Sleep Disturbance on Stroke Patients: A Narrative Review

Abstract

Purpose of Review: Sleep disturbance is one of the most prevalent yet systematically neglected consequences of stroke. It affects between one-third and more than half of all stroke survivors, yet it receives a fraction of the clinical attention devoted to motor or cognitive impairment. This review was undertaken to examine the prevalence and clinical spectrum of post-stroke sleep disturbance, to understand the neurobiological mechanisms through which stroke disrupts sleep architecture, and to evaluate the clinical consequences of poor sleep quality for functional recovery, neuroplasticity, depression, cognitive function, and quality of life in stroke survivors.

Methods: A comprehensive narrative literature search was conducted across PubMed, Google Scholar, ScienceDirect, CINAHL, Embase, PsycINFO, and the Cochrane Library. The final search was performed on March 2026. Search terms included combinations of "stroke," "sleep quality," "insomnia," "sleep disturbance," "sleep architecture," "post-stroke sleep," "neuroplasticity," "motor recovery," "functional outcomes," "Pittsburgh Sleep Quality Index," "polysomnography," "actigraphy," "quality of life," "depression," "cognitive decline," and "circadian rhythm." Studies published between January 2015 and March 2026 were included. Eligible studies included randomized controlled trials, observational studies, systematic reviews, and meta-analyses examining sleep quality and its consequences in adult stroke populations. Non-English publications, case reports, editorials, and conference abstracts were excluded.

Results: Post-stroke sleep disturbance is highly prevalent, affecting 32–56% of stroke survivors across study designs and diagnostic criteria, with evidence that it persists into the chronic phase of recovery in the majority of affected patients. Neurobiological mechanisms include direct structural damage to hypothalamic, thalamic, and brainstem sleep-regulatory circuits; neuroinflammatory disruption of sleep homeostasis; and secondary behavioural perpetuating factors including irregular schedules, excessive time in bed, and post-stroke depression. Poor sleep quality independently predicts worse motor outcomes, slower functional recovery, greater depression severity, accelerated cognitive decline, reduced quality of life, and elevated stroke recurrence risk. Fewer than 6% of stroke survivors receive formal sleep evaluation in the first three post-stroke months despite this burden.

Conclusion: Sleep quality is a core determinant of stroke recovery outcomes, not a peripheral quality-of-life concern. The mechanistic evidence establishing sleep as an active component of rehabilitation-relevant neuroplasticity, combined with clinical evidence that poor sleep independently predicts functional and psychological outcomes, justifies its integration into standard post-stroke rehabilitation assessment and management. Routine sleep screening using validated instruments should be implemented immediately. Prospective longitudinal research examining the causal pathways between specific sleep architecture deficits and rehabilitation outcomes in diverse populations is urgently needed.