Central Serous Chorioretinopathy

Etiology, Diagnosis, and Treatment

Background: Central serous chorioretinopathy (CSC) is a rare eye disease (estimated prevalence 1.4 per 10 000 people) characterized by a serous fluid collection under the central portion of the retina. Its pathogenesis and optimal treatment remain incompletely understood.

Methods: In this narrative review, we discuss the risk factors, pathophysiology, diagnostic evaluation, and treatment of CSC.

Results: Systemic corticosteroids are considered a well-documented precipitating factor for the disease (odds ratio 4.29, 95% confidence interval [2.01; 9.15]). Potential psychosomatic factors have been inadequately studied. The pathophysiology is likewise incompletely understood; choroidal vascular dysregulation and hyperpermeability appear to be key mechanisms. The resulting fluid collection under the retina can markedly impair photoreceptor function and vision. In 80%–90% of acute cases, the fluid is spontaneously resorbed. Various treatments, ranging from laser therapy to medication-based approaches, have been proposed for patients who do not experience spontaneous remission, but non of them has been found to yield superior functional outcomes in network meta-analyses. Morphologically, in two randomized trials, subretinal fluid regressed in 67% and 78%, respectively, of patients treated with photodynamic therapy, compared to 29% and 17% after micropulse laser treatment or oral eplerenone.

Conclusion: CSC is still incompletely understood, and the treatment options for it are a matter of debate. There is an urgent need for further controlled prospective trials with an adequate period of observation and functional endpoints.

Cite this as: Lange C, Lahmann C, Pauleikhoff L: Central serous chorioretinopathy: Etiology, diagnosis, and treatment. Dtsch Arztebl Int 2026; 123: 189–94. DOI: 10.3238/arztebl.m2026.0007

Central serous chorioretinopathy (CSC, formerly also referred to as retinopathia centralis serosa [RCS]) is a macular disease characterized by acute serous fluid collection under the central portion of the retina due to choroidal thickening and increased vascular permeability. Clinically, CSC typically presents with an acute reduction in visual acuity, wavy vision (metamorphopsia), and a relative central visual field defect, which may lead to irreversible visual loss in chronic cases (Figure 1) (1).

Figure 1

An artist’s representation of the symptoms of central serous chorioretinopathy (CSC) as perceived by patients. The pictures by the artist, who is herself affected by the disease, illustrate the symptoms often reported by patients with chronic CSC: metamorphopsia, dyschromatopsia, and a relative central visual field defect (“gray disc”).

With an estimated prevalence of approximately 1.4 per 10 000 people, CSC is one of the most common macular diseases (2). In contrast to age-related macular degeneration (AMD), CSC, with a male-to-female ratio of 3:1, primarily affects men of working age (40–50 years), which can have a significant socioeconomic impact (1).

Since its first description in 1866 by Albrecht von Graefe (3), founder of the German Society of Ophthalmology and a doyen of modern ophthalmology, a number of risk factors for the development of CSC have been discussed (4), including a stress-induced etiology, which has earned the disease the label “manager disease” in popular reporting.

However, many other disease-promoting factors and potential pathogenetic associations have been identified in recent years, casting new light on the disease.

Our review article aims to present possible theories on the pathophysiology and risk factors of CSC and to provide an overview of the diagnostic and therapeutic options available.

Methods

For this narrative review, relevant articles on the risk factors, pathophysiology, diagnosis evaluation, and treatment of the disease were collected and evaluated. To this end, the PubMed database was searched for meta-analyses and randomized controlled trials (RCTs) using the search term “central serous chorioretinopathy” (as of October 2025). In addition, national and international guidelines on CSC were evaluated.

Pathophysiology

The precise cause of CSC remains unknown (5, 6). However, some years ago, choroidal thickening and large-caliber choroidal vessels were identified beneath the fovea in patients with CSC, leading to the disease being classified as part of the “pachychoroid” disease spectrum (Greek: “pachýs” = thick; “chorioid” = choroid) (7, 8). Using indocyanine green angiography (ICGA), these vessels have been shown to represent collateral vessels between different vortex veins (5, 9, 10). Following this, it was postulated that scleral thickening, together with various exogenous events, may lead to venous congestion in the choroidal vessels, a phenomenon referred to as venous overload choroidopathy (6, 7). This venous overload can then cause fluid leakage from the large choroidal vessels, presenting as focal or diffuse hyperpermeability on ICGA (5). If the retinal pigment epithelium (RPE) is damaged at one or more sites, proteins and plasma fluid can seep into the subretinal space and lead to the accumulation of subretinal fluid. Consistent with this, it was shown that mutations in the PTPRB gene are associated with both an increased incidence of CSC and the occurrence of venous varicosis (11).

Clinical presentation and diagnosis

Three-quarters of patients with CSC notice a worsening of their central visual function, prompting them to visit an ophthalmologist. When questioned in more detail, 50% of affected individuals report metamorphopsia and/or a relative central visual field defect (often described as a gray disc). Approximately 20% of patients report blurred vision, while around 10% report altered color perception (dyschromatopsia) (1). Figure 1 shows an artist’s representation of the typical symptom complex experienced by an affected individual. However, the subjective symptoms do not always correlate with the severity of the disease. For example, many patients still report visual loss in the inactive phase of the disease, whereas they do not always notice an increase in edema, particularly in chronic stages.

Morphologically, the characteristic changes seen in CSC can be demonstrated using multimodal ophthalmological imaging (12). An overview of the most commonly used imaging modalities and their typical findings in CSC can be found in Table 1, while examples of imaging findings are presented in Figure 2. In general, invasive angiography is of particular relevance for the diagnosis and treatment planning of the disease, whereas optical coherence tomography (OCT) is particularly suited for monitoring the disease course. Multimodal imaging is able to visualize the degree of chronicity of the disease, thereby helping to differentiate the disorder from other maculopathies, such as neovascular age-related macular degeneration (nAMD), diabetic macular edema, and ocular tumors, which has significant therapeutic implications (13).

Figure 2

Multimodal imaging in a 40-year-old female patient with a healthy right eye (a–e) and acute central serous chorioretinopathy in the left eye (f–j). The best-corrected visual acuity in the right eye was 1.0 (refraction +0.0 –0.5 40°) and in the left eye 0.8 (refraction +2.0 –1.50 100°). On the fundus images (a and f), the left eye shows a pocket of subretinal fluid (dotted line), which is marked with an asterisk (*) on the infrared (IR) images (b and g) and on the optical coherence tomography (OCT) images (c and h). In addition, pigment epithelial detachment is visible in the region of the leakage point (arrowhead). On indocyanine green angiography (ICGA) (d and i) and on fluorescence angiography (FAG) (e and j), choroidal thickening in the left eye (arrow), and in this region, hyperfluorescence due to vascular leakage (“chimney phenomenon,” arrow) are visible.

Table 1

Overview of the most important imaging modalities for central serous chorioretinopathy and typical findings with each modality

Classification and spontaneous course

Clinically, CSC is divided into an acute and a chronic form. The acute form is characterized by the rapid onset of impaired choroidal permeability and subretinal fluid accumulation. The spontaneous course generally has a good prognosis and is self-limiting; in approximately 80–90% of patients, the subretinal fluid spontaneously resorbs within 6 months and vision is largely restored to baseline (14). Imaging typically shows only few pathological lesions, with the exception of areas of choroidal leakage and pockets of subretinal fluid. However, approximately 50% of cases of acute CSC recur (15).

In chronic forms, on the other hand, subretinal fluid persists for a period of 4–6 months, without any resorption occurring during that time. Imaging reveals increasing retinal thinning and diffuse degeneration of the RPE and photoreceptors, which can lead to irreversible morphological as well as functional defects (12). As part of the European CSC registry, retina.net e. V. (www.ccs-register.de), chronic changes of this kind were detected in half of all patients with CSC—a finding, however, that is likely attributable to recruitment at large tertiary care centers (1).

Systemic and psychosomatic risk factors

In addition to the abovementioned local choroidal changes, numerous systemic and psychosomatic factors are believed to promote the development and chronification of CSC (4, 16). The use of both systemic and locally applied corticosteroids is an established risk factor and is associated with an approximately fourfold increased likelihood of developing the disease (odds ratio [OR] 4.29, 95% confidence interval [2.01; 9.15]) (4). Furthermore, certain autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus, as well as Helicobacter pylori infections, have been proposed as possible triggers (17, 18). Cardiovascular risk factors such as hypertension and smoking may promote venous overload choroidopathy (6), whereas sleep disturbances related to sleep apnea are thought to contribute to the development of CSC via dysregulation of the hypothalamic–pituitary–adrenal axis and altered cortisol rhythms (19). The most important risk factors along with their corresponding confidence intervals are shown in Table 2.

Table 2

Risk factors for the development of central serous chorioretinopathy together with the associated odds ratio and 95% confidence intervals

However, many of these risk factors have been postulated on the basis of small cohorts or case reports; a large-scale, systematic assessment of risk factors is currently being conducted by the CSC registry funded by retina.net e. V. (1). This involves the standardized recording of patient history, clinical findings, disease course, and treatment decisions in patients with CSC at large European treatment centers. The fact that more than 1000 individuals have already been included and that follow-up periods exceed 10 years in some cases may lead to a better understanding of the effects of the various risk factors on disease course and prognosis.

Given the well-established risk associated with exogenous corticosteroid therapy, it has been suggested that elevated endogenous steroid levels may promote CSC. For example, previous studies suggested an association between CSC and Cushing syndrome; however, this has not been confirmed by more recent investigations (20). Along similar lines, elevated endogenous steroid levels due to psychological stress as well as other psychosomatic and psychiatric factors have also been discussed as possible triggers of CSC (21). A 1978 publication based on clinical observations first reported an association between CSC and the type-A personality profile, characterized by competitive drive, impatience, and low frustration tolerance (22). The author suggested that stress, via hormonal mechanisms, particularly through cortisol regulation, triggers vascular changes in the choroid, thereby contributing to the development of CSC (22). A meta-analysis also found an increased risk for individuals with type-A personality traits as well as those using psychopharmacological drugs (Table 2) (4). The stereotype of the highly competitive, impatient young man led to CSC being referred to as “manager’s disease.” However, this classification of individuals into different personality types is a historical concept dating back to the 1950s (23) and is no longer routinely used in modern psychosomatics. Instead, the focus is placed on individual features such as stress management, emotional lability (neuroticism), hostility, perfectionism, and alexithymia. These features are assessed in research and clinical practice using validated questionnaires to identify psychological stress factors in a targeted manner and address them therapeutically. Psychological stress in particular has been intensively researched: A number of studies have shown that patients with CSC have significantly higher stress levels compared to control groups (24, 25). Moreover, affected individuals often report stressful life events or inadequate coping strategies in conjunction with the onset of eye symptoms (26). Having a generalized anxiety disorder also appears to increase the recurrence rate (27, 28).

Stress as a risk factor: cause or consequence?

These studies, however, provide no unequivocal evidence that stress is a cause rather than merely a consequence of the disease. Most studies were conducted retrospectively using small sample sizes and were susceptible to bias due to subjective recall. A larger, prospective, and standardized investigation based on validated questionnaires to assess stress levels reported significantly higher stress levels in patients with CSC compared to healthy control subjects (24). Similarly elevated stress levels were also observed in patients with macular edema following branch retinal vein occlusion, for which stress is not considered a triggering factor (24). Thus, vision loss appears to lead to increased stress levels independent of the underlying disease (29), as has also been described for a number of other ophthalmological disorders (30, 31, 32).

In order to demonstrate the causal nature of a psychosomatic predisposition to the disease, at-risk individuals would need to be assessed prior to disease onset using validated questionnaires. Since the psychodiagnostic tools used to date are highly heterogeneous, it would be beneficial to develop a standardized, ophthalmology-specific screening tool. Only in this way might it be possible to distinguish between cause and effect. Furthermore, the clinically highly relevant question of the extent to which a reduction in psychosocial stressors can favorably influence the disease course should be investigated in larger studies.

Treatment strategies

Given its good spontaneous prognosis, uncomplicated acute CSC can be treated conservatively in many cases. Since best-corrected visual acuity often remains good, most activities of everyday life are still possible. However, in professions that place high demands on vision (for example, pilots and professional drivers), individuals may be temporarily unable to work. In such cases, discontinuation of potential triggering drugs such as corticosteroids, optimization of systemic risk factors, and close follow-up are recommended (33). Interventional procedures are indicated in chronic CSC with persistent or recurrent subretinal fluid and relevant visual impairment (34).

Half-dose photodynamic therapy (HD-PDT) is currently considered the treatment of choice (34), based in particular on two large RCTs: In the PLACE trial, which included a total of 179 patients, 67% of those treated with HD-PDT showed complete resolution of subretinal fluid, whereas this was the case in only 29% of those receiving micropulse laser treatment (35). In the SPECTRA trial with 107 patients, 78% of those treated with HD-PDT showed complete resolution of subretinal fluid, while this was the case in only 17% of those treated with oral eplerenone (36). PDT works by reducing choroidal hyperpermeability in a targeted manner in the selected treatment area, thereby treating the cause of fluid leakage (level of evidence 1b) (37).

Focal argon laser therapy of solitary leakage sites has been used as a treatment option in patients with CSC since the 1990s, despite the fact that large-scale randomized trials are still lacking. Previous studies show that this method is able to accelerate the resorption of subretinal fluid (6 weeks in the treatment group versus 16 weeks in the untreated group) (38); however, no significant effects on visual acuity, color vision, or recurrence rates have been demonstrated (level of evidence 2b) (39). A direct comparison of focal laser therapy with other treatment methods is challenging, since it can only be used in patients with focal, extrafoveal leakage points.

Subthreshold laser techniques are now established as an additional treatment alternative. The micropulse laser (MPL) uses modulated, non-thermal impulses to stimulate the regeneration mechanism of the RPE without damaging the photoreceptors. Randomized controlled trials have shown accelerated fluid resorption and improvements in visual acuity of approximately one line (logMAR BCVA −0.1 ± 0.21) within 3–6 months (level of evidence 1b) (40, e1, e2); however, study protocols vary with regard to power, pulse duration, and interval, which is why there is currently no standardized recommendation for the use of MPL.

Three recent network meta-analyses (39, e3, e4) compared the efficacy of various treatments for chronic CSC (level of evidence 1a). It was determined that the endpoints used in the underlying studies were highly heterogeneous, thereby complicating any analysis across the various treatment methods. While many of the abovementioned RCTs used the anatomical endpoint of subretinal fluid resorption as their primary endpoint, the meta-analyses focused on changes in visual acuity, which were reported in almost every RCT (Table 3) (39). However, the subjective symptoms of patients with CSC often correlate only poorly with their measured visual acuity (e5).

Table 3

Effect sizes for changes in visual acuity with various CSC treatments based on the largest network meta-analysis on the disease*

Even though there was no significant difference in the final visual acuity outcomes (Table 3), the studies identified photodynamic therapy and subthreshold laser procedures as currently the most effective treatments for subretinal fluid resorption. Mineralocorticoid receptor antagonists such as eplerenone, on the other hand, showed no significant benefit compared with placebo in the meta-analyses and are therefore currently considered to be of limited value (e6). If secondary choroidal neovascularization (CNV) occurs—as is the case in 2–15% of patients with chronic CSC—intraocular anti-vascular endothelial growth factor (VEGF) therapy remains the treatment of choice (e7), although in an RCT it showed no significant effect on central visual acuity compared with placebo injections (+ 5.02 ETDRS letters; [−3.12; 13.16], n = 23) (e8).

Discussion and outlook

A comprehensive assessment of CSC reveals that it is unlikely to be a monocausal, stress-induced disease, but instead represents a complex interplay between local choroidal vascular barrier deficiency, choroidal venous overload, and various systemic and psychosomatic risk factors. Although many patients perceive psychological stress as a trigger, there are as yet no prospective studies using validated questionnaires and corresponding biomolecular parameters that would provide evidence of direct causality. There is also no clear evidence of efficacy for psychotherapeutic or psychopharmacological interventions.

In terms of treatment, photodynamic therapy stands out due to its consistent efficacy data and favorable effect sizes. Subthreshold and conventional laser techniques broaden the treatment spectrum, particularly in cases where photodynamic therapy is contraindicated (verteporfin intolerance) or there is insufficient treatment response. Eplerenone and anti-VEGF show only a limited effect.

Four key research directions can be identified for the future: First, research into prognostic biomarkers using multimodal imaging with the aim of identifying predictors of chronicity and, from these, deriving individualized treatment approaches; second, the standardization and prospective validation of protocols for subthreshold laser techniques in randomized trials to determine optimal treatment parameters; third, conducting longitudinal cohort studies to systematically record and analyze psychosomatic factors using validated questionnaires and correlative endocrine and immunological markers; and fourth, in addition to etiological factors and treatment options, future research should also focus on improving visual acuity. Only through these integrative approaches can treatment be further optimized and the quality of life of those affected be durably improved.

Conflict of interest statement
The authors declare that no conflict of interest exists.

Manuscript received on 30 July 2025, revised version accepted on 20 January 2026.

Translated from the original German by Christine Rye.

Corresponding author
Prof. Dr. Dr. med. Clemens Lange

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