Beyond Conventional Sleep Parameters: Circadian Rhythm Disruption in Adolescents with Juvenile Myoclonic Epilepsy: An Actigraphy Study

Background/Objectives: Juvenile myoclonic epilepsy (JME) is characterized by seizures clustering in the early morning hours, reflecting circadian modulation of cortical excitability. To the best of our knowledge, circadian rest–activity rhythms have not previously been objectively characterized in adolescents with JME, a gap that may be relevant to understanding seizure timing in this population. This study aimed to characterize circadian rest–activity rhythms and sleep parameters in adolescents with JME compared to healthy controls (HCs) and to explore whether chronotype relates to the strength of circadian rhythm. Methods: This pilot case–control study analyzed data from 11 adolescents with JME and 10 age- and sex-matched HCs who underwent 14-day continuous wrist actigraphy. Non-parametric circadian rhythm analysis (NPCRA) and cosinor analysis were conducted, and conventional sleep–wake parameters and night-to-night variability were derived. Subjective data from the Morningness–Eveningness Questionnaire (MEQ), the Pittsburgh Sleep Quality Index, a modified Epworth Sleepiness Scale, and the Pediatric Sleep Questionnaire were included. Between-group comparisons used the Mann–Whitney U test with an effect size of r. Results: Patients showed significantly lower interdaily stability (p = 0.002, r = 0.692), higher intradaily variability (p = 0.022, r = 0.500), reduced peak daytime activity (p = 0.002, r = 0.672), and attenuated cosinor (p = 0.013, r = 0.544) and mesor (p = 0.001, r = 0.754) amplitude, all with large effect sizes. Night-to-night variability was significantly greater for sleep efficiency (p = 0.010, r = 0.561), the fragmentation index (p = 0.003, r = 0.653), and mean sleep-bout duration (p = 0.020, r = 0.509). The MEQ score correlated positively with cosinor amplitude (rho = 0.679, p = 0.022) and peak daytime activity (rho = 0.615, p = 0.044). No significant group differences were found in conventional sleep–wake parameters. Given the exploratory nature of this pilot study, no correction for multiple comparisons was applied, and these findings should be considered hypothesis-generating. Conclusions: This pilot study provides preliminary evidence of circadian rest–activity rhythm disruption in a small and clinically heterogeneous adolescent cohort, with large effect sizes in JME, despite preserved conventional sleep parameters, underscoring the potential value of NPCRA-based actigraphy monitoring in this population and the need for replication in larger cohorts.