Microstructural changes in CSC have attracted much interest in recent years. And the improvements of technologies in the field of OCT has enabled reproducible, in-vivo, automatic and quantitative measurements of retinal layer thicknesses even in pathologic eyes [16, 17].
In the present study of the OCT findings in unilateral resolved acute CSC, we found a decrement in the ONL thickness in the central 1-mm circle of the affected eyes. There might be possible explanations; first, the current understanding of the pathogenesis of CSC emphasizes the role of the choroid, which is the main source of blood supply to the foveal avascular zone. And a great portion of retina in the foveal avascular zone is composed of the ONL . Focal ischemia of the choriocapillaris may result in photoreceptor apoptosis leading to ONL thinning. Second, experimental animal models have shown that retinal detachment and reattachment can induce a variety of cellular changes that can decrease visual acuity [19–21]. Retinal detachment can cause photoreceptor cell loss, found as early as 1 to 3 days after retinal detachment [22, 23]. Although the estimated onset of the CSC is based on the symptom perception of participant and is not completely definite, our results are consistent with experimental retinal detachment models in which the number of photoreceptor cells reduces within a few days, suggesting that ONL thinning may begin in the very early stage of CSC [22, 23]. The baseline ONL thinning determined in our study can be explained by rapid affect of short-term retinal detachment. With reattachment, the retina can recover to some degree, but this recovery is accompanied by morphological abnormalities such as decreased number of cells in ONL . Similarly in our study, the finding that the average ONL thickness increased 6 months after complete resolution of SRF, but still low compared to uninvolved fellow eye supporting that retina can recover to some degree. Third, Maruko et al. , reported that after reattachment, the ONL was thinner in eyes with CSC than in eyes with rhegmatogenous retinal detachment, although the duration of SRF did not differ between the two groups. This finding reveals that in CSC, not only detachment of neurosensorial retina from the RPE induces apoptosis of photoreceptors and also SRF, which is composed of leaking from the choroidal vascular system, may contribute to apoptosis. However, Goktas , investigated the correlation of SRF volume with choroidal thickness and macular volume in acute CSC and reported that SRF volume does not correlate with macular volume suggesting that formation of SRF is not solely responsible from changes in macular volume in acute CSC. Hata et al. , reported that ONL thickness starts to decrease with the occurrence of SRF, progresses until the resolution of SRF and showed no significant change for at least 6 months after complete resolution of SRF indicating that the loss of photoreceptors does not proceed after SRF resolution. However, Ersoz et al. , reported that decrease in ONL thickness starts with development of RPE alterations before SRF accumulation in pachychoroid pigment epitheliopathy. In our study, we found that the mean ONL thickness was increased 6 months after complete resolution of SRF, but the increment was not statistically significant. Similar to our results, Nakamura et al. , reported that the cone density remained lower after resolution of SRF in the eyes with CSC than in the normal eyes. Additionally, they found that the cone density increased throughout the follow-up period.
The ONL in affected eyes of patients with CSC was consistently thinner than in unaffected fellow eyes, despite the fact that unaffected fellow eyes may not always be completely normal; characteristic findings of CSC, such as hypoperfusion or hyperpermeability of the vessels in the choroid, can frequently be seen in both eyes [29, 30]. For this reason we compared unaffected fellow eyes and healthy controls and we found that ONL thicknesses of eyes with CSC and unaffected fellow eyes were reduced compared to healthy control group, however the decrement was statistically significant only in eyes with CSC.
Previous OCT studies have shown that the thinning of ONL was related to poor visual outcomes. The ONL is composed of the nuclei of photoreceptors and its thinning reflects loss of photoreceptors . According to a common assumption, ONL thinning in patients with CSC is a consequence of disturbed regeneration of photoreceptor outer segments due to the failure of phagocytosis [7, 9]. Nakamura et al. , reported that the mean cone densities of eyes with CSC after SRF resolution were significantly decreased compared to the healthy control eyes. Similarly, a significant correlation of visual acuity and the ONL thickness was also observed in the current study at baseline and 6 months after complete resolution of SRF. Moreover, since the size and brightness of images determined by the number of stimulated cones, most of the patients reported micropsia and darkness after resolution of CSC despite good BCVA.
There were several limitations in our study, including the small number of cases, the short period of follow up, the retrospective nature of the study. Furthermore, only assessment of visual acuity is insufficient to assess macular function. Further studies are needed to investigate the relationship of foveal microstructural changes and retinal function.
In conclusion, ONL thickness is thinned in cases with acute CSC, and although there is some increase in ONL thickness 6 months after complete resolution of the SRF, it is still thinner compared to the unaffected fellow eyes. Additionally, ONL thickness was correlated with the BCVA in eyes with CSC before and after resolution of SRF.