Central Serous Chorioretinopathy

1. Disease Information

Overview

Central serous chorioretinopathy (CSC/CSCR), first described by Albrecht von Graefe in 1866, is characterized by focal serous detachment of the neural retina and/or retinal pigment epithelium (RPE) in the posterior pole (zhang2023centralserouschorioretinopathy pages 1-2). It is recognized as the first-described pachychoroid spectrum disorder, defined by chronic choroidal thickening and choriocapillaris dysfunction with or without RPE abnormalities overlying pachyvessels (zhang2023centralserouschorioretinopathy pages 1-2). CSC exists in acute and chronic subtypes: acute CSC is typically self-limiting within 2–3 months, while chronic CSC involves persistent subretinal fluid (SRF) beyond 4–6 months with RPE decompensation, potentially leading to permanent visual impairment from photoreceptor damage or RPE atrophy (zhang2023centralserouschorioretinopathy pages 1-2, kim2025treatmentofcentral pages 2-3).

Disease Identifiers and Classification

The following table summarizes disease identifiers, synonyms, and classification for CSC:

Table: This table summarizes the main disease identifiers, synonyms, and classification terms for Central Serous Chorioretinopathy. It is useful for harmonizing disease knowledge-base entries across clinical, ontology, and research resources.

Synonyms: Central serous retinopathy, central serous choroidopathy, central serous pigment epitheliopathy, CSCR, CSC (zhang2023centralserouschorioretinopathy pages 1-2).

Key Ontology Terms: - MONDO: MONDO:0007381 (central serous retinopathy) - EFO: EFO_0009784 (central serous retinopathy); EFO_0009363 (chronic central serous retinopathy) (OpenTargets Search: central serous chorioretinopathy) - ICD-10: H35.71 - MeSH: D056833

2. Etiology

Disease Causal Factors

CSC is a complex, multifactorial disease whose precise etiology remains incompletely understood. The pathogenesis involves dysfunction at the choroidal level with hyperpermeability, choriocapillaris remodeling, and RPE barrier breakdown (zhang2023centralserouschorioretinopathy pages 1-2). A "venous overload choroidopathy" hypothesis has recently been proposed, emphasizing morphological and pathological characteristics including choroidal thickening, choriocapillaris hyperpermeability, and intervortex venous anastomoses (ramo2024raregeneticvariation pages 30-33, zhang2023centralserouschorioretinopathy pages 1-2).

Risk Factors

Environmental and Lifestyle Risk Factors: - Corticosteroid use (systemic, nasal, topical, intravenous, and intravitreal routes) — the most consistently identified modifiable risk factor (kim2025treatmentofcentral pages 2-3, zhang2023centralserouschorioretinopathy pages 2-4) - Psychological stress and Type A personality — neuroendocrine activation with catecholamine and corticosteroid release affects choroidal vascular permeability (zhang2023centralserouschorioretinopathy pages 2-4) - Sleep apnea — associated with approximately 5× increased risk (kim2025treatmentofcentral pages 2-3) - H. pylori infection — may increase tissue sensitivity to inflammatory reactions and oxidative stress (zhang2023centralserouschorioretinopathy pages 2-4) - Sympathomimetic agents and antipsychotic medications (kim2025treatmentofcentral pages 2-3) - Endogenous hormonal changes (Cushing syndrome, pregnancy) (kim2025treatmentofcentral pages 2-3) - Additional factors: hypertension, alcohol use, kidney disease (zhang2023centralserouschorioretinopathy pages 2-4) - Sleep quality: CSC patients demonstrate significantly poorer sleep quality (58.2% vs. 23.9% in controls) (zhang2023centralserouschorioretinopathy pages 2-4)

Genetic Risk Factors: CSC has a polygenic, multifactorial inheritance pattern. Multiple genome-wide association studies (GWAS) have identified susceptibility loci, including CFH, PTPRB, TNFRSF10A, GATA5, ARMS2, VIPR2, CDH5, and NR3C2 (mori2025genomewideassociationand pages 2-3, ramo2025raregeneticvariation pages 1-2, mori2025genomewideassociationand pages 11-11). The most significant novel finding is a low-frequency missense variant (rs113791087) in PTPRB encoding vascular endothelial protein tyrosine phosphatase (VE-PTP), with OR = 3.06 (P = 7.4 × 10⁻¹⁵) in a meta-analysis of 2,452 CSC patients and 865,767 controls (ramo2025raregeneticvariation pages 1-2, ramo2024raregeneticvariation pages 1-4).

Protective Factors

The rs113791087 variant in PTPRB, while conferring CSC risk, was paradoxically associated with reduced risk of glaucoma (OR = 0.82, P = 6.9 × 10⁻⁹), suggesting complex pleiotropic effects of vascular endothelial signaling (ramo2025raregeneticvariation pages 1-2, ramo2024raregeneticvariation pages 1-4). No robust genetic or environmental protective factors have been consistently identified for CSC prevention specifically.

Gene-Environment Interactions

Corticosteroids have been shown to regulate the expression of CDH5 (cadherin 5), a CSC susceptibility gene, providing a molecular link between environmental corticosteroid exposure and genetic susceptibility (mori2025genomewideassociationand pages 11-11). The mineralocorticoid receptor gene NR3C2 has been associated with chronic CSC susceptibility, and mineralocorticoid receptor antagonists can effectively treat the condition, further linking the glucocorticoid/mineralocorticoid pathway to genetic predisposition (matet2020lipocalin2as pages 6-6, zhang2023centralserouschorioretinopathy pages 2-4).

3. Phenotypes

Symptoms and Clinical Signs

CSC presents as a predominantly unilateral condition (bilateral in 5–18% of cases) with the following symptoms (zhang2023centralserouschorioretinopathy pages 4-5): - Blurred vision (HP:0000572) - Central scotoma (HP:0000575) - Micropsia (HP:0012508) - Metamorphopsia (HP:0012507) - Reduced contrast sensitivity (HP:0030452)

HPO Terms: - HP:0000572 Visual loss - HP:0007401 Macular atrophy - HP:0011506 Choroidal neovascularization - HP:0000580 Pigmentary retinopathy - HP:0001103 Subretinal fluid

Phenotype Characteristics

• Age of onset: Predominantly middle-aged adults aged 30–50 years (zhang2023centralserouschorioretinopathy pages 1-2, ramo2024raregeneticvariation pages 1-4)
• Severity: Variable from mild self-limited acute episodes to severe chronic disease with legal blindness (12.8% developing legal blindness after mean 11.3-year follow-up in chronic CSC) (mori2025genomewideassociationand pages 1-2)
• Progression: Episodic in acute CSC; progressive in chronic CSC with RPE atrophy and photoreceptor deterioration (zhang2023centralserouschorioretinopathy pages 5-7)
• Frequency: Men account for 72–87.5% of patients (zhang2023centralserouschorioretinopathy pages 1-2)

Quality of Life Impact

Patients with CSC demonstrate significantly poorer sleep quality (58.2% vs. 23.9% in controls) and higher prevalence of stress, depression, and anxiety compared to healthy controls (zhang2023centralserouschorioretinopathy pages 2-4). Vision loss, metamorphopsia, and central scotoma significantly impact daily functioning, particularly for individuals of working age.

4. Genetic/Molecular Information

Susceptibility Genes and GWAS Findings

A meta-analysis of three GWAS comprising 8,811 Asians and Caucasians with replication in 4,338 additional Asians identified seven genome-wide significant loci (mori2025genomewideassociationand pages 2-3, mori2025genomewideassociationand pages 1-2). The most comprehensive genetic findings are summarized in the following table:

Table: This table summarizes the main genetic susceptibility loci reported for central serous chorioretinopathy, emphasizing loci supported by recent GWAS and multi-omics work. It is useful for quickly distinguishing loci with quantified effect sizes from those currently reported mainly as significant associations without effect estimates in the retrieved evidence.

Key findings include: - CFH (complement factor H, 1q31.3): A major susceptibility locus with 26 CFH- or CFHR-related pathways showing significant associations, indicating the complement pathway's importance in CSC pathogenesis (mori2025genomewideassociationand pages 2-3, chen2026thecfh–cfhr5locus pages 10-10). OpenTargets identifies CFH as the highest-scoring disease-target association (score 0.485) for central serous retinopathy (OpenTargets Search: central serous chorioretinopathy). - PTPRB (VE-PTP, 12q15): The novel rs113791087 missense variant (allele frequency 0.5%) shows OR = 3.06 in meta-analysis. Predicted loss-of-function variants showed even stronger association (OR = 17.09, P = 0.018) (ramo2025raregeneticvariation pages 1-2, ramo2024raregeneticvariation pages 1-4). - TNFRSF10A (8p21.3): TNF receptor superfamily member 10a, identified in Japanese GWAS and replicated across populations. OpenTargets association score 0.364 (OpenTargets Search: central serous chorioretinopathy, mori2025genomewideassociationand pages 2-3). - LINC01924-CDH7 (rs12960630): Novel locus showing positive correlation between CSC risk allele and plasma cortisol concentration (mori2025genomewideassociationand pages 1-2).

Multi-Omics Insights

Expression/splicing quantitative trait loci (QTL) analyses showed association of identified GWAS hits with expression and/or splicing of genes in genital organs, potentially explaining the sex differences in CSC (mori2025genomewideassociationand pages 1-2). Protein QTL analysis suggested protein-level contribution of the complement factor H pathway to CSC pathogenesis (mori2025genomewideassociationand pages 1-2).

Epigenetic Information

Limited epigenetic data are available specifically for CSC. The mineralocorticoid receptor pathway and glucocorticoid-responsive gene regulation (including CDH5) suggest corticosteroid-mediated transcriptional changes may contribute to disease susceptibility (mori2025genomewideassociationand pages 11-11).

5. Environmental Information

Environmental Factors

Corticosteroid exposure remains the most well-documented environmental trigger. Among corticosteroid users in South Korea (2011–2015), CSC prevalence was 9.4 per 10,000 in men and 3.0 per 10,000 in women (zhang2023centralserouschorioretinopathy pages 2-4). Corticosteroid-treated patients experience higher recurrence rates and more severe disease features including bilateral involvement, multiple pigment epithelial detachments, greater fluorescein leakage sites, and increased choroidal thickness (zhang2023centralserouschorioretinopathy pages 2-4).

Lifestyle Factors

Depression is associated with increased risk of recurrent CSC (zhang2023centralserouschorioretinopathy pages 2-4). Sleep disorders, psychological stress, and Type A personality are consistently identified environmental contributors to disease onset and recurrence (kim2025treatmentofcentral pages 2-3, zhang2023centralserouschorioretinopathy pages 2-4).

Infectious Agents

H. pylori infection has been associated with CSC, potentially through increasing tissue sensitivity to inflammatory reactions triggered by oxidative stress and reducing cellular antioxidant capacity (zhang2023centralserouschorioretinopathy pages 2-4).

6. Mechanism/Pathophysiology

Molecular Pathways

The pathophysiology of CSC involves multiple interconnected pathways:

1. Choroidal vascular dysfunction: Dysautoregulation of choroidal circulation leads to hyperpermeability and fluid accumulation beneath the RPE (zhang2023centralserouschorioretinopathy pages 4-5). Choroidal changes include higher vascularity index, enlarged vessels, and increased choroidal thickness (kim2025treatmentofcentral pages 2-3). GO terms: GO:0045766 (positive regulation of angiogenesis), GO:0001974 (blood vessel remodeling).

2. Complement factor H pathway: Protein QTL analysis and GWAS data implicate the CFH-CFHR pathway in CSC pathogenesis. FHR proteins compete with factor H in complement regulation through the alternative complement pathway (chen2026thecfh–cfhr5locus pages 8-9, mori2025genomewideassociationand pages 2-3). GO term: GO:0006956 (complement activation).

3. Vascular endothelial phosphatase (VE-PTP) dysfunction: PTPRB variants alter vascular endothelial signaling, and abnormal choroidal veins in CSC patients share morphological similarities with varicose veins, supporting a "venous overload choroidopathy" hypothesis (ramo2025raregeneticvariation pages 1-2, ramo2024raregeneticvariation pages 30-33).

4. Mineralocorticoid receptor pathway: High levels of glucocorticoids, mineralocorticoids, and testosterone are found in CSC patients. The mineralocorticoid receptor pathway contributes to RPE and choroidal dysfunction (zhang2023centralserouschorioretinopathy pages 2-4, matet2020lipocalin2as pages 6-6).

5. Neuroendocrine activation: Psychological stress activates the neuroendocrine system with catecholamine and corticosteroid release, affecting choroidal vascular permeability (zhang2023centralserouschorioretinopathy pages 2-4).

Cellular Processes

• RPE barrier dysfunction: Glucocorticoids alter RPE, Bruch's membrane, and choriocapillaris permeability (zhang2023centralserouschorioretinopathy pages 2-4). CL term: CL:0002586 (retinal pigment epithelial cell).
• Oxidative stress susceptibility: Decreased lipocalin 2 (LCN2) in CSC patients contributes to excessive oxidative stress and RPE barrier dysfunction. LCN2 normally enhances antioxidant enzyme expression (HMOX1 and SOD2) in RPE cells (matet2020lipocalin2as pages 5-6, matet2020lipocalin2as pages 1-2, matet2020lipocalin2as pages 2-3). GO term: GO:0006979 (response to oxidative stress).
• Inflammation: LCN2 suppresses ocular inflammation through NF-κB pathway inhibition; its deficiency may promote innate immune dysregulation (matet2020lipocalin2as pages 6-6, matet2020lipocalin2as pages 1-2).
• Choroidal congestion: Dilation of outer choroidal vessels (Haller's layer) with attenuation of inner layers (Sattler's layer and choriocapillaris) (zhang2023centralserouschorioretinopathy pages 4-5).

Biomarkers

• Lipocalin 2 (LCN2/NGAL): Serum LCN2 is significantly lower in CSC patients than controls (81.4 ± 48.7 vs. 107.3 ± 44.5 ng/ml, p < 0.0001). An 80 ng/ml cutoff discriminates acute/recurrent CSC from controls with 80.3% sensitivity and 75.8% specificity (matet2020lipocalin2as pages 3-5, matet2020lipocalin2as pages 1-2).
• NGAL/MMP-9 complex: Lower in CSC patients (47.2 ± 40.7 vs. 74.1 ± 42.6 ng/ml, p < 0.0001). A 38 ng/ml cutoff provides 69.6% sensitivity and 80.3% specificity (matet2020lipocalin2as pages 3-5).
• Plasma cortisol: The novel CSC risk allele at rs12960630 (LINC01924-CDH7) shows positive correlation with plasma cortisol concentration (mori2025genomewideassociationand pages 1-2).

7. Anatomical Structures Affected

Organ Level

• Primary organ: Eye (UBERON:0000970)
• Specific structure: Macula lutea (UBERON:0000053), posterior pole of the eye
• Body system: Visual system

Tissue and Cell Level

• Retina (UBERON:0000966): Neural retina with serous detachment
• Retinal pigment epithelium (CL:0002586): RPE dysfunction, atrophy, hyperplasia, and barrier breakdown (zhang2023centralserouschorioretinopathy pages 5-7, zhang2023centralserouschorioretinopathy pages 4-5)
• Choroid (UBERON:0001776): Thickened with dilated vessels in Haller's layer, attenuated Sattler's layer and choriocapillaris (zhang2023centralserouschorioretinopathy pages 7-10, zhang2023centralserouschorioretinopathy pages 4-5)
• Choriocapillaris (UBERON:0002208): Hyperpermeability and attenuation (kim2025treatmentofcentral pages 3-5)
• Photoreceptors (CL:0000210): Outer segment elongation, ellipsoidal band disruption correlating with visual acuity loss (zhang2023centralserouschorioretinopathy pages 7-10)

Localization

• Predominantly unilateral; bilateral in 5–18% of cases (zhang2023centralserouschorioretinopathy pages 4-5)
• Posterior pole/macular region preferentially affected
• Subretinal fluid accumulation beneath neurosensory retina

8. Temporal Development

Onset

• Typical age: 30–50 years (zhang2023centralserouschorioretinopathy pages 1-2, ramo2024raregeneticvariation pages 1-4)
• Onset pattern: Acute, often related to stress or corticosteroid exposure

Progression

• Acute CSC: Self-limiting in approximately 90–95% of cases with spontaneous SRF resorption within 2–3 months; expected visual recovery to 20/20 or better (zhang2023centralserouschorioretinopathy pages 10-12, zhang2023centralserouschorioretinopathy pages 1-2)
• Chronic CSC: Persistent SRF >4–6 months with progressive RPE decompensation (kim2025treatmentofcentral pages 2-3)
• Risk factors for chronicity: Subfoveal choroidal thickness >500 µm, PED height >50 µm, age >40 years (kim2025treatmentofcentral pages 2-3)
• Recurrence rates: 15–50% depending on study methodology and follow-up duration; 19–51% in various series (kim2025treatmentofcentral pages 2-3, zhang2023centralserouschorioretinopathy pages 5-7)
• Complications: Choroidal neovascularization (CNV) in 2–15.6% of chronic CSC cases; RPE atrophy; photoreceptor loss (zhang2023centralserouschorioretinopathy pages 5-7, kim2025treatmentofcentral pages 3-5)

Disease Course Patterns

• Episodic/relapsing in acute form
• Progressive with accumulating damage in chronic form
• Critical period: Decision to treat typically at 3–4 months if SRF persists (zhang2023centralserouschorioretinopathy pages 10-12)

9. Inheritance and Population

Epidemiology

• Annual incidence: Approximately 5.8–10 per 100,000 (age-adjusted); approximately 10 per 100,000 in men (zhang2023centralserouschorioretinopathy pages 1-2, ramo2024raregeneticvariation pages 1-4)
• Prevalence: Among corticosteroid users in South Korea: 9.4 per 10,000 in men, 3.0 per 10,000 in women (zhang2023centralserouschorioretinopathy pages 2-4)

Inheritance Pattern

CSC is a complex/multifactorial disease with polygenic susceptibility rather than Mendelian inheritance. Multiple common and rare genetic variants contribute to disease risk (mori2025genomewideassociationand pages 2-3, ramo2025raregeneticvariation pages 1-2).

Population Demographics

• Sex ratio: Males represent 72–87.5% of patients; however, older women show similar prevalence rates to men (zhang2023centralserouschorioretinopathy pages 1-2)
• Racial/ethnic distribution: More prevalent in Asians compared to Caucasians and African Americans (zhang2023centralserouschorioretinopathy pages 2-4, zhang2023centralserouschorioretinopathy pages 1-2)
• Age distribution: Peak incidence at 30–50 years of age (zhang2023centralserouschorioretinopathy pages 1-2, ramo2024raregeneticvariation pages 1-4)
• Geographic variant distribution: The PTPRB rs113791087 variant has a low frequency of 0.5% (enriched in FinnGen/Finnish population) (ramo2025raregeneticvariation pages 1-2, ramo2024raregeneticvariation pages 1-4)

10. Diagnostics

Clinical Tests and Imaging

Optical Coherence Tomography (OCT): The primary diagnostic modality, revealing SRF accumulation, pigment epithelial detachment (PED), increased subfoveal choroidal thickness, dilated vessels in Haller's layer, thinning of Sattler's layer, choriocapillaris attenuation, photoreceptor outer segment elongation, and ellipsoidal band disruption (zhang2023centralserouschorioretinopathy pages 5-7, zhang2023centralserouschorioretinopathy pages 7-10, zhang2023centralserouschorioretinopathy pages 4-5).

Fluorescein Angiography (FA): Demonstrates characteristic leakage patterns — "ink-blot" pattern in 53–93% and "smoke-stack" pattern in approximately 7% of acute cases; multifocal diffuse leakage in chronic CSC (zhang2023centralserouschorioretinopathy pages 5-7).

Indocyanine Green Angiography (ICGA): Shows delayed choroidal filling, dilation of large choroidal veins, and multifocal hyperfluorescence indicating choroidal hyperpermeability — present in 93% of CSC patients (zhang2023centralserouschorioretinopathy pages 5-7, kim2025treatmentofcentral pages 3-5).

OCT Angiography (OCTA): Reveals abnormal choriocapillaris dilation, high signal intensity areas, and surrounding hyperperfusion patterns indicating focal choroidal ischemia; useful for detecting type 1 CNV (zhang2023centralserouschorioretinopathy pages 7-10, kim2025treatmentofcentral pages 11-11).

Fundus Autofluorescence (FAF): Shows hyperautofluorescence (RPE dysfunction) or hypoautofluorescence (atrophic areas); "fluid tracks" visible in chronic CSC (kim2025treatmentofcentral pages 3-5, zhang2023centralserouschorioretinopathy pages 10-12).

Advanced Modalities: Ultra-widefield imaging, flavoprotein fluorescence (FPF), fluorescence lifetime imaging ophthalmoscopy (FLIO), multispectral imaging, and multicolor imaging are emerging diagnostic tools (zhang2023centralserouschorioretinopathy pages 1-2, zhang2023centralserouschorioretinopathy pages 10-12).

Artificial Intelligence in Diagnosis

Deep learning models, particularly CNN architectures (DenseNet, ResNet-50, VGG-16), have demonstrated exceptional performance in automated CSC diagnosis from OCT images, with DenseNet achieving 99.78% accuracy, 99.68% sensitivity, and 100% specificity (shojaeinia2025acomprehensiveoverview pages 1-2). AI-based systems can also differentiate acute from chronic CSC subtypes (94.2% accuracy), predict treatment persistence, forecast treatment response, and estimate post-treatment visual acuity (shojaeinia2025acomprehensiveoverview pages 14-16, shojaeinia2025acomprehensiveoverview pages 13-14, shojaeinia2025acomprehensiveoverview pages 8-9).

Biomarker-Based Diagnostics

Serum LCN2 (cutoff 80 ng/ml) and NGAL/MMP-9 complex (cutoff 38 ng/ml) represent potential systemic biomarkers for CSC diagnosis (matet2020lipocalin2as pages 3-5).

Differential Diagnosis

Key conditions to differentiate include: age-related macular degeneration (AMD), polypoidal choroidal vasculopathy (PCV), diabetic macular edema (DME), choroidal neovascularization from other causes, and Vogt-Koyanagi-Harada disease.

11. Outcome/Prognosis

Visual Outcomes

• Acute CSC: Favorable prognosis with 90–95% spontaneous resolution and expected recovery to ≥20/20 vision (zhang2023centralserouschorioretinopathy pages 10-12, zhang2023centralserouschorioretinopathy pages 1-2)
• Chronic CSC: 12.8% develop legal blindness after mean 11.3-year follow-up (mori2025genomewideassociationand pages 1-2); with half-dose PDT treatment, approximately 95% achieve visual acuity of 20/30 or better (zhang2023centralserouschorioretinopathy pages 1-2)

Recurrence and Complications

• Recurrence rates: 15–50% overall; untreated patients 51% vs. 25% in PDT-treated patients in acute CSC (kim2025treatmentofcentral pages 2-3, kim2025treatmentofcentral pages 8-9)
• CNV develops in 2–15.6% of chronic cases (zhang2023centralserouschorioretinopathy pages 5-7, kim2025treatmentofcentral pages 3-5)
• Progressive RPE atrophy, photoreceptor deterioration, and ganglion cell loss contribute to long-term morbidity (zhang2023centralserouschorioretinopathy pages 5-7)

Prognostic Factors

Poor prognostic indicators include persistent SRF >3–4 months, subfoveal choroidal thickness >500 µm, PED height >50 µm, age >40 years, bilateral involvement, and corticosteroid use (kim2025treatmentofcentral pages 2-3, zhang2023centralserouschorioretinopathy pages 2-4).

12. Treatment

The following table summarizes current and experimental treatment modalities for CSC:

Table: This table summarizes current treatment options for central serous chorioretinopathy, including mechanisms, indications, comparative efficacy, and the strength of supporting evidence. It is useful for quickly distinguishing standard-of-care therapies such as half-dose PDT from conditional, off-label, or investigational options.

Key Treatment Details

Half-Dose Photodynamic Therapy (PDT): The mainstay of treatment for chronic CSC, with SRF resolution rates of 91% at 19 months and 81% at 50 months follow-up. PDT reduces recurrence risk to approximately 20% compared to 53.8% with observation alone over ≥3-year follow-up (kim2025treatmentofcentral pages 8-9). PDT works through choriocapillaris vascular remodeling and decreased choroidal hyperpermeability (zhang2023centralserouschorioretinopathy pages 1-2). MAXO term: MAXO:0000127 (phototherapy).

Mineralocorticoid Receptor Antagonists (Eplerenone/Spironolactone): The randomized VICI trial showed eplerenone failed to meet its primary endpoint of improving BCVA at 12 months in chronic CSC, making its routine use controversial (kim2025treatmentofcentral pages 9-10, zhang2023centralserouschorioretinopathy pages 1-2). MAXO term: MAXO:0000010 (pharmacotherapy).

Anti-VEGF Therapy: Standard treatment specifically for CSC complicated by active choroidal neovascularization (type 1 CNV), supported by the MINERVA trial. Not effective as monotherapy for uncomplicated CSC (kim2025treatmentofcentral pages 9-10, kim2025treatmentofcentral pages 9-9). MAXO term: MAXO:0001298 (intravitreal injection).

Subthreshold Micropulse Laser: Complete SRF resolution in 36–100% of chronic CSC patients across studies; the PLACE trial showed inferiority to half-dose PDT (kim2025treatmentofcentral pages 7-8, zhang2023centralserouschorioretinopathy pages 14-15).

Focal Laser Photocoagulation: Appropriate for extrafoveal leakage points identified on FA/ICGA (kim2025treatmentofcentral pages 9-10, kim2025treatmentofcentral pages 7-8). MAXO term: MAXO:0010022 (laser photocoagulation).

Active Clinical Trials

Current recruiting trials include studies evaluating gut microbiota associations (NCT06527326), micropulse laser treatment (NCT06346405), choroidal blood flow assessment (NCT05589974), and subthreshold nanosecond laser (NCT05570591). A phase 2/3 trial evaluating oral melatonin for acute CSC (NCT06809751) is not yet recruiting.

13. Prevention

Primary Prevention

• Corticosteroid avoidance/minimization: The most important modifiable risk factor. Discontinuation of corticosteroids (oral, inhaled, nasal, topical) is recommended when possible (kim2025treatmentofcentral pages 2-3, zhang2023centralserouschorioretinopathy pages 2-4)
• Stress management: Given the strong association with psychological stress and Type A personality, stress reduction strategies may reduce onset and recurrence risk (zhang2023centralserouschorioretinopathy pages 2-4)
• Sleep disorder management: Treatment of obstructive sleep apnea (5× increased risk) may be preventive (kim2025treatmentofcentral pages 2-3)

Secondary Prevention

• Risk factor modification: Corticosteroid discontinuation and stress reduction can enhance vision recovery in acute CSC (zhang2023centralserouschorioretinopathy pages 10-12)
• Early treatment: Early half-dose PDT for recurrent or non-resolving cases reduces recurrence from 24% to 4% (kim2025treatmentofcentral pages 8-9)

Tertiary Prevention

• Monitoring for CNV: Regular OCT/OCTA follow-up for chronic CSC patients to detect type 1 CNV early (kim2025treatmentofcentral pages 3-5)
• Appropriate treatment escalation: Transition from observation to PDT treatment when SRF persists >3–4 months (zhang2023centralserouschorioretinopathy pages 10-12)

Genetic Counseling

CSC is a complex, multifactorial disease without a defined Mendelian inheritance pattern. While genetic risk factors have been identified (particularly CFH, PTPRB), genetic counseling is not routinely recommended as no single gene drives disease (mori2025genomewideassociationand pages 2-3, ramo2025raregeneticvariation pages 1-2).

14. Other Species / Natural Disease

Animal Models

Several animal models have been developed to study CSC pathogenesis:

• Aldosterone-induced rat model: Melatonin has been shown to prevent experimental CSC in rats treated with aldosterone, supporting the mineralocorticoid receptor pathway in pathogenesis (Yu et al. 2022, doi:10.1111/jpi.12802)
• Choroidal congestion mouse model: Matsumoto et al. (2021) developed a choroidal congestion model as a potential pachychoroid model (doi:10.1371/journal.pone.0246115)
• Adrenaline-induced chinchilla rabbit model: Intravenous adrenaline injection produces temporal topographic changes mimicking CSC features (Yan et al. 2023, doi:10.2147/dddt.s381957)
• Adenosine A2A receptor antagonist model: KW6002 has been shown to mitigate aldosterone-induced CSC in mice (Liu et al. 2026, doi:10.1016/j.neuropharm.2026.111036)

These models recapitulate aspects of choroidal thickening, subretinal fluid accumulation, and RPE dysfunction but do not fully reproduce the complex multifactorial nature of human CSC.

15. Model Organisms

Available Models

• Rat (Rattus norvegicus, NCBI Taxon:10116): Aldosterone-induced model showing subretinal fluid and RPE changes
• Mouse (Mus musculus, NCBI Taxon:10090): Choroidal congestion model; adenosine receptor-related models
• Rabbit (Oryctolagus cuniculus, NCBI Taxon:9986): Adrenaline-induced model

Model Limitations

Current models primarily address individual pathogenic mechanisms (hormonal, vascular congestion) rather than the full spectrum of genetic susceptibility, complement pathway involvement, and chronic disease features seen in human CSC. No transgenic or knockout models specifically targeting CSC susceptibility genes (CFH, PTPRB, TNFRSF10A) have been reported in the retrieved literature.

Summary of Key Ontology Annotations

Disease: MONDO:0007381; EFO_0009784; ICD-10: H35.71 Phenotypes (HPO): HP:0000572 (visual loss), HP:0007401 (macular atrophy), HP:0011506 (choroidal neovascularization), HP:0000580 (pigmentary retinopathy) Anatomical structures (UBERON): UBERON:0000966 (retina), UBERON:0001776 (choroid), UBERON:0000053 (macula lutea) Cell types (CL): CL:0002586 (retinal pigment epithelial cell), CL:0000210 (photoreceptor cell) Biological processes (GO): GO:0006956 (complement activation), GO:0006979 (response to oxidative stress), GO:0001974 (blood vessel remodeling), GO:0045766 (positive regulation of angiogenesis) Treatments (MAXO): MAXO:0000127 (phototherapy), MAXO:0000010 (pharmacotherapy), MAXO:0001298 (intravitreal injection), MAXO:0010022 (laser photocoagulation) Chemical entities (CHEBI): CHEBI:50858 (corticosteroid), CHEBI:6781 (mineralocorticoid), CHEBI:145022 (eplerenone), CHEBI:50267 (verteporfin)

This report integrates evidence from 10 primary literature sources, 13 clinical trials, and OpenTargets disease-target association data. Disease information is derived from aggregated disease-level resources including comprehensive reviews, GWAS meta-analyses, and clinical trial data rather than individual patient electronic health records.

References

1. (zhang2023centralserouschorioretinopathy pages 1-2): Xinyuan Zhang, Connie Zhi Fong Lim, Jay Chhablani, and Yew Meng Wong. Central serous chorioretinopathy: updates in the pathogenesis, diagnosis and therapeutic strategies. Eye and Vision, Jul 2023. URL: https://doi.org/10.1186/s40662-023-00349-y, doi:10.1186/s40662-023-00349-y. This article has 84 citations and is from a peer-reviewed journal.

2. (kim2025treatmentofcentral pages 2-3): Yoon Jeon Kim, Sobha Sivaprasad, Tariq Aslam, Polona Jaki Mekjavić, Vilma Jūratė Balčiūnienė, Linda Visser, Antonia M. Joussen, Young Hee Yoon, Timothy Y. Y. Lai, and Annabelle A. Okada. Treatment of central serous chorioretinopathy: new options for an old disease. Eye, 39:2375-2388, Jul 2025. URL: https://doi.org/10.1038/s41433-025-03894-z, doi:10.1038/s41433-025-03894-z. This article has 9 citations and is from a peer-reviewed journal.

3. (OpenTargets Search: central serous chorioretinopathy): Open Targets Query (central serous chorioretinopathy, 3 results). Buniello, A. et al. (2025). Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery. Nucleic Acids Research.

4. (zhang2023centralserouschorioretinopathy pages 2-4): Xinyuan Zhang, Connie Zhi Fong Lim, Jay Chhablani, and Yew Meng Wong. Central serous chorioretinopathy: updates in the pathogenesis, diagnosis and therapeutic strategies. Eye and Vision, Jul 2023. URL: https://doi.org/10.1186/s40662-023-00349-y, doi:10.1186/s40662-023-00349-y. This article has 84 citations and is from a peer-reviewed journal.

5. (ramo2024raregeneticvariation pages 30-33): Joel T Rämö, Bryan Gorman, Lu-Chen Weng, Sean J Jurgens, Panisa Singhanetr, Marisa G Tieger, Elon HC van Dijk, Christopher W Halladay, Xin Wang, Joost Brinks, Seung Hoan Choi, Yuyang Luo, Saiju Pyarajan, Cari L Nealon, Michael B Gorin, Wen-Chih Wu, Lucia Sobrin, Kai Kaarniranta, Suzanne Yzer, Aarno Palotie, Neal S Peachey, Joni A Turunen, Camiel JF Boon, Patrick T Ellinor, Sudha K Iyengar, Mark J Daly, and Elizabeth J Rossin. Rare genetic variation in ve-ptp is associated with central serous chorioretinopathy, venous dysfunction and glaucoma. medRxiv, May 2024. URL: https://doi.org/10.1101/2024.05.08.24307013, doi:10.1101/2024.05.08.24307013. This article has 1 citations.

6. (mori2025genomewideassociationand pages 2-3): Yuki Mori, E. H. V. van Dijk, M. Miyake, Yoshikatsu Hosoda, A. D. den Hollander, S. Yzer, Akiko Miki, Li Jia Chen, Jeeyun Ahn, Ayako Takahashi, Kazuya Morino, Shin-Ya Nakao, C. Hoyng, D. S. Ng, Ling-Ping Cen, Haoyu Chen, T. Ng, C. P. Pang, Kwangsic Joo, Takehiro Sato, Yasuhiko Sakata, Atsushi Tajima, Y. Tabara, Yasuharu Takeo Akihiro Shinji Fumihiko Tabara Nakayama Sekine Kosugi Matsuda, Takeo Nakayama, Akihiro Sekine, S. Kosugi, Fumihiko Matsuda, Kyu Hyung Park, K. Yamashiro, Shigeru Honda, Masao Nagasaki, C. Boon, and A. Tsujikawa. Genome-wide association and multi-omics analyses provide insights into the disease mechanisms of central serous chorioretinopathy. Scientific Reports, Mar 2025. URL: https://doi.org/10.1038/s41598-025-92210-6, doi:10.1038/s41598-025-92210-6. This article has 6 citations and is from a peer-reviewed journal.

7. (ramo2025raregeneticvariation pages 1-2): Joel T. Rämö, Bryan R. Gorman, Lu-Chen Weng, Sean J. Jurgens, Panisa Singhanetr, Marisa G. Tieger, Elon HC van Dijk, Christopher W. Halladay, Xin Wang, Blake M. Hauser, Soo Hyun Kim, Joost Brinks, Seung Hoan Choi, Yuyang Luo, Saiju Pyarajan, Cari L. Nealon, Michael B. Gorin, Wen-Chih Wu, Scott A. Anthony, David P. Roncone, Lucia Sobrin, Kai Kaarniranta, Suzanne Yzer, Aarno Palotie, Neal S. Peachey, Joni A. Turunen, Camiel JF Boon, Patrick T. Ellinor, Sudha K. Iyengar, Mark J. Daly, and Elizabeth J. Rossin. Rare genetic variation in ptprb is associated with central serous chorioretinopathy, varicose veins and glaucoma. Nature Communications, May 2025. URL: https://doi.org/10.1038/s41467-025-58686-6, doi:10.1038/s41467-025-58686-6. This article has 13 citations and is from a highest quality peer-reviewed journal.

8. (mori2025genomewideassociationand pages 11-11): Yuki Mori, E. H. V. van Dijk, M. Miyake, Yoshikatsu Hosoda, A. D. den Hollander, S. Yzer, Akiko Miki, Li Jia Chen, Jeeyun Ahn, Ayako Takahashi, Kazuya Morino, Shin-Ya Nakao, C. Hoyng, D. S. Ng, Ling-Ping Cen, Haoyu Chen, T. Ng, C. P. Pang, Kwangsic Joo, Takehiro Sato, Yasuhiko Sakata, Atsushi Tajima, Y. Tabara, Yasuharu Takeo Akihiro Shinji Fumihiko Tabara Nakayama Sekine Kosugi Matsuda, Takeo Nakayama, Akihiro Sekine, S. Kosugi, Fumihiko Matsuda, Kyu Hyung Park, K. Yamashiro, Shigeru Honda, Masao Nagasaki, C. Boon, and A. Tsujikawa. Genome-wide association and multi-omics analyses provide insights into the disease mechanisms of central serous chorioretinopathy. Scientific Reports, Mar 2025. URL: https://doi.org/10.1038/s41598-025-92210-6, doi:10.1038/s41598-025-92210-6. This article has 6 citations and is from a peer-reviewed journal.

9. (ramo2024raregeneticvariation pages 1-4): Joel T Rämö, Bryan Gorman, Lu-Chen Weng, Sean J Jurgens, Panisa Singhanetr, Marisa G Tieger, Elon HC van Dijk, Christopher W Halladay, Xin Wang, Joost Brinks, Seung Hoan Choi, Yuyang Luo, Saiju Pyarajan, Cari L Nealon, Michael B Gorin, Wen-Chih Wu, Lucia Sobrin, Kai Kaarniranta, Suzanne Yzer, Aarno Palotie, Neal S Peachey, Joni A Turunen, Camiel JF Boon, Patrick T Ellinor, Sudha K Iyengar, Mark J Daly, and Elizabeth J Rossin. Rare genetic variation in ve-ptp is associated with central serous chorioretinopathy, venous dysfunction and glaucoma. medRxiv, May 2024. URL: https://doi.org/10.1101/2024.05.08.24307013, doi:10.1101/2024.05.08.24307013. This article has 1 citations.

10. (matet2020lipocalin2as pages 6-6): A. Matet, T. Jaworski, E. Bousquet, J. Canonica, C. Gobeaux, A. Daruich, Min Zhao, M. Zola, Magda A. Meester-Smoor, D. Mohabati, F. Jaisser, S. Yzer, and F. Behar-Cohen. Lipocalin 2 as a potential systemic biomarker for central serous chorioretinopathy. Scientific Reports, Nov 2020. URL: https://doi.org/10.1038/s41598-020-77202-y, doi:10.1038/s41598-020-77202-y. This article has 26 citations and is from a peer-reviewed journal.

11. (zhang2023centralserouschorioretinopathy pages 4-5): Xinyuan Zhang, Connie Zhi Fong Lim, Jay Chhablani, and Yew Meng Wong. Central serous chorioretinopathy: updates in the pathogenesis, diagnosis and therapeutic strategies. Eye and Vision, Jul 2023. URL: https://doi.org/10.1186/s40662-023-00349-y, doi:10.1186/s40662-023-00349-y. This article has 84 citations and is from a peer-reviewed journal.

12. (mori2025genomewideassociationand pages 1-2): Yuki Mori, E. H. V. van Dijk, M. Miyake, Yoshikatsu Hosoda, A. D. den Hollander, S. Yzer, Akiko Miki, Li Jia Chen, Jeeyun Ahn, Ayako Takahashi, Kazuya Morino, Shin-Ya Nakao, C. Hoyng, D. S. Ng, Ling-Ping Cen, Haoyu Chen, T. Ng, C. P. Pang, Kwangsic Joo, Takehiro Sato, Yasuhiko Sakata, Atsushi Tajima, Y. Tabara, Yasuharu Takeo Akihiro Shinji Fumihiko Tabara Nakayama Sekine Kosugi Matsuda, Takeo Nakayama, Akihiro Sekine, S. Kosugi, Fumihiko Matsuda, Kyu Hyung Park, K. Yamashiro, Shigeru Honda, Masao Nagasaki, C. Boon, and A. Tsujikawa. Genome-wide association and multi-omics analyses provide insights into the disease mechanisms of central serous chorioretinopathy. Scientific Reports, Mar 2025. URL: https://doi.org/10.1038/s41598-025-92210-6, doi:10.1038/s41598-025-92210-6. This article has 6 citations and is from a peer-reviewed journal.

13. (zhang2023centralserouschorioretinopathy pages 5-7): Xinyuan Zhang, Connie Zhi Fong Lim, Jay Chhablani, and Yew Meng Wong. Central serous chorioretinopathy: updates in the pathogenesis, diagnosis and therapeutic strategies. Eye and Vision, Jul 2023. URL: https://doi.org/10.1186/s40662-023-00349-y, doi:10.1186/s40662-023-00349-y. This article has 84 citations and is from a peer-reviewed journal.

14. (mori2025genomewideassociationand pages 10-11): Yuki Mori, E. H. V. van Dijk, M. Miyake, Yoshikatsu Hosoda, A. D. den Hollander, S. Yzer, Akiko Miki, Li Jia Chen, Jeeyun Ahn, Ayako Takahashi, Kazuya Morino, Shin-Ya Nakao, C. Hoyng, D. S. Ng, Ling-Ping Cen, Haoyu Chen, T. Ng, C. P. Pang, Kwangsic Joo, Takehiro Sato, Yasuhiko Sakata, Atsushi Tajima, Y. Tabara, Yasuharu Takeo Akihiro Shinji Fumihiko Tabara Nakayama Sekine Kosugi Matsuda, Takeo Nakayama, Akihiro Sekine, S. Kosugi, Fumihiko Matsuda, Kyu Hyung Park, K. Yamashiro, Shigeru Honda, Masao Nagasaki, C. Boon, and A. Tsujikawa. Genome-wide association and multi-omics analyses provide insights into the disease mechanisms of central serous chorioretinopathy. Scientific Reports, Mar 2025. URL: https://doi.org/10.1038/s41598-025-92210-6, doi:10.1038/s41598-025-92210-6. This article has 6 citations and is from a peer-reviewed journal.

15. (chen2026thecfh–cfhr5locus pages 10-10): Zhen Ji Chen, Jun Yu, Mary Ho, Danny S.C. Ng, Marten E. Brelen, Alvin L. Young, Jason C.S. Yam, Clement C. Tham, Chi Pui Pang, and Li Jia Chen. The cfh–cfhr5 locus in wet age-related macular degeneration, polypoidal choroidal vasculopathy, and central serous chorioretinopathy. Ophthalmology Science, 6(2):101043, Feb 2026. URL: https://doi.org/10.1016/j.xops.2025.101043, doi:10.1016/j.xops.2025.101043. This article has 1 citations.

16. (chen2026thecfh–cfhr5locus pages 8-9): Zhen Ji Chen, Jun Yu, Mary Ho, Danny S.C. Ng, Marten E. Brelen, Alvin L. Young, Jason C.S. Yam, Clement C. Tham, Chi Pui Pang, and Li Jia Chen. The cfh–cfhr5 locus in wet age-related macular degeneration, polypoidal choroidal vasculopathy, and central serous chorioretinopathy. Ophthalmology Science, 6(2):101043, Feb 2026. URL: https://doi.org/10.1016/j.xops.2025.101043, doi:10.1016/j.xops.2025.101043. This article has 1 citations.

17. (matet2020lipocalin2as pages 5-6): A. Matet, T. Jaworski, E. Bousquet, J. Canonica, C. Gobeaux, A. Daruich, Min Zhao, M. Zola, Magda A. Meester-Smoor, D. Mohabati, F. Jaisser, S. Yzer, and F. Behar-Cohen. Lipocalin 2 as a potential systemic biomarker for central serous chorioretinopathy. Scientific Reports, Nov 2020. URL: https://doi.org/10.1038/s41598-020-77202-y, doi:10.1038/s41598-020-77202-y. This article has 26 citations and is from a peer-reviewed journal.

18. (matet2020lipocalin2as pages 1-2): A. Matet, T. Jaworski, E. Bousquet, J. Canonica, C. Gobeaux, A. Daruich, Min Zhao, M. Zola, Magda A. Meester-Smoor, D. Mohabati, F. Jaisser, S. Yzer, and F. Behar-Cohen. Lipocalin 2 as a potential systemic biomarker for central serous chorioretinopathy. Scientific Reports, Nov 2020. URL: https://doi.org/10.1038/s41598-020-77202-y, doi:10.1038/s41598-020-77202-y. This article has 26 citations and is from a peer-reviewed journal.

19. (matet2020lipocalin2as pages 2-3): A. Matet, T. Jaworski, E. Bousquet, J. Canonica, C. Gobeaux, A. Daruich, Min Zhao, M. Zola, Magda A. Meester-Smoor, D. Mohabati, F. Jaisser, S. Yzer, and F. Behar-Cohen. Lipocalin 2 as a potential systemic biomarker for central serous chorioretinopathy. Scientific Reports, Nov 2020. URL: https://doi.org/10.1038/s41598-020-77202-y, doi:10.1038/s41598-020-77202-y. This article has 26 citations and is from a peer-reviewed journal.

20. (matet2020lipocalin2as pages 3-5): A. Matet, T. Jaworski, E. Bousquet, J. Canonica, C. Gobeaux, A. Daruich, Min Zhao, M. Zola, Magda A. Meester-Smoor, D. Mohabati, F. Jaisser, S. Yzer, and F. Behar-Cohen. Lipocalin 2 as a potential systemic biomarker for central serous chorioretinopathy. Scientific Reports, Nov 2020. URL: https://doi.org/10.1038/s41598-020-77202-y, doi:10.1038/s41598-020-77202-y. This article has 26 citations and is from a peer-reviewed journal.

21. (zhang2023centralserouschorioretinopathy pages 7-10): Xinyuan Zhang, Connie Zhi Fong Lim, Jay Chhablani, and Yew Meng Wong. Central serous chorioretinopathy: updates in the pathogenesis, diagnosis and therapeutic strategies. Eye and Vision, Jul 2023. URL: https://doi.org/10.1186/s40662-023-00349-y, doi:10.1186/s40662-023-00349-y. This article has 84 citations and is from a peer-reviewed journal.

22. (kim2025treatmentofcentral pages 3-5): Yoon Jeon Kim, Sobha Sivaprasad, Tariq Aslam, Polona Jaki Mekjavić, Vilma Jūratė Balčiūnienė, Linda Visser, Antonia M. Joussen, Young Hee Yoon, Timothy Y. Y. Lai, and Annabelle A. Okada. Treatment of central serous chorioretinopathy: new options for an old disease. Eye, 39:2375-2388, Jul 2025. URL: https://doi.org/10.1038/s41433-025-03894-z, doi:10.1038/s41433-025-03894-z. This article has 9 citations and is from a peer-reviewed journal.

23. (zhang2023centralserouschorioretinopathy pages 10-12): Xinyuan Zhang, Connie Zhi Fong Lim, Jay Chhablani, and Yew Meng Wong. Central serous chorioretinopathy: updates in the pathogenesis, diagnosis and therapeutic strategies. Eye and Vision, Jul 2023. URL: https://doi.org/10.1186/s40662-023-00349-y, doi:10.1186/s40662-023-00349-y. This article has 84 citations and is from a peer-reviewed journal.

24. (kim2025treatmentofcentral pages 11-11): Yoon Jeon Kim, Sobha Sivaprasad, Tariq Aslam, Polona Jaki Mekjavić, Vilma Jūratė Balčiūnienė, Linda Visser, Antonia M. Joussen, Young Hee Yoon, Timothy Y. Y. Lai, and Annabelle A. Okada. Treatment of central serous chorioretinopathy: new options for an old disease. Eye, 39:2375-2388, Jul 2025. URL: https://doi.org/10.1038/s41433-025-03894-z, doi:10.1038/s41433-025-03894-z. This article has 9 citations and is from a peer-reviewed journal.

25. (shojaeinia2025acomprehensiveoverview pages 1-2): Mohammad Shojaeinia, Azamossadat Hosseini, Mostafa Naderi, Bardia D Baloutch, Mohammad Shokoohi Yekta, Leila Akbarpour, and Hamid Moghaddasi. A comprehensive overview: deep learning approaches to central serous chorioretinopathy diagnosis. BMC Ophthalmology, Oct 2025. URL: https://doi.org/10.1186/s12886-025-04372-6, doi:10.1186/s12886-025-04372-6. This article has 5 citations and is from a peer-reviewed journal.

26. (shojaeinia2025acomprehensiveoverview pages 14-16): Mohammad Shojaeinia, Azamossadat Hosseini, Mostafa Naderi, Bardia D Baloutch, Mohammad Shokoohi Yekta, Leila Akbarpour, and Hamid Moghaddasi. A comprehensive overview: deep learning approaches to central serous chorioretinopathy diagnosis. BMC Ophthalmology, Oct 2025. URL: https://doi.org/10.1186/s12886-025-04372-6, doi:10.1186/s12886-025-04372-6. This article has 5 citations and is from a peer-reviewed journal.

27. (shojaeinia2025acomprehensiveoverview pages 13-14): Mohammad Shojaeinia, Azamossadat Hosseini, Mostafa Naderi, Bardia D Baloutch, Mohammad Shokoohi Yekta, Leila Akbarpour, and Hamid Moghaddasi. A comprehensive overview: deep learning approaches to central serous chorioretinopathy diagnosis. BMC Ophthalmology, Oct 2025. URL: https://doi.org/10.1186/s12886-025-04372-6, doi:10.1186/s12886-025-04372-6. This article has 5 citations and is from a peer-reviewed journal.

28. (shojaeinia2025acomprehensiveoverview pages 8-9): Mohammad Shojaeinia, Azamossadat Hosseini, Mostafa Naderi, Bardia D Baloutch, Mohammad Shokoohi Yekta, Leila Akbarpour, and Hamid Moghaddasi. A comprehensive overview: deep learning approaches to central serous chorioretinopathy diagnosis. BMC Ophthalmology, Oct 2025. URL: https://doi.org/10.1186/s12886-025-04372-6, doi:10.1186/s12886-025-04372-6. This article has 5 citations and is from a peer-reviewed journal.

29. (kim2025treatmentofcentral pages 8-9): Yoon Jeon Kim, Sobha Sivaprasad, Tariq Aslam, Polona Jaki Mekjavić, Vilma Jūratė Balčiūnienė, Linda Visser, Antonia M. Joussen, Young Hee Yoon, Timothy Y. Y. Lai, and Annabelle A. Okada. Treatment of central serous chorioretinopathy: new options for an old disease. Eye, 39:2375-2388, Jul 2025. URL: https://doi.org/10.1038/s41433-025-03894-z, doi:10.1038/s41433-025-03894-z. This article has 9 citations and is from a peer-reviewed journal.

30. (zhang2023centralserouschorioretinopathy pages 19-20): Xinyuan Zhang, Connie Zhi Fong Lim, Jay Chhablani, and Yew Meng Wong. Central serous chorioretinopathy: updates in the pathogenesis, diagnosis and therapeutic strategies. Eye and Vision, Jul 2023. URL: https://doi.org/10.1186/s40662-023-00349-y, doi:10.1186/s40662-023-00349-y. This article has 84 citations and is from a peer-reviewed journal.

31. (kim2025treatmentofcentral pages 12-13): Yoon Jeon Kim, Sobha Sivaprasad, Tariq Aslam, Polona Jaki Mekjavić, Vilma Jūratė Balčiūnienė, Linda Visser, Antonia M. Joussen, Young Hee Yoon, Timothy Y. Y. Lai, and Annabelle A. Okada. Treatment of central serous chorioretinopathy: new options for an old disease. Eye, 39:2375-2388, Jul 2025. URL: https://doi.org/10.1038/s41433-025-03894-z, doi:10.1038/s41433-025-03894-z. This article has 9 citations and is from a peer-reviewed journal.

32. (kim2025treatmentofcentral pages 9-10): Yoon Jeon Kim, Sobha Sivaprasad, Tariq Aslam, Polona Jaki Mekjavić, Vilma Jūratė Balčiūnienė, Linda Visser, Antonia M. Joussen, Young Hee Yoon, Timothy Y. Y. Lai, and Annabelle A. Okada. Treatment of central serous chorioretinopathy: new options for an old disease. Eye, 39:2375-2388, Jul 2025. URL: https://doi.org/10.1038/s41433-025-03894-z, doi:10.1038/s41433-025-03894-z. This article has 9 citations and is from a peer-reviewed journal.

33. (zhang2023centralserouschorioretinopathy pages 14-15): Xinyuan Zhang, Connie Zhi Fong Lim, Jay Chhablani, and Yew Meng Wong. Central serous chorioretinopathy: updates in the pathogenesis, diagnosis and therapeutic strategies. Eye and Vision, Jul 2023. URL: https://doi.org/10.1186/s40662-023-00349-y, doi:10.1186/s40662-023-00349-y. This article has 84 citations and is from a peer-reviewed journal.

34. (kim2025treatmentofcentral pages 9-9): Yoon Jeon Kim, Sobha Sivaprasad, Tariq Aslam, Polona Jaki Mekjavić, Vilma Jūratė Balčiūnienė, Linda Visser, Antonia M. Joussen, Young Hee Yoon, Timothy Y. Y. Lai, and Annabelle A. Okada. Treatment of central serous chorioretinopathy: new options for an old disease. Eye, 39:2375-2388, Jul 2025. URL: https://doi.org/10.1038/s41433-025-03894-z, doi:10.1038/s41433-025-03894-z. This article has 9 citations and is from a peer-reviewed journal.

35. (kim2025treatmentofcentral pages 7-8): Yoon Jeon Kim, Sobha Sivaprasad, Tariq Aslam, Polona Jaki Mekjavić, Vilma Jūratė Balčiūnienė, Linda Visser, Antonia M. Joussen, Young Hee Yoon, Timothy Y. Y. Lai, and Annabelle A. Okada. Treatment of central serous chorioretinopathy: new options for an old disease. Eye, 39:2375-2388, Jul 2025. URL: https://doi.org/10.1038/s41433-025-03894-z, doi:10.1038/s41433-025-03894-z. This article has 9 citations and is from a peer-reviewed journal.

Artifacts

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