Abstracts

Rationale: Childhood absence epilepsy (CAE) is characterized by a self-limited period of absence seizures and bursts of bifrontally predominant generalized spike and wave discharges on EEG. Impairments in attention and executive function are common comorbidities in CAE, though the cause is unknown. Epileptic spikes disrupt sleep spindles, a cardinal sleep oscillation, in animal models of absence epilepsy and focal epilepsy in humans. Changes in spindle rate predict IQ and cognitive symptoms in control children and children with Rolandic epilepsy. We hypothesized that children with CAE would have transiently reduced sleep spindles during the active disease state. As antiseizure medication (ASM) reduces epileptic activity in CAE, we further hypothesized that ASM would improve sleep spindle rate in children with active disease.


Methods: We performed a retrospective case-control study. All patients diagnosed with CAE with EEGs capturing N2 sleep between 3/2002-3/2024 available for analysis were included (n=73 total; n=23, active untreated, 17F, 5.9±1.2 years old; n=29 active treated, 19F, 6.3±1.1 years old; n=7 resolved untreated, 5F, 6.3±0.7 years old; n=14 resolved treated, 11F, 6.7±2.6 years old). Age-matched children without a history of neurological disease or psychoactive medications and with normal EEG recordings capturing N2 sleep between 2/2002-4/2021 were included as controls (n=52, 34F, 7.0±2.2 years old). Age, sex, anti-seizure medication, and disease stage at the time the EEG was performed were collected from chart review. A validated, automated spindle detector was applied to epochs containing N2 sleep. Spindle rate was computed at Fp1, Fp2, and Fz electrodes referenced to average from the clinical 19-channel scalp EEG. Linear mixed-effects models were used to estimate differences in spindle rate between groups at each channel with sex and age as covariables.

Results: Patients with untreated active CAE had a lower frontal sleep spindle rate during N2 (3.5 spindles/min) compared to patients with untreated resolved CAE (mean 7.4 spindles/min, p< 0.0001), and compared to control children (mean 6.3 spindles/min, p=0.0001;