Elie Gottlieb1, Mohamed S Khlif2, Laura Bird2, Emilio Werden2, Thomas Churchward3, Matthew P Pase4, Natalia Egorova5, Mark E Howard6, Amy Brodtmann2. 1. The Florey Institute of Neuroscience and Mental Health, Melbourne, VIC, Australia; University of Melbourne, Melbourne, VIC, Australia. Electronic address: Elie.Gottlieb@Florey.edu.au. 2. The Florey Institute of Neuroscience and Mental Health, Melbourne, VIC, Australia; University of Melbourne, Melbourne, VIC, Australia. 3. Institute for Breathing and Sleep, Melbourne, VIC, Australia; Austin Health, Heidelberg, VIC, Australia. 4. Turner Institute for Brain and Mental Health, School of Psychological Sciences, Monash University, VIC, Australia; Harvard T.H. Chan School of Public Health, Harvard University, MA, USA. 5. The Florey Institute of Neuroscience and Mental Health, Melbourne, VIC, Australia; University of Melbourne, Melbourne, VIC, Australia; Melbourne School of Psychological Sciences, University of Melbourne, Melbourne, VIC, Australia. 6. University of Melbourne, Melbourne, VIC, Australia; Institute for Breathing and Sleep, Melbourne, VIC, Australia; Austin Health, Heidelberg, VIC, Australia.
Abstract
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=ηp2 >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.
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 strokepatients in the chronic recovery phase compared to healthy controls. PATIENTS/ METHODS: Radiologically confirmed ischemic strokepatients (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 strokepatients (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 strokepatients (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, strokepatients 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. CONCLUSIONS: Fifty-seven percent of chronic strokepatients 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.