Selective Slow-wave Sleep Deprivation Research Articles

Going Local: Insights from EEG and Stereo-EEG Studies of the Human Sleep-Wake Cycle

In the present paper, we reviewed a large body of evidence, mainly from quantitative EEG studies of our laboratory, supporting the notion that sleep is a local and use-dependent process. Quantitative analyses of sleep EEG recorded from multiple cortical derivations clearly indicate that every sleep phenomenon, from sleep onset to the awakening, is strictly local in nature. Sleep onset first occurs in frontal areas, and a frontal predominance of low-frequency power persists in the first part of the night, when the homeostatic processes mainly occur, and then it vanishes. Upon awakening, we showed an asynchronous EEG activation of different cortical areas, the more anterior ones being the first to wake up. During extended periods of wakefulness, the increase of sleepiness-related low-EEG frequencies is again evident over the frontal derivations. Similarly, experimental manipulations of sleep length by total sleep deprivation, partial sleep curtailment or even selective slow-wave sleep deprivation lead to a slow-wave activity rebound localized especially on the anterior derivations. Thus, frontal areas are crucially involved in sleep homeostasis. According to the local use-dependent theory, this would derive from a higher sleep need of the frontal cortex, which in turn is due to its higher levels of activity during wakefulness. The fact that different brain regions can simultaneously exhibit different sleep intensities indicates that sleep is not a spatially global and uniform state, as hypothesized in the theory. We have also reviewed recent evidence of localized effects of learning and plasticity on EEG sleep measures. These studies provide crucial support to a key concept in the theory, the one claiming that local sleep characteristics should be use-dependent. Finally, we have reported data corroborating the notion that sleep is not necessarily present simultaneously in the entire brain. Our stereo-EEG recordings clearly indicate that sleep and wakefulness can co-exist in different areas, suggesting that vigilance states are not necessarily temporally discrete states. We conclude that understanding local variations in sleep propensity and depth, especially as a result of brain plasticity, may provide in the near future insightful hints into the fundamental functions of sleep.

Antidepressant effects of selective slow wave sleep deprivation in major depression: A high-density EEG investigation

Sleep deprivation can acutely reverse depressive symptoms in some patients with major depression. Because abnormalities in slow wave sleep are one of the most consistent biological markers of depression, it is plausible that the antidepressant effects of sleep deprivation are due to the effects on slow wave homeostasis. This study tested the prediction that selectively reducing slow waves during sleep (slow wave deprivation; SWD), without disrupting total sleep time, will lead to an acute reduction in depressive symptomatology. As part of a multi-night, cross-over design study, participants with major depression (non-medicated; n = 17) underwent baseline, SWD, and recovery sleep sessions, and were recorded with high-density EEG (hdEEG). During SWD, acoustic stimuli were played to suppress subsequent slow waves, without waking up the participant. The effects of SWD on depressive symptoms were assessed with both self-rated and researcher-administered scales. Participants experienced a significant decrease in depressive symptoms according to both self-rated (p = .007) and researcher-administered (p = .010) scales, while vigilance was unaffected. The reduction in depressive symptoms correlated with the overnight dissipation of fronto-central slow wave activity (SWA) on baseline sleep, the rebound in right frontal all-night SWA on recovery sleep, and the amount of REM sleep on the SWD night. In addition to highlighting the benefits of hdEEG in detecting regional changes in brain activity, these findings suggest that SWD may help to better understand the pathophysiology of depression and may be a useful tool for the neuromodulatory reversal of depressive symptomatology.

Effects of selective slow-wave sleep deprivation on nocturnal blood pressure dipping and daytime blood pressure regulation

Nocturnal blood pressure (BP) decline or "dipping" is an active, central, nervously governed process, which is important for BP regulation during daytime. It is, however, not known whether the sleep process itself or, more specifically, slow-wave sleep (SWS) is important for normal dipping. Therefore, in the present study, healthy subjects (6 females, 5 males) were selectively deprived of SWS by EEG-guided acoustic arousals. BP and heart rate (HR) were monitored during experimental nights and the following day. Additionally, nocturnal catecholamine excretion was determined, and morning baroreflex function was assessed by microneurographic measurements of muscle sympathetic nerve activity (MSNA) and heart rate variability (HRV). Data were compared with a crossover condition of undisturbed sleep. SWS was successfully deprived leading to significantly attenuated mean arterial BP dipping during the first half (P < 0.05), but not during the rapid-eye-movement-dominated second half of total sleep; however, dipping still evolved even in the absence of SWS. No differences were found for nighttime catecholamine excretion. Moreover, daytime resting and ambulatory BP and HR were not altered, and morning MSNA and HRV did not differ significantly, indicating that baroreflex-mediated sympathoneural BP regulation was not affected by the preceding SWS deprivation. We conclude that in healthy humans the magnitude of nocturnal BP dipping is significantly affected by sleep depth. Deprivation of SWS during one night does not modulate the morning threshold and sensitivity of the vascular and cardiac baroreflex and does not alter ambulatory BP during daytime.

Antero-posterior functional coupling at sleep onset: changes as a function of increased sleep pressure

The use of the directed transfer function (DTF), an advanced computational analysis of electroencephalogaphic (EEG) data, which provides an estimation of the direction of the information flow underlying cortico-cortical functional coupling, has shown that the presleep period is characterized by posterior-to-anterior functional cortical coupling, while at sleep onset there is an inversion of that direction. This finding supported the idea that anterior cortical areas first synchronize sleep EEG activity. The aim of the present study was to assess the changes of functional coupling between anterior and posterior midline cortical areas during the sleep onset process when sleep pressure is heightened by a selective slow-wave sleep (SWS) deprivation. The hypothesis was that the anterior-to-posterior direction of the cortical functional coupling at sleep onset is enhanced by SWS deprivation. Ten normal right-handed male students slept for six consecutive nights in the laboratory (1: adaptation, 2: baseline, 3: baseline with awakenings, 4 and 5: SWS deprivations, 6: recovery), with standard polysomnographic recordings. The DTF was computed on data recorded during nights two and six from anterior (Fz A1) and posterior (Pz A1, Oz A1) derivations. Results showed that, during the recovery night, the anterior-to-posterior direction of functional cortical coupling is already present in the presleep period, indicating that SWS deprivation advances the shift to an anterior-to-posterior directionality of functional cortical coupling, possibly as a consequence of heightened sleep pressure. These findings support the notion that a spread of synchronizing signals from associative prefrontal to posterior areas play a role in the wake–sleep transition.

Regional Differences of the Human Sleep Electroencephalogram in Response to Selective Slow-wave Sleep Deprivation

The purpose of this study was to assess the topographic changes in sleep recuperative processes in response to selective slow-wave sleep (SWS) deprivation. SWS was suppressed on two consecutive nights by means of acoustic stimulation. The electroencephalogram (EEG) power of baseline, deprivation and recovery nights was analysed in 1 Hz bins. During the SWS deprivation nights, large decreases of EEG power were found at frontopolar, central and parietal derivations encompassing the delta, theta and alpha range, while only slow delta (0.5-2 Hz) was affected at the frontal derivation. Recovery sleep was characterized by a generalized increase of power during non-REM sleep encompassing the delta, theta and alpha bands, with a clear antero-posterior gradient. The coherent behaviour of different EEG bands with traditionally different electrophysiological meanings during non-REM sleep suggests that, in light of the recent advances in sleep neurophysiology, a re-examination of the functional role of EEG rhythms during sleep is needed. The 'resistance' to selective SWS deprivation of the frontal area, together with its larger increase of EEG power during recovery, may be interpreted as a sign of a greater sleep need of the frontal cortical areas, confirming that some aspects of the regulatory processes of human sleep are local in nature and may show use-dependent characteristics.

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

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. 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. 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. 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.

Plasma Catecholamines and Selective Slow Wave Sleep Deprivation

The present study evaluated the effect of slow wave sleep (SWS) deprivation on plasma levels of catecholamines in healthy male volunteers. Eleven volunteers spent 4 nights in the sleep laboratory (2 nights of habituation and 2 further nights); during the latter, 1 night served as control, and in the other, SWS deprivation was performed. Blood was drawn at 30-min intervals. SWS was reduced by 86%; no sleep stage 4 was observed during the SWS-deprived nights. SWS reduction was found not to correlate with catecholamine levels. However, epinephrine levels were found to be sensitive to sleep fragmentation. The time interval between arousals in the SWS-deprived night as well as the difference in sleep efficiency were related to increases in epinephrine levels (p < 0.01 and p < 0.025, respectively). These results support the view that continuity rather than the duration of SWS is important for the recuperative value of sleep.

Interhemispheric asymmetry of human sleep EEG in response to selective slow-wave sleep deprivation.

Recent evidence suggests that the human sleep electroencephalogram (EEG) shows regional differences over both the sagittal and coronal planes. In the present study, in a group of 10 right-handers, the authors investigated the presence of hemispheric asymmetries in the homeostatic regulation of human sleep EEG power during and after selective slow-wave sleep (SWS) deprivation. The SWS deprivation was slightly more effective over the right hemisphere, but the left hemisphere showed a markedly larger increase of EEG power in the 1.00-24.75 Hz range during recovery-night non-REM sleep, and a larger increase of EEG power during both deprivation-night and recovery-night REM sleep. These results support the greater need for sleep recuperative processes of the left hemisphere, suggesting that local sleep regulation processes may also act during REM sleep.

Interhemispheric asymmetry of human sleep EEG in response to selective slow-wave sleep deprivation.

Interhemispheric asymmetry of human sleep EEG in response to selective slow-wave sleep deprivation.

EEG arousals in normal sleep: variations induced by total and selective slow-wave sleep deprivation.

Aim of the present study was to assess changes in arousal rates after selective slow-wave (SWS) and total sleep deprivations. Two-way mixed design comparing the arousal index (Al), as expressed by the number of EEG arousals divided by sleep duration, in totally or selectively sleep deprived subjects. Sleep laboratory. Nineteen normal male subjects [mean age=23.3 years (S.E.M.=0.55)]. Al was measured in baseline nights and after selective SWS (N=10) and total sleep deprivation (N=9). During the baseline nights AI values changed across sleep stages as follows: stage 1 > stage 2 and REM > SWS, but did not present any significant variations as a function of time elapsed from sleep onset. The recovery after deprivation showed a reduction in EEG arousals, more pronounced after total sleep deprivation; this decrease affected NREM but not REM sleep. During the baseline nights Al showed a close-to-significance negative correlation with REM duration, while during the recovery nights a significant positive relation with stage 1 duration was found. The present results suggest that recuperative processes after sleep deprivation are also associated with a higher sleep continuity as defined by the reduction of EEG arousals.

Effect of slow-wave sleep deprivation on topographical distribution of spindles

Spindle activity, visually scored in the 12–15 Hz range over antero-posterior midline derivations, has been assessed in ten normal subjects during a baseline and a recovery sleep after 2 nights of selective slow-wave sleep (SWS) deprivation. The recovery sleep, characterized by a significant increase of stage 4 and SWS as compared to the baseline, revealed that sleep spindles are reduced in the first NREM sleep cycle. The size of this reduction in spindle density progressively decreased in the course of the night, paralleling the depletion of SWS rebound. Topographical distribution of spindle activity showed a global linear increase over consecutive NREM-REM sleep cycles, regarding to the whole antero-posterior midline EEG derivations except the occipital one. It is concluded that the SWS rebound after 2 nights of selective SWS deprivation is associated with a reduction of spindles during stage 2.

Selective slow‐wave sleep deprivation and time‐of‐night effects on cognitive performance upon awakening

We evaluated the effects of selective slow-wave sleep (SWS) deprivation and time-of-night factors on cognitive performance upon awakening. Ten normal men slept for 6 consecutive nights in the laboratory: 1 adaptation, 2 baseline, 2 selective SWS deprivation, and 1 recovery night. Cognitive performance was assessed by means of a Descending Subtraction Task after 2, 5, and 7.5 h of sleep. There was an almost complete selective SWS suppression during both deprivation nights, and a significant SWS rebound during the recovery sleep. Regarding cognitive performance, a progressive linear decrease of sleep inertia upon successive awakenings was found during all experimental nights except for the recovery night. In addition, a significant decrease of sleep inertia was observed upon the morning awakening of the second deprivation night for the measure of performance speed, and a significant increase of sleep inertia upon the morning awakening of the recovery night for the measure of performance accuracy. The results show that cognitive performance upon awakening is adversely affected by sleep depth and that, during the sleep-wake transition, cognitive performance accuracy is more impaired than performance speed.

Selective slow-wave sleep deprivation and time-of-night effects on cognitive performance upon awakening

Selective slow-wave sleep deprivation and time-of-night effects on cognitive performance upon awakening

The relationship between frequency of rapid eye movements in REM sleep and SWS rebound.

Previous studies have shown a decrease in rapid eye movement (REM) frequency during desynchronized sleep in recovery nights following total or partial sleep deprivation. This effect has been ascribed to an increase in sleep need or sleep depth consequent to sleep length manipulations. The aims of this study were to assess REM frequency variations in the recovery night after two consecutive nights of selective slow-wave sleep (SWS) deprivation, and to evaluate the relationships between REM frequency and SWS amount and auditory arousal thresholds (AAT), as an independent index of sleep depth. Ten normal males slept for six consecutive nights in the laboratory: one adaptation, two baseline, two selective SWS deprivation and one recovery night. SWS deprivation allowed us to set the SWS amount during both deprivation nights close to zero, without any shortening of total sleep time. In the ensuing recovery night a significant SWS rebound was found, accompanied by an increase in AAT. In addition, REM frequency decreased significantly compared with baseline. This effect cannot be attributed to a variation in prior sleep duration, since there was no sleep loss during the selective SWS deprivation nights. Stepwise regression also showed that the decrease in REM frequency is not correlated with the increase in AAT, the traditional index of sleep depth, but is correlated with SWS rebound.

The effects of slow-wave sleep (SWS) deprivation and time of night on behavioral performance upon awakening

The aim of the present study is to evaluate the effects of selective SWS deprivation on the motor and sensory motor performance impairment immediately after awakening from nocturnal sleep at different times of the night. Ten normal males slept for 6 consecutive nights in the laboratory: one adaptation, two baseline, two selective SWS deprivation, and one recovery night. During the last 4 nights performance was assessed four times: (a) before sleep, as a baseline measure; (b) within 30 s from the first nighttime awakening, after 2 h of sleep; (c) within 30 s from the second nighttime awakening, after 5 h of sleep; (d) within 30 s from the final morning awakening. After each awakening, following a 3-min cognitive test, a simple Auditory Reaction Time task (ART, about 5 min) and a Finger Tapping Task (FTT, 3 min) were administered. Median of Reaction Times (RT) and of Intertapping Intervals (ITI), 10% fastest RT, 10% slowest RT, and number of misses were considered as dependent variables. The selective SWS deprivation was very effective: SWS percentage during both the deprivation nights was close to zero. This strong manipulation of SWS amount interacted with time-of-night factors in influencing sleep inertia. The SWS deprivation procedure caused a worsening of behavioral performance during the deprivation nights, as well as upon the final awakening of the recovery night. Behavioral performance slowing upon awakening is accounted for by: (1) a general decrement in overall response speed (median of RT); (2) an “optimum response shift”, i.e., a decrease in speed of the fastest responses; (3) an increase of lapsing, with more marked response delays resulting in a further decrease in response speed in the “lapse domain”. Finally, our results do not support the existence of a circadian rhythm of sleep inertia linked to body temperature rhythm.

Auditory arousal thresholds after selective slow-wave sleep deprivation

Objectives: The aim of this study is to assess Auditory Arousal Thresholds (AATs) three times during an undisturbed baseline night and to compare them to AATs during the recovery night that follows two consecutive nights of selective SWS deprivation. The presence of a time-of-night effect on AATs will also be assessed. Methods: Ten male Ss slept in the laboratory for 6 consecutive nights. The first two 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. In the last 4 nights Ss were awakened three times, after 2, 5 and 7.5 h of sleep, respectively. All the awakenings were carried out from stage 2 (after at least 5 consecutive min of stage 2), by means of 1000 Hz ascending tone series. The AAT determination was based on EEG-EMG criteria: at least 10-s of clear alpha rhythm and/or a 10 s movement arousal. Results: During both deprivation nights, SWS amount was close to zero. In the ensuing recovery night a significant SWS rebound was found, accompanied by a significant increase of AATs with respect to the baseline. Furthermore, there was a significant linear decrease of AATs during the night. Finally, the individual correlations between AATs and SWS amount were significant in 4 out of 10 Ss. Conclusions: These results confirm that AATs are a reliable index of sleep depth by showing that the SWS rebound following selective SWS deprivation is paralleled by a significant AAT enhancement. The experimental paradigm also allows us to claim that AATs show a decreasing linear trend during the night, having excluded any procedural bias. Finally, AATs can be directly related to SWS amount that preceded the awakening, although the individual correlations between AATs and SWS have to be considered with caution, given the high inter-subject variability and the small number of observations.

Selective slow-wave sleep deprivation influences blood serotonin profiles and serum melatonin concentrations in healthy subjects

Internal desynchronization in circadian rhythms provoked by shift work in susceptible individuals may interfere with the time-keeping system and circadian rhythms of the sleep-wake cycle, vital signs, neurotransmitters, and hormone concentrations in blood. It may lead to an abnormal relationship between the central circadian pacemaker and higher cognitive brain centers causing a higher frequency of health complaints among nightshift workers than among day workers (Moore-Ede et al 1982). It has been speculated that continued desynchronization precipitates a homeostatic imbalance which may result in depressive illness; thus depression has been hypothesized to be a disorder of time-keeping (van Cauter and Turek 1986; Aschoff 1981; Wehr and Goodwin 1983). Serotonin and melatonin are neuromodulators involved in the regulation of sleep and circadian rhythmicity. Serotonin's role in sleep regulation has been shown by Koella (1984), Borbely et al (1980), Matussek and Patschke (1963), Wauquier and Dugovic (1990), and others, although it is still debated whether a change in serotonin turnover is actually associated with insomnia. The suprachiasmatic nucleus which accommodates the internal clock is innervated with serotonergic neurons, and serotonin is the