Quantification of Sleepiness: A New Approach

The Stanford Sleepiness Scale (SSS) is a self-rating scale which is used to quantify progressive steps in sleepiness. The present study investigated whether the SSS cross-validates with performance on mental tasks and whether the SSS demonstrates changes in sleepiness with sleep loss. Five college student Ss were given a brief test of memory and the Wilkinson Addition Test in 2 test sessions and The Wilkinson Vigilance Test in 2 other sessions spaced throughout a 16-hr day for 6 days. Ss made SSS ratings every 15 min during their waking activities. On night 4, Ss underwent all night sleep deprivation. On all other nights, Ss were allowed only 8 hrs in bed. Mean SSS ratings correlated r= .68 with performance on the Wilkinson Tests. Discrete SSS ratings correlated r= .47 with performance on the memory test. Moreover, mean baseline SSS ratings were found to be significantly lower than corresponding ratings of the deprivation period.     

Interaction of REM Deprivation and Stage 4 Deprivation With Total Sleep Loss: Experiment 2

To determine whether prior deprivation of stage REM or stage 4 sleep would potentiate the effects of total sleep loss, 7 young adult males were denied REM sleep and 7 were denied stage 4 sleep for 3 nights before 1 night of total sleep loss. Measures of autonomic and EEG activity, mood, anxiety, Rorschach CET and on several performance tasks were obtained during baseline, following stage deprivation, total sleep loss, and during recovery. There were no marked changes in any area following 3 nights of stage REM and stage 4 deprivation. The changes following total sleep loss were similar for both groups. Prior deprivation of stage REM or stage 4 did not potentiate sleep loss effects. Ss who had no stage deprivation prior to 1 night of sleep loss had more impairment following sleep loss than did the Ss of this study.     

Relationship of Rapid Eye Movement Density to the Prior Accumulation of Sleep and Wakefulness

Ocular activity during the REM stage of sleep was studied for the purpose of determining what effect previous sleep and waking would have on the intensity of that activity. Eleven Ss slept to satiation during a 54-hr session and then, after a day of waking, slept for another night. REM density (i.e., number of eye mvts per min of REM period) rose progressively during the first night and morning, and then remained at a high level for the remainder of the 54 hrs; the mean REM density for Night 2 and also for Night 3 was about double the REM density of Night 1. Multiple regression analysis indicated that the amount of prior sleep was positively correlated with REM density whereas the amount of waking was negatively correlated. Peak REM density occurred after a mean of 9.88 hrs of sleep. Thereafter, periods of waking alternated with periods of sleep while the REM density oscillated at its peak level. It was concluded that REM density reflects the output of a sleep-waking negative feedback circuit.     

The Recuperative Effects of REM Sleep and Stage 4 Sleep on Human Performance After Complete Sleep Loss: Experiment 1

Twelve young (17–21 yrs) male Navy recruits volunteered for a sleep loss study. After 4 baseline days, the Ss were completely deprived of sleep for 2 days and nights. Next followed an experimental phase of 2 days and nights after which all Ss received 2 nights of uninterrupted sleep. During the experimental phase, the 4 Ss in the REM-deprived group were aroused whenever they showed signs of REM sleep. The 4 Ss of the stage 4-deprived group were aroused whenever they showed signs of entering stage 4 sleep, and the 4 Ss of the Control group had uninterrupted sleep. All tests (speed and accuracy of addition, speed and accuracy of self-paced vigilance, errors of omission in experimenter paced vigilance, immediate recall of word lists, and mood) showed significant impairment after the first night of complete sleep loss. But during the experimental (sleep-stage-deprivation) and recovery phases, all three groups showed equal rates of recovery. Depriving the S of stage REM or stage 4 during recovery sleep does not affect the recuperation rate. Frequent arousals (50–100 per night) also do not impair recovery. The amount of sleep is probably more important than the kind of sleep.     

Performance and Mood During and After Gradual Sleep Reduction

Long-term gradual sleep reduction effects were investigated on 4 young adult collegiate couples. The battery of assessment tools included a sleep log, Stanford Sleepiness Scale, Profile of Mood States, Feeling Tone Checklist, a measure of circadian oral temperature, Williams Word Memory test, Digit Span test, Wilkinson Auditory Vigilance task, Wilkinson Addition task, Minnesota Multiphasic Personality Inventory, Rapid Alternation task, psychiatric and medical examinations, and a subjective effects questionnnaire. It was concluded that 6–8 months of gradual sleep restriction, down to 4.5–5.5 hrs per night, does not result in behavioral effects measurable by the instruments used. Subjective fatigue appears to be the limiting factor in determining tolerability of gradual sleep restriction. At the end of an additional 12-month follow-up period, total sleep time was still 1–2.5 hrs below baseline, but measures of well-being had returned to baseline levels.     

Effects of different sleep reductions on daytime sleepiness.

This study evaluated the effects of different amounts of sleep and SWS restriction on the ensuing day-time sleepiness. Six healthy selected males, after one adaptation night and an initial 8-hr baseline night, were allowed to sleep 5, 4, 3, 2, and 1 hr with a 1-week interval between conditions. The following day, 4 sleep onset MSLT trials and 2 Wilkinson Auditory Vigilance Task (WAVT) were administered. Before each MSLT, self evaluations of sleepiness and activation on a visual analogue scale (ADAS) were assessed. Each restriction night was followed by an 8-hr recovery night, and a final 8-hr baseline night was recorded. The day after each night the same diurnal tests were repeated. Results indicated a linear increase in the propensity to sleep (MSLT) and of subjective sleepiness as a function of the increase in sleep restrictions. Performance scores (WAVT) showed that vigilance is partially affected by sleep restrictions. For each measure, regression analyses showed that the effect of sleep reduction is better predicted by the total duration of sleep than by the amount of SWS. Correlations between measures were negligible with the exception of those between performance and subjective sleepiness measures.     

Sleep During and After Gradual Sleep Reduction

To determine: 1) the minimum amounts of sleep subjects would tolerate, 2) the changes in EEG sleep measures, and 3) whether subjects would revert to baseline sleep after study termination, 4 couples gradually reduced their sleep. Three couples reduced their TST in 30-min steps from a baseline of 8 hrs and one couple from a baseline of 6.5 hrs. Subjective estimates of sleep time, sleep quality, and mood were collected daily. Home EEG sleep recordings were obtained 3 nights a week. Two of the 8-hr sleepers reduced their sleep to 5.5 hrs, 2 to 5.0 hrs, and 2 reached 4.5 hrs. These 6 subjects continued sleeping 1 to 2.5 hrs below baseline amounts a year after reduction terminated. The 6.5-hr baseline couple reached 5.0 hrs and returned to 6.5 hrs TST during follow-up. Stages W, 2, and REM decreased significantly in absolute amounts. Percentage of stages W and 2 also decreased significantly. REM percent remained constant. Stage 3 was constant while stage 4 increased in both absolute and relative amounts. REM cycle length remained constant. Stage 4 rebound on 7-hr nights was not observed during times of greatest sleep reduction. Occurrences of stage REM within 10 min of stage 1 onset were observed in 2 subjects when their TST was below 6.5 hrs. Our results are consistent with other studies of shortened sleep, indicating that TST is the major determinant of sleep-stage characteristics.     

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.     

Body Movements During Sleep After Sleep Loss

Following 4 baseline nights, 7 Ss were deprived of REM sleep for 3 nights and 7 were deprived of stage 4 sleep. Both groups were then deprived of total sleep for 1 night and then allowed 2 nights of uninterrupted recovery sleep. Compared to baseline nights, on the first recovery night the number of body movements was significantly reduced in all sleep stages and for total sleep. On the second recovery night, the number of movements was back to baseline level. The increased amount of slow-wave sleep (stages 3 and 4) during recovery sleep was not the primary reason for the reduced body motility.     

Cumulative Effects of Sleep Restriction on Daytime Sleepiness

Sleep and daytime sleepiness were evaluated in 10 young adult subjects to determine whether restricting nocturnal step by a constant amount produces cumulative impairment. Subjects were studied for 12 consecutive days, including 3 baseline days with a 10-hr time in bed, 7 days with sleep restricted to 5 hrs, and 2 recovery days. In 5 subjects, recovery included a 10-hr time in bed; in the remaining subject, recovery induced a 5-hr time in bed with a 1-hr daytime nap. Sleepiness was measured using two self-rating scales and the multiple sleep latency test. During sleep restriction, nocturnal stage 2 and REM sleep were reduced and slow wave sleep was unaffected. Stanford Sleepiness Scales showed an immediate increase in daytime sleepiness that reached a plateau after 4 days. An analog sleepiness rating scale showed increased sleepiness after 2 restricted nights and leveled off after the fourth restricted night. The multiple sleep latency tests showed no effect of sleep restriction until the second day, followed by a progressive increase in sleepiness that persisted through the seventh sleep restriction day. During the recovery period, daytime sleepiness returned to basal values on all three measures following one full night of sleep; with a daytime nap, no further cumulative effects of sleep restriction were seen.     

Sleep deprivation and phasic activity of REM sleep: independence of middle-ear muscle activity from rapid eye movements

In the recovery nights after total and partial sleep deprivation there is a reduction of rapid eye movements during REM sleep as compared to baseline nights; recent evidence provided by a selective SWS deprivation study also shows that the highest percentage of variance of this reduction is explained by SWS rebound. The present study assesses whether the reduction of rapid eye movements (REMs) during the recovery night after total sleep deprivation is paralleled by a decrease of middle-ear muscle activity (MEMA), another phasic muscle activity of REM sleep. Standard polysomnography, MEMA and REMs of nine subjects were recorded for three nights (one adaptation, one baseline, one recovery); baseline and recovery night were separated by a period of 40 hours of continuous wake. Results show that, in the recovery night, sleep deprivation was effective in determining an increase of SWS amount and of the sleep efficiency index, and a decrease of stage 1, stage 2, intra-sleep wake, and NREM latencies, without affecting REM duration and latency. However, MEMA frequency during REM sleep did not diminish during these nights as compared to baseline ones, while there was a clear effect of REM frequency reduction. Results indicate an independence of phasic events of REM sleep, suggesting that the inverse relation between recovery sleep after sleep deprivation and REM frequency is not paralleled by a concomitant variation in MEMA frequency.     

The Effects on Subsequent Sleep of an Acute Restriction of Sleep Length

This experiment was designed to test the effects on subsequent sleep of a restriction in sleep length on the previous night. Eight male subjects were studied. After baseline recordings were made, sleep was restricted to either a period between 4-8 am or to a period between 6–8 am. On the night following the restriction of sleep the subjects retired at 11 pm and they were permitted to sleep ad lib in the morning. The restricted sleep periods resulted in differential sleep deprivation. Stages REM and 2 were markedly reduced whereas stages 3 and 4 showed little or no reduction in amount. There were significant reductions in sleep latencies and in the amount of lime spent in stages 0 and 1. The first 8 hrs of ad lib sleep following the 2 restricted sleep periods did not differ in any significant way from the 8 hrs of baseline sleep. When sleep was permitted to continue until the subjects awakened spontaneously, the sleep after the restriction of sleep to‘i hrs was significantly longer and displayed significantly more of stages REM and 2 when compared with the baseline ad lib sleep condition. The ad lib sleep period following the 4 hr condition showed similar changes although the differences were not statistically significant. The significant reductions in stages KEM and 2 during the restricted sleep periods were attributed to the effects of reduced steep length per se. The increases in sleep length and specifically the increases in stages REM and 2 during the ad lib sleep periods were attributed to a differential sleep “debt” accruing from restricted sleep length.     

REM Sleep Interruption: Experimental Shortening of REM Period Duration

This experiment concerns itself with the extent to which psychological factors can influence normal sleep patterns. After 4 baseline nights of uninterrupted sleep, each of 4 Ss was awakened in the course of 2 nights during every REM period about 10 min following each REM onset. Ss, however, were not REM deprived. The interruption nights were followed by a recovery night of uninterrupted sleep. All nights were consecutive. The results show that during recovery nights all Ss continued to have significantly shorter than normal REM periods by going into NREM sleep at about the time they would have been awakened during the interruption nights. These shortened REM periods occurred even during early morning hours, when REM periods normally become longer. Arguments are advanced that this finding may best be explained in terms of a conditioned avoidance response.     

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.     

Sleepiness after glucose in narcolepsy

SUMMARY  The issue of whether a high carbohydrate intake affects sleepiness and sleep variables has been studied in normals but not in patients suffering from narcolepsy, despite anecdotal evidence that sugars may facilitate sleepiness in this population. This study investigated whether the intake of 50g glucose exacerbated sleepiness in narcolepsy subjects. A double-blind cross-over study, involving 12 narcolepsy subjects and 12 matched controls, measured behaviour after a light lunch supplemented with a drink of either 50g glucose or placebo (artificially sweetened drink). The main dependent variables were the performance and EEG measures from the Wilkinson Auditory Vigilance Task (WAVT) and sleep variables from a 45 minute nap. The results indicate that in the narcolepsy subjects glucose was associated with decreased wake duration, reduced sleep onset latency and more spontaneous and induced sleep stage changes during the WAVT, while the nap revealed an increased intensity of sleepiness after glucose as measured by the Polygraphic Score of Sleepiness. Eleven of the twelve narcolepsy subjects showed increased REM duration in the nap after glucose. The findings are discussed in relation to serotonin synthesis, basal sleepiness and possible irregularities in the action of insulin.     

Biperiden administration during REM sleep deprivation diminished the frequency of REM sleep attempts.

Sixteen subjects were assigned to a group using either placebo or biperiden, with eight subjects in each group. Both groups were studied for one acclimatization night, one baseline night, four nights of rapid eye movement (REM) sleep deprivation and two recovery nights. All the subjects received either placebo or 4 mg biperiden 1 hour before sleep during the four nights of REM sleep deprivation. During the baseline and the recovery nights both groups received placebo capsules. The results showed that REM sleep time during the REM sleep deprivation was reduced by 70-75% below the baseline night in both groups. The number of attempts to enter REM sleep was significantly reduced by biperiden as compared to placebo for each of the four REM sleep deprivation nights. Because the total sleep time in the biperiden group was reduced, the number of REM sleep attempts was corrected by the total sleep time. The adjusted number of REM sleep attempts was also significantly reduced in the biperiden group. REM sleep latency showed a reduction in the placebo group, whereas in the biperiden group REM sleep latency was unchanged throughout the deprivation nights. In the recovery night REM sleep time was increased in both groups, with no differences between the groups. The REM sleep latency showed a reduction in the first recovery night in both groups that persisted through the second recovery night. The above findings support the role of biperiden as a REM sleep suppressive drug.     

Modafinil, d-amphetamine and placebo during 64 hours of sustained mental work. II. Effects on two nights of recovery sleep

Polysomnograms were obtained from 37 volunteers, before (baseline) and after (two consecutive recovery nights) a 64-h sleep deprivation, with (d-amphetamine or modafinil) or without (placebo) alerting substances. The drugs were administered at 23.00 hours during the first sleep deprivation night (after 17.5 h of wakefulness), to determine whether decrements in cognitive performance would be prevented; at 05.30 hours during the second night of sleep deprivation (after 47.5 h of wakefulness), to see whether performance would be restored; and at 15.30 hours during the third day of continuous work, to study effects on recovery sleep. The second recovery night served to verify whether drug-induced sleep disturbances on the first recovery night would carry over to a second night of sleep. Recovery sleep for the placebo group was as expected: the debt in slow-wave sleep (SWS) and REM sleep was paid back during the first recovery night, the rebound in SWS occurring mainly during the first half of the night, and that of REM sleep being distributed evenly across REM sleep episodes. Recovery sleep for the amphetamine group was also consistent with previously published work: increased sleep latency and intrasleep wakefulness, decreased total sleep time and sleep efficiency, alterations in stage shifts, Stage 1, Stage 2 and SWS, and decreased REM sleep with a longer REM sleep latency. For this group, REM sleep rebound was observed only during the second recovery night. Results for the modafinil group exhibited decreased time in bed and sleep period time, suggesting a reduced requirement for recovery sleep than for the other two groups. This group showed fewer disturbances during the first recovery night than the amphetamine group. In particular, there was no REM sleep deficit, with longer REM sleep episodes and a shorter REM latency, and the REM sleep rebound was limited to the first REM sleep episode. The difference with the amphetamine group was also marked by less NREM sleep and Stage 2 and more SWS episodes. No REM sleep rebound occurred during the second recovery night, which barely differed from placebo. Hence, modafinil allowed for sleep to occur, displayed sleep patterns close to that of the placebo group, and decreased the need for a long recovery sleep usually taken to compensate for the lost sleep due to total sleep deprivation.     

Performance and Sleepiness as a Function of Frequency and Placement of Sleep Disruption

Eight normal young adult sleepers spent 4 nonconsecutive weeks in the laboratory. Each week consisted of a baseline night followed by 2 consecutive nights of disrupted sleep, followed by 2 recovery nights. Disruption conditions included: a) brief awakening after each minute of accumulated sleep, b) brief awakening after each 10 min of accumulated sleep, c) 2.5 hrs of normal sleep followed by a brief awakening at each sleep onset, and d) total sleep deprivation. Morning testing revealed that all disruption conditions decreased sleep latency in a morning nap test. Performance after 1-min disruptions approximated that seen after total sleep loss. Performance decrements were less in the 10-min condition and least in the 2.5-hr sleep condition. Performance under baseline and total sleep loss conditions was used to predict performance during the sleep deprivation condition using four sleep stage rules. Total time asleep and total time asleep minus stage 1 predicted performance poorly. Total SWS plus REM predicted performance best but could not differentiate the 10-min and 2.5-hr conditions. Therefore, it was concluded that the data were most parsimoniously explained by the Sleep Continuity Theory—i.e., that periods of uninterrupted sleep in excess of 10 min are required for sleep to be restorative.     

Exercise before bed does not impact sleep inertia in young healthy males

Sleep inertia is the transitional state marked by impaired cognitive performance and reduced vigilance upon waking. Exercising before bed may increase the amount of slow‐wave sleep within the sleep period, which has previously been associated with increased sleep inertia. Healthy males (n = 12) spent 3 nights in a sleep laboratory (1‐night washout period between each night) and completed one of the three conditions on each visit – no exercise, aerobic exercise (30 min cycling at 75% heart rate), and resistance exercise (six resistance exercises, three sets of 10 repetitions). The exercise conditions were completed 90 min prior to bed. Sleep was measured using polysomnography. Upon waking, participants completed five test batteries every 15 min, including the Karolinska Sleepiness Scale, a Psychomotor Vigilance Task, and the Spatial Configuration Task. Two separate linear mixed‐effects models were used to assess: (a) the impact of condition; and (b) the amount of slow‐wave sleep, on sleep inertia. There were no significant differences in sleep inertia between conditions, likely as a result of the similar sleep amount, sleep structure and time of awakening between conditions. The amount of slow‐wave sleep impacted fastest 10% reciprocal reaction time on the Psychomotor Vigilance Task only, whereby more slow‐wave sleep improved performance; however, the magnitude of this relationship was small. Results from this study suggest that exercise performed 90 min before bed does not negatively impact on sleep inertia. Future studies should investigate the impact of exercise intensity, duration and timing on sleep and subsequent sleep inertia.     

Awakening Latency From Sleep For Meaningful and Non-Meaningful Stimuli

Personally significant and non-significant low intensity sound stimuli were used to determine awakening latencies from sleep stages REM and 2. Latency was measured from stimulus onset to a) the sleeper's own acknowledgement of waking, and b) alpha rhythm onset. Both stimuli were presented twice, once in each sleep stage, to 8 Ss. Voluntary response latencies in REM were shorter than in stage 2 (p <.025) but no difference was found for the latency of alpha rhythm onset. The personally significant stimulus, however, caused a significantly shorter awakening latency using both criteria. The results suggest that perceptual thresholds are low in both sleep stages 2 and REM but that the ability or willingness to organize a response is greater in REM sleep.