Selective REM sleep deprivation in humans: effects on sleep and sleep EEG

Abstract

To investigate rapid eye movement (REM) sleep regulation, eight healthy young men were deprived of REM sleep for three consecutive nights. In a three-night control sleep deprivation (CD) session 2 wk later, the subjects were repeatedly awakened from non-REM sleep in an attempt to match the awakenings during the REM sleep deprivation (RD) nights. During the RD nights the number of sleep interruptions required to prevent REM sleep increased within and across consecutive nights. REM sleep was reduced to 9.2% of baseline (CD nights: 80.7%) and rose to 140.1% in the first recovery night. RD gave rise to changes in the EEG power spectra of REM sleep. Power in the 8.25- to 11-Hz range was reduced in the first recovery night, an effect that gradually subsided but was still present in the third recovery night. The rising REM sleep propensity, as reflected by the increase of interventions within and across RD nights, and the moderate REM sleep rebound during recovery can be accounted for by a compensatory response that serves REM sleep homeostasis. The changes in the electroencephalogram power spectra, which were observed during enhanced REM sleep propensity, may be a sign of an altered quality of REM sleep.

Effect of Chronic Phenelzine Treatment on REM Sleep Report of Three Patients

“…Nevertheless, two weeks of rebound appear unlikely to be long enough to regain all REM sleep, which had been lost during the months of phenelzine treatment. It has previously been hypothesized that accumulated REM sleep pressure may be reduced and/or replaced by wakefulness (Endo et al 1998;Horne 2000). The enhancement of TFA in waking during treatment and its weak inverse relationship with REM sleep is consistent with this view, and may be evidence for compensatory REM sleep mechanisms occurring during wakefulness.…”

Is the nonREM–REM sleep cycle reset by forced awakenings from REM sleep?

“…In SRSD, the interventions and the remaining REM sleep activity aggregate in clusters reminding of the REM episodes in undisturbed nights [15,16]. This phenomenon was confirmed in the present study.…”

“…These include an increasing number of awakenings required to prevent REM sleep, a decreasing REM latency, a rise of the wakening threshold and an increase in REM sleep immediately after SRSD [14]. In the course of SRSD nights, the REM pressure increases, but still varies with the circadian phase and decreases during the remaining REM activity to an extent depending on the effectiveness of the procedure [15,16]. Typically, the interventions are not equally distributed in the course of SRSD recordings.…”

“…Then, all of a sudden this behavior is abandoned and nonREM sleep prevails. Treatment nights therefore exhibit clusters of interrupted REM sleep activity alternating with bouts of nonREM sleep [15,16].…”

“…Obviously, this second model is also able to explain the clustering of interventions in SRSD: chances for stage REM to reoccur after the awakenings are high, because SRSD generates a considerable REM pressure [15,16]. Sleep is therefore repeatedly interrupted and the interventions will accumulate until nonREM sleep activity is chosen for the first time.…”