Central Sleep Apnea After Stroke: Prevalence, Mechanisms, and Clinical Implications

Central sleep apnea (CSA) and Cheyne-Stokes respiration (CSR) are common but underrecognized forms of sleep-disordered breathing after stroke. Although OSA dominates poststroke research, CSA and CSR are neglected because they rarely appear in isolation.

The reported prevalence of CSA and CSR after stroke shows substantial variability across individual studies (1%-72%), whereas meta-analyses suggest pooled estimates of approximately 7% to 12%. Longitudinal data suggest that CSA and CSR improve in some patients, reflecting a component of an acute injury, yet persist in others, indicating sustained ventilatory instability. CSA may act both as a mediator of physiologic stress and as a marker of cerebral, sleep, and cardiovascular vulnerability. Its pathophysiologic characteristics are multifactorial, combining neurogenic (eg, disruption of central autonomic and respiratory networks, altered CO₂ sensitivity, and lesion topography) and nonneurogenic (eg, cardiac dysfunction, medication, and sleep fragmentation) mechanisms. Evidence of CSA as a risk factor for stroke recurrence or long-term outcomes is limited and inconclusive. Although few reports suggested watchful waiting or symptom-based positive airway pressure trials, recommendations on management including diagnostics, optimal timing, and treatment strategies remain unclear.

CSA after stroke is prevalent, pathophysiologically complex, and therapeutically underexplored. A need exists for standardized definitions, longitudinal phenotyping, sex-specific analyses, and physiologic metrics beyond the apnea-hypopnea index to inform better individualized, mechanism-based care for CSA in stroke survivors.