0720 Sleep Microarchitecture Determinants of Sleepiness in Central Disorders of Hypersomnolence

Abstract Introduction Canonical measures of sleep macroarchitecture correlate only loosely with measures of daytime sleepiness in central disorders of hypersomnolence. It is important to evaluate whether sleep microarchitecture measures such as slow wave activity around K complexes (Delta-SWAK), odds ratio product (ORP), and wake/N1 index potentially distinguish NT1, NT2, and IH and whether these values are predictive of subjective and objective measures of sleepiness. Methods We reviewed NPSG’s performed at Mount Sinai between 2018 and 2025 from 16 patients with central hypersomnia (5 NT1, 6 NT2 and 5 IH) and 14 demographically-matched control patients with no sleep disorders per history or PSG. We used validated automated signal progressing algorithms to measure Delta-SWAK and ORP. The Wake/N1 Index (the number of transitions from any sleep stage to wake or NREM stage 1 normalized by total sleep time) was derived from the hypnogram. Delta-SWAK was available in a subset of 3 NT1, 4 NT2, and 2 IH patients. Results Mean N1 index was: 3.2 ± 1.4 in NT1, 2.8 ± 1.5 in NT2, 3.1 ± 2.3 in IH, and 3.7 ± 1.8 in controls. Mean wake index was 3.0 ± 1.1 in NT1, 1.8 ± 0.8 in NT2, 3.1 ± 1.7 in IH, and 2.1 ± 1.0 in controls. The N1/W index was 6.2 ± 1.8 in NT1, 4.6 ± 2.1 in NT2, 6.3 ± 2.5 in IH, and 5.8 ± 2.0 in controls. Mean Delta-SWAK was 6.2 ± 8.1 in NT1, 4.2 ± 2.0 in NT2, and 3.5 ± 1.1 in IH. No statistically significant differences between groups were observed for each sleep architecture variable (one-way ANOVA). Among the 9 subjects with hypersomnia of any cause with Delta-SWAK data, the Pearson correlation coefficient was 0.42 for Delta-SWAK and Epworth sleepiness score and was -0.05 for Delta-SWAK and mean sleep latency. Conclusion Prior work has suggested that daytime sleepiness was associated with a high N1/Wake index in pediatric narcolepsy and a low Delta-SWAK in OSA. Within the currently limited dataset, we are not observing significant differences in these sleep architecture variables between hypersomnia groups nor significant associations between these variables and subjective or objective measures of sleepiness. Support (if any)