Introduction Obstructive Sleep Apnea Is Believed to Cause Sleepi- Ness in 3% of Adults,1 but the Mechanism by Which Sleepiness and Other Cognitive Changes Are Pro- Duced Is Not Completely

OBSTRUCTIVE SLEEP APNEA IS BELIEVED TO CAUSE SLEEPINESS IN 3% OF ADULTS,1 BUT THE MECHANISM BY WHICH SLEEPINESS AND OTHER COGNITIVE CHANGES ARE PRODUCED IS NOT COMPLETELY UNDERSTOOD.2 Although hypoxemia may play some role,3 much attention has focused on the role of arousals, which typically occur at the termination of each apnea, hypopnea, or transient period of increased respiratory effort.4,5 Arousals induced experimentally and designed to approximate those seen in sleep-disordered breathing (SDB) can cause excessive daytime sleepiness.6,7 However, clinical studies repeatedly fail to find close associations between rates of apneic events or scored arousals and measures of excessive daytime sleepiness.8-10 Part of the reason may be that many patients, and especially children, do not always show visually recognizable electroencephalography (EEG) arousals after apneic events.11 A desire to improve the ability of polysomnograms to predict SDB outcomes has given rise to new equipment and strategies to monitor breathing or breathing effort, such as esophageal pressure monitoring,12 nasal pressure monitoring,13 and the forced oscillation technique.14 Other approaches have focused on nonvisible EEG changes detected by signal analysis,15-19 on body movements,20 or on subtle autonomic changes.21,22 However, none of these methods, all of which are linked to the concept that discrete apneic events in some way cause sleepiness, have substantially improved the prediction of important SDB outcomes. Meanwhile, some data suggest that information as crude as a history of snoring still predicts sleepiness even after rates of recorded apneic events are taken into account.23 Among children, a history of snoring more readily distinguishes hyperactive and nonhyperactive children than does full laboratory-based polysomnography.24 These observations suggest that important aspects of SDB physiology, including some critical links between SDB and sleepiness, remain to be discovered. In this context, we developed a novel hypothesis: that partial obstruction of the many respiratory cycles that occur between scored apneas and hypopneas could cause numerous microarousals, invisible to the human eye, but able to produce significant impact on cortical activity and neurobehavioral outcomes. To test this hypothesis, we developed a computerized signal analysis algorithm that demonstrated respiratory cycle-related EEG changes (RCREC) for the first time.25 We now explore the physiologic significance and clinical utility of RCREC using data recorded from 10 subjects enrolled in an ongoing study of polysomnographic methods and outcomes in childhood SDB.