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Ganglion Cell Loss in the Course of Central Serous Chorioretinopathy
Maciej Gawęcki1, Andrzej Grzybowski2,3
1Dobry Wzrok Ophthalmological Clinic, 80-822, Gdańsk, Poland.
Introduction:
Central serous chorioretinopathy (CSCR) as a clinical entity is potentially damaging and may significantly affect retinal morphology and function, especially in the chronic form. Our study aimed to determine the amount of deficit of best corrected visual acuity (BCVA) and individual retinal layers, including ganglion cells, in different types of CSCR and with reference to its duration.
Methods:
The retrospective analysis included 69 eyes of patients with resolved CSCR managed in Dobry Wzrok Ophthalmological Clinic between 1 January 2019 and 30 June 2022. The diagnosis of CSCR was based on the criteria outlined by the Central Serous Chorioretinopathy International Group. The analysis included data obtained from medical history, BCVA testing, and spectral domain optical coherence tomography (SD-OCT) measurements, with specific thickness values for individual retinal layers. The results were compared among affected eyes, unaffected fellow eyes, and healthy controls.
Results:
BCVA values were significantly lower in acute (0.08 ± 0.12 logMAR) and chronic (0.26 ± 0.19 logMAR) cases versus controls (0.0 logMAR). The thickness of all retinal layers (central subfoveal thickness, CST; inner retina with ganglion cell complex, GC; outer retina, ORT; and photoreceptor outer segments, POS) and macular volume (MV) were significantly decreased in chronic eyes versus controls (p < 0.01). Acute eyes had significant thinning of the outer retina and POS only compared to control eyes (p < 0.01). The amount of deficit in CST, ORT, GC, and MV was strongly correlated with poorer BCVA (p < 0.001), and the deficit of CST, ORT, and GC was correlated with disease duration (p < 0.05). The subfoveal choroidal thickness was significantly greater in affected and fellow eyes versus controls (p < 0.001).
Conclusion:
Damage to the outer retina and photoreceptors occurs early in the course of CSCR, with a deficit in ganglion cells noted adjunctively in chronic forms of the disease. Further studies are required to precisely determine correlation between visual loss in CSCR and deficits in individual retinal layers.
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