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Co-activated yet disconnected-Neural correlates of eye closures when trying to stay awake.

Ju Lynn Ong, Danyang Kong, Tiffany T Y Chia, Jesisca Tandi, B T Thomas Yeo, Michael W.L. Chee

Neuroimage September 1, 2015 DOI: 10.1016/j.neuroimage.2015.03.085 (opens in new tab) via PubMed

Summary

AI-generated from the abstract

When people are sleep-deprived, spontaneous eye closures that signal the onset of sleep become more frequent. Using task-free fMRI in sleep-deprived participants, the study found that these eye closures are accompanied by widespread co-activation of sensory cortices (visual, auditory, somatosensory) and the default mode network, consistent with internal sensory activity without external input. Co-activation of fronto-parietal attentional areas may reflect resistance to sleep or engagement of mental imagery. These brain activity patterns differed from those during cued eye closures in rested participants and from mind-wandering or light sleep. Eye closures also reduced functional connectivity within the default mode and dorsal attention networks, adding to reductions already caused by sleep deprivation. Thalamic deactivation occurred during eye closures in the sleep-deprived state but similar changes appeared when well-rested.

Study at a glance

Characteristics Observational study Peer reviewed
Population Sleep-deprived participants
Topics Dreaming
Keywords Eye closure Sleep deprivation Sleep mentation FMRI
Key finding Spontaneous eye closures during sleep deprivation trigger extensive co-activation of sensory cortices and default mode network, distinct from cued eye closures in rested individuals.

Abstract

Spontaneous eye-closures that herald sleep onset become more frequent when we are sleep deprived. Although these are typically associated with decreased responsiveness to external stimuli, it is less clear what occurs in the brain at these transitions to drowsiness and light sleep. To investigate this, task-free fMRI of sleep-deprived participants was acquired. BOLD activity associated with periods of spontaneously occurring eye closures were marked and analyzed. We observed concurrent and extensive hypnagogic co-activation of the extrastriate visual, auditory, and somatosensory cortices as well as the default mode network, consistent with internal sensory activity without external stimulation. Co-activation of fronto-parietal areas known to mediate attentional control could correspond with participants resisting sleep or additional engagement of mental imagery. This constellation of signal changes differed from those elicited by cued eye closures of similar duration and distribution in the same, rested participants. They also differ from signal changes associated with mind-wandering and consolidated light sleep. Concurrent with the observed event-related changes, eye closures elicited additional reduction in functional connectivity within nodes of the DMN and DAN, superposed on already reduced connectivity associated with sleep deprivation. There was concurrent deactivation of the thalamus during eye-closure during the sleep-deprived state but almost similar changes occurred in the well-rested state that may also be relevant. These findings highlight the dynamic shifts in brain activity and connectivity at border between wakefulness and sleep.

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