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dc.contributor.authorGottlieb, Elie-
dc.contributor.authorEgorova, Natalia-
dc.contributor.authorKhlif, Mohamed S-
dc.contributor.authorKhan, Wasim-
dc.contributor.authorWerden, Emilio-
dc.contributor.authorPase, Matthew P-
dc.contributor.authorHoward, Mark E-
dc.contributor.authorBrodtmann, Amy-
dc.identifier.citationSleep 2020; 43(9): zsaa054en
dc.description.abstractSleep-wake disruption is a key modifiable risk factor and sequela of stroke. The pathogenesis of poststroke sleep dysfunction is unclear. It is not known whether poststroke sleep pathology is due to focal infarction to sleep-wake hubs or to accelerated poststroke neurodegeneration in subcortical structures after stroke. We characterize the first prospective poststroke regional brain volumetric and whole-brain, fiber-specific, white matter markers of objectively measured sleep-wake dysfunction. We hypothesized that excessively long sleep (>8 h) duration and poor sleep efficiency (<80%) measured using the SenseWear Armband 3-months poststroke (n = 112) would be associated with reduced regional brain volumes of a priori-selected sleep-wake regions of interest when compared to healthy controls with optimal sleep characteristics (n = 35). We utilized a novel technique known as a whole-brain fixel-based analysis to investigate the fiber-specific white matter differences in participants with long sleep duration. Stroke participants with long sleep (n = 24) duration exhibited reduced regional volumes of the ipsilesional thalamus and contralesional amygdala when compared with controls. Poor sleep efficiency after stroke (n = 29) was associated with reduced ipsilesional thalamus, contralesional hippocampus, and contralesional amygdala volumes. Whole-brain fixel-based analyses revealed widespread macrostructural degeneration to the corticopontocerebellar tract in stroke participants with long sleep duration, with fiber reductions of up to 40%. Neurodegeneration to subcortical structures, which appear to be vulnerable to accelerated brain volume loss after stroke, may drive sleep-wake deficiencies poststroke, independent of lesion characteristics and confounding comorbidities. We discuss these findings in the context of the clinicopathological implications of sleep-related neurodegeneration and attempt to corroborate previous mechanistic-neuroanatomical findings.en
dc.subjectascending arousal systemen
dc.subjectregional brain volumeen
dc.subjectsleep durationen
dc.subjectsleep efficiencyen
dc.titleRegional neurodegeneration correlates with sleep-wake dysfunction after stroke.en
dc.typeJournal Articleen
dc.identifier.affiliationDepartment of Neuroimaging, Institute of Psychiatry, Psychology, and Neuroscience (IoPPN), King's College, London, UKen
dc.identifier.affiliationTurner Institute for Brain and Mental Health, School of Psychological Sciences, Monash University, Melbourne, Victoria, Australiaen
dc.identifier.affiliationHarvard T.H. Chan School of Public Health, Harvard University, MAen
dc.identifier.affiliationThe Florey Institute of Neuroscience and Mental Healthen
dc.identifier.affiliationUniversity of Melbourne, Melbourne, Victoria, Australiaen
dc.identifier.affiliationAustin Healthen
dc.identifier.affiliationInstitute for Breathing and Sleepen
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