A Combination of Structural and Neuromus- Cular Control Factors Contribute to the Pathogenesis of Childhood Obstructive Sleep

403 A COMBINATION OF STRUCTURAL AND NEUROMUSCULAR CONTROL FACTORS CONTRIBUTE TO THE PATHOGENESIS OF CHILDHOOD OBSTRUCTIVE SLEEP APNEA syndrome (OSAS).1-6 However, the cause of the neuromuscular abnormalities is not well understood. Previous work has shown that, compared to normal controls, children with OSAS have selectively elevated arousal thresholds to respiratory stimuli, such as mechanical and hypercapnic stimuli.7,8 Children with OSAS also have impaired upper airway reflex responses to subatmospheric pressure during sleep.1 On the other hand, children with OSAS have normal arousal thresholds to nonrespiratory (e.g., auditory) stimuli.9 The underlying causes of the altered arousal and upper airway responses to respiratory stimuli in OSAS remain unknown. It is also not known whether these altered responses reflect a cause or effect of the OSAS phenomenology. It is possible that, compared to normal controls, children with OSAS have altered afferent processing of mechanoreceptor responses in the upper airway to the negative pressure generated by breathing against occlusions. Such alterations in processing may be secondary to anatomic differences in the physical properties of upper airway tissue affecting their ability to transduce pressure changes into afferent neural signals. Alternatively, they may reflect alterations in the central processing of the afferent information. Respiratory related evoked potentials (RREPs) are one way to measure the central nervous system processing of respiratory afferent information.10-12 RREPs are the averaged surface EEG responses to multiple brief occlusions or loads applied during inspiration.10,11 During wakefulness, a series of early components is evident in the RREPs, reflecting initial sensory and motor processing13,14 and a subsequent series of late components reflecting cognitive processing of the stimuli.15,16 During Non-REM (NREM) sleep, a different series of later components is produced that reflect the elicitation of phasic EEG responses (such as vertex sharp waves and K-complexes) to stimuli.17-19 Stimuli relating to increases in inspiratory effort reliably induce RREPs,20 which in turn provide a unique way to investigate the afferent processing pathway for respiratory load mechanoreception during both wakefulness and sleep.17,21 We have recently demonstrated that inspiratory occlusions reliably produce RREPs in children in stage 2, SWS, and REM sleep.22 While similar to the sleep RREPs previously reported in adults, the predominant late component in children was the N350 waveform rather than the N550, and the scalp topography of the components was more broadly distributed than typically seen in adults. Compared to normal adults, adults with OSAS have fewer K-complexes evoked by inspiratory occlusion stimuli during Obstructive sleep ApneA in children