4.6 Article

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

Journal

SLEEP MEDICINE
Volume 83, Issue -, Pages 45-53

Publisher

ELSEVIER
DOI: 10.1016/j.sleep.2021.04.011

Keywords

Sleep architecture; Sleep apnea; Stroke; Brain ischemia; Polysomnography

Funding

  1. National Heart Foundation [102052]
  2. National Health and Medical Research Council [GTN1158384, GTN1094974, GTN1020526]
  3. National Institute on Aging [1R01AG062531-01A1]
  4. Alzheimer's Association [2018-AARG-591358]
  5. Australian Research Council [DE180100893]
  6. Heart Foundation Future Leader Fellowship [100784]

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In chronic stroke patients, 57% had undiagnosed moderate-severe obstructive sleep apnea and exhibited reduced slow-wave sleep with potentially compensatory increases in NREM 1-2 sleep compared to controls. Formal sleep studies are necessary after stroke, even in the absence of self-reported history of sleep-wake pathology.
Objective/background: 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. Patients/methods: 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. Results: 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=eta p2 >0.07). We observed no differences in ipsilesionally versus contralesionally scored sleep architecture. Conclusions: 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. (C) 2021 Elsevier B.V. All rights reserved.

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