Post-stroke insomnia: multidimensional mechanisms, clinical heterogeneity, and toward mechanism-informed, objectively quantified management.

Stroke survivors frequently experience sleep disturbance, among which post-stroke insomnia (PSI) is common yet often underrecognized across the post-stroke course. Although its clinical expression may vary over time, PSI is associated with reduced rehabilitation engagement, impaired quality of life, and potentially adverse long-term outcomes. Accumulating evidence suggests that PSI is not a unitary entity; rather, it reflects interacting neurobiological and psychosocial processes, including injury to sleep-wake regulatory networks, neurotransmitter and circadian disruption, neuroinflammation, hypothalamic-pituitary-adrenal (HPA) axis and autonomic hyperarousal, hemodynamic and neurovascular dysfunction, and comorbid conditions such as pain, nocturia, and sleep-disordered breathing. Despite growing interest, PSI management in clinical practice largely follows general insomnia strategies, and interpretation of treatment effects is constrained by heterogeneous intervention protocols, limited objective sleep assessment, and short follow-up.

Methods

This narrative review was informed by searches of PubMed, Web of Science, Google Scholar, and Chinese databases (CNKI and Wanfang) from inception to February 2026, complemented by reference screening. This review synthesizes key mechanistic domains and sources of heterogeneity in post-stroke insomnia (PSI) and discusses a pragmatic, mechanism-informed approach emphasizing objective sleep phenotyping and coordinated management of dominant drivers. We highlight controversies, current research gaps, and near-term opportunities to advance PSI care through standardized definitions, combined subjective-objective outcomes, and stratified interventions aligned with patient-level mechanisms.