CSC usually affects young or middle-aged male adults and is usually unilateral (13). In its typical presentation, localized serous detachment of the neurosensory retina containing the macula is observed and spreads to the surrounding retina over time. One or more pigment epithelial detachments may be observed in some of the eyes with CSC. Patients generally complain of metamorphopsy, scotoma in the visual field and blurred vision. Micropsy, dyschromatopsy, or reduced contrast sensitivity may also develop. CSC could also be asymptomatic in rare cases (14).
Choroid and RPE dysfunction; subretinal fluid (SRF) is the most important causes of leakage (15, 16). Vascular hyperpermeability and obstruction belong to pachicoroid vascular changes. Lobular choroidal ischemia and venous obstruction have been shown to be the cause of fluid leakage from the choriocapillaris. Low perfusion and hydrostatic pressure due to subretinal fluid may be the cause of secondary damage on RPE (17). SRF originates from choriocapillaries, so photoreceptors can feed enough to survive despite long-term separation. CSC associated detached retina may induce the release of vascular endothelial growth factor (VEGF) into the subretinal area, and trigger the development of choroidal neovascularization in the eye (18).
Beside OCT and FFA, OCT angiography (OCTA) and indocyanine green (ICG) angiography are helpful in diagnosis of CSC. In typical cases, one or more fluorescent spots appear in FFA, indicating fluid leakage. A fluorescent leak area that expands with a serous separation and late accumulation occurs in 10–15% of cases. The Amsler grid test may be useful in demonstrating metamorphopsy. Hyperopia often develops in the affected eye (19–23). All cases we included in our study had typical CSC findings in both FFA and OCT imaging (Fig. 1).
In CSC, pathology is usually self-limiting and resolved. Visual acuity often turn back to previous level after a few months after the SRF dissolves, but visual problems may sustain after the fluid has dissipated (3). Even most of the cases has only one attack, recurrence may develop in the first year in 30–50% of patients. We did not include the eyes that had a second attack in our study. It has been reported that chronic CSC, called Type II, may develop in 5% of eyes. The time threshold considered to be for chhronic CSC ranges from 3 to 6 months (9, 24). In our study, we did not include the eyes that improved spontaneously before 3 months. From this perspective, it can be said that the eyes in our study were not acute but might be chronic.
Since there is a high possibility of spontaneous recovery in acute cases, follow-up without treatment is generally recommended (25). In chronic CSC management, most ophthalmology clinics recommend treatment (26–30). Intravitreal injection of acetazolamide or finasteride, eplerenone, spironolactone, propranolol, vitamins and non-steroidal anti-inflammatory drugs, photodynamic therapy, anti-VEGF agents, transpupillary thermotherapy and subthreshold lasers are the main treatment options (31–37). Treatment is recommended if resorption does not develop within 3–4 months or the patient has bilateral involvement or acute CSC recurrence and chronic CSC is diagnosed (26, 30). The patients we included in our study were started orally with acetazolamide and propranolol treatment, starting 3 months after the CSC attack developed.
Some of the most important risk factors for CSC development are aggressive personality and physiological stress. CSC often affects freelancers, managers, entrepreneurs and actively working men with a high stress burden. In the literature, CSC; It has been reported in many publications that it is more common in people with type-A or narcissistic personality (38–41). Therefore, it has been reported that psychological intervention, sleep patterns or beta-blocker drug treatments may prevent relapses or progression to chronic CSC (42–44). The patients in this study were followed-up without applying medical treatment and advice stress-reducing recommendations for the first 3 months.
There are publications in the literature indicating that shift work and sleep disorders can be important and independent risk factors for CSC. In these individuals, cortisol and catecholamine changes that develop with disruption of the circadian rhythm may be the triggering element of CSC. Although the relationship between CSC and melatonin level has not been shown yet; there are studies claiming that providing sleep patterns by melatonin may be useful in patients with CSC (45). There are publications claiming that early diagnosis and treatment of obstructive sleep apnea (OSA) may decrease the risk of CSC. Although the prevalence of OSA has been shown to be high in cases with CSC, objective evidence to support OSA screening in these patients is not sufficient today (40, 41). It is also suggested that glucocorticoids, mineralocorticoids and testosterone play a role in the pathogenesis of CSC. There is widespread proof that cortisol has a significant effect on the capillary permeability of the choroid. It has been reported that 5–10% of cases with Cushing's syndrome characterized by high cortisol develop simultaneous CSC (41, 46, 47). None of our cases had a history of OSA or exogenous glucocorticoid use that could be the cause of endogenous steroid elevation.
There are also some publications reporting that CSC may also be associated with catecholamines. In a meta-analysis, the relationship between CSC and catecholamine and drugs that can raise blood pressure was determined. High risk of CSC has been shown with the use of agents that increasing sympathetic activity (pseudoephedrine, amphetamine and oxymetazoline) (41). None of our cases had a history of sympathomimetic drug use.
Most of our cases also were male patients with high stress load. Our suggestions to rearrange the lifestyle may contributed to the high spontaneous improvement that developed especially in the first 6 months. SSRIs are also widely used today as an anxiolytic drug. Discontinuation of these drugs sometimes causes psychiatrists to worry about anxiety in the patient going out of control. This worry was the most important reason why SSRIs were not interrupted in Grup 2. There was no other antidepressant or anxiolytic drug was started in patients in Group 3 whose SSRI was discontinued. The first thing that makes our study special is that it is the article in the literature that reports the association of SSRI and CSC with the most cases. The most important contribution of our study to the literature might be demonstrating the discontinuation of SSRI could accelerate SRF resolution in CSC.
Propranolol is a non-selective adrenergic beta receptor blocker. Since it has a lipophilic molecular structure, its effect on central nervous system and neurons is strong. Propranolol treatment, which was initiated later in stress and anxiety control in patients in SSRI discontinued Group 3, may have contributed positively. Because beta blockers are drugs that inhibit the adrenergic system and cause sedation and anxiolytic effects. Propranolol also strongly blocks 𝛽2 adreno-receptors and causes evidet vasoconstriction. This vasoconstriction may be another reason for propranolol to positively contribute to CSC treatment (1). Because there are studies in the literature that argue that there may be a relationship between vasodilation and CSC. Fraunfelder et al. has been reported the inhibitors of phosphodiesterase type 5 enzym (tadalafil, sildenafil, vardenafil) that used in the treatment of erectile dysfunction might be the etiological cause of CSC. (25). Propranolol treatment was started to all patients in Group 3 on the recommendation of the clinic of psychiatry after the SSRI was discontinued. Therefore, it may be thought that the main reason for the difference between the groups could be due to propranolol.
This study has some limitations. Firstly, small sample size and short follow-up time can be meaningful. Another point to consider is that it is not clear whether the earlier developed SRF resolution in Group 3 was due to discontinuation of the SSRI or the initiation of propranolol.