|Year : 2016 | Volume
| Issue : 3 | Page : 151-156
Sub-foveal choroidal thickness in acute central serous chorioretinopathy and its correlation with central macular thickness
Hossam T Al-Sharkawy MD , Rania K Farag
Ophthalmology Department Center, Faculty of Medicine, Mansoura University, Mansoura, Egypt
|Date of Submission||09-Jul-2016|
|Date of Acceptance||28-Sep-2016|
|Date of Web Publication||6-Dec-2016|
Hossam T Al-Sharkawy
Ophthalmology Center, Faculty of Medicine, Mansoura University, Mansoura - 35516
Source of Support: None, Conflict of Interest: None
The aim of the study was to measure subfoveal choroidal thickness (SFCT) in eyes with central serous chorioretinopathy (CSCR), to compare it with that of contralateral clinically unaffected eyes and with that of other healthy persons, and to study its correlation with central macular thickness (CMT).
Patients and methods
Fifty-four eyes of 36 (23 male and 13 female patients) patients were included in this study under three groups: 18 eyes with recent unilateral CSCR, 18 free fellow eyes of patients with unilateral CSCR, and 18 healthy eyes of age-matched normal controls. Spectral-domain optical coherence tomography was performed to measure SFCT in all eyes and CMT in eyes with CSCR.
The mean patient age was 37.4 years, whereas that of normal controls was 38.0 years. The mean SFCT was 332.0 μm in eyes with CSCR, 247.25 μm in the unaffected fellow eyes, and 248.74 μm in normal control eyes. SFCT in eyes with CSCR was significantly greater than that in each of the unaffected fellow eyes and normal control eyes, whereas there was no significant difference between fellow eyes and control eyes. The mean CMT in eyes with CSCR was 477.62 μm with a significant positive correlation with SFCT.
Subfoveal choroid in eyes with acute unilateral CSCR was significantly thicker than that in contralateral clinically unaffected eyes and that in healthy eyes of age-matched normal controls, whereas it was not significantly different between contralateral unaffected eyes and normal eyes. CMT was positively correlated with SFCT in eyes with CSCR.
Keywords: central serous chorioretinopathy, choroidal thickness, optical coherence tomography
|How to cite this article:|
Al-Sharkawy HT, Farag RK. Sub-foveal choroidal thickness in acute central serous chorioretinopathy and its correlation with central macular thickness. Delta J Ophthalmol 2016;17:151-6
|How to cite this URL:|
Al-Sharkawy HT, Farag RK. Sub-foveal choroidal thickness in acute central serous chorioretinopathy and its correlation with central macular thickness. Delta J Ophthalmol [serial online] 2016 [cited 2022 Jul 2];17:151-6. Available from: http://www.djo.eg.net/text.asp?2016/17/3/151/195259
| Introduction|| |
Central serous chorioretinopathy (CSCR) is a relatively common idiopathically acquired chorioretinal disorder that was first described by von Graefe in 1866 ,. It usually affects young and middle-aged men between the ages of 20 and 50 years . It is characterized by well-defined serous neurosensory retinal detachment in the posterior pole  with leakage of fluid through the retinal pigment epithelium (RPE) into the subretinal space .
The precise pathophysiology of CSCR is still not fully understood . Impairment in the absorptive capacity and barrier function in the RPE was previously thought to be an important contributing factor . However, Negi and Marmor , concluded that simple dysfunction of the RPE could not lead to CSCR. Gass  postulated that choriocapillaris hyperpermeability might result in exudation of fluid into the subretinal space. More recent studies using indocyanine green angiography revealed abnormalities of the choroidal vasculature, including delayed infusion, venous dilatation, vascular congestion, and hyperpermeability ,,,,,,, suggesting that a generalized choroidal vascular disturbance occurs in CSCR . Other studies using high-resolution ultrasonography also demonstrated hyperdynamic circulation within the choroid of eyes with CSCR ,,. Increased choroidal pressure from hyperpermeable vessels may cause RPE damage and detachment and ultimately result in neurosensory detachment . It is now generally accepted that the choroid is the primary site involved in CSCR pathology . However, no method was available to observe the choroidal thickness in vivo .
Optical coherence tomography (OCT) is a noninvasive imaging technique that has been one of the most important ancillary tests used extensively for diagnosis and monitoring of many posterior segment diseases by providing high-resolution, cross-sectional images of the retina, the retinal nerve fiber layer, and the optic nerve head. However, clear imaging of the choroid using OCT has often been difficult as the RPE hinders the penetration process and is highly light scattering, resulting in attenuation of the relatively weak reflection signal from the choroid . This is because the wavelength of the light source in conventional OCT (840–870 nm) is not long enough to penetrate into the choroid, which needs a wavelength in the 1060 nm range for clear imaging . However, the recent advances in OCT technology and software now enable sufficient visualization of the choroid for measuring its thickness .
The aim of this study was to measure the subfoveal choroidal thickness in eyes with acute unilateral CSCR using spectral-domain (SD)-OCT, to compare it with that of contralateral clinically unaffected eyes and with that of other healthy persons, and to study its possible correlation with central macular thickness (CMT).
| Patients and methods|| |
This prospective cross-sectional study included 54 eyes of 36 patients from among those who attended the Nile Ophthalmology Center in Mansoura, Egypt, between January and December 2015. The Ethics Committee of the Faculty of Medicine, Mansoura University, approved the study protocol, and written informed consent was obtained from each patient. There were 23 (63.89%) men and 13 (36.11%) women and their mean age was 37.69±8.81 years with a range from 24 to 52 years. The eyes were enrolled under three groups;
- Group I: 18 eyes with recent unilateral CSCR.
- Group II: 18 free fellow eyes of patients with unilateral CSCR.
- Group III: 18 healthy eyes of age-matched normal controls.
All participants underwent a complete bilateral ophthalmic examination that included assessment of refraction and best-corrected visual acuity, slit-lamp biomicroscopy, dilated fundus examination, intraocular pressure measurement, and OCT. In addition, fundus photography and fluorescein angiography were performed for patients with CSCR.
Inclusion criteria for CSCR were symptom duration of less than 1 month, presence of circumscribed area of subretinal fluid involving the macula confirmed by OCT, and evidence of idiopathic leakage from the RPE on fluorescein angiography in one eye.
Exclusion criteria included bilateral CSCR, chronic CSCR, refractive error more than ±4.0 D, other ocular diseases that might produce subretinal fluid such as polypoidal choroidal vasculopathy, choroidal neovascularization, age-related macular degeneration, pathological myopia, intraocular inflammation or infection, retinal dystrophies, macular hole, epiretinal membrane, and macular edema not associated with CSCR, glaucoma or ocular hypertension (intraocular pressure >21 mmHg), dense media opacity that might result in a poor image, history of ocular surgery or photocoagulation, pregnancy, systemic diseases that might affect choroidal thickness, such as diabetes mellitus and malignant hypertension, and intake of medication that might alter the choroidal vasculature, including corticosteroid and sildenafil ,.
Optical coherence tomography measurements
A three-dimensional OD-OCT system, which is combined with a nonmydriatic retinal camera (3D OCT 2000, version 8.10; Topcon Corp., Tokyo, Japan), was used to measure the subfoveal choroidal thickness (SFCT) in all eyes included in the study and to measure CMT in eyes with CSCR. This system has ∼5 µm axial resolution and 20 µm horizontal resolution. three-dimensional data were obtained using the raster scanning technique centered on the fovea, covering a square area measuring 6 mm horizontal, 6 mm vertical, and 1.7 mm axial depth.
An internal fixation target was used to improve reproducibility, and pupil dilatation with tropicamide 1% and phenylephrine 2.5% was done before scanning. The choroidal mode, included in the OCT system software, was used to examine the macular area. All OCT images were captured between noon and 2 O’clock. OCT enabled clear visualization of the individual layers; the presumed fovea was first defined as the central area without the inner retinal layers. These layers, which were well delineated in the periphery, were traced to the central area until the area where these layers disappeared was determined. All OCT measurements were taken by one experienced examiner (R.K.F.) who was blinded to the state of the contralateral (group II) eyes. The SFCT was defined as the vertical distance between the outer border of the hyper-reflective line corresponding to the RPE-Bruch’s membrane complex and innermost hyper-reflective line of chorioscleral interface directly beneath the center of the fovea and was manually measured in all eyes using the built-in caliper tool ([Figure 1]). The retinal thickness at the central fovea (CMTs) was defined as the distance from the inner retinal surface to the RPE including the serous retinal detachment and was automatically measured in all CSCR eyes with OCT software.
|Figure 1 Subfoveal choroidal thickness measured manually using the built-in caliper tool. (a) Eye with central serous chorioretinopathy (330 μ). (b) Clinically unaffected fellow eye (250 μ). (c) Healthy control eye (207 μ).|
Click here to view
Observed data were presented as means and standard deviations, and statistical analysis was performed using the statistical package for the social sciences (SPSS, version 18.0; SPSS Inc., Chicago, Illinois, USA) for windows. Multiple values were compared by analysis of variance, and when differences were significant post hoc multiple comparisons were performed (least significant difference). Correlations were investigated using Pearson’s correlation coefficient. A P value of up to 0.05 was considered statistically significant.
| Results|| |
[Table 1] shows age and sex in the three groups. Patients of groups I and II (eyes with CSCR and their clinically unaffected fellow eyes, respectively) were composed of 12 (66.6%) men and six (33.4%) women and their mean age was 37.4±7.77 years with a range from 24 to 49 years, whereas patients of group III (normal control eyes) were composed of 11 (61.1%) men and seven (38.9%) women and their mean age was 38.0±10.1 years with a range from 26 to 52 years. There was no statistically significant difference in age between the groups (t=−0.180 and P=0.858). The correlation between SFCT and age was not significant in total eyes (r=−0.127 and P=0.480), in group I eyes with CSCR (r=0.070 and P=0.805), or in group II eyes (fellow eyes) (r=0.412 and P=0.359), whereas there was a significant negative correlation between SFCT and age in group III normal control eyes (r=−0.747 and P=0.008).
[Table 2] shows SFCT in the three groups. The mean SFCT in group I (eyes with CSCR) was 332.0±36.46 μm with a range from 282 to 398 μm, whereas in the unaffected fellow eyes (group II) the mean SFCT was 247.25±41.24 μm with a range from 218 to 346 μm. Normal control eyes had a mean SFCT of 248.74±13.26 μm with a range from 219 to 274 μm. By analysis of variance test, there was a statistically significant difference in SFCT among the three groups (F=41.24 and P<0.001). SFCT in eyes with CSCR was significantly greater than that in each of the unaffected fellow eyes (P<0.001) and normal control eyes (P<0.001), whereas there was no statistically significant difference in SFCT between the unaffected fellow eyes and normal control eyes (P=0.906).
CMT, including the serous retinal detachment, was automatically measured in group I eyes with CSCR to determine whether there was a correlation between SFCT and CMT. The mean CMT in eyes with CSCR was 477.62±142.56 μm with a range from 273 to 715 μm, and there was a statistically significant positive correlation between SFCT and CMT in these eyes (r=0.622 and P=0.023).
| Discussion|| |
Choroidal thickness may be affected by age, axial length, refractive error, and diurnal variation ,,,,,. Age was not significantly different among the current study groups. Eyes with refractive error more than ±4.0 D were excluded from the study to avoid the effect of high refractive errors on choroidal thickness. Usui et al.  and Tan et al.  reported that choroidal thickness was greatest in the morning and progressively decreased throughout the day, with a relatively small diurnal variation of 20–30 μm. All OCT images in the present study were captured between noon and 2 O’clock to avoid the effect of diurnal variation on choroidal thickness.
Mean patient age was 37.4 years (12 men and six women), whereas that of normal controls was 38 years (11 men and seven women). This was similar to the mean age reported by Goktas  for CSCR patients and controls. Yang et al.  had moderately older patients and controls, whereas this age was much younger than that reported by Kuroda et al. , by Manabe et al. , and by Jirarattanasopa et al. , who included cases of chronic and/or resolved CSCR as well.
In the current study, the mean SFCT of eyes with CSCR (332 μm) was significantly greater than that in the unaffected fellow eyes (247.25 μm) and in normal control eyes (248.74 μm), whereas the thickness was not significantly different between unaffected fellow eyes and normal control eyes. These results are in agreement with those obtained by Jirarattanasopa et al. , who used the longer wavelength swept-source OCT to measure the mean whole macular choroidal thickness in unaffected fellow eyes (254.2 μm) and found it less than that in unilateral CSCR eyes (326.6 μm) but it did not differ from normal control eyes (233.0 μm). Using enhanced depth imaging OCT, Maruko et al.  also found subfoveal choroid in symptomatic eyes to be significantly thicker than that in fellow eyes (414 vs. 350 µm, respectively) and Kuroda et al.  reported that mean SFCT in eyes with CSCR (475 μm) was significantly greater than that in age-matched control eyes (372 μm).
In CSCR, the choroid may not be thickened only in the subfoveal area but in other retinal zones as well. Manabe et al. , using SD-OCT in the choroidal mode, measured the mean choroidal thicknesses in the center, inner circle, and outer circle of the macula in active chronic CSCR and found them significantly greater than in normal controls before treatment with photodynamic therapy. After treatment, the thickness was reduced to the normal values in the center and inner circle but not in the outer circle of the macula. Kim et al.  also used the choroidal mode to measure choroidal thicknesses at five points (center of the fovea, 500 μm temporal and nasal to the fovea, and 1500 μm temporal and nasal to the fovea) and found them significantly higher for CSCR eyes than for controls at all locations.
The present study did not find significant difference in SFCT between clinically unaffected fellow eyes and normal control eyes. However, Dang et al. , using enhanced depth imaging OCT, found the mean SFCT in symptomatic eyes with CSCR (422 µm) to be significantly greater than that in fellow eyes (367 µm) and the mean SFCT in fellow eyes to be significantly greater than that in the control group (274 µm). This was also consistent with the study conducted by Goktas , who reported significant differences in mean SFCT among CSCR eyes (461.4 µm), fellow eyes (375.3 µm), and control eyes (287.6 µm). Similarly, Yang et al.  concluded that the mean SFCT was significantly larger in the affected CSCR eyes (455 µm) than in the contralateral unaffected eyes (387 µm), which was significantly larger than that in the eyes of the control group (289 µm).
Choroidal thickening in CSCR may reflect increased choriocapillary permeability through accumulation of fluid and expansion of the choroidal vessels. Maruko et al.  found that the subfoveal choroid in the fellow eyes of patients with CSCR was significantly thicker (mean 410 μm) in eyes with choroidal vascular hyperpermeability visualized with indocyanine green angiography than in eyes without choroidal vascular hyperpermeability (mean 239 μm) and concluded that measuring the choroidal thickness with OCT might be a useful noninvasive method to evaluate the subclinical abnormalities in CSCR. Dang et al.  did not find significant differences in SFCT between the fellow eyes without hyperfluorescence and the control eyes, indicating that choroidal vascular hyperpermeability played an important role in the pathophysiology of CSCR.
Bilaterality of the choroidal vasculopathy in many studies suggests a systemic etiology for the disease  causing hyperperfusion of the choroid, which may be attributed to increased sympathetic nerve activity . This produces high hydrostatic pressure within the choroid, eventually leading to RPE leaks and serous retinal detachment ,. Subretinal fluid accumulates when the exudation of serous fluid from choroidal vessels exceeds the barrier and the pump functions of RPE . Kang and Kim  found that the thickness of the choroid in eyes with CSCR decreased after spontaneous resolution of subretinal fluid but not to the normal level. This corresponds to the study of Iida et al. , which demonstrated persistence of the choroidal vascular abnormalities on indocyanine green angiography, even after cessation of RPE leakage, explaining the common recurrences in CSCR.
Several studies have recognized patient age as the most important factor determining choroidal thickness in normal eyes ,,,, but this may not apply for CSCR patients. In the present study, there was a significant negative correlation between SFCT and age in normal control eyes but not in eyes with CSCR or fellow eyes. This is consistent with the study of Margolis and Spaide , who reported a mean decrease in choroidal thickness of 15.6 µm/year in normal eyes. Ikuno et al.  and Kim et al.  also concluded that age was the most strongly associated factor with choroidal thickness rather than refractive error in healthy eyes. On the other hand, Imamura et al.  found no correlation between SFCT and age in CSCR patients, whereas Jirarattanasopa et al.  reported that the mean macular choroidal thickness was negatively correlated with age in eyes with CSCR.
The current study also investigated the correlation between SFCT and CMT, including elevation of the serous retinal detachment, in eyes with CSCR and found a significant positive correlation. Goktas , instead, studied the correlation of SFCT and subretinal fluid volume, which was estimated using a built-in segmentation-modifying tool of SD-OCT, and found no association between these two parameters in eyes with acute CSCR. Therefore, he suggested that formation of subretinal fluid might not solely be associated with choroidal vasculature and that some additional factors such as RPE dysfunction could have a role in the pathogenesis of CSCR, which might need further studies to clarify.
Limitations of this study included its cross-sectional design, with selection of only unilateral acute CSCR with no follow-up of choroidal thickness after resolution or in chronic cases. The number of cases was small as the disease might be less common in Egypt than in the Far-East. Choroidal thickness was measured manually by a single observer because there was no automatic detection and segmentation software available for measurement of choroidal thickness. Light scattering by RPE and choroid made visualization of the choroidoscleral interface difficult in some eyes, especially in those with thick choroid. In addition, measurement was taken at a single point only (subfoveal), although the choroid might be thicker elsewhere in some cases.
| Conclusion|| |
OD-OCT is a noninvasive easy, reproducible tool to image the choroid and may be a valuable method in the diagnosis and understanding of the pathophysiology of CSCR. Subfoveal choroid in eyes with acute unilateral CSCR was significantly thicker than that in contralateral clinically unaffected eyes and that in healthy eyes of age-matched normal controls, whereas there was no significant difference in SFCT between contralateral clinically unaffected eyes and normal control eyes. This study supports the concept that CSCR is a primary choroidal disorder. The CMT including the serous retinal detachment was positively correlated with SFCT in eyes with CSCR.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Kim YK, Ryoo NK, Woo SJ, Park KH. Choroidal thickness changes after photodynamic therapy and recurrence of chronic central serous chorioretinopathy. Am J Ophthalmol 2015; 160:72–84.
Dang Y, Sun X, Xu Y, Mu Y, Zhao M, Zhao J et al.
Subfoveal choroidal thickness after photodynamic therapy in patients with acute idiopathic central serous chorioretinopathy. Ther Clin Risk Manag 2014; 10:37–43.
Abouammoh MA. Advances in the treatment of central serous chorioretinopathy. Saudi J Ophthalmol 2015; 29:278–286.
Kim DY, Joe SG, Yang SJ, Lee JY, Kim JG, Yoon YH. The association between choroidal thickness variations and response to intravitreal bevacizumab in central serous chorioretinopathy. Korean J Ophthalmol 2015; 29:160–167.
Goktas A. Correlation of subretinal fluid volume with choroidal thickness and macular volume in acute central serous chorioretinopathy. Eye 2014; 28:1431–1436.
Kuroda S, Ikuno Y, Yasuno Y, Nakai K, Usui S, Sawa M et al.
Choroidal thickness in central serous chorioretinopathy. Retina 2013; 33:302–308.
Negi A, Marmor MF. The resorption of subretinal fluid after diffuse damage to the retinal pigment epithelium. Invest Ophthalmol Vis Sci 1983; 24:1475–1479.
Negi A, Marmor MF. Experimental serous retinal detachment and focal pigment epithelial damage. Arch Ophthalmol 1984; 102:445–449.
Gass JD. Pathogenesis of disciform detachment of the neuroepithelium. Am J Ophthalmol 1967; 63(Suppl 3):1–139.
Jirarattanasopa P, Ooto S, Tsujikawa A, Yamashiro K, Hangai M, Hirata M et al.
Assessment of macular choroidal thickness by optical coherence tomography and angiographic changes in central serous chorioretinopathy. Ophthalmology 2012; 119:1666–1678.
Iida T, Kishi S, Hagimura N, Shimizu K. Persistent and bilateral choroidal vascular abnormalities in central serous chorioretinopathy. Retina 1999; 19:508–512.
Spaide RF, Hall L, Haas A, Campeas L, Yannuzzi LA, Fisher YL et al.
Indocyanine green videoangiography of older patients with central serous chorioretinopathy. Retina 1996; 16:203–213.
Spaide RF, Goldbaum M, Wong DW, Tang KC, Iida T Serous detachment of the retina. Retina 2003; 23:820–846.
Chan WM, Lam DS, Lai TY, Tam BS, Liu DT, Chan CK. Choroidal vascular remodelling in central serous chorioretinopathy after indocyanine green guided photodynamic therapy with verteporfin: a novel treatment at the primary disease level. Br J Ophthalmol 2003; 87:1453–1458.
Chan WM, Lai TY, Lai RY, Tang EW, Liu DT, Lam DS Safety enhanced photodynamic therapy for chronic central serous chorioretinopathy: one-year results of a prospective study. Retina 2008; 28:85–93.
Yannuzzi LA, Slakter JS, Gross NE, Spaide RF, Costa D, Huang SJ et al.
Indocyanine green angiography-guided photodynamic therapy for treatment of chronic central serous chorioretinopathy: a pilot study. Retina 2003; 23:288–298.
Imamura Y, Fujiwara T, Margolis R, Spaide RF. Enhanced depth imaging optical coherence tomography of the choroid in central serous chorioretinopathy. Retina 2009; 29:1469–1473.
Doro D, Visentin S, Maimone PE, Pilotto E. High-resolution ultrasonography in central serous chorioretinopathy. Am J Ophthalmol 2005; 139:550–552.
Tittl M, Polska E, Kircher K, Kruger A, Maar N, Stur M, Schmetterer L. Topical fundus pulsation measurement in patients with active central serous chorioretinopathy. Arch Ophthalmol 2003; 121:975–978.
Tittl M, Maar N, Polska E, Weigert G, Stur M, Schmetterer L. Choroidal hemodynamic changes during isometric exercise in patients with inactive central serous chorioretinopathy. Invest Ophthalmol Vis Sci 2005; 46:4717–4721.
Manabe S, Shiragami C, Hirooka K, Izumibata S, Tsujikawa A, Shiraga F. Change of regional choroid thickness after reduced-fluence photodynamic therapy for chronic central serous chorioretinopathy. Am J Ophthalmol 2015; 159:644–651.
Adhi M, Duker JS. Optical coherence tomography − current and future applications. Curr Opin Ophthalmol 2013; 24:213–221.
Maruko I, Iida T, Sugano Y, Ojima A, Sekiryu T. Subfoveal choroidal thickness in fellow eyes of patients with central serous chorioretinopathy. Retina 2011; 31:1603–1608.
Hamzah F, Shinojima A, Mori R, Yuzawa M. Choroidal thickness measurement by enhanced depth imaging and swept-source optical coherence tomography in central serous chorioretinopathy. BMC Ophthalmol 2014; 14:145.
Kim SW, Oh J, Kwon SS, Yoo J, Huh K. Comparison of choroidal thickness among patients with healthy eyes, early age-related maculopathy, neovascular age-related macular degeneration, central serous chorioretinopathy, and polypoidal choroidal vasculopathy. Retina 2011; 31:1904–1911
Jampol LM, Weinreb R, Yannuzzi L. Involvement of corticosteroids and catecholamines in the pathogenesis of central serous chorioretinopathy: A rationale for new treatment strategies. Ophthalmology 2002; 109:1834–1837.
Vance SK, Imamura Y, Freund KB. The effects of sildenafil citrate on choroidal thickness as determined by enhanced depth imaging optical coherence tomography. Retina 2011; 31:332–335.
Pryds A, Larsen M. Choroidal thickness following extrafoveal photodynamic treatment with verteporfin in patients with central serous chorioretinopathy. Acta Ophthalmol 2012; 90:738–743.
Wei WB, Xu L, Jonas JB, Shao L, Du KF, Wang S et al.
Subfoveal choroidal thickness: the Beijing Eye Study. Ophthalmology 2013; 120:175–180.
Usui S, Ikuno Y, Akiba M, Maruko I, Sekiryu T, Nishida K, Iida T. Circadian changes in subfoveal choroidal thickness and the relationship with circulatory factors in healthy subjects. Invest Ophthalmol Vis Sci 2012; 53:2300–2307.
Tan CS, Ouyang Y, Ruiz H, Sadda SR. Diurnal variation of choroidal thickness in normal, healthy subjects measured by spectral domain optical coherence tomography. Invest Ophthalmol Vis Sci 2012; 53:261–266.
Barteselli G, Chhablani J, El-Emam S, Wang H, Chuang J, Kozak I et al.
Choroidal volume variations with age, axial length, and sex in healthy subjects: a three-dimensional analysis. Ophthalmology 2012; 119:2572–2578.
Ouyang Y, Heussen FM, Mokwa N, Walsh AC, Durbin MK, Keane PA et al.
Spatial distribution of posterior pole choroidal thickness by spectral domain optical coherence tomography. Invest Ophthalmol Vis Sci 2011; 52:7019–7026.
Yang L, Jonas JB, Wei W. Choroidal vessel diameter in central serous chorioretinopathy. Acta Ophthalmol 2013; 91:e358–e362.
Tewari HK, Gadia R, Kumar D, Venkatesh P, Garg SP. Sympathetic-parasympathetic activity and reactivity in central serous chorioretinopathy: a case-control study. Invest Ophthalmol Vis Sci 2006; 47:3474–3478.
Gass JDM. Pathogenesis of disciform detachment of the neuroepithelium, II: idiopathic central serous chorioretinopathy. Am J Ophthalmol 1967; 63:587–615.
Uetani R, Ito Y, Oiwa K, Ishikawa K, Terasaki H. Half-dose vs one-third-dose photodynamic therapy for chronic central serous chorioretinopathy. Eye (Lond) 2012; 26:640–649.
Kang NH, Kim YT. Change in subfoveal choroidal thickness in central serous chorioretinopathy following spontaneous resolution and low-fluence photodynamic therapy. Eye (Lond) 2013; 27:387–391.
Margolis R, Spaide RF. A pilot study of enhanced depth imaging optical coherence tomography of the choroid in normal eyes. Am J Ophthalmol 2009; 147:811–815.
Spaide RF. Age-related choroidal atrophy. Am J Ophthalmol 2009; 147:801–810.
Ikuno Y, Kawaguchi K, Nouchi T, Yasuno Y. Choroidal thickness in healthy Japanese subjects. Invest Ophthalmol Vis Sci 2010; 51:2173–2176.
Ramrattan RS, van der Schaft TL, Mooy CM, de Bruijn WC, Mulder PG, de Jong PT. Morphometric analysis of Bruch’s membrane, the choriocapillaris, and the choroid in aging. Invest Ophthalmol Vis Sci 1994; 35:2857–2864.
[Table 1], [Table 2]