Pathomechanisms in central serous chorioretinopathy: A recent update

Abstract

Background Central serous chorioretinopathy (CSCR) is a potentially blinding choroidal disease. Despite decades of research, the pathological mechanisms of CSCR are still poorly understood. In recent years, there has been a strong emphasis on choroidal dysfunction as a primary cause of CSCR. Main Body The concept of the pachychoroid disease spectrum and pachychoroid-driven processes are central to current theories regarding the pathophysiological underpinnings of CSCR. Choroidal hyperpermeability and subsequent leakage of fluid seen in CSCR may be due to several causes. Among them are venous congestion, inflammation, mineralocorticoid receptor activation, systemic factors including hemodynamic changes, obstructive sleep apnea, phosphodiesterase inhibitor use, pregnancy, and genetic predispositions. Congestion of vortex veins that drain blood from the choroid may contribute to the dilation of Haller vessels and cause fluid leakage. Vortex veins exit the eye through the sclera; thus, increased scleral thickness has been proposed to be a factor in venous congestion. Asymmetric vortex vein drainage may similarly result in congestion of the local venous system. Vortex vein anastomoses may overload the venous system and form secondary to venous congestion. Recent studies suggest inflammation and mineralocorticoid activation may factor into the development of CSCR, though more research in these areas is called for. Systemic conditions and genetics may predispose individuals to develop CSCR. Conclusions By striving to understand the molecular and physiological mechanisms of this disease, we can better diagnose and treat CSCR to improve outcomes for patients.

Ocular Manifestations in a Context of Primary Hyperparathyroidism: A Report of Two Cases

“…Central serous chorioretinopathy belongs to the pachychoroid disease spectrum. Much research work has been conducted to elucidate the exact pathophysiology of pachychoroid and CSCR, with some theories including venous congestion, mineralocorticoid receptor (MR) activation, inflammatory processes, and systemic conditions with hemodynamics alterations 12 . Recent studies have demonstrated an increased vulnerability of choroidal blood flow to vascular variations in patients with CSCR 13 , 14 .…”

Evaluation of the Retinal Vessel Density and Subfoveal Choroidal Thickness in Central Cerous Chorioretinopathy Using Optical Coherence Tomography

“…The alteration is primarily localized in the macular area, with fluid accumulating in the subretinal space. Several explanations concerning the disease's pathophysiology have been offered, two of which are accepted: choroidal dysfunction and pigment epithelial dysfunction [ 5 , 16 ]. Although the exact mechanism of the disease has not been determined, radiographic studies have revealed that the predominant alteration in the CSCR eye is due to increased permeability, which results in systemic fluid leakage from choroidal capillaries into the subretinal area [ 17 ].…”

Efficacy of Subthreshold Micropulse Laser for Central Serous Chorioretinopathy

“…Effektivität der Subthreshold-Micropulse-Laser-Therapie bei der Chorioretinopathia centralis serosa Background/Introduction Central serous chorioretinopathy (CSCR) is a disease of the pachychoroid spectrum. The currently most accepted pathophysiological mechanism includes primary choroidal dysfunction, possibly due to venous congestion, inflammation, aberrant steroid metabolism, and genetic factors [1,2]. Besides choroidal dysfunction, acute CSCR is defined by subretinal fluid (SRF) accumulation resulting from one or more leakage points due to a micro-tear in the retinal pigment epithelium (RPE) [3].…”