Cognitive dysfunction, either alone or as an element in the syndrome of delirium, is a common
occurrence with an incidence as high as 75% in intensive care unit (ICU) patients and can
independently result in serious consequences including higher mortality rate. Delirium
develops through a complex interaction between the patient's baseline vulnerability (risk
factors) and precipitating factors such as disruption of sleep that may occur during
hospitalization. While sedative-hypnotic agents that are used to facilitate hypnosis and the
management of mechanically ventilated patients converge on the neural substrate that mediate
endogenous sleep, they do so at different juncture points depending on its molecular
mechanism of hypnotic action. Hypnotic agents that modulate the GABAA receptor converge at
the level of the hypothalamus while α2 adrenergic agonists converge on sleep pathways within
the brainstem. This translational project seeks to determine whether sedation mediated by
activation of α2 adrenoceptors (dexmedetomidine) is more like natural sleep than that
provided by a sedative agent that modulates the GABAA receptor (propofol). The investigators
will examine volunteers who will be monitored continuously by electroencephalography (EEG)
and whole-brain functional connectivity by magnetoencephalography (MEG) during each of three
sleep stages, namely, that induced by dexmedetomidine, propofol, or saline (natural sleep,
control). The two drug-induced sleep regimens will be compared to natural sleep using EEG and
brain connectivity by MEG