The effect of sleepiness on performance monitoring: I know what I am doing,but do I care?

The behavioral, cognitive, and psychophysiological effects of extended wakefulness are well known. As time awake increases, errors become more common and are often attributed to lapses in attention. Such lapses can be reflected in the error-related negativity (Ne/ERN), a negative electroencephalogram deflection occurring after errors and is thought to be related to error detection or response conflict. Following the Ne/ERN, a positive deflection (error positivity, Pe) is also observed and is thought to reflect further evaluation of the error. To elicit Ne/ERNs, the Eriksen Flanker Task was administered to 17 women (aged 19-45 years) at two levels of alertness (4 and 20 h awake). After extended wakefulness, participants reported being subjectively sleepier and performing worse, but showed no significant difference in subjective effort. Across alertness conditions, they reported a similar number of subjective errors which closely matched an objective analysis of the errors. The Ne/ERN was not significantly reduced by sleepiness in contrast to the Pe which was reduced. Behavioral slowing after errors was larger in the alert than in the sleepy condition. These results show that after 20 h of wakefulness, individuals are reacting to their errors. However, further evaluation of the error, and remediation of these errors may be impaired despite continued effort.     

错误相关电位的任务诱导模式及其在神经系统疾病中的应用进展

错误相关电位（ErrP）是脑在错误事件后出现的特定脑电电位改变,隶属于事件相关电位。本研究就ErrP的任务诱导模式和其在神经系统疾病中的应用进行归纳总结,首先阐述错误相关负波、错误正波和反馈相关负波这3种ErrP成分的神经来源及其在错误加工中的意义,然后总结当前主要的ErrP任务诱导模式,其次介绍了ErrP在神经系统疾病中的应用,最后对ErrP未来的研究方向和应用趋势作出展望。     

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.     

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.     

Performance monitoring during sleep inertia after a 1‐h daytime nap

Performance monitoring is an essential function involved in the correction of errors. Deterioration of this function may result in serious accidents. This function is reflected in two event‐related potential (ERP) components that occur after erroneous responses, specifically the error‐related negativity/error negativity (ERN/Ne) and error positivity (Pe). The ERN/Ne is thought to be associated with error detection, while the Pe is thought to reflect motivational significance or recognition of errors. Using these ERP components, some studies have shown that sleepiness resulting from extended wakefulness may cause a decline in error‐monitoring function. However, the effects of sleep inertia have not yet been explored. In this study, we examined the effects of sleep inertia immediately after a 1‐h daytime nap on error‐monitoring function as expressed through the ERN/Ne and Pe. Nine healthy young adults participated in two different experimental conditions (nap and rest). Participants performed the arrow‐orientation task before and immediately after a 1‐h nap or rest period. Immediately after the nap, participants reported an increased effort to perform the task and tended to estimate their performance as better, despite no objective difference in actual performance between the two conditions. ERN/Ne amplitude showed no difference between the conditions; however, the amplitude of the Pe was reduced following the nap. These results suggest that individuals can detect their own error responses, but the motivational significance ascribed to these errors might be diminished during the sleep inertia experienced after a 1‐h nap. This decline might lead to overestimation of their performance.     

Odor identification accuracy declines following 24 h of sleep deprivation

Brain imaging studies demonstrate that sleep deprivation reduces glucose metabolism and blood flow in the prefrontal cortex, and such reductions are associated with impairments in cognitive functioning. Although some of the greatest metabolic declines occur within the orbitofrontal cortex, little is known about the effects of sleep loss on the types of processes mediated by this region, including emotion, motivation, feeding, and olfaction. The present study tested odor identification accuracy when individuals were well rested and again following 24 h of wakefulness. Relative to rested baseline performance, sleep-deprived individuals demonstrated a significant decline in the ability to identify specific odors on the Smell Identification Test. This decrement in olfactory functioning occurred concomitantly with slowed psychomotor speed and increased ratings of self-reported sleepiness. Performance on a task that required complex mental set shifting did not change significantly following sleep deprivation, suggesting that the decrements in odor identification could not be attributed to task difficulty. Finally, while there was no relationship between subjective sleepiness and odor identification at rested baseline, greater subjective sleepiness was associated with better odor identification ability following 24 h of sleep loss. Possible implications of these findings are discussed.     

The pendulum technique for paradoxical sleep deprivation in rats

A new technique for paradoxical sleep (PS) deprivation in rats is presented. Animals are prevented from entering into PS by allowing them to sleep for only brief periods of time. This is accomplished by an apparatus which moves the animals' cages backwards and forwards like a pendulum. At the extremes of the motion postural imbalance is produced in the animals forcing them to walk downwards to the other side of their cages. A minimal amount of PS and a moderate amount of slow wave sleep (SWS) were detected during a deprivation period of 72 hrs. Following the deprivation treatment the recovery of sleep was monitored for 3 hrs; at the beginning of the light period for one group and at the beginning of the dark period for a second group. The sleep-waking patterns of two baseline groups were established at the time when the recovery sleep was examined in the deprivation groups. The deprivation treatment resulted in a significant increase in the amount of PS and a significant decrease in the amount of SWS. The extent of PS increase was similar in both deprivation groups, in spite of a large difference in the amount of SWS. The decrease of SWS mainly occurred during recovery sleep in the light. It was observed that sleep in the dark differs from sleep in the light in behavioural aspects.     

Slow-wave sleep deprivation and waking function

SUMMARY  Slow-wave sleep (SWS) has been theorized to be an intense form of nonREM sleep, but selective deprivation of SWS or Stage 4 sleep has not been shown to cause greater decrements in alertness or performance, compared to deprivation or disruption of the other stages of sleep. The present experiment examined the effects of marked SWS deprivation (SD) for two nights, a control sleep disruption (CD) condition in which minutes of SWS were preserved, and a no sleep disruption (ND) condition. Daytime sleepiness was assessed with the multiple sleep latency test (MSLT) and performance was evaluated with the simulated assembly line task (SALT), neither of which was used in previous studies of SWS or Stage 4 sleep deprivation. In agreement with prior studies, two nights of SD did not cause greater daytime sleepiness than did CD, although sleepiness in both conditions was increased compared to the ND condition. In addition, neither SD nor CD caused declines in performance or mood. However, post hoc analysis suggests an interaction between SWS and sleep duration, such that sufficient SWS may tend to prevent adverse effects of mild sleep loss on waking function.     

Unihemispheric sleep deprivation in bottlenose dolphins

SUMMARY  Unihemispheric and bihemispheric sleep deprivation were performed in bottlenose dolphins. One brain hemisphere was capable of being deprived of delta (0.5-3.0 Hz) sleep in the former condition. Here, an increase in sleep pressure was observed during sleep deprivation in the deprived hemisphere. In the recovery sleep, following unihemispheric sleep deprivation, there was a rebound of delta sleep only in the deprived hemisphere. Following bihemispheric sleep deprivation the animals exhibited an increase in delta sleep in both hemispheres.     

Electrophysiological correlates of error correction

Evidence in the literature for the proposed relationship between the error-related negativity (ERN) and error correction is rather limited and inconsistent. We investigated corrective behavior and the ERN in two groups of participants who performed a flanker task. The correction-instructed group was asked to immediately correct all encountered errors. The noninstructed group was unaware that corrective responses were recorded. We found a negative deflection following corrected errors that peaked at 200-240 ms after the error. We refer to this negativity in the ERP waveform as correction-related negativity (CoRN). We assume that the correction-related negativity reflects evaluative functions of the motor system necessary for error corrections. ERN latency and amplitude were modulated by the occurrence and temporal characteristics of immediate corrections. These results are discussed within the framework of current models of performance monitoring.     

Impaired decision making following 49 h of sleep deprivation

Sleep deprivation reduces regional cerebral metabolism within the prefrontal cortex, the brain region most responsible for higher-order cognitive processes, including judgment and decision making. Accordingly, we hypothesized that two nights of sleep loss would impair decision making quality and lead to increased risk-taking behavior on the Iowa Gambling Task (IGT), which mimics real-world decision making under conditions of uncertainty. Thirty-four healthy participants completed the IGT at rested baseline and again following 49.5 h of sleep deprivation. At baseline, volunteers performed in a manner similar to that seen in most samples of healthy normal individuals, rapidly learning to avoid high-risk decks and selecting more frequently from advantageous low-risk decks as the game progressed. After sleep loss, however, volunteers showed a strikingly different pattern of performance. Relative to rested baseline, sleep-deprived individuals tended to choose more frequently from risky decks as the game progressed, a pattern similar to, though less severe than, previously published reports of patients with lesions to the ventromedial prefrontal cortex. Although risky decision making was not related to participant age when tested at rested baseline, age was negatively correlated with advantageous decision making on the IGT, when tested following sleep deprivation (i.e. older subjects made more risky choices). These findings suggest that cognitive functions known to be mediated by the ventromedial prefrontal cortex, including decision making under conditions of uncertainty, may be particularly vulnerable to sleep loss and that this vulnerability may become more pronounced with increased age.     

Effects of age on recovery of body weight following REM sleep deprivation of rats

Chronically enforced rapid eye (paradoxical) movement sleep deprivation (REM-SD) of rats leads to a host of pathologies, of which hyperphagia and loss of body weight are among the most readily observed. In recent years, the etiology of many REM-SD-associated pathologies have been elucidated, but one unexplored area is whether age affects outcomes. In this study, male Sprague-Dawley rats at 2, 6, and 12 months of age were REM sleep-deprived with the platform (flowerpot) method for 10-12 days. Two-month-old rats resided on 7-cm platforms, while 10-cm platforms were used for 6- and 12-month-old rats; rats on 15-cm platforms served as tank controls (TCs). Daily changes in food consumption (g/kg(0.67)) and body weight (g) during baseline, REM-SD or TCs, and post-experiment recovery in home cages were determined. Compared to TCs, REM-SD resulted in higher food intake and decreases in body weight. When returned to home cages, food intake rapidly declined to baseline levels. Of primary interest was that rates of body weight gain during recovery differed between the age groups. Two-month-old rats rapidly restored body weight to pre-REM-SD mass within 5 days; 6-month-old rats were extrapolated by linear regression to have taken about 10 days, and for 12-month-old rats, the estimate was about 35 days. The observation that restoration of body weight following its loss during REM-SD may be age-dependent is in general agreement with the literature on aging effects on how mammals respond to stress.     

Relationships between affect, vigilance, and sleepiness following sleep deprivation

This pilot study examined the relationships between the effects of sleep deprivation on subjective and objective measures of sleepiness and affect, and psychomotor vigilance performance. Following an adaptation night in the laboratory, healthy young adults were randomly assigned to either a night of total sleep deprivation (SD group; n = 15) or to a night of normal sleep (non-SD group; n = 14) under controlled laboratory conditions. The following day, subjective reports of mood and sleepiness, objective sleepiness (Multiple Sleep Latency Test and spontaneous oscillations in pupil diameter, PUI), affective reactivity/regulation (pupil dilation responses to emotional pictures), and psychomotor vigilance performance (PVT) were measured. Sleep deprivation had a significant impact on all three domains (affect, sleepiness, and vigilance), with significant group differences for eight of the nine outcome measures. Exploratory factor analyses performed across the entire sample and within the SD group alone revealed that the outcomes clustered on three orthogonal dimensions reflecting the method of measurement: physiological measures of sleepiness and affective reactivity/regulation, subjective measures of sleepiness and mood, and vigilance performance. Sleepiness and affective responses to sleep deprivation were associated (although separately for objective and subjective measures). PVT performance was also independent of the sleepiness and affect outcomes. These findings suggest that objective and subjective measures represent distinct entities that should not be assumed to be equivalent. By including affective outcomes in experimental sleep deprivation research, the impact of sleep loss on affective function and their relationship to other neurobehavioral domains can be assessed.     

Increased cerebral response during a divided attention task following sleep deprivation

We recently reported that the brain showed greater responsiveness to some cognitive demands following total sleep deprivation (TSD). Specifically, verbal learning led to increased cerebral activation following TSD while arithmetic resulted in decreased activation. Here we report data from a divided attention task that combined verbal learning and arithmetic. Thirteen normal control subjects performed the task while undergoing functional magnetic resonance imaging (FMRI) scans after a normal night of sleep and following 35 h TSD. Behaviourally, subjects showed only modest impairments following TSD. With respect to cerebral activation, the results showed (a) increased activation in the prefrontal cortex and parietal lobes, particularly in the right hemisphere, following TSD, (b) activation in left inferior frontal gyrus correlated with increased subjective sleepiness after TSD, and (c) activation in bilateral parietal lobes correlated with the extent of intact memory performance after TSD. Many of the brain regions showing a greater response after TSD compared with normal sleep are thought to be involved in control of attention. These data imply that the divided attention task required more attentional resources (specifically, performance monitoring and sustained attention) following TSD than after normal sleep. Other neuroimaging results may relate to the verbal learning and/or arithmetic demands of the task. This is the first study to examine divided attention performance after TSD with neuroimaging and supports our previous suggestion that the brain may be more plastic during cognitive performance following TSD than previously thought.     

Photically evoked potentials in the visual cortex following paradoxical sleep deprivation in rats

Immediately following 72 hr of paradoxical sleep (PS) deprivation, the P3-N3 amplitude of the photically evoked response in the visual cortex was measured in waking rats. PS deprivation was achieved instrumentally by one of three different techniques: the classical platform, the multiple platform, or the pendulum technique. For each of the techniques a control condition was run additionally. The PS deprivation effect consisted of a decrement in the P3-N3 amplitude, which was interpreted as indicating an increase in tonic arousal having a depressing influence on cortical excitability. Concomitantly, a relatively large technique effect occurred, in which the difference between the two platform techniques on the one hand, and the pendulum technique on the other, was most apparent. The same factors did not influence behavioural activity taking place during the presentation of photic stimulation, but did during the preceding 5 min adaptation period. Although the present findings are in contrast with previous reports in animals, they may not be inconsistent with the basic idea of the neural excitability hypothesis of PS.     

Effects of sleep deprivation on wound healing

Sleep deprivation is widely regarded as a stressor and has been shown to have significant effects on host defences. Severely sleep-deprived rats develop lesions on their paws and tails, suggesting possible deficits in the healing process. The purpose of this study was to assess the impact of rapid eye-movement (REM) sleep deprivation (RSD) on wound healing in a rat model. Male dark-hooded Long-Evans rats, 2-4 months old, were subjected to dorsal application of two sterile punch biopsies, each 3.5 mm in size. Biopsies were performed either immediately before or immediately after 5 days of sleep deprivation. Wound healing in REM sleep-deprived animals was compared with home cage control and yoked control animals. RSD did not produce differences in the rate of healing, regardless of the timing of the biopsy punch. RSD does not appear to have significant effects on wound healing and thus appears to act differently from other types of stressors on wound healing.     

The effects of total sleep deprivation, selective sleep interruption and sleep recovery on pain tolerance thresholds in healthy subjects

The aim of this study was to compare the effects of total sleep deprivation (TSD), rapid eye movement (REM) sleep and slow wave sleep (SWS) interruption and sleep recovery on mechanical and thermal pain sensitivity in healthy adults. Nine healthy male volunteers (age 26--43 years) were randomly assigned in this double blind and crossover study to undergo either REM sleep or SWS interruption. Periods of 6 consecutive laboratory nights separated by at least 2 weeks were designed as follows: N1 Adaptation night; N2 Baseline night; N3 Total sleep deprivation (40 h); N4 and N5 SWS or REM sleep interruption; N6 Recovery. Sleep was recorded and scored using standard methods. Tolerance thresholds to mechanical and thermal pain were assessed using an electronic pressure dolorimeter and a thermode operating on a Peltier principle. Relative to baseline levels, TSD decreased significantly mechanical pain thresholds (-8%). Both REM sleep and SWS interruption tended to decrease mechanical pain thresholds. Recovery sleep, after SWS interruption produced a significant increase in mechanical pain thresholds (+ 15%). Recovery sleep after REM sleep interruption did not significantly increase mechanical pain thresholds. No significant differences in thermal pain thresholds were detected between and within periods. In conclusion this experimental study in healthy adult volunteers has demonstrated an hyperalgesic effect related to 40 h TSD and an analgesic effect related to SWS recovery. The analgesic effect of SWS recovery is apparently greater than the analgesia induced by level I (World Health Organization) analgesic compounds in mechanical pain experiments in healthy volunteers.     

Effects of two nights sleep deprivation and two nights recovery sleep on response inhibition

This study examined the effects of two nights of total sleep deprivation (TSD) and two nights of recovery sleep on response inhibition. Thirty-eight young, healthy adults performed a Go-NoGo task at 14 : 00 after: (1) a normal night of sleep; (2) each of two consecutive nights of TSD; and (3) each of two consecutive nights of recovery sleep; they also performed the task at 05 : 00 during the first night of sleep deprivation. We hypothesized that TSD would lead to an impaired ability to withhold a response that would be reversed with recovery sleep. Subjects did experience a significant increase in false positive responses throughout all of TSD, errors of omission (i.e. missed 'go' targets) were not significant until after the second night of TSD. Both components (withholding a response and automatic responding) of the task returned to baseline levels after one night of recovery sleep. These data suggest that individuals experience difficulty in withholding an inappropriate response during TSD, even when they are able to attend to the incoming stimuli and respond accurately to appropriate stimuli.     

Effects of adaptogens on granulocytopoiesis during paradoxical sleep deprivation

We studied the effects of extracts from Siberian ginseng, Rhodiola rosea, bergenia, and ginseng (G115) and pantohematogen on granulocytopoiesis after paradoxical sleep deprivation. The effects of adaptogens on the blood system were most pronounced during hyperplasia of granulocytopoiesis. Natural preparations were divided into groups depending on their activity. Extracts of Siberian ginseng and Rhodiola rosea did not modulate granulocytopoiesis. Ginseng G115 extract suppressed granulocytopoiesis. Bergenia extract and pantohematogen produced ambiguous effects on the granulocytic hemopoietic stem.     

Reward prediction error signals associated with a modified time estimation task

The feedback error-related negativity (fERN) is a component of the human event-related brain potential (ERP) elicited by feedback stimuli. A recent theory holds that the fERN indexes a reward prediction error signal associated with the adaptive modification of behavior. Here we present behavioral and ERP data recorded from participants engaged in a modified time estimation task. As predicted by the theory, our results indicate that fERN amplitude reflects a reward prediction error signal and that the size of this error signal is correlated across participants with changes in task performance.