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.     

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.     

Dry mouth upon awakening in obstructive sleep apnea

The aim was to assess the significance of dry mouth upon awakening as a symptom of obstructive sleep apnea (OSA). The participants were 668 consecutive adults referred for polysomnographic evaluation (PSG) because of snoring and suspected OSA, and 582 adults who were attending a general health check‐up. Data were obtained from self‐administered questionnaires and PSG evaluation. The participants were asked to answer the following question: ‘During the last month, did you experience waking up in the morning with a dry mouth?’. The response scale consisted of five categories: ‘never’, ‘rarely’, ‘sometimes’, often’, or ‘almost always’. We classified patients as having dry mouth upon awakening complaint only if they reported experiencing the symptom ‘almost always’. The prevalence of dry mouth upon awakening was twofold higher in patients with OSA (31.4%) than in primary snorers (16.4%, P < 0.001), and increased linearly from 22.4%, to 34.5%, and 40.7% in mild, moderate, and severe OSA respectively (P < 0.001). The prevalence of dry mouth upon awakening in the control group was 3.2%. Logistic regression results indicated that this symptom significantly differentiated OSA patients from primary snorers after adjusting for age, BMI, gender, hypertension, and other classical OSA symptoms (OR 2.33, 95% CI 1.34–4.07). Dry mouth upon awakening appears as a significant symptom of OSA. We suggest that increased sleep time spent with an open mouth is a likely explanation for these findings.     

Homeostasis of REM sleep after total and selective sleep deprivation in the rat

During specific rapid eye movement (REM) sleep deprivation its homeostatic regulation is expressed by progressively more frequent attempts to enter REM and by a compensatory rebound after the deprivation ends. The buildup of pressure to enter REM may be hypothesized to depend just on the time elapsed without REM or to be differentially related to non-REM (NREM) and wakefulness. This problem bears direct implications on the issue of the function of REM and its relation to NREM. We compared three protocols that combined REM-specific and total sleep deprivation so that animals underwent similar 3-h REM deprivations but different concomitant NREM deprivations for the first 2 (2T1R), 1 (1T2R), or 0 (3R) hours. Deprivation periods started at hour 6 after lights on. Twenty-two chronically implanted rats were recorded. The median amount of REM during all three protocols was approximately 1 min. The deficits of median amount of NREM in minutes within the 3-h deprivation periods as compared with their baselines were, respectively for 2T1R, 1T2R, and 3R, 35 (43%), 25 (25%), and 7 (7%). Medians of REM rebound in the three succeeding hours, in minutes above baseline, were, respectively, 8 (44%), 9 (53%), and 9 (50%), showing no significant differences among protocols. Attempted transitions to REM showed a rising trend during REM deprivations reaching a final value that did not differ significantly among the three protocols. These results support the hypothesis that the build up of REM pressure and its subsequent rebound is primarily related to REM absence independent of the presence of NREM.     

Auditory evoked responses upon awakening from sleep in human subjects

The hypothesis that a state of hypoarousal upon awakening should lead to a decrease in amplitude and an increase in latency of the N1-P2 components of the Auditory Evoked Potentials (AEPs) as compared to presleep wakefulness levels, was evaluated after two nocturnal awakenings and after the final morning awakening from a 7.5-h night of sleep. The amplitude of the N1-P2 complex was reduced upon awakening as compared to presleep wakefulness levels, but only following the first nocturnal awakening, scheduled after the first 2 h of sleep. This result is interpreted as indicating a link between slow wave sleep amount, mainly present during the first part of the night, and lowered levels of brain activation upon awakening. The reaction times, recorded concomitantly to AEPs, were more sensitive to the negative effects of sleep inertia.     

Self‐awakening improves alertness in the morning and during the day after partial sleep deprivation

The ability to awaken at a predetermined time without an alarm is known as self‐awakening. Self‐awakening improves morning alertness by eliminating sleep inertia; however, the effects of self‐awakening on daytime alertness and alertness that has deteriorated as a result of sleep loss are unknown. The aim of this study was to determine the effects of self‐awakening on both morning and daytime alertness after partial sleep deprivation. Fifteen healthy males without the habit of self‐awakening participated in a cross‐over trial including forced awakening and self‐awakening conditions. In each condition, participants' sleep was restricted to 5 h per night in their homes for 4 consecutive days. They completed a psychomotor vigilance task and subjective ratings of sleepiness immediately upon awakening each morning. On the fourth day, participants completed subjective ratings of sleepiness, a psychomotor vigilance task and sleep latency tests in the laboratory seven times at 1‐h intervals during the day. The response speed on the psychomotor vigilance task, in the morning and during the day, was higher in the self‐awakening than the forced awakening condition. Our results showed that self‐awakening improved alertness (assessed by response speeds) by reducing sleep inertia and alleviated daytime sleepiness heightened by partial sleep deprivation.     

Error correction maintains post-error adjustments after one night of total sleep deprivation

Previous behavioral and electrophysiologic evidence indicates that one night of total sleep deprivation (TSD) impairs error monitoring, including error detection, error correction, and posterror adjustments (PEAs). This study examined the hypothesis that error correction, manifesting as an overtly expressed self-generated performance feedback to errors, can effectively prevent TSD-induced impairment in the PEAs. Sixteen healthy right-handed adults (seven women and nine men) aged 19–23 years were instructed to respond to a target arrow flanked by four distracted arrows and to correct their errors immediately after committing errors. Task performance and electroencephalogram (EEG) data were collected after normal sleep (NS) and after one night of TSD in a counterbalanced repeated-measures design. With the demand of error correction, the participants maintained the same level of PEAs in reducing the error rate for trial N +  1 after TSD as after NS. Corrective behavior further affected the PEAs for trial N +  1 in the omission rate and response speed, which decreased and speeded up following corrected errors, particularly after TSD. These results show that error correction effectively maintains posterror reduction in both committed and omitted errors after TSD. A cerebral mechanism might be involved in the effect of error correction as EEG beta (17–24 Hz) activity was increased after erroneous responses compared to after correct responses. The practical application of error correction to increasing work safety, which can be jeopardized by repeated errors, is suggested for workers who are involved in monotonous but attention-demanding monitoring tasks.     

Age, performance and sleep deprivation

Young subjects are frequently involved in sleep-related accidents. They could be more affected than older drivers by sleep loss and therefore worsen their driving skills quicker, or have a different perception of their level of impairment. To test these hypotheses we studied variations of reaction time (RT), a fundamental prerequisite for safe performing, as measured by lapses, i.e. responses > or = 500 ms and self-assessment of performance and sleepiness after a night awake and after a night asleep in a balanced crossover design in young versus older healthy subjects. Ten young (20-25 years old) and 10 older volunteers (52-63 years old) were tested with and without 24 h of sleep deprivation. Without sleep deprivation, RTs were slower in older subjects than in the younger ones. However, after sleep deprivation, the RTs of young subjects increased while that of the older subjects remained almost unaffected. Sleepiness and self-perception of performance were equally affected in both age groups showing different perception of performance in the age groups. Our findings are discussed in terms of vulnerability to sleep-related accidents.     

Recovery sleep and performance following sleep deprivation with dextroamphetamine

Twelve subjects were studied to determine the after-effects of using three 10-mg doses of dextroamphetamine to sustain alertness during sleep deprivation. Sleep architecture during recovery sleep was evaluated by comparing post-deprivation sleep beginning 15 h after the last dextroamphetamine dose to post-deprivation sleep after placebo. Performance and mood recovery were assessed by comparing volunteers who received dextroamphetamine first (during sleep deprivation) to those who received placebo first. Stages 1 and 2 sleep, movement time, REM latency, and sleep latency increased on the night after sleep deprivation with dextroamphetamine vs. placebo. Stage 4 was unaffected. Comparisons to baseline revealed more stage 1 during baseline than during either post-deprivation sleep period and more stage 2 during baseline than during sleep following placebo. Stage 4 sleep was lower during baseline than it was after either dose, and REM sleep was lower during baseline and after dextroamphetamine than after placebo. Sleep onset was slowest on the baseline night. Next-day performance and mood were not different as a function of whether subjects received dextroamphetamine or placebo during deprivation. These data suggest dextroamphetamine alters post-deprivation sleep architecture when used to sustain alertness during acute sleep loss, but next-day performance and subjective mood ratings are not substantially affected. A recovery sleep period of only 8 h appears to be adequate to regain baseline performance levels after short-term sleep deprivation.     

Vascular resistance in the rat during baseline, chronic total sleep deprivation, and recovery from total sleep deprivation

Rats subjected to total sleep deprivation (TSD) by the disk-over-water method exhibit an elevated temperature set point, increased energy expenditure (EE), and increased circulating norepinephrine--all of which should militate for an increase in body temperature. Instead, after a small rise early in TSD, intraperitoneal temperature (T(ip)) fell progressively, indicating a reduced ability to retain body heat. To evaluate whether vasoconstrictor defenses against heat loss in the regions of major heat dissipation in the rat (hindpaws and tail) were impaired, peripheral vascular resistance (PVR) was calculated from aortic blood pressure (BP) and blood flow (BF) (BP and BF were continuously recorded at the aortic-iliac junction). TSD rats and their yoked control (TSC) rats were subjected to TSD for 10 to 22 days. As in earlier studies, TSD rats showed excessive heat loss indicated by a falling T(ip) (after an initial rise) while EE was elevated. Temperature set point was presumably raised throughout deprivation as shown previously. Although a small decline in PVR early in deprivation could have increased heat loss, there was no evidence of a massive vasodilation in the region examined which could, in itself, account for the progressive inability to retain heat over the course of TSD. In fact, PVR was near baseline levels during the latter half of TSD. Nevertheless, there was evidence of impaired vasoconstrictive defenses in TSD rats inasmuch as they showed significantly lower PVR than TSC rats during most of the deprivation period in spite of indications that they were farther below set point. It is not yet clear whether this impairment was a major determinant of the heat loss in TSD rats. A rapid PVR rebound during recovery suggested a release from a TSD-linked blockage of vasomotor compensation for excessive heat loss.     

Phosphorous31 magnetic resonance spectroscopy after total sleep deprivation in healthy adult men

STUDY OBJECTIVES: To investigate chemical changes in the brains of healthy adults after sleep deprivation and recovery sleep, using phosphorous magnetic resonance spectroscopy. DESIGN: Three consecutive nights (baseline, sleep deprivation, recovery) were spent in the laboratory. Objective sleep measures were assessed on the baseline and recovery nights using polysomnography. Phosphorous magnetic resonance spectroscopy scans took place beginning at 7 am to 8 am on the morning after each of the 3 nights. SETTING: Sleep laboratory in a private psychiatric teaching hospital. PARTICIPANTS: Eleven healthy young men. INTERVENTIONS: Following a baseline night of sleep, subjects underwent a night of total sleep deprivation, which involved supervision to ensure the absence of sleep but was not polysomnographically monitored. MEASUREMENTS AND RESULTS: No significant changes in any measure of brain chemistry were observed the morning after a night of total sleep deprivation. However, after the recovery night, significant increases in total and beta-nucleoside triphosphate and decreases in phospholipid catabolism, measured by an increase in the concentration of glycerylphosphorylcholine, were observed. Chemical changes paralleled some changes in objective sleep measures. CONCLUSIONS: Significant chemical changes in the brain were observed following recovery sleep after 1 night of total sleep deprivation. The specific process underlying these changes is unclear due to the large brain region sampled in this exploratory study, but changes may reflect sleep inertia or some aspect of the homeostatic sleep mechanism that underlies the depletion and restoration of sleep. Phosphorous magnetic resonance spectroscopy is a technique that may be of value in further exploration of such sleep-wake functions.     

Electrodermal activity during total sleep deprivation and its relationship with other activation and performance measures

The present study analyses the variations of the skin resistance level (SRL) during 48 h of total sleep deprivation (TSD) and its relationship to body temperature, self-informed sleepiness in the Stanford Sleepiness Scale (SSS), and reaction time (RT). All of the variables were evaluated every 2 h except for the SSS, which was evaluated every hour. A total of 30 healthy subjects (15 men and 15 women) from 18 to 24 years old participated in the experiment. Analyses of variance (ANOVAs) with TSD days and time-of-day as factors showed a substantial increase of SRL, SSS, and RT, and a decrease in body temperature marked by strong circadian oscillations. The interaction between day by time-of-day was only significant for RT. Furthermore, Pearson's correlations showed that the increase of SRL is associated to the decrease in temperature (mean r=-0.511), the increase of SSS (mean r=0.509), and the deterioration of RT (mean r=0.425). The results support previous TSD reports and demonstrate the sensitivity of SRL to TSD. The non-invasive character of SRL, its simplicity, and its relationships with other activation parameters, widely validated by previous literature, convert SRL into an interesting and useful measure in this field.     

Direct comparison of total sleep deprivation and late partial sleep deprivation in the treatment of major depression

BACKGROUND: There are clinical as well as experimental indications that--contrary to what is generally assumed--late partial sleep deprivation (LPSD) is not as effective as total sleep deprivation (TSD) in the treatment of depression. METHOD: We conducted a randomised balanced crossover study with 39 in-patients with major depression (mainly unipolar) in which both procedures LPSD and TSD were compared within a 1-week interval. Response was defined as a reduction of > or =30% in the 6-item Hamilton Depression Rating Scale and/or one of two self-rating scales (Adjective Mood Scale, Visual Analogue Scale). RESULTS: Overall response rate on the day after was low (0-53%, depending on the rating used). TSD proved slightly and in about half of the comparisons also significantly more effective than LPSD. In general, first treatments were more effective than second treatments; there were 10-20% second day responses; in up to 10% of the treatments patients worsened after sleep deprivation (using the same absolute criteria as for therapeutic response). LIMITATIONS: Non-blind rating, intentional and unintentional napping (microsleep) was not recorded, mainly unipolar depressives. CONCLUSIONS: Total sleep deprivation seems to be more effective than late partial sleep deprivation. We believe that there might be a dose-response relationship between hours of lost sleep and therapeutic effect within the range of 1 night.     

Residual,differential neurobehavioral deficits linger after multiple recovery nights following chronic sleep restriction or acute total sleep deprivation

Study ObjectivesThe amount of recovery sleep needed to fully restore well-established neurobehavioral deficits from sleep loss remains unknown, as does whether the recovery pattern differs across measures after total sleep deprivation (TSD) and chronic sleep restriction (SR).MethodsIn total, 83 adults received two baseline nights (10–12-hour time in bed [TIB]) followed by five 4-hour TIB SR nights or 36-hour TSD and four recovery nights (R1–R4; 12-hour TIB). Neurobehavioral tests were completed every 2 hours during wakefulness and a Maintenance of Wakefulness Test measured physiological sleepiness. Polysomnography was collected on B2, R1, and R4 nights.ResultsTSD and SR produced significant deficits in cognitive performance, increases in self-reported sleepiness and fatigue, decreases in vigor, and increases in physiological sleepiness. Neurobehavioral recovery from SR occurred after R1 and was maintained for all measures except Psychomotor Vigilance Test (PVT) lapses and response speed, which failed to completely recover. Neurobehavioral recovery from TSD occurred after R1 and was maintained for all cognitive and self-reported measures, except for vigor. After TSD and SR, R1 recovery sleep was longer and of higher efficiency and better quality than R4 recovery sleep.ConclusionsPVT impairments from SR failed to reverse completely; by contrast, vigor did not recover after TSD; all other deficits were reversed after sleep loss. These results suggest that TSD and SR induce sustained, differential biological, physiological, and/or neural changes, which remarkably are not reversed with chronic, long-duration recovery sleep. Our findings have critical implications for the population at large and for military and health professionals.     

Recovery sleep following different visual conditions during total sleep deprivation in man.

The findings of visual impairment during total sleep deprivation were used as a basis for a possible link between vision and sleep. It was proposed that the level of visual load imposed during sleep deprivation was an important variable, and would have a substantial effect upon recovery sleep. Six young male subjects underwent two conditions of 64 h of sleep deprivation on separate occasions. One condition incorporated a high visual load, and the other a low load. Exercise and sound were balanced. All night sleep EEGs were taken for two baseline nights, and also for two recovery nights following each condition. There was a significant increase of stage 4 on all recovery nights and a REM rebound on the second recovery night. SWS, particularly stage 4, TST and REM density, were significantly greater following the high load. Implications of these findings for sleep theories and for sleep deprivation research are discussed.     

Effect of 64 hours of sleep deprivation upon sleep in geriatric normals and insomniacs

Fifty-eight geriatric normal and chronic insomniac sleepers were screened with sleep recordings to define groups of 12 Normal (Sleep Efficiency greater than 85%) and Insomniac (Sleep Efficiency less than 80%) sleepers. All subjects then had 4 baseline sleep nights, 64 hours of total sleep loss, and 4 recovery nights. Insomniacs, had lower sleep efficiencies and less REM than Normals during baseline. Sleep efficiency was high (97%) in both groups on the first recovery night but decreased toward baseline values in both groups between the second (Normal) and fourth (Insomniac) recovery night. The groups had relatively little slow wave sleep, but had a significant increase on the first recovery night. Five Normals and one Insomniac had REM latency of less than 15 min on their first recovery night. This REM latency was found to be significantly correlated with the amount of slow wave sleep on baseline. Decreased REM latency in initial recovery sleep was interpreted as evidence of decreased pressure for slow wave sleep in aging.     

Prolonged effects of 24-h total sleep deprivation on sleep and sleep EEG in the rat

Long-term effects of 24-h sleep deprivation (SD) on sleep and sleep EEG were analyzed in male rats during 4 recovery days (Rec). An increase of total sleep time and non-rapid eye-movement (NREM) sleep was present during Rec 1-4, and of REM sleep in Rec 1 and in the dark periods of Rec 2 and 3. After the initial increase of slow-wave activity (SWA, mean EEG power density in the 0.75-4.0 Hz range) in NREM sleep, SWA declined below baseline until Rec 3. Sleep continuity was increased in Rec 1. The persistent effects of SD which are probably due to homeostatic and circadian facets of sleep regulation, must be taken into account in the design of SD studies.     

One night of sleep deprivation decreases treadmill endurance performance

The aim was to test the hypothesis that one night of sleep deprivation will impair pre-loaded 30 min endurance performance and alter the cardio-respiratory, thermoregulatory and perceptual responses to exercise. Eleven males completed two randomised trials separated by 7 days: once after normal sleep (496 (18) min: CON) and once following 30 h without sleep (SDEP). After 30 h participants performed a 30 min pre-load at 60% $ \dot{V}{\text{O}}_{2\max } $ followed by a 30 min self-paced treadmill distance test. Speed, RPE, core temperature (T _re), mean skin temperature (T _sk), heart rate (HR) and respiratory parameters ( $ \dot{V}{\text{O}}_{2} $ , $ \dot{V}{\text{CO}}_{2} $ , $ \dot{V}{\text{E}} $ , RER pre-load only) were measured. Less distance (P = 0.016, d = 0.23) was covered in the distance test after SDEP (6037 (759) 95%CI 5527 to 6547 m) compared with CON (6224 (818) 95%CI 5674 to 6773 m). SDEP did not significantly alter T _re at rest or thermoregulatory responses during the pre-load including heat storage (0.8°C) and T _sk. With the exception of raised $ \dot{V}{\text{O}}_{2} $ at 30 min on the pre-load, cardio-respiratory parameters, RPE and speed were not different between trials during the pre-load or distance test (distance test mean HR, CON 174 (12), SDEP 170 (13) beats min^?1: mean RPE, CON 14.8 (2.7), SDEP 14.9 (2.6)). In conclusion, one night of sleep deprivation decreased endurance performance with limited effect on pacing, cardio-respiratory or thermoregulatory function. Despite running less distance after sleep deprivation compared with control, participants’ perception of effort was similar indicating that altered perception of effort may account for decreased endurance performance after a night without sleep.