DyssomniaNN: Multi-Scale Spiking Neural Modeling of Human Sleep Disorders and Perceived Restedness

Özetle: Clinical sleep medicine repeatedly documents profound divergences between objective sleep duration and subjective daytime impairment, notably exemplified by sleep state misperception in paradoxical insomnia and boundary…

Özet

Clinical sleep medicine repeatedly documents profound divergences between objective sleep duration and subjective daytime impairment, notably exemplified by sleep state misperception in paradoxical insomnia and boundary instability in narcolepsy type 1. Here, we present DyssomniaNN: a multi-scale biophysical computational framework coupling Borbély's two-process regulation of sleep homeostasis and circadian drive with Saper's hypothalamic reciprocal flip-flop circuit and a recurrent corticothalamic leaky integrate-and-fire spiking neural network. We formalize five clinical cohorts across an identical 72-hour photoperiod: healthy control, circadian rhythm sleep-wake disorder (delayed-phase), chronic insomnia, paradoxical insomnia, and narcolepsy type 1. The synthetic local field potential converges closely with empirical human electroencephalography spectra from the PhysioNet Sleep-EDF database across all canonical frequency bands (spectral mean absolute error of 0.33–0.35). Furthermore, we introduce the Well-Rested Index to quantify restorative efficacy. Simulations reveal that sleep duration fails to predict restorative recovery: paradoxical insomnia achieves normal total sleep time (21.15 h) yet yields low restoration (37.6%) from unsuppressed cortical beta-band intrusion, whereas hypocretin deficiency in narcolepsy produces severe nocturnal fragmentation (781 min of wake after sleep onset) and 35 sleep-onset rapid eye movement periods. DyssomniaNN provides an in silico platform for mechanistic sleep research and virtual neuropharmacology.

Orijinal Özet (İngilizce)

Clinical sleep medicine repeatedly documents profound divergences between objective sleep duration and subjective daytime impairment, notably exemplified by sleep state misperception in paradoxical insomnia and boundary instability in narcolepsy type 1. Here, we present DyssomniaNN: a multi-scale biophysical computational framework coupling Borbély's two-process regulation of sleep homeostasis and circadian drive with Saper's hypothalamic reciprocal flip-flop circuit and a recurrent corticothalamic leaky integrate-and-fire spiking neural network. We formalize five clinical cohorts across an identical 72-hour photoperiod: healthy control, circadian rhythm sleep-wake disorder (delayed-phase), chronic insomnia, paradoxical insomnia, and narcolepsy type 1. The synthetic local field potential converges closely with empirical human electroencephalography spectra from the PhysioNet Sleep-EDF database across all canonical frequency bands (spectral mean absolute error of 0.33–0.35). Furthermore, we introduce the Well-Rested Index to quantify restorative efficacy. Simulations reveal that sleep duration fails to predict restorative recovery: paradoxical insomnia achieves normal total sleep time (21.15 h) yet yields low restoration (37.6%) from unsuppressed cortical beta-band intrusion, whereas hypocretin deficiency in narcolepsy produces severe nocturnal fragmentation (781 min of wake after sleep onset) and 35 sleep-onset rapid eye movement periods. DyssomniaNN provides an in silico platform for mechanistic sleep research and virtual neuropharmacology.

Kaynak: arXiv:2610.13918 · PDF