Sleep Smarter: Optimal Sleep May Preserve Cognition and Reduce Dementia Risk in Focal Epilepsy

Commentary

Epilepsy is a common neurological disorder with its highest incidence in older adults. ¹ A growing body of epidemiologic, molecular, and experimental evidence supports a bidirectional relationship between epilepsy and dementia: individuals with epilepsy have a two- to threefold increased risk of developing dementia, while those with dementia have up to a tenfold higher incidence of seizures compared with age-matched controls.^1–3 These comorbidities are particularly relevant in an aging population, yet effective strategies to prevent cognitive decline in epilepsy remain limited.

Sleep may represent a critical link between epilepsy and dementia. Sleep disruption is common in epilepsy, where slow-wave sleep can facilitate epileptiform activity and sleep deprivation lowers seizure threshold. Dementia is likewise associated with fragmented sleep and circadian dysregulation, while tau and β-amyloid—proteins implicated in both conditions—are cleared via glymphatic pathways that are most active during sleep.^4–6 Collectively, these observations suggest that sleep may represent a key physiological state during which pathological hyperexcitability and neurodegeneration converge, contributing to cognitive decline.

Whether poor sleep and epilepsy interact synergistically to accelerate cognitive decline or instead independently increase dementia risk remains uncertain. Existing evidence linking sleep and cognition in epilepsy is limited; small studies suggest associations between disrupted sleep architecture and poorer memory performance, but are constrained by small sample sizes, suboptimal controls, and heterogeneous comparators.^4,6,7 Longitudinal data examining sleep and incident dementia in epilepsy are particularly scarce. To address this gap, Tai and colleagues analyzed data from the prospective UK Biobank, which included 482,207 participants without dementia at baseline. ⁸ Of these, 3788 had epilepsy, 6372 had a history of stroke, and 472,047 served as controls. Participants were followed for a median of 12 years. Habitual sleep duration was self-reported and categorized as optimal (6-8 h per night) or nonoptimal (<6 or >8 h), and executive function was assessed using standardized cognitive testing.

Four key findings emerged. ⁸ First, optimal sleep duration was associated with better executive function across all groups; however, the magnitude of benefit was significantly greater in individuals with focal epilepsy than in healthy controls, a pattern not observed in the stroke cohort. Second, nonoptimal sleep was associated with poorer executive function up to eight years prior to the diagnosis of focal epilepsy. Third, individuals with focal epilepsy and nonoptimal sleep had an approximately fivefold higher risk of developing dementia compared with controls with optimal sleep, exceeding that observed in individuals with stroke and poor sleep. Finally, optimal sleep substantially attenuated dementia risk in focal epilepsy, whereas no comparable protective effect was observed in the stroke cohort.

These findings have several clinical implications. Across all groups, optimal sleep was associated with better cognitive performance; however, the effect size was greatest in epilepsy, suggesting that adequate sleep may partially mitigate the cognitive burden of the disease. ⁸ This underscores sleep as a potentially important determinant of cognitive health in focal epilepsy. Clinically, these results support routine sleep assessment in epilepsy care and highlight sleep optimization as an accessible strategy for preserving cognitive function.

Second, greater epilepsy severity was associated with worse executive function, but this relationship was attenuated among individuals reporting optimal sleep. This raises the possibility that sleep may modify the cognitive impact of disease severity and represents a potentially actionable therapeutic target.^4–7 Accordingly, identification and treatment of sleep disorders—including insomnia, sleep fragmentation, and obstructive sleep apnea—should be considered integral to comprehensive epilepsy care. That said, sleep quality is likely more relevant than duration alone and remains difficult to measure at scale. Emerging approaches, including wearable accelerometry and long-term EEG monitoring, may provide more precise phenotyping of sleep in future studies. ⁹

Third, optimal sleep appeared to reduce dementia risk in focal epilepsy, with a stronger protective association than that observed in controls and no comparable effect in stroke. Several mechanisms may underlie this observation. Subclinical interictal epileptiform discharges may disrupt sleep physiology and impair cognition, while epileptic activity may suppress slow-wave sleep, the state in which glymphatic clearance of tau and β-amyloid is maximal.^3–6,10 Impaired clearance of these neurodegenerative proteins may accelerate cognitive decline and contribute to the increased dementia risk observed in focal epilepsy.^5–7,10 These findings further support sleep as a modifiable risk factor and provide rationale for sleep-focused interventions as part of long-term epilepsy management.

Finally, individuals with focal epilepsy and nonoptimal sleep demonstrated poorer executive function up to eight years before epilepsy diagnosis, with the cognitive gap widening over time. ⁸ This suggests that sleep disturbances may precede clinical diagnosis and may represent an early marker of evolving network dysfunction or neurodegeneration. Cognitive complaints in epilepsy should therefore prompt careful evaluation of sleep quality as a potentially reversible contributor. However, whether sleep disruption contributes causally to disease progression or instead reflects early pathology remains uncertain. ¹⁰

Despite its strengths, including large sample size and long follow-up, several limitations should be considered. Clinical data were derived from hospital records, death certificates, and self-report, introducing potential misclassification. Epilepsy was identified using diagnostic coding, limiting granularity regarding seizure localization, frequency, underlying pathology, and other disease-specific factors relevant to cognition. Sleep duration was self-reported rather than objectively measured, limiting assessment of sleep architecture, fragmentation, quality, and comorbid sleep disorders. As an observational study, causality cannot be inferred, and residual confounding from seizure burden, antiseizure medications, psychiatric comorbidities, and other unmeasured variables is possible. Sleep was assessed only at baseline, which may not reflect longitudinal changes over the follow-up period. Future studies incorporating objective sleep measures, detailed epilepsy phenotyping, and interventional designs are needed to determine whether sleep optimization can meaningfully preserve cognition and reduce dementia risk in focal epilepsy.

In conclusion, the highlighted study ⁸ supports a more proactive, sleep-centered approach to cognitive preservation in focal epilepsy. In the absence of disease-modifying therapies for epilepsy-related cognitive decline, routine assessment and management of sleep disorders represent practical, low-cost strategies that may support long-term brain health. Integrating sleep-focused care into routine epilepsy management may therefore be an important component of neuroprotective practice. Although these findings associate adequate sleep with better cognition and lower dementia risk, the observational design precludes causal inference. Future randomized and mechanistic studies using objective sleep measures are needed to determine whether sleep improvement can modify cognitive outcomes in focal epilepsy. In the interim, clinicians may reasonably encourage patients to “sleep smarter”—prioritizing sufficient, high-quality sleep as a simple and actionable strategy to support long-term cognitive health in focal epilepsy.