Background: Optical coherence tomography angiography (OCT-A) has emerged as a novel, fast, safe and non-invasive imaging technique of analyzing the retinal and choroidal microvasculature in vivo. OCT-A captures multiple sequential B-scans performed repeatedly over a specific retinal area at high speed, thus enabling the composition of a vascular map with areas of contrast change (high flow zones) and areas of steady contrast (slow or no flow zones). It therefore provides unique insight into the exact retinal or choroidal layer and location at which abnormal blood flow develops. OCTA has evolved into a useful tool for understanding a number of retinal pathologies such as diabetic retinopathy, age-related macular degeneration, central serous chorioretinopathy, vascular occlusions, macular telangiectasia and choroidal neovascular membranes of other causes. OCT-A technology is also increasingly being used in the evaluation of optic disc perfusion and has been suggested as a valuable tool in the early detection of glaucomatous damage and monitoring progression. Objective: To review the existing literature on the applications of optical coherence tomography angiography in neurodegenerative diseases. Summary: A meticulous literature was performed until the present day. Google Scholar, PubMed, Mendeley search engines were used for this purpose. We used 123 published manuscripts as our references. OCT-A has been utilized so far to describe abnormalities in multiple sclerosis (MS), Alzheimer's disease, arteritic and non-arteritic optic neuropathy (AION and NAION), Leber's hereditary optic neuropathy (LHON) papilloedema, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis (ALS), Wolfram syndrome, migraines, lesions of the visual pathway and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). It appears that OCT-A findings correlate quite well with the severity of the aforementioned diseases. However, OCT-A has its own limitations, namely its lack of wide-field view of the peripheral retina and the inaccurate interpretation due to motion artifacts in uncooperative groups of patients (e.g. children). Larger prospective longitudinal studies will need to be conducted in order to eliminate the aforementioned limitations.

Purpose: To compare visual outcomes, complications and vision-related quality-of-life (QoL) following micro-thin Descemet stripping automated endothelial keratoplasty (MT-DSAEK) versus Descemet membrane endothelial keratoplasty (DMEK) for the management of corneal endothelial dysfunction in Fuchs dystrophy. Design: Prospective, double-blinded randomized controlled clinical trial Methods: Patients with visually significant endothelial decompensation from Fuchs dystrophy were prospectively randomized to receive MT-DSAEK or DMEK surgery. The primary outcome was best spectacle-corrected visual acuity (BSCVA) at 12 months. Secondary outcomes included refraction, keratometry, endothelial cell count, complications and vision-related QoL at 6 and 12 months postoperatively.Results: A total of 56 eyes of 56 patients were enrolled, 28 in each group. Post-operatively, LogMAR mean BSCVA in the MT-DSAEK group was 0.17±0.08 and 0.11±0.09 at 6 and 12 months compared to 0.09±0.13 and 0.04±0.13 following DMEK (p=0.03, p=0.002 respectively) with the DMEK cohort achieving 3.5logMAR letters better BSCVA at 1 year compared to MT-DSAEK. Complication rates were similar with 3.5% rebubbling rate in both groups, 1 primary graft failure in DMEK and a single endothelial rejection in the MT-DSAEK arm. Vision-related QoL was comparable at 6 and 12 months post-operatively and no eyes demonstrated loss of vision from pre-operative BSCVA.Conclusion: DMEK surgery resulted in significantly better BSCVA at 1, 3, 6 and 12 months post-operatively compared to MT-DSAEK. Patient satisfaction was similar with no differences reported in vision-related QoL scores, as was the complications profile between groups. Thus, our results favor DMEK as the better choice procedure for eyes with Fuchs-related corneal decompensation without ocular comorbidities.

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BackgroundSarcoidosis constitutes one of the leading causes of ocular inflammation. Chronic ocular sarcoidosis can affect any segment of the eye and its adnexa, producing a wide range of clinical manifestations and severity. If left untreated, permanent visual impairment or even blindness may ensue. Treatment approaches vary from topical therapy to systemic agents that induce immunosuppression to different levels according to disease severity.ObjectiveTo review the published literature on the management options for chronic ocular sarcoidosis and provide a comprehensive list of available treatment strategies, including the newer biologics.SummaryOcular disease remains a challenging aspect of sarcoidosis and may even be the presenting sign of the disease. Prompt and effective therapy may reverse visual damage and prevent permanent loss of vision. Because of the complexity of the disease, a multidisciplinary approach is often required, with a view to addressing both the ocular and other systemic manifestations of sarcoidosis. Recent data suggest that achieving overall optimal systemic control is of paramount importance in controlling eye inflammation as well. Cytotoxic immunosuppressive agents for refractory chronic ocular disease, as well as biologic anti-TNFα therapies, have advanced the management of chronic disease and should be considered corticosteroid-sparing strategies before the onset of significant steroid-induced morbidity.