Background and purpose: In patients with obstructive sleep apnea (OSA) syndrome the episodes of upper airway obstruction lead to hypoxemia during sleep. The aim of the study was to establish the influence of sleep hypoxemia on the function of the visual tract in OSA patients.
Material and methods: The latency and amplitude of wave P100 of visual evoked potentials have been studied in 35 patients with OSA syndrome (mean apnea index 48+/-19). The diagnosis of OSA was established on the basis of continuous recordings of the respiratory function during sleep with additional full polysomnography in 17 patients.
Results: Mean absolute latency of P100 was longer in OSA patients than in healthy controls (117.0+/-8.8 ms vs. 104.3+/-4.6 ms, p<0.001). The differences in the amplitude of P100 were not significant (5.9+/-2.6 mV in OSA patients and 7.62+/-3.04 mV in healthy persons). In 60% of patients the latency of P100 exceeded 118 ms; in this group of patients the mean SaO2 during sleep apneas was lower than in patients with normal P100 latency (46+/-15% vs. 69+/-10%, p<0.05). Full polysomnographic studies revealed that in patients with prolonged latencies as compared with patients with normal P100 latencies there were lower: minimal SaO2 during NREM sleep (63+/-12% vs. 78+/-8%, p<0.05), as well as mean and minimal SaO2 during REM sleep (53+/-15% vs. 80+/-5% and 46+/-15% vs. 69+/-10%, p<0.05), without differences in apnea index or apnea duration.
Conclusions: In patients with OSA syndrome the electrophysiological abnormalities suggesting damage of the optical tract may develop probably as a consequence of profound sleep hypoxemia.