Age-related macular degeneration (AMD) was described for the first time in the 1840s and is currently the leading cause of blindness for patients over 65 years in Western Countries. This disease impacts the eye’s posterior segment and damages the macula, a retina section with high levels of photoreceptor cells and responsible for the central vision. Advanced AMD stages are divided into the atrophic (dry) form and the exudative (wet) form. Atrophic AMD consists in the progressive atrophy of the retinal pigment epithelium (RPE) and the outer retinal layers, while the exudative form results in the anarchic invasion by choroidal neo-vessels of RPE and the retina. This invasion is responsible for fluid accumulation in the intra/sub-retinal spaces and for a progressive dysfunction of the photoreceptor cells. To date, the few existing anti-AMD therapies may only delay or suspend its progression, without providing cure to patients. However, in the last decade, an outstanding number of research programs targeting its different aspects have been initiated by academics and industrials. This review aims to bring together the most recent advances and insights into the mechanisms underlying AMD pathogenicity and disease evolution, and to highlight the current hypotheses towards the development of new treatments, i.e., symptomatic vs. curative. The therapeutic options and drugs proposed to tackle these mechanisms are analyzed and critically compared. A particular emphasis has been given to the therapeutic agents currently tested in clinical trials, whose results have been carefully collected and discussed whenever possible.

Aim To assess the effectiveness and safety of intravitreal dexamethasone implants for treating post-surgical macular oedema, including Irvine-Gass syndrome refractory to first-line treatments. Methods Descriptive, observational, retrospective, consecutive, uncontrolled, multicentre, national case series. 50 patients were included in the study between March 2011 and June 2013 with a minimum 6 months follow-up. At baseline, each patient received a dexamethasone implant 0.7 mg (Ozurdex). Best-corrected visual acuity (BCVA), central subfield macular thickness (CSMT), and intraocular pressure (IOP) were measured at baseline and then monthly. The main outcome measure was the mean change in BCVA (in ETDRS letters (Early Treatment Diabetic Retinopathy Study): L) Results Baseline mean±SD BCVA was 55.7±15.4 L. At month 2, BCVA was 71.8±10.5 L and 61.2% of patients had an increase of more than 15 letters. Baseline mean CSMT was 544±117.2 μm and this decreased to 302 μm at month 2. Anatomic and functional recurrences were both first detected from month 3 and continued throughout follow-up, with values consistently above baseline. The peak in IOP was reached in month 1 with mean IOP of 15.3±4.6 mm Hg. Of the 39/50 patients followed up for 12 months, 49% received a second injection. The anatomic and functional response and safety patterns were similar to that obtained with the first intravitreal injection, demonstrating Ozurdex’s reproducibility. However, more than half of the patients followed-up for at least 1 year presented neither functional nor anatomical recurrence. Conclusions Ozurdex would appear to be an interesting alternative therapy for treating post-surgical macular oedema, including Irvine-Gass syndrome refractory to first-line treatments.

Purpose. To compare subfoveal choroidal thickness (SFCT) before and after uneventful cataract surgery using enhanced depth imaging optical coherence tomography (EDI-OCT). Methods. A prospective study was conducted on 115 eyes of 95 patients who had phacoemulsification. Measurements of SFCT were performed preoperatively, 1 day (D1), 7 days (D7), 1 month (M1), and 3 months (M3) after surgery using the EDI-OCT technique. Central retinal thickness (CRT) was measured before surgery and at M1 and M3. Results. The 95 patients had a mean age of 76 ± 8.3 years. The mean SFCT at baseline was 224 ± 75 μm. It showed a negative correlation with age and axial length (P = 0.03). The SFCT significantly increased after surgery with a mean value of 232 ± 76 μm at D1 (P < 0.001), 237 ± 78 μm at M1 (P < 0.001), and 232 ± 76 μm at M3 (P < 0.001). The mean CRT increased from 234 ± 48 μm at baseline to 248 ± 48 μm at M1 (P = 0.005), and 252 ± 81 μm at M3 (P = 0.001). Three (2.6%) patients developed a pseudophakic cystoid macular edema (PCME). The greatest progression of SFCT after phacoemulsification was observed for these patients. It preceded the occurrence of pseudophakic cystoid macular edema (PCME) by 1 month. Conclusions. Mean SFCT increased after cataract surgery. The changes in baseline SFCT were greater in PCME patients and preceded the increase in CRT.

Purpose: To determine the specific location of the initial lesion in acute retinal pigment epitheliitis. Methods: Four patients diagnosed with acute retinal pigment epitheliitis were studied. Fundus photographs, fluorescein angiography and indocyanine green angiography, and spectral-domain optical coherence tomography findings were reviewed. Results: Four healthy young patients presented with acute onset of unilateral decreased vision. Ophthalmoscopy showed macular pigment mottling with surrounding yellow hypopigmented areas at the level of the retinal pigment epithelium (RPE). Fluorescein angiography revealed transmission hyperfluorescence. Early-phase and midphase indocyanine green angiography images showed a patchy macular hyperfluorescence. At late phase of indocyanine green angiography, a hyperfluorescent halo with a cockadelike appearance of the macular area was observed. Spectral-domain optical coherence tomography showed a disruption of the photoreceptors' inner segment and outer segment interface associated with a wider disruption of the RPE inner band. These disrupted lines were replaced by a dome-shaped highly reflective lesion involving the RPE inner layer, the photoreceptors' inner segment and outer segment layers, and, in two cases, the outer nuclear layer. With time, indocyanine green angiography showed resolution of the observed lesions. Spectral-domain optical coherence tomography showed restored and continuous inner segment and outer segment layers and RPE inner band. Conclusion: Spectral-domain optical coherence tomography findings suggest that the initial lesion in acute retinal pigment epitheliitis is located at the junction between the photoreceptor outer segments and the apical side of the RPE cells. Indocyanine green angiography and spectral-domain optical coherence tomography show that the RPE appears to be more widely involved than the neurosensory retina.