Researchers have demonstrated considerable interest in investigating associations with both normal-tension glaucoma (NTG) and advancing primary open angle glaucoma (POAG) in patients with comorbidities, particularly sleep apnea. This study published in December in the Journal of Glaucoma found a high prevalence of NTG but not POAG among patients with obstructive sleep apnea/hypopnea syndrome (OSAHS). This link with NTG is particularly strong among those with moderate to severe OSAHS.
These results indicate that glaucoma patients should be screened or questioned about obstructive sleep apnea as part of their glaucoma evaluation. Likewise, the study’s authors conclude that the presence of glaucoma should be considered in patients with moderate and severe OSAHS.
The study included 247 patients with symptoms of sleep-related breathing disorders, such as loud snoring, observed apnea or excessive daytime sleepiness consecutively admitted to a medical center in Taiwan for overnight polysomnography. Patients with a history of stroke with central apnea, chronic uveitis, glaucoma, optic neuropathy, earlier ocular trauma or ocular surgery were excluded.
The authors found that 209 patients had OSAHS and 38 were classified as normal. Among the OSAHS group, NTG was diagnosed in 12 patients (5.7 percent), which was significantly greater than in the normal group (P=0.003), which had no patients with any type of glaucoma. Among those with NTG, one was classified as having mild OSAHS, three as moderate and eight as severe. The prevalence of NTG among moderate/severe OSAHS patients was 7.1 percent, which was significantly higher (P=0.033) than among normal/mild OSAHS patients.
The authors also found that mean saturation of oxygen and lowest saturation of oxygen correlated with average RNFL thickness among OSAHS patients, and the severity of OSAHS was inversely correlated with RNFL thickness.
No cases of POAG or chronic angle-closure glaucoma were identified among the patients in the study. The authors think that NTG is an optic neuropathy compromised by hypoxia and vascular dysregulation in patients with OSAHS, even with IOP below 21 mmHg, and the pathophysiology of NTG may be fundamentally different from that of POAG.