Poster sessions

Introduction: An electrophysiological explanation for mechanisms \nunderlying Insomnia Disorder (ID) should be sought in sleep protection \nmechanisms that ensure sleep stability and continuity. The \nK-Complex (KC), a typical waveform of Non-Rapid Eye Movement \n(NREM) sleep stage 2 (N2), is a cortical event that plays a key role in \nsleep protection and as a forerunner of slow waves. This exploratory \nstudy aims to evaluate the transition probabilities between N2 epochs \ncharacterized by low (lKC) and high (hKC) KC frequency into deepening \nor lightning sleep stages, and to test differences between ID \npatients and Healthy Controls (HCs). \nMethod: Twenty IDs (mean age: 43.5 ± 12.7; 7M/13F) and eighteen \nmatched HCs (mean age: 41.6 ± 11.9; 8M/10F) were recruited and \nunderwent a nocturnal polysomnography recording. The Markovian \nChains methodology was applied during the First NREM sleep Cycle \n(FC) and the Total Sleep Time (TST). The transition probabilities were \ncalculated between sleep stages according to N2 epochs with lKC and \nhKC frequency based on the median of both groups. \nResults: Wilcoxon signed-rank tests in the whole sample showed that \nduring the FC, the probability of transitioning from hKC N2 epochs to \nNREM sleep Stage 3 (N3) was higher than the probabilities of transit \nfrom hKC to NREM sleep stage 1 (N1) (hKCàN3 vs. hKCàN1: 0.117 \n± 0.104 vs. 0.019 ± 0.026; W = 361, p < 0.001) or to wake (hKCàN3 \nvs. hKCàwake: 0.117 ± 0.104 vs. 0.012 ± 0.021; W = 344, p < 0.001). \nMoreover, the same finding resulted considering the TST (hKCàN3 \nvs. hKCàN1: 0.059 ± 0.042 vs. 0.028 ± 0.018; W = 362.5, p < 0.001; \nhKCàN3 vs. hKCàwake: 0.059 ± 0.042 vs. 0.025 ± 0.017; W = 439, \np < 0.001). We repeated the tests separating HCs and IDs, showing the \nsame pattern of results. However, when comparing the probability of \ntransit from hKC to N3 between the two groups, this was higher in HCs \nthan IDs during the FC (ID vs. HC: 0.155 ± 0.104 vs. 0.081 ± 0.094; \nU = 242.5, p = 0.029), not attributable to group differences in the hKC \npercentage (U = 184, p = 0.704). \nConclusion: These findings confirm the role of KC as forerunner of \ndeep sleep, both in FC and in TST, regardless of the presence of \nID. However, the transition probabilities from hKC epochs to N3 during \nFC were significantly reduced in ID patients compared to HCs, \nsuggesting a possible breakdown of neurophysiological mechanisms \nrelated to KC in this condition.