# Choroidal neovascularization as a trigger for central serous chorioretinopathy

## TL;DR

This study suggests that choroidal neovascularization can trigger central serous chorioretinopathy in some patients with pachychoroid features.

## Contribution

The study provides evidence that CNV can act as a direct trigger for acute CSCR episodes, not just a complication.

## Key findings

- Four patients with CNV and a first episode of CSCR showed leakage colocalized within the CNV lesion.
- CNV was subfoveal and mature, with subretinal fluid fluctuations not always linked to anti-VEGF treatment.
- The findings suggest CNV may trigger acute CSCR episodes in the pachychoroid spectrum.

## Abstract

To investigate whether choroidal neovascularization (CNV) may occasionally precipitate central serous chorioretinopathy (CSCR) in patients with pachychoroid features, by analyzing cases where fluorescein angiography (FA)-confirmed leakage originated directly within the CNV lesion.

In this retrospective case series conducted at two tertiary referral centers, we reviewed patients with no prior history or signs of CSCR who presented with a first episode of CSCR and coexisting CNV between December 2024 and April 2025. Inclusion required at least one FA-confirmed leakage point located within the neovascular complex. Multimodal imaging—including FA, spectral-domain optical coherence tomography (SD-OCT), and optical coherence tomography angiography (OCTA)—was performed to detect CNV and evaluate its topographical relationship with leakage.

Among 202 patients screened, four met inclusion criteria (two males, two females; age range 54–58 years). All presented with a unilateral first episode of CSCR. In each case, FA and OCTA demonstrated precise colocalization of the leakage point within the CNV lesion. CNV was predominantly subfoveal and exhibited a mature morphology. Three patients were diagnosed simultaneously with CSCR and a neovascular membrane, while one developed CSCR during follow-up of a previously identified pachychoroid neovasculopathy. Subretinal fluid fluctuations were observed in all cases and often appeared independent of anti-VEGF treatment, suggesting a mechanism not exclusively driven by VEGF-mediated CNV activity.

This case series suggests that, within the pachychoroid spectrum, CNV may not only complicate chronic or complex CSCR but may also act as a direct trigger of acute episodes. These findings underscore the importance of multimodal imaging, particularly FA and OCTA, for comprehensive assessment of CSCR. Given the small sample size and retrospective design, these observations should be interpreted as hypothesis-generating and warrant confirmation in larger prospective studies.

The online version contains supplementary material available at 10.1186/s40942-025-00761-7.