Topographical changes in N1-P2 amplitude upon awakening from recovery sleep after slow-wave sleep deprivation

Objectives: To assess auditory evoked potentials (AEPs) before sleep and upon 3 awakenings during an undisturbed baseline night and to compare them to AEPs during a night characterized by a recuperative increase in the amount of slow-wave sleep (SWS) as a consequence of two consecutive nights of selective SWS deprivation. Methods: Ten male subjects slept in the laboratory for 6 consecutive nights. The first 2 nights were undisturbed. The 3rd night was considered as baseline. During the 4th and 5th nights, selective SWS deprivation was obtained by means of acoustic stimulation. The 6th night was a recovery. The data reported here were collected during the baseline and the recovery night. Subjects were awakened 3 times: after 2 h, 5 h (nocturnal awakenings) and 7.5 h (final morning awakening) of sleep, respectively. All the awakenings were carried out from stage 2. The AEP recordings were carried out in bed, while subjects were performing a simple auditory reaction time task. Results: The amplitude of the N1-P2 complex decreased upon the first awakening of the baseline night as compared to pre-sleep wakefulness levels; during the recovery night, the decrease of N1-P2 amplitude was present also upon the second and final awakening. N1 latency increased upon the two nocturnal awakenings regardless of the night, while P2 latency was not affected. Moreover, the N1-P2 amplitude increased during recovery at the frontal midline derivation as compared to baseline, while it decreased at Pz and Oz. Conclusions: The N1-P2 amplitude and, to a lesser extent, the N1 latency, are sensitive in showing a state of brain deactivation during the sleep-wake transition. The decrease of N1-P2 amplitude at the parieto-occipital locations during recovery is coherent with the hypothesis of a functional link between SWS amount and cortical hypoarousal upon awakening. The unexpected increase of the same variable at Fz can be interpreted as the effect of a compensatory effort of the frontal areas for the increased homeostatic drive for sleep during the recovery night. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.