Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/26451
Title: Sleep architectural dysfunction and undiagnosed obstructive sleep apnea after chronic ischemic stroke.
Austin Authors: Gottlieb, Elie;Khlif, Mohamed S;Bird, Laura ;Werden, Emilio ;Churchward, Thomas J ;Pase, Matthew P;Egorova, Natalia;Howard, Mark E ;Brodtmann, Amy 
Affiliation: Harvard T.H. Chan School of Public Health, Harvard University, MA, USA
Melbourne School of Psychological Sciences, University of Melbourne, Melbourne, VIC, Australia
Turner Institute for Brain and Mental Health, School of Psychological Sciences, Monash University, VIC, Australia
The Florey Institute of Neuroscience and Mental Health, Melbourne, VIC, Australia
University of Melbourne, Melbourne, VIC, Australia
Institute for Breathing and Sleep
Austin Health
Issue Date: 15-Apr-2021
metadata.dc.date: 2021-04-15
Publication information: Sleep Medicine 2021; 83: 45-53
Abstract: 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.
URI: https://ahro.austin.org.au/austinjspui/handle/1/26451
DOI: 10.1016/j.sleep.2021.04.011
PubMed URL: 33991892
Type: Journal Article
Subjects: Brain ischemia
Polysomnography
Sleep apnea
Sleep architecture
Stroke
Appears in Collections:Journal articles

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