Central serous chorioretinopathy

Central serous chorioretinopathy
An occurrence of central serous retinopathy of the fovea centralis imaged using optical coherence tomography.
SpecialtyOphthalmology 

Central serous chorioretinopathy (CSC or CSCR), also known as central serous retinopathy (CSR), is an eye disease that causes visual impairment, often temporary, usually in one eye.[1] When the disorder is active, it is characterized by leakage of fluid under the retina that has a propensity to accumulate under the central macula. This results in blurred or distorted vision (metamorphopsia). A blurred or gray spot in the central visual field is common when the retina is detached. Reduced visual acuity may persist after the fluid has disappeared.[1]

The disease is considered of unknown cause. It mostly affects white males in the age group 20 to 50 (male:female ratio 6:1)[2] and occasionally other groups. The condition is believed to be exacerbated by stress or corticosteroid use.[3]

Pathophysiology

Recently, central serous chorioretinopathy has been understood to be part of the pachychoroid spectrum.[4][5] In pachychoroid spectrum disorders, of which CSC represents stage II, the choroid, the highly vascularized layer below the retina, is thickened and congested with increased blood vessel diameter, especially in the deep choroid (the so-called Haller's layer). This results in increased pressure from the deep choroid against the superficial choroid close to the retina, damaging the fine blood vessels (capillaries) needed to supply oxygen and nutrients to the retinal pigment epithelium and retina. Additionally, fluid can leak from these damaged vessels and accumulate under the retina.

Different stages of the pachychoroid are defined depending on the amount of cumulative damage.[4][5] If there are defects in the retinal pigment epithelium without accumulation of fluid below the retina, a pachychoroid pigment epitheliopathy (PPE) is present. Accumulation of fluid results in central serous chorioretinopathy (CSC). The development of secondary blood vessels, so-called choroidal neovascularization (CNV) leads to pachychoroid neovasculopathy (PNV). If parts of these new vessels bulge outward, so-called aneurysms develop within this CNV, defining pachychoroid aneurysmal type 1 CNV (or, still widely used, polypoidal choroidal vasculopathy (PCV)).

Since the individual stages develop one after the other from the respective preliminary stage, pachychoroidal diseases of the macula are divided into 4 stages according to Siedlecki, Schworm and Priglinger:[6]

Pachychoroid spectrum disorders of the macula (after Siedlecki et al.[6])
0 Uncomplicated pachychoroid (UCP)
I Pachychoroid pigment epitheliopathy (PPE)
II Central serous chorioretinopathy (CSC)
III Pachychoroid neovasculopathy (PNV)
a) with neurosensory detachment (subretinal fluid)
b) without neurosensory detachment (no subretinal fluid)
IV Pachychoroid aneurysmal type 1 choroidal neovascularization (PAT1)

(also polypoidal choroidal vasculopathy, PCV)

Risk factors

CSC is sometimes called idiopathic CSC which means that its cause is unknown. Nevertheless, stress appears to play an important role. An oft-cited but potentially inaccurate conclusion is that persons in stressful occupations, such as airplane pilots, have a higher incidence of CSC.

CSC has also been associated with cortisol and corticosteroids. Persons with CSC have higher levels of cortisol.[7] Cortisol is a hormone secreted by the adrenal cortex which allows the body to deal with stress, which may explain the CSC-stress association. There is extensive evidence to the effect that corticosteroids (e.g. cortisone), commonly used to treat inflammations, allergies, skin conditions and even certain eye conditions, can trigger CSC, aggravate it and cause relapses.[8][9][10] A study of 60 persons with Cushing's syndrome found CSC in 3 (5%).[11] Cushing's syndrome is characterized by very high cortisol levels. Certain sympathomimetic drugs have also been associated with causing the disease.[12]

Evidence has also implicated Helicobacter pylori (see gastritis) as playing a role.[13][14] It would appear that the presence of the bacteria is well correlated with visual acuity and other retinal findings following an attack.

Evidence also shows that people with MPGN type II kidney disease can develop retinal abnormalities, including CSC caused by deposits of the same material that originally damaged the glomerular basement membrane in the kidneys.[15]

Diagnosis

The diagnosis usually starts with a dilated examination of the retina, followed by confirmation by optical coherence tomography, fluorescein angiography, and indocyanine green angiography. The angiography test will usually show one or more fluorescent spots with fluid leakage. In 10%-15% of the cases, these will appear in a classic smokestack shape. Differential diagnosis should be immediately performed to rule out retinal detachment, which is a medical emergency. A clinical record should be taken to keep a timeline of the detachment. The affected eye will sometimes exhibit a refractive spectacle prescription that is more far-sighted than the fellow eye due to the decreased focal length caused by the raising of the retina.

Indocyanine green angiography is a key diagnostic tool to assess the extent of choroidal abnormalities, showing different leakage patterns that correlate with disease severity and possibly treatment outcome.[17] Laser Doppler imaging can be used to reveal the underlying swollen choroidal vessels under the retinal pigment epithelium and assess the health of the retina in the affected area which can be useful in making a treatment decision.

Treatment

Any ongoing corticosteroid treatment should be tapered and stopped, where possible. It is important to check current medication, including nasal sprays and creams, for ingredients of corticosteroids; if found, seek advice from a medical practitioner for an alternative.

Most eyes with CSC undergo spontaneous resorption of subretinal fluid within 3–4 months. Recovery of visual acuity usually follows. Treatment should be considered if resorption does not occur within 3–4 months, spontaneously or as a result of counselling. The available evidence suggests that half-dose (or half-fluence) photodynamic therapy is the treatment of choice for CSC with subretinal fluid for longer than 3–4 months.[1]

Due to the natural disease course of CSC – in which spontaneous resolution of subretinal fluid often occurs in first-episode cases – retrospective studies may erroneously report positive treatment outcomes and should, therefore, be evaluated with caution.[1]

Laser treatments

Full-dose photodynamic therapy (PDT) with verteporfin was first described in CSC in 2003.[18] Later, reduced-settings PDT (half-dose, half-fluence, and half-time) was found to have the same efficacy and a very low chance of complications. Follow-up studies have confirmed the treatment's long-term effectiveness[19] including its effectiveness for the chronic variant of the disease.[20] In the prospective randomized PLACE trial, half-dose photodynamic therapy was found to be superior compared to high-density subthreshold micropulse laser in chronic CSC, both with regard to anatomical and functional outcomes.[21] In the prospective randomized SPECTRA trial, half-dose PDT was shown to be more successful in treating chronic CSC.[22][23] At long-term follow-up, PDT in CSC is safe, also when treating the central macula (fovea).[24] Indocyanine green angiography may be used to predict how the patient will respond to PDT.[25][26]

Laser photocoagulation, which effectively burns the leak area shut (in contrast to PDT), may be considered in cases where there is little improvement in a 3- to 4-month duration, and the leakage is confined to a single or a few sources of leakage at a safe distance from the fovea. Laser photocoagulation is not indicated for cases where the leak is very near the central macula or for cases where the leakage is widespread and its source is difficult to identify. Laser photocoagulation can permanently damage vision where applied. Carefully tuned lasers can limit this damage.[27] Even so, laser photocoagulation is not a preferred treatment for leaks in the central vision and is considered an outdated treatment by some doctors.[28] Foveal attenuation has been associated with more than 4 months' duration of symptoms, however a better long-term outcome has not been demonstrated with laser photocoagulation than without photocoagulation.[29]

In chronic cases, transpupillary thermotherapy has been suggested as an alternative to laser photocoagulation where the leak is in the central macula.[30]

Yellow micropulse laser has shown promise in very limited retrospective trials.[3]

A Cochrane review updated in 2025, seeking to compare the effectiveness of various treatments for CSC, found low-quality evidence that half-dose PDT treatment resulted in improved visual acuity and less recurrence of CSC in patients with acute CSC, compared to patients in the control group.[31] The review also found benefits in micropulse laser treatments, where patients with acute and chronic CSC had improved visual acuity compared to control patients.[31] The review did not demonstrate the superiority of one treatment option over another.[31]

An evidence-based treatment guideline published in 2024 by an international expert panel concluded that half-dose or half-fluence PDT is the treatment of choice in chronic and recurrent CSC.[1] Likewise, an international expert consensus-based guideline concluded that half-dose PDT is the preferred first-line treatment for chronic CSC.[32]

Oral medications

Spironolactone is a mineralocorticoid receptor antagonist that may help reduce the fluid associated with CSC. In a retrospective study noted by Acta Ophthalmologica, spironolactone improved visual acuity in CSC patients over the course of 8 weeks.[33]

Eplerenone is another mineralocorticoid receptor antagonist that has been thought to reduce the subretinal fluid that is present with CSC. In a study noted in the International Journal of Ophthalmology, results showed Epleronone decreased the subretinal fluid both horizontally and vertically over time.[34] However, a large investigator-initiated randomized controlled trial (VICI) showed that eplerenone has no significant effect on chronic CSC.[35][36]

Topical treatment

Though no topical treatment has been proven to be effective in the treatment of CSC. Some doctors have attempted to use nonsteroidal topical medications to reduce the subretinal fluid associated with CSC. The nonsteroidal topical medications that are sometimes used to treat CSC are ketorolac, diclofenac, or bromfenac, but the level of evidence to support their use is limited.[37]

Lifestyle changes

People who have irregular sleep patterns, type A personalities, sleep apnea, or systemic hypertension have been described to be more susceptible to CSC, although the level of evidence to support lifestyle interventions such as stress reduction is limited.

Prognosis

The prognosis for acute CSC is generally excellent. While immediate vision loss may be as poor as 20/200 in the affected eye, clinically, over 90% of patients regain 20/25 vision or better within 45 days.[29] Once the fluid has resolved, either spontaneously or through treatment, distortion is reduced and visual acuity improves as the eye heals. However, some visual abnormalities can remain even where visual acuity is measured at 20/20. This includes localized reductions in light sensitivity as assessed by visual field testing (microperimetry).[38] Lasting problems include decreased night vision, reduced color discrimination, and localized distortion caused by scarring of the sub-retinal layers.[39] Complications include subretinal neovascularization and pigment epithelial detachment.[40]

The disease can re-occur causing progressive vision loss. The prognosis of chronic CSC is less favorable, with continued clinical consultation and treatment generally being advised.[1]

See also

References

  1. ^ a b c d e f Feenstra, Helena M. A.; van Dijk, Elon H. C.; Cheung, Chui Ming Gemmy; Ohno-Matsui, Kyoko; Lai, Timothy Y. Y.; Koizumi, Hideki; Larsen, Michael; Querques, Giuseppe; Downes, Susan M.; Yzer, Suzanne; Breazzano, Mark P.; Subhi, Yousif; Tadayoni, Ramin; Priglinger, Siegfried G.; Pauleikhoff, Laurenz J. B. (July 2024). "Central serous chorioretinopathy: An evidence-based treatment guideline". Progress in Retinal and Eye Research. 101 101236. doi:10.1016/j.preteyeres.2024.101236. ISSN 1873-1635. PMID 38301969.
  2. ^ Sartini F, Figus M, Nardi M, Casini G, Posarelli C (July 2019). "Non-resolving, recurrent and chronic central serous chorioretinopathy: available treatment options". Eye. 33 (7): 1035–1043. doi:10.1038/s41433-019-0381-7. PMC 6707196. PMID 30824822.
  3. ^ a b André Maia (February 2010). "A New Treatment for Chronic Central Serous Retinopathy". Retina Today. Archived from the original on 2012-08-09. Retrieved 2013-08-11.
  4. ^ a b Cheung CM, Lee WK, Koizumi H, Dansingani K, Lai TY, Freund KB (January 2019). "Pachychoroid disease". Eye. 33 (1): 14–33. doi:10.1038/s41433-018-0158-4. PMC 6328576. PMID 29995841.
  5. ^ a b Akkaya S (October 2018). "Spectrum of pachychoroid diseases". International Ophthalmology. 38 (5): 2239–2246. doi:10.1007/s10792-017-0666-4. PMID 28766279. S2CID 4022900.
  6. ^ a b Siedlecki J, Schworm B, Priglinger SG (December 2019). "The Pachychoroid Disease Spectrum-and the Need for a Uniform Classification System". Ophthalmology. Retina. 3 (12): 1013–1015. doi:10.1016/j.oret.2019.08.002. PMID 31810570. S2CID 208813687.
  7. ^ Garg SP, Dada T, Talwar D, Biswas NR (November 1997). "Endogenous cortisol profile in patients with central serous chorioretinopathy". The British Journal of Ophthalmology. 81 (11): 962–4. doi:10.1136/bjo.81.11.962. PMC 1722041. PMID 9505819.
  8. ^ Pizzimenti JJ, Daniel KP (August 2005). "Central serous chorioretinopathy after epidural steroid injection". Pharmacotherapy. 25 (8): 1141–6. doi:10.1592/phco.2005.25.8.1141. PMID 16207106. S2CID 23535867.
  9. ^ Bevis T, Ratnakaram R, Smith MF, Bhatti MT (August 2005). "Visual loss due to central serous chorioretinopathy during corticosteroid treatment for giant cell arteritis". Clinical & Experimental Ophthalmology. 33 (4): 437–9. doi:10.1111/j.1442-9071.2005.01017.x. PMID 16033370. S2CID 1224694.
  10. ^ Fernández Hortelano A, Sádaba LM, Heras Mulero H, García Layana A (April 2005). "Coroidopatía serosa central como complicación de epitelitis en tratamiento con corticoides" [Central serous chorioretinopathy as a complication of epitheliopathy under treatment with glucocorticoids]. Archivos de la Sociedad Española de Oftalmología. 80 (4): 255–8. doi:10.4321/S0365-66912005000400010. PMID 15852168.
  11. ^ Bouzas EA, Scott MH, Mastorakos G, Chrousos GP, Kaiser-Kupfer MI (September 1993). "Central serous chorioretinopathy in endogenous hypercortisolism". Archives of Ophthalmology. 111 (9): 1229–33. doi:10.1001/archopht.1993.01090090081024. PMID 8363466.
  12. ^ Michael JC, Pak J, Pulido J, de Venecia G (July 2003). "Central serous chorioretinopathy associated with administration of sympathomimetic agents". American Journal of Ophthalmology. 136 (1): 182–5. doi:10.1016/S0002-9394(03)00076-X. PMID 12834690.
  13. ^ Ahnoux-Zabsonre A, Quaranta M, Mauget-Faÿsse M (December 2004). "[Prevalence of Helicobacter pylori in central serous chorioretinopathy and diffuse retinal epitheliopathy: a complementary study]" [Prevalence of Helicobacter pylori in central serous chorioretinopathy and diffuse retinal epitheliopathy: a complementary study]. Journal Français d'Ophtalmologie (in French). 27 (10): 1129–33. doi:10.1016/S0181-5512(04)96281-X. PMID 15687922.
  14. ^ Cotticelli L, Borrelli M, D'Alessio AC, Menzione M, Villani A, Piccolo G, et al. (2006). "Central serous chorioretinopathy and Helicobacter pylori". European Journal of Ophthalmology. 16 (2): 274–8. doi:10.1177/112067210601600213. PMID 16703546. S2CID 37258065.
  15. ^ Colville D, Guymer R, Sinclair RA, Savige J (August 2003). "Visual impairment caused by retinal abnormalities in mesangiocapillary (membranoproliferative) glomerulonephritis type II ("dense deposit disease")". American Journal of Kidney Diseases. 42 (2): E2-5. doi:10.1016/S0272-6386(03)00665-6. PMID 12900843.
  16. ^ Puyo, Léo; Paques, Michel; Fink, Mathias; Sahel, José-Alain; Atlan, Michael (2019). "Choroidal vasculature imaging with laser Doppler holography". Biomedical Optics Express. 10 (2): 995–1012. doi:10.1364/BOE.10.000995. PMC 6377881. PMID 30800528.
  17. ^ Pauleikhoff, Laurenz J. B.; Diederen, Roselie M. H.; Chang-Wolf, Jennifer M.; Moll, Annette C.; Schlingemann, Reinier O.; van Dijk, Elon H. C.; Boon, Camiel J. F. (September 2024). "Choroidal hyperpermeability patterns correlate with disease severity in central serous chorioretinopathy: CERTAIN study report 2". Acta Ophthalmologica. 102 (6): e946–e955. doi:10.1111/aos.16679. hdl:1887/4212307. ISSN 1755-3768. PMID 38561630.
  18. ^ Yannuzzi, L. A. (2003). "Indocyanine green angiography-guided photodynamic therapy for treatment of chronic central serous chorioretinopathy: a pilot study". Retina. 23 (3): 288–98. doi:10.1097/00006982-200306000-00002. PMID 12824827.
  19. ^ Chan WM, Lai TY, Lai RY, Liu DT, Lam DS (October 2008). "Half-dose verteporfin photodynamic therapy for acute central serous chorioretinopathy: one-year results of a randomized controlled trial". Ophthalmology. 115 (10): 1756–65. doi:10.1016/j.ophtha.2008.04.014. PMID 18538401.
  20. ^ Karakus SH, Basarir B, Pinarci EY, Kirandi EU, Demirok A (May 2013). "Long-term results of half-dose photodynamic therapy for chronic central serous chorioretinopathy with contrast sensitivity changes". Eye. 27 (5): 612–20. doi:10.1038/eye.2013.24. PMC 3650272. PMID 23519277.
  21. ^ van Dijk, Elon (2018-05-20). "Half-Dose Photodynamic Therapy versus High-Density Subthreshold Micropulse Laser Treatment in Patients with Chronic Central Serous Chorioretinopathy: The PLACE Trial". Ophthalmology. 125 (10): 1547–1555. doi:10.1016/j.ophtha.2018.04.021. hdl:2066/196622. PMID 29776672.
  22. ^ van Rijssen, Thomas J.; van Dijk, Elon H. C.; Tsonaka, Roula; Feenstra, Helena M. A.; Dijkman, Greet; Peters, Petrus J. H.; Diederen, Roselie M. H.; Hoyng, Carel B.; Schlingemann, Reinier O.; Boon, Camiel J. F. (January 2022). "Half-Dose Photodynamic Therapy Versus Eplerenone in Chronic Central Serous Chorioretinopathy (SPECTRA): A Randomized Controlled Trial". American Journal of Ophthalmology. 233: 101–110. doi:10.1016/j.ajo.2021.06.020. ISSN 1879-1891. PMID 34214454.
  23. ^ Feenstra, Helena M. A.; van Dijk, Elon H. C.; van Rijssen, Thomas J.; Tsonaka, Roula; Diederen, Roselie M. H.; Hoyng, Carel B.; Schlingemann, Reinier O.; Boon, Camiel J. F. (March 2023). "Long-term follow-up of chronic central serous chorioretinopathy patients after primary treatment of oral eplerenone or half-dose photodynamic therapy and crossover treatment: SPECTRA trial report No. 3". Graefe's Archive for Clinical and Experimental Ophthalmology. 261 (3): 659–668. doi:10.1007/s00417-022-05836-x. ISSN 1435-702X. PMC 9988736. PMID 36202933.
  24. ^ Feenstra, Helena M. A.; Diederen, Roselie M. H.; Lamme, Martine J. C. M.; Tsonaka, Roula; Fauser, Sascha; Yzer, Suzanne; van Rijssen, Thomas; Gkika, Theodora; Downes, Susan M.; Schlingemann, Reinier O.; Hoyng, Carel B.; van Dijk, Elon H. C.; Boon, Camiel J. F. (2023-03-01). "Increasing Evidence for the Safety of Fovea=Involving Half-Dose Photodynamic Therapy for Chronic Central Serous Chorioretinopahty". Retina. 43 (3): 379–388. doi:10.1097/IAE.0000000000003686. ISSN 1539-2864. PMC 9935620. PMID 36727801.
  25. ^ Inoue R, Sawa M, Tsujikawa M, Gomi F (March 2010). "Association between the efficacy of photodynamic therapy and indocyanine green angiography findings for central serous chorioretinopathy". American Journal of Ophthalmology. 149 (3): 441–6.e1–2. doi:10.1016/j.ajo.2009.10.011. PMID 20172070.
  26. ^ van Rijssen, Thomas J.; van Dijk, Elon H. C.; Dijkman, Greet; Boon, Camiel J. F. (August 2018). "Clinical characteristics of chronic central serous chorioretinopathy patients with insufficient response to reduced-settings photodynamic therapy". Graefe's Archive for Clinical and Experimental Ophthalmology. 256 (8): 1395–1402. doi:10.1007/s00417-018-4003-z. ISSN 1435-702X. PMC 6060777. PMID 29732468.
  27. ^ Roider J, Brinkmann R, Wirbelauer C, Laqua H, Birngruber R (August 1999). "Retinal sparing by selective retinal pigment epithelial photocoagulation". Archives of Ophthalmology. 117 (8): 1028–34. doi:10.1001/archopht.117.8.1028. PMID 10448745.
  28. ^ Boscia F (April 2010). "When to Treat and Not to Treat Patients With Central Serous Retinopathy". Retina Today. Archived from the original on 2012-10-17.
  29. ^ a b Wang M, Munch IC, Hasler PW, Prünte C, Larsen M (March 2008). "Central serous chorioretinopathy". Acta Ophthalmologica. 86 (2): 126–45. doi:10.1111/j.1600-0420.2007.00889.x. PMID 17662099. S2CID 42537355.
  30. ^ Wei SY, Yang CM (2005). "Transpupillary thermotherapy in the treatment of central serous chorioretinopathy". Ophthalmic Surgery, Lasers & Imaging. 36 (5): 412–5. doi:10.3928/1542-8877-20050901-11. PMID 16238041.
  31. ^ a b c Lange, Clemens Ak; Qureshi, Riaz; Pauleikhoff, Laurenz (2025-06-16). "Interventions for central serous chorioretinopathy: a network meta-analysis". The Cochrane Database of Systematic Reviews. 2025 (6) CD011841. doi:10.1002/14651858.CD011841.pub3. ISSN 1469-493X. PMC 12169103. PMID 40522203.
  32. ^ Radke, Nishant V.; van Dijk, Elon H. C.; Spaide, Richard F.; Holz, Frank G.; Koizumi, Hideki; Freund, K. Bailey; Subhi, Yousif; Lange, Clemens; Singh, Sumit Randhir; Chen, Haoyu; Chen, Li Jia; Chen, San-Ni; Chhablani, Jay; Behar-Cohen, Francine; Das, Taraprasad (2025-10-15). "International consensuses and guidelines on central serous chorioretinopathy (CSC) by the Asia Pacific Vitreo-retina Society (APVRS), the Academy of Asia-Pacific Professors of Ophthalmology (AAPPO) and the Academia Retina Internationalis (ARI)". Asia-Pacific Journal of Ophthalmology. 14 (5) 100252. doi:10.1016/j.apjo.2025.100252. ISSN 2162-0989. PMID 41106484.
  33. ^ Lee J.Y. (2016). "Spironolactone in the treatment of non-resolving central serous chorioretinopathy: a comparative analysis". Acta Ophthalmologica. 94 j.1755-3768.2016.0285. doi:10.1111/j.1755-3768.2016.0285.
  34. ^ Singh RP, Sears JE, Bedi R, Schachat AP, Ehlers JP, Kaiser PK (2015). "Oral eplerenone for the management of chronic central serous chorioretinopathy". International Journal of Ophthalmology. 8 (2): 310–4. doi:10.3980/j.issn.2222-3959.2015.02.17. PMC 4413566. PMID 25938046.
  35. ^ Lotery A, Sivaprasad S, O'Connell A, Harris RA, Culliford L, Ellis L, et al. (January 2020). "Eplerenone for chronic central serous chorioretinopathy in patients with active, previously untreated disease for more than 4 months (VICI): a randomised, double-blind, placebo-controlled trial". Lancet. 395 (10220): 294–303. doi:10.1016/S0140-6736(19)32981-2. hdl:1983/c40782ba-12d7-428b-8724-bbffb45d7bcf. PMID 31982075.
  36. ^ Trials Centre, Bristol. "VICI Trial YouTube video". Twitter.
  37. ^ "Retinal Physician - Central Serous Chorioretinopathy and Topical NSAIDs". Retinal Physician. Archived from the original on 30 August 2017. Retrieved 15 October 2017.
  38. ^ Pfau M, van Dijk EHC, van Rijssen TJ, Schmitz-Valckenberg S, Holz FG, Fleckenstein M; et al. (2021). "Estimation of current and post-treatment retinal function in chronic central serous chorioretinopathy using artificial intelligence". Scientific Reports. 11 (1) 20446. Bibcode:2021NatSR..1120446P. doi:10.1038/s41598-021-99977-4. PMC 8516921. PMID 34650220.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  39. ^ Baran NV, Gürlü VP, Esgin H (August 2005). "Long-term macular function in eyes with central serous chorioretinopathy". Clinical & Experimental Ophthalmology. 33 (4): 369–72. doi:10.1111/j.1442-9071.2005.01027.x. PMID 16033348. S2CID 21817531.
  40. ^ Kanyange ML, De Laey JJ (2002). "Long-term follow-up of central serous chorioretinopathy (CSCR)". Bulletin de la Société Belge d'Ophtalmologie (284): 39–44. PMID 12161989.
This article is issued from Wikipedia. The text is available under Creative Commons Attribution-Share Alike 4.0 unless otherwise noted. Additional terms may apply for the media files.