Abstract

Defective arousal mechanisms are viewed as contributory to sleep hypopnea disorders and Sudden Infant Death Syndrome. Arousal has traditionally been viewed as an “all or none” event defined behaviorally as“full arousal” (eyes open, cry) or electrophysiologically as >3 sec of altered EEG-activity. In contrast, our own recent studies suggest that arousal is a stepwise process beginning with a sleep startle which then may or may not progress to “full arousal”. However startles have not traditionally been viewed as arousal related phenomena in infants since the associated EEG changes last < 3sec and are mostly due to movement artifacts. We hypothesized that, if startles are the initial event in a sequential arousal process, then they might be associated with less obvious electrophysiological events intermediate between those of sleep and“full arousal”. We monitored EEG sleep spindles since activation of the primary arousal mechanisms in the brainstem reticular activating system eliminates spindle activity generated in the thalamus. We studied spontaneous sleep startles (n=23) as well as those elicited by briefly occluding the infants face mask airway (n=128) in 12 normal infants (age 10-19 weeks) during sleep. We recorded EEG (C3-P3), ECG, O2-Saturation, limb and nuchal EMG and video of the infant. The intensity of startles was scored on a scale of 0 to 3 based on the limb EMG magnitude and video recorded movements. We focused on the β-spindle frequency range (13-18 Hz). Spindle periodicity was analysed by using a threshold over a compressed spectral band array. Spontaneous sleep startles were immediately followed by a prolongation of the inter spindle interval from a mean of 7.9 sec (+/- 0.16 SE) during the control period to 20.4 sec (+/- 0.94 SE) after startle (p<0.005); following occlusion related startles inter spindle period increased to 24.8 sec (+/- 0.92 SE) (p<0.001). Furthermore the intensity of evoked startles was positively correlated with the inter spindle interval period (p<0.01). Conclusion: Spontaneous as well as evoked startles are immediately followed by elimination of sleep spindles. This phenomenon strongly suggests a linkage between sleep startles and increased activity in subcortical arousal mechanisms. These findings support the concept that infant arousal is not an“all or none” event but a process that begins as a series of subcortical events and reflex behaviors that potentially progress to a“full” or unambiguous EEG arousal.HD 10993

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