- Shared neurobiology: thalamocortical synchronisation, circadian genes, adenosine and orexin systems underpin NREM promotion of epileptiform activity and REM protection.
- Bidirectional clinical impact: epileptic activity fragments sleep architecture and microstructure, while sleep loss and obstructive sleep apnoea lower seizure threshold and worsen epilepsy.
- Therapeutic priority: multidisciplinary management with sleep disorder screening, antiseizure medication optimisation, obstructive sleep apnoea treatment, behavioural sleep interventions to improve seizures and quality of life.
Front Neurol. 2026 Sep 17;17:1882139. doi: 10.3389/fneur.2026.1882139. eCollection 2026.
ABSTRACT
BACKGROUND: Epilepsy and sleep disorders are highly prevalent conditions that frequently coexist, exerting reciprocal adverse effects through shared neurobiological mechanisms.
OBJECTIVE: We conducted a narrative review of the literature addressing the bidirectional relationship between epilepsy and sleep disorders, aiming to provide a comprehensive synthesis of its neurophysiological basis, clinical implications, and therapeutic consequences.
RESULTS: The epilepsy-sleep relationship is mediated by multiple neurobiological mechanisms, including thalamocortical network dynamics, circadian clock gene regulation, adenosinergic and orexinergic tone, synaptic homeostasis, and glymphatic clearance. A key pathophysiological concept underlying this relationship is that NREM sleep promotes interictal epileptiform discharges and seizure propagation through thalamocortical synchronization, whereas REM sleep exerts a protective effect. Epileptic activity disrupts both sleep macro- and microarchitecture, reducing total sleep time, sleep efficiency, and REM sleep, increasing wake after sleep onset, and destabilizing NREM microarchitecture as reflected by altered cyclic alternating pattern rates. Conversely, sleep disturbances lower the seizure threshold and contribute to disease progression: sleep deprivation is an independent seizure-precipitating factor, and comorbid obstructive sleep apnea further lowers the seizure threshold through intermittent hypoxia and arousal instability. Specific epileptic syndromes with a privileged sleep relationship are also reviewed, including sleep-related hypermotor epilepsy, epileptic encephalopathy with spike-wave activation in sleep, and self-limited childhood focal epilepsies. The differential diagnosis between NREM parasomnias and sleep-related epilepsies remains challenging; the diagnostic workup should always include a thorough clinical history characterizing the episodes, followed by video-polysomnography, which represents the gold standard. From a therapeutic standpoint, antiseizure medications exert heterogeneous effects on sleep architecture, and polytherapy is independently associated with worse sleep quality; targeting sleep disturbances therefore represents a modifiable strategy capable of improving seizure control, cognitive function, and quality of life.
CONCLUSION: A multidisciplinary approach integrating systematic screening for sleep disorders, optimization of antiseizure medication timing and selection, treatment of comorbid obstructive sleep apnea, and behavioral sleep interventions has the potential to meaningfully improve outcomes in patients with epilepsy. Wider implementation of these strategies in routine clinical practice is both a priority and an opportunity.
PMID:42824487 | PMC:PMC13628168 | DOI:10.3389/fneur.2026.1882139
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