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Purpose To determine anatomical and functional retinal modifications in patients with idiopathic epiretinal membrane (ERM) without objective symptoms. Methods This prospective monocentric study included 28 eyes of 28 patients with ERM having a best corrected visual acuity greater than 20/25. All patients underwent a complete ophthalmic examination, including the measurement of the visual acuity on the ETDRS scale, a macular SD‐OCT and a microperimetry at 0, 6 and 12 months. We assessed macular abnormalities on SD‐OCT namely: retinal folds, retrofoveolar deposits, cystoid cavities and external retinal layers alterations. Results At baseline the mean visual acuity was 85±4 letters, the mean macular sensitivity was 14.3±1.3 decibels, the mean macular thickness was 357±32 micrometers and the score of the SD‐OCT retinal abnormalities per patient was 2.5±0.8. At one year, the score of the SD‐OCT retinal abnormalities per patient was significantly higher: 3.3±1.3 (p=0.007). At one year, the mean visual acuity, the mean macular sensitivity and the mean macular thickness were stable at 84±5 letters (p=0.8), 14.4±1.7 decibels (p=0.8) and 356±43 micrometers (p=0.3), respectively. Conclusion This study showed an increased number of retinal lesions observed on SD‐OCT with a stable visual acuity and a stable retinal sensitivity measured with the microperimetry after one year of follow‐up.

PurposeThe catabolism of cholesterol in neurons leads to a more hydrophilic compound soluble form, the 24‐S‐hydroxycholesterol by means of an enzyme the CYP46A1.The aim of this study was to analyse the implication of 24‐S‐hydroxycholesterol (24‐S‐OHC) on Müller glial cells (MGC) membrane dynamics in the rat.MethodsMGC were grown in vitro from retinas of 10‐day‐old Long Evans rats. Cells were treated with 24‐S‐OHC (treatment) or ethanol (control) for 2 min or 6 h. From twenty millions of MGC in each group, lipid‐rafts were obtained after a 1% Lubrol lysis and an ultra centrifugation (180,000 g – 20 h – 4°C). The following proteins: caveolin, flottilin, connexin 30 and 43, CRALBP, DHAPAT, GFAP and vimentin were analysed using Western blotting on all fractions (lipid‐rafts and non‐rafts). MGC membrane fluidity was studied in vitro with two different techniques: anisotropy measurements performed with the lipophilic fluorescent probe TMA‐DPH and fluorescence recovery after photobleaching (FRAP) observed using confocal microscopy.Results24‐S‐OHC treatment on in vitro MGC increased the expression of GFAP and delocalized GFAP in the lipid‐raft fraction; 24‐S‐OHC treatment induced a delocalization of DHAPAT protein out of the lipid‐rafts fraction. Anisotropy was decreased with the 24‐S‐OHC treatment (difference: 5.1 × 10−3; p < 0.01) revealing an increase of the membrane fluidity. This increase was confirmed by the FRAP technique, which showed a shorter time of fluorescence recovery for the treated cells.ConclusionsThis study showed that 24‐S‐OHC could be a candidate leading a key role in the activation of MGC, disturbing lipid‐raft organization by changing the localization of signalization proteins and increasing membrane's fluidity.