Abstract

Abstract Introduction The sleep onset period, involving so-called stage N1 sleep largely, is characterized by a reduction in the amount of alpha activity compared to wakefulness. Various kinds of physiological and psychological changes are also apparent, such as slow eye movements, changes in muscle tonus, and the hypnagogic dream-like mentation. These phenomena are thought to be the reflection of dynamic alterations in the brain during the transition period, however, details of these changes have still been uncovered. Methods We aimed to investigate a dynamic shift in the brain connectivity at sleep onset using the method of EEG-fMRI simultaneous recording. Twenty-three healthy subjects participated. EEG/fMRI were recorded simultaneously during an hour’s nap in a 3T-MRI scanner and real-time monitoring of EEG was performed. To record the transition period between multiple times, an experimenter inside a scanner room touched a subject’s foot for inducing arousal when a shift to NREM sleep stage 1 was observed. EEG data were scored according to the AASM criteria. Based on sleep stages defined by polysomnographic findings, we investigated alterations in functional connectivity of sleep- and wake- promoting regions within the hypothalamus and other areas including the thalamus. Results Posterior alpha power showed significant positive correlation with BOLD signals in the anterior and medial dorsal thalamus. Connectivity between the thalamus and cortical regions reduced sharply in the descent to sleep stage. Meanwhile, BOLD signals of the sleep- and wake- promoting regions within the hypothalamus fluctuated with certain temporal lags from fluctuations of alpha rhythm at sleep onset. Conclusion Present findings provide preliminary evidence of dynamics of wake- and sleep- promoting regions in the human brain in vivo. Our data also support the hypothesis that reduced thalamocortical connectivity which limits the capacity to integrate information is associated with the transition of consciousness at sleep onset. Support None

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