https://doi.org/10.1140/epjs/s11734-026-02321-y
Regular Article
Slow-wave sleep fragmentation and spike-wave discharges: a bidirectional relationship in absence epilepsy
1
Institute of Higher Nervous Activity and Neurophysiology of Russian Academy of Sciences, Butlerova Str., 5A, 117485, Moscow, Russian Federation
2
Siberian Center for the Study of Artificial Intelligence and Digital Technologies, Novosobornaya 1, Lenin Avenue, 67, 634029, Tomsk, Russian Federation
a
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Received:
29
December
2025
Accepted:
15
April
2026
Published online:
24
April
2026
Abstract
Absence epilepsy is characterized by spike-wave discharges (SWDs) observed on electroencephalogram and is often linked to fragmented slow-wave sleep (SWS). However, the causal relationship between SWS and SWDs remains unclear. To investigate this, we employed a machine learning approach in WAG/Rij rats, developing a high-throughput gradient boosting algorithm for automated detection of SWDs and SWS (F-score > 0.88). Using 6-h EEG recordings from 22 rats, we applied Kaplan–Meier survival analysis and Cox regression to model SWS duration as a function of the latency to the next SWD (the SWS–SWD interval). We defined three temporal categories: zero (< 2 s), short (2–25 s), and long (> 25 s). The results revealed a complex, bidirectional relationship. SWDs occurring with zero or short latency significantly increased the hazard of SWS termination (hazard ratio up to 1.84), actively fragmenting sleep. This effect was modulated by SWS duration: shorter episodes were most susceptible to immediate (zero-interval) SWDs, while longer episodes were disrupted by both zero and short intervals. In contrast, long-interval SWDs had no significant effect on prior SWS structure (hazard ratio ≈ 1.02). We propose a cyclical model in which inherent SWS instability generates epileptogenic slow-wave activity that triggers imminent SWDs (zero interval), which in turn exacerbate sleep fragmentation. These findings identify specific SWS–SWD temporal microstates as critical digital biomarkers, highlighting their potential for advancing targeted neurotherapeutic strategies.
Supplementary Information The online version contains supplementary material available at https://doi.org/10.1140/epjs/s11734-026-02321-y.
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© The Author(s), under exclusive licence to EDP Sciences, Springer-Verlag GmbH Germany, part of Springer Nature 2026
Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
