Sleep architectural dysfunction and undiagnosed obstructive sleep apnea after chronic ischemic stroke

• Published in: Sleep medicine Vol. 83; pp. 45 - 53
• Main Authors: Gottlieb, Elie, Khlif, Mohamed S., Bird, Laura, Werden, Emilio, Churchward, Thomas, Pase, Matthew P., Egorova, Natalia, Howard, Mark E., Brodtmann, Amy
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.07.2021
• Subjects: Brain ischemia; Polysomnography; Sleep apnea; Sleep architecture; Stroke; Brain ischemia; Stroke; Sleep apnea; Sleep architecture; Polysomnography
• ISSN: 1389-9457; 1878-5506
• DOI: 10.1016/j.sleep.2021.04.011

Sleep-wake dysfunction is bidirectionally associated with the incidence and evolution of acute stroke. It remains unclear whether sleep disturbances are transient post-stroke or are potentially enduring sequelae in chronic stroke. Here, we characterize sleep architectural dysfunction, sleep-respiratory parameters, and hemispheric sleep in ischemic stroke patients in the chronic recovery phase compared to healthy controls. Radiologically confirmed ischemic stroke patients (n = 28) and matched control participants (n = 16) were tested with ambulatory polysomnography, bi-hemispheric sleep EEG, and demographic, stroke-severity, mood, and sleep-circadian questionnaires. Twenty-eight stroke patients (22 men; mean age = 69.61 ± 7.4 years) were cross-sectionally evaluated 4.1 ± 0.9 years after mild-moderate ischemic stroke (baseline NIHSS: 3.0 ± 2.0). Fifty-seven percent of stroke patients (n = 16) exhibited undiagnosed moderate-to-severe obstructive sleep apnea (apnea-hypopnea index >15). Despite no difference in total sleep or wake after sleep onset, stroke patients had reduced slow-wave sleep time (66.25 min vs 99.26 min, p = 0.02), increased time in non-rapid-eye-movement (NREM) stages 1–2 (NREM-1: 48.43 vs 28.95, p = 0.03; NREM-2: 142.61 vs 115.87, p = 0.02), and a higher arousal index (21.46 vs 14.43, p = 0.03) when compared to controls. Controlling for sleep apnea severity did not attenuate the magnitude of sleep architectural differences between groups (NREM 1-3=ηp2 >0.07). We observed no differences in ipsilesionally versus contralesionally scored sleep architecture. Fifty-seven percent of chronic stroke patients had undiagnosed moderate-severe obstructive sleep apnea and reduced slow-wave sleep with potentially compensatory increases in NREM 1–2 sleep relative to controls. Formal sleep studies are warranted after stroke, even in the absence of self-reported history of sleep-wake pathology. •Patients with chronic ischemic stroke exhibit slow-wave sleep reductions and compensatory increases to NREM 1-2.•Although no patients self-reported a history of OSA, almost 60% exhibited moderate-to-severe obstructive sleep apnea.•We observed no differences in sleep architecture between the ipsi- and contra-lesional hemispheres.•Formal sleep studies are warranted after ischemic stroke to detect undiagnosed OSA and sleep architectural dysfunction.