“…Developments in retinal and choroidal imaging, especially during the last decade, have revealed that CSC is linked to a thicker choroid, i.e., pachychoroid, and that this pachychoroid is seen in a spectrum of conditions, which appear to share both clinical nature and etiological findings [ 7 , 8 , 9 , 10 ]. It is hypothesized that pachychoroid reflects a choroidal venous overload, which is supported by angiographic evidence of choroidal vascular hyperpermeability, dilated veins, vortex venous anastomoses, and delayed filling of the choroidal veins [ 7 , 8 , 9 , 10 ]. These circumstances are hypothesized to explain a disease progression of first a gradual development of a pachychoroid phenotype; followed by a pachychoroid pigment epitheliopathy (PPE), i.e., pigment epithelium detachment (PED) without any subretinal fluid or intraretinal fluid; followed by CSC; and CSC complicated by neovascularizations, e.g., seen as polypoidal choroidal vasculopathy (PCV)/aneurysmal type 1 neovascularization [ 7 , 8 , 9 , 10 ].…”