Conversely, Berg et al were unable to find a difference in the frequency of brief arousals between symptomatic snorers and asymptomatic nonsnoring control subjects. Significantly more respiratory events were found in the snoring group, mostly in the form of IUAR, although the same percentage of respiratory events resulted in arousals in both groups. The authors questioned whether differences in the arousal duration between the two groups accounted for the difference in symptoms, although this parameter was not examined. They also postulated a possible qualitative difference between respiratory and nonrespiratory arousals. These are provocative and, as yet, unanswered questions.
Regardless, the majority of the available data favors brief arousals as the cause of daytime symptoms in UARS, especially given the lack of oxyhemoglobin desaturation in this syndrome.
The next logical step in understanding the pathogenesis of symptoms in this disorder is to elucidate the mechanism(s) leading to arousal. Stoohs and Guilleminault hypothesized in 1991 that the arous-als in UARS were, at least partly, due to flow limitation and the mechanical changes reflected by increased negative Pes. In fact, Gleeson et al had previously demonstrated a close correlation between arousal (defined as increased electromyogram [EMG] activity and a shift to alpha in the EEG) and the magnitude of Pes nadir just prior to arousal in a group of normal male subjects Link birth control. There was no lower limit imposed on the duration of these arousals; therefore, brief arousals similar to those seen in UARS were included in the analysis. The researchers demonstrated that arousal occurred at approximately the same Pes nadir (about —15 cm H2O), regardless of the primary stimulus used to induce the arousal, including increased external resistive load, hypoxia, and hypercapnea. Furthermore, the level of hypoxia or hypercapnea correlated poorly between different arousals resulting from the manipulation of the other stimuli.