This study evaluated a group of patients with acute CSC using mfERG and EDI-OCT. mfERG is an objective examination that provides a regional map of retinal function across the posterior pole. Many studies have demonstrated abnormal mfERG responses in the detached retina in an affected eye.[9–12, 15–17] However, debate persists regarding the mfERG abnormalities in areas without serous detachment and in the normal fellow eye. Marmor and Tan were the first to show abnormal mfERG responses in the peripheral retina without SRD, but subsequent studies revealed that reductions in mfERG responses were limited to the central rings of affected eyes.[10, 11, 15–17] Unfortunately, these studies were not able to resolve this debate because of the relatively small numbers of patients enrolled. Timothy et al. performed a cross-sectional study in 45 eyes with acute CSC using mfERG and found a reduction in the second-order mfERG response for the more peripheral macular area. 
In the present study, mfERG examination in 57 patients with acute CSC showed that retinal responses and the implicit time of mfERG were significantly impaired in the area with SRD, which is consistent with previous reports. The P1 amplitude and implicit time of rings 4–5 was found to be significantly impaired in affected eyes when compared with the controls. This finding suggested that the area of retinal dysfunction in CSC is larger than the SRD observed clinically. In contrast with the mfERG results in affected eyes, the retinal response in fellow eyes was less severely impaired over the entire area examined. However, a post hoc analysis revealed that the patients with a better reduction in SRD showed a less impaired mfERG response in fellow eyes than the patients whose retinal detachments were not spontaneously decreased by more than 90% after 3 months. This finding means that some of the patients with unilateral CSC had fellow eyes with good retinal responses and others did not. For this reason, there has been debate regarding whether normal fellow eyes in patients with CSC have abnormal retinal responses on mfERG examination. This study clearly indicates that the pathogenesis of CSC involves areas beyond the SRD in affected eyes and areas throughout the posterior pole of non-affected eyes; this finding support the view that CSC is a disease affected by systemic humoral factors or by diffuse underlying choroidal vascular disease.[18, 19]
The advent of EDI-OCT has provided a non-invasive method for examination of the choroid and has contributed greatly to current understanding of the pathogenesis underlying CSC. EDI-OCT imaging has shown that the choroid is abnormally thickened in both the affected and non-affected eye during the acute phase of CSC and that the choroidal thickness gradually decreases with regression of the disease. The EDI-OCT imaging measurements in this study also showed that the choroid thickness was increased in both the affected and normal fellow eyes but decreased significantly as SRD regressed. In addition to measuring choroidal thickness, various parameters from the OCT images, including SRFT, CRT, and CMT were measured manually and correlations were sought between the mfERG and OCT parameters. Previous studies that investigated patients with CSC using mfERG and OCT performed similar analyses to identify associations between the functional and structural changes in CSC.[9, 20] In those studies, there was no significant association of OCT parameters, including SRFT, CCT, and CMT, with mfERG parameters and none performed correlation analysis, including for choroidal thickness, in patients with CSC because EDI-OCT was not available at the time when the studies were conducted. In the present study, subfoveal choroidal thickness was the only OCT parameter that was negatively associated with mfERG. Ignacio et al. reported significant correlations between choroidal thickness and the results of mfERG. The choroid dissipates heat from retinal metabolism and supplies nutrients and oxygen to the outer retina. Furthermore, pathological change in the choroid has been proposed to be involved in the pathogenesis of CSC. Therefore, a thickened choroid implies that a pathological change in the choroid, compromised photoreceptor metabolism, and an ischemic outer retinal layer causes the retinal dysfunction. In this study, retinal dysfunction become more prominent as the choroid thickened.
The major limitation of this study is the lack of follow-up mfERG results. There has been debate as to whether retinal dysfunction is fully recovered after resolution of SRD.[10, 11] This study was not able to answer this question. A further prospective study that includes follow-up mfERG evaluation in a large number of patients with CSC is needed for a better understanding of retinal dysfunction in CSC. The second limitation is that only the thickness of the choroid was measured, in spite of EDI-OCT allowing for in-depth observation of the choroid and the analysis was unable to compare the exact location between OCT images and mfERG measurements.  These limitations may have contributed to the lack of a significant correlation between the choroidal thickness of fellow eyes and the mfERG results (data not presented), unlike with affected eyes. The mfERG results and choroidal thickness in the fellow eye were not perfectly normal, and gross measurement of choroidal thickness could not detect subtle differences, which may have resulted in failure to identify a correlation between OCT and mfERG in fellow eyes. Evaluation of structural components of the choroid by EDI-OCT, along with functional evaluation by mfERG, will provide new insights into the pathogenesis of CSC. The small number of control subjects and short follow-up period were further weaknesses of this study.
In spite of these limitations, this study is the first to examine patients with acute CSC using a combination of EDI-OCT and mfERG and found bilateral diffuse impairment of the retinal response. The retinal response of the unaffected eye was associated with regression of SRD, suggesting that the mfERG results for the unaffected eye may serve as an indicator of spontaneous regression. By applying the mfERG in routine clinical examination for CSC, patients will be able to obtain more precise information regarding their course of disease. Furthermore, pathological changes in the choroid identified by EDI-OCT had a negative correlation with retinal function measured with mfERG. These findings imply that structural and functional impairment of the choroid plays an important role in the pathogenesis of CSC. Further evaluation using EDI-OCT and mfERG will improve current understanding of the choroid in patients with CSC and explain the subtle variation in disease progression from patient to patient.