Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/26451
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dc.contributor.authorGottlieb, Elie-
dc.contributor.authorKhlif, Mohamed S-
dc.contributor.authorBird, Laura-
dc.contributor.authorWerden, Emilio-
dc.contributor.authorChurchward, Thomas J-
dc.contributor.authorPase, Matthew P-
dc.contributor.authorEgorova, Natalia-
dc.contributor.authorHoward, Mark E-
dc.contributor.authorBrodtmann, Amy-
dc.date2021-04-15-
dc.date.accessioned2021-05-17T05:47:00Z-
dc.date.available2021-05-17T05:47:00Z-
dc.date.issued2021-04-15-
dc.identifier.citationSleep Medicine 2021; 83: 45-53en
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/26451-
dc.description.abstractSleep-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.en
dc.language.isoeng
dc.subjectBrain ischemiaen
dc.subjectPolysomnographyen
dc.subjectSleep apneaen
dc.subjectSleep architectureen
dc.subjectStrokeen
dc.titleSleep architectural dysfunction and undiagnosed obstructive sleep apnea after chronic ischemic stroke.en
dc.typeJournal Articleen
dc.identifier.journaltitleSleep Medicineen
dc.identifier.affiliationHarvard T.H. Chan School of Public Health, Harvard University, MA, USAen
dc.identifier.affiliationMelbourne School of Psychological Sciences, University of Melbourne, Melbourne, VIC, Australiaen
dc.identifier.affiliationTurner Institute for Brain and Mental Health, School of Psychological Sciences, Monash University, VIC, Australiaen
dc.identifier.affiliationThe Florey Institute of Neuroscience and Mental Health, Melbourne, VIC, Australiaen
dc.identifier.affiliationUniversity of Melbourne, Melbourne, VIC, Australiaen
dc.identifier.affiliationInstitute for Breathing and Sleepen
dc.identifier.affiliationAustin Healthen
dc.identifier.doi10.1016/j.sleep.2021.04.011en
dc.type.contentTexten
dc.identifier.pubmedid33991892
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