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Editors Selection IGR 11-2

Clinical Forms of Glaucoma: GOOD NIGHT - SLEEP TIGHT - to save your sight

Comment by George Lambrou on:

27378 Normal tension glaucoma in patients with obstructive sleep apnea/hypopnea syndrome, Lin P-W; Friedman M; Lin H-C et al., Journal of Glaucoma, 2010;

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Obstructive sleep apnea/hypopnea syndrome (OSAHS) is a condition ‐ predominantly prevalent in male adults with central obesity ‐ characterized by recurrent complete or partial airway obstruction during sleep, lasting for up to two minutes each. These respiratory episodes, which may number up to several hundred per night, cause severe hypoxia, hypercapnia and sympathetic activation, which in turn result in sleep disturbances and, occasionally, in hypertensive peaks and cardiac arrythmias. Sleep apnea is now recognized as an important risk factor for cardiovascular and neurovascular diseases, like hypertension (both systemic and pulmonary), myocardial infarction, congestive heart failure and stroke. Could it be that, through hypo-oxygenation of the blood and sympathetic vasoconstriction, sleep apnea may also contribute to optic nerve hypoxia and development of normal-tension glaucoma?

Could it be that, through hypo-oxygenation of the blood and sympathetic vasoconstriction, sleep apnea may also contribute to optic nerve hypoxia and development of normal-tension glaucoma?

This is the hypothesis that Lin et al. (1787) set out to explore, by evaluating for ocular signs of NTG 256 patients submitted to an allnight diagnostic sleep study. After excluding patients with prior stroke or ocylar disease, they divided the 247 remaining patients into four groups (no OSAHS; mild; moderate; severe OSAHS), then grouped them back into a No/Mild OSAHS group (1) and a Moderate/Severe OSAHS group (2).

The number of patients with NTG (defined on tonometric, ophthalmoscopic, HFA-SITA 30-2 and OCT RNFL criteria) was relatively high (n = 12 or 5%) for this age group (early forties) and showed a suggestive and statistically significant frequency distribution: 0% among the 38 normal participants, 1.8% among the 56 mild, 5.8% among the 52 moderate and 7.9% among the 101 severe OSAHS patients. The prevalence of NTG was significantly higher in group 2, where a significantly lower oxygen saturation was also found. Interestingly, Body Mass Index correlated with IOP but neither with perimetric MD nor with RNFL, whereas oxygen saturation did correlate with RNFL thickness.

These results support the initial hypothesis that sleep apnea may contribute to retinal nerve fiber damage by inducing hypoxic conditions, without a direct effect on IOP (interestingly, there was not a single case of POAG among the 247 study participants). However, as the authors acknowledge, their sample size was small and the sex- and age-distributions biased by patient recruitment (predominantly severe OSAHS patients referred to a tertiary care center). Further studies with age- and sex-matched subgroups of different OSAHS severities are required to confirm whether sleep apnea is indeed a risk factor for the development or progression of glaucoma, of the normal-tension or primary varieties.

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