# Ocular Implications in Patients with Sleep Apnea
## 3 Results
### Glaucoma  
Glaucoma is a progressive optic neuropathy that associates accelerated apoptosis of the lymph node cells in the retina. The classification of different types of glaucoma dependson the anatomical condition of the iridocorneal angle and the etiology of glaucoma (primary or secondary). There are several types of glaucoma, but those related to SAS are normal blood pressure glaucoma and primary open-angle glaucoma [7; 30; 39]. The prevalence of glaucoma in SAS patients has been investigated by numerous studies, the results ranging from 5.9% [40], 12.9% ([PERSON] et al., 2013) [41], 27% ([PERSON] et al., 2008) to 30% ([PERSON] et al., 2019 [42]. The connection between SAS and glaucoma has been confirmed over time by several studies, which investigated several glaucoma-specific ocular parameters, including: increased IOP, thinning of SFNR (retinal nerve fiber layer) peripapillary, field impairment visually, and glaucomatous changes of the optic nerve [43]. [PERSON] et al. state that patients who do not have glaucoma but have SAS may develop glaucoma if SAS is not well controlled. Thus, strict control of this condition can contribute to a better management of glaucoma and stabilization of visual fields [44]. In 2019, [PERSON] et al. conducted a study for the evaluation of SFNR and lymph node complex in patients with SAS, which confirmed that 40% of retinal lymph node axons are already lost before visual field defects [45], [PERSON] et al. tried to see the influence of apnea on the IOP; therefore, they examined the immediate dynamic response of the parameter in relation to the altered respiratory events in patients' sleep. \"The mean IOP was lower in patients free of apnea\". They concluded that \"the variation in IOP in patients with SAS is influenced to some extent by the circadian rhythm, while apnea and hypopnea occur accidentally during sleep, regardless of the evolution of IOP\". Only obstructive sleep apnea influences the value of intraocular pressure, in terms of keeping breathing [46]. [PERSON] et al. published an article investigating the association between SAS and glaucoma in young adults. They evaluated a sample of 858 patients aged 19-21, all healthy, who were re-evaluated at ages 21-24, 20% of whom were diagnosed with SAS. Following this study, they concluded that patients diagnosed with SAS had an increase in SFNR of approximately 4 \(\upmu\)m (especially in the infratemporal and supratemporal segments), compared to the control group [43]. The change in the thickness of SNFR (retinal nerve fiber layer) was also highlighted by [PERSON] et al. (2014) and [PERSON] et al. (2011) [47] in patients who had a severe type of SAS compared to the control group. In their studies, the authors consisted at a thinning in the early SNFR superolateral time, these two sectors being most severely affected in SAS. Thinning of SFNR is a change found in early glaucoma, which may indicate an increased risk of SAS- associated glaucoma from a young age [43]. In our recent prospective study of 65 eyes in 65 patients, the association of glaucoma with the severity of sleep apnea syndrome was demonstrated. Within the studied group, patients with mild or moderate primary open-angle glaucoma, with moderate or severe dry-eye syndrome, patients with floppy-eyelid syndrome, with optical non-arteritis ischemic neuropathy, and a patient with retinal central vein occlusion were identified. The increased rate of the apnea syndrome during sleep produces a severe disorder of the ocular surface and a retinal neuro- degenerative disorder [8]. Regarding the role of SAS treatment by CPAP in the variation of intraocular pressure (IOP), there are several contradictory studies: Some claim that this treatment causes increased IOP [5], while others claim that it would help prevent glaucoma and optic nerve neuropathy [37].