Sleep characteristics have been reported as predictors of neurodevelopmental outcome (14,15,16) and there is general agreement that indices of stability in SWC over time are positively correlated with improved clinical outcomes. SWC is described as smooth sinusoidal variations, mostly in the minimum amplitude. Phases with broader bandwidth represent discontinuous background activity during quiet sleep, whilst the phases with narrower bandwidth correspond to the more continuous activity during wakefulness and active sleep. SWC develops with increasing maturation of the child. From 31 to 32 weeks' gestational age, quiet sleep periods are clearly discernable in the aEEG trace as distinct periods with increased bandwidth. At term-equivalent age these periods represent trace alternant electroencephalography (EEG) patterns (17). The average duration of quiet sleep periods is 24 to 28 minutes for infants between 32 and 36 weeks' gestational age. These periods are slightly longer at night but are otherwise relatively stable and are not affected by incubator covers or developmental care interventions (18). The internal trigger for SWC is located in the brainstem and the presence of SWC in healthy term newborns is considered a sign of brain stem integrity (19,20). In newborns with hypoxic-ischemic encephalopathy sleep organization can be altered and the presence of SWC on aEEG is considered to be a good prognostic sign (21). Timing of onset of SWC has been shown to predict neurodevelopmental outcome based on whether the SWC returns before or after 36 hours of a presumed hypoxic insult (22).