow impairment in AION disease.

No abstract

The pathogenesis of diabetic macular edema (DME) is complex. Persistently high blood glucose activates multiple cellular pathways and induces inflammation, oxidation stress, and vascular dysfunction. Retinal ganglion cells, macroglial and microglial cells, endothelial cells, pericytes, and retinal pigment epithelium cells are involved. Neurodegeneration, characterized by dysfunction or apoptotic loss of retinal neurons, occurs early and independently from the vascular alterations. Despite the increasing knowledge on the pathways involved in DME, only limited therapeutic strategies are available. Besides antiangiogenic drugs and intravitreal corticosteroids, alternative therapeutic options tackling inflammation, oxidative stress, and neurodegeneration have been considered, but none of them has been currently approved.