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Valerio Fabiani, Andrea Rea, Mario Fabiani; Subclinical Neurosensorial Damage In Patients With Osas. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3515.
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Repeated episodes of partial or complete upper airway obstruction, which characterize the obstructive sleep apnea syndrome (OSAS), produce reduction of oxygen saturation in arterial blood (SaO2) and therefore hypoxia. Hypoxia might be linked to damage to the neurosensorial structures both visual and cochlear. The aim of this study was to investigate the effect of hypoxia on the cochlear external ciliated cells and the retinal nerve fiber layer in patients with severe OSAS.
We studied 20 patients with severe obstructive sleep apnea. The group of OSAS patients, consisted of 7 males and 13 females, their ages were between 40 and 70 years (mean age = 55.05). The group of OSAS patients was compared with a control group consisting of 20 healthy subjects. All patients underwent polysomnographic examination, transient evoked acoustic emissions (TEOAE), distortion product otoacoustic emissions (DPOAE) and retinal nerve fiber layer evaluation (RNFL).
16 out of 20 OSAS patients presented pathological TEOAE and DPOAE, as compared to the control group, showing a significant reduction in the amplitude of the DP-gram for frequencies between 2.0 and 4.0 kHz (P=.006). In addition we found a positive correlation between AHI, TEOAE and DPOAE with an increase in the AHI associated with an increase of cochlear damage. The mean RNFL thickness was 105.35 ± 6.7 µm in glaucomatous eyes, less than in normal (113.18 ± 7.7 µm) with no significant statistical difference between the two study groups.
Repeated episodes of hypoxia might be responsible of cochlear external ciliated cells and retinal nerve fiber layer alterations. Otoacustic emissions and RNFL might be useful clinical test in order to detect subclinical neurosensorial damage due to chronic hypoxia. Lifelong nocturnal continuous positive airway pressure is the treatment of choice to prevent episodes of apneas and hypoxia.
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