AbstractEpilepsy, as one of the most prevalent neurological diseases in childhood, has a strong reciprocal relationship with sleep. Sleep-associated epilepsy syndromes in childhood are mostly genetic and can be divided into (a) the group of self-limited focal epilepsies of childhood including self-limited epilepsy with autonomic seizures (SeLEAS) and self-limited epilepsy with centrotemporal spikes (SeLECTS) and (b) (non-self-limited) sleep-related hypermotor epilepsy (SHE). Sleep-accentuated (developmental and) epileptic encephalopathies (DEE/EE-SWAS, Landau–Kleffner syndrome [LKS]) are either genetic (possible transition from SeLEAS or SeLECTS) or structural, and they are characterized by continuous bilateral focal or generalized epileptic activity throughout the night with a clinical manifestation of stagnation or regression, in particular of cognition (verbal agnosia in LKS). Epilepsy syndromes with increased seizure frequency after sleep deprivation or with seizures in the transition to awakening include juvenile generalized epilepsy syndromes such as epilepsy with generalized tonic-clonic seizures alone (GTCA) or juvenile myoclonic epilepsy (JME), but also SeLECTS. Sleep is a very active process: Regeneration, reorganization, and consolidation of memory facilitate development and cognitive functioning. Epilepsy can alter sleep architecture and vice versa, which can appear as a vicious circle in epilepsies that are sleep related. Macrostructural elements of sleep such as sleep efficiency, sleep onset latency, wakefulness after sleep onset, REM and non-REM sleep fraction, as well as microstructural sleep elements such as slow-wave activity, slope of slow waves, cyclic alternating pattern (CAP), and physiological sleep figures, are important biomarkers with which to understand clinical symptoms such as cognitive stagnation and regression, to monitor treatment, but also to determine prognostic factors and will be an important tool for future studies.
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