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.     

Impaired motor memory for a pursuit rotor task following Stage 2 sleep loss in college students

SUMMARY  It has recently been reported that selective REM sleep deprivation (REMD) in college students results in memory impairment of the application of a set of rules in a logic task, but not recall of a paired associate task. The present experiments were designed to examine the effects of Total Sleep Deprivation (TSD) and (REMD) following acquisition of a pure motor task, the pursuit rotor. In Experiment 1, subjects ( N = 90) were exposed to TSD for one of several nights following training. Results showed that TSD on the same night as training resulted in poorer performance on retest one week later. In Experiment 2, subjects ( N = 42) were exposed to various kinds of sleep deprivation on the night of task acquisition. One group was subjected to REMD. Other groups included a non-REM awakening control group (NREMA), a TSD group, a normally rested Control group and a group allowed the first 4h of sleep in the night before being subjected to TSD (LH-TSD) for the rest of the night. Results showed the REMD and Control groups to have excellent memory for this task while the TSD and LH - TSD subjects had significantly poorer memory for the task. The NREMA group showed a slight, but not significant deficit. It was concluded that Stage 2 sleep, rather than REM sleep was the important stage of sleep for efficient memory processing of the pursuit rotor task.     

Effects of sleep deprivation on memory in mice: role of state-dependent learning

Study Objectives:

A considerable amount of experimental evidence suggests that sleep plays a critical role in learning/memory processes. In addition to paradoxical sleep, slow wave sleep is also reported to be involved in the consolidation process of memories. Additionally, sleep deprivation can induce other behavioral modifications, such as emotionality and alternations in locomotor activity in rodents. These sleep deprivation-induced alterations in the behavioral state of animals could produce state-dependent learning and contribute, at least in part, to the amnestic effects of sleep deprivation. The aim of the present study was to examine the participation of state-dependent learning during memory impairment induced by either paradoxical sleep deprivation (PSD) or total sleep deprivation (TSD) in mice submitted to the plus-maze discriminative avoidance or to the passive avoidance task.

Design:

Paradoxical sleep deprivation (by the multiple platform method) and total sleep deprivation (by the gentle handling method) were applied to animals before training and/or testing.

Conclusions:

Whereas pre-training or pre-test PSD impaired retrieval in both memory models, pre-training plus pre-test PSD counteracted this impairment. For TSD, pre-training, pre-test, and pre-training plus pre-test TSD impaired retrieval in both models. Our data demonstrate that PSD- (but not TSD-) memory deficits are critically related to state-dependent learning.

Citation:

Patti CL; Zanin KA; Sanday L; Kameda SR; Fernandes-Santos L; Fernandes HA; Andersen ML; Tufik S; Frussa-Filho R. Effects of sleep deprivation on memory in mice: role of state-dependent learning. SLEEP 2010;33(12):1669-1679.     

Sleep deprivation, cognitive performance, and hormone therapy in postmenopausal women

OBJECTIVE: To study the effects of sleep deprivation on cognitive performance in postmenopausal women and to evaluate whether hormone therapy (HT) has a modifying effect on coping. DESIGN: Twenty-six postmenopausal women, aged 58 to 72 years (mean 64 years), volunteered for the study (HT users, n = 16; nonusers, n = 10). They spent four consecutive nights in the sleep laboratory. The cognitive tests were performed three times: after the baseline night, after one night of sleep deprivation, and after the rebound night. The cognitive measures included visual episodic memory, visuomotor performance, verbal attention, and shared attention. RESULTS: The practice effect typically occurring in cognitive tests was blunted during sleep deprivation, which indicated deterioration of performance. At rebound, performance improved in visual episodic memory (immediate recall P < 0.01; delayed recall P < 0.05), visuomotor performance (P < 0.001), verbal attention (P < 0.0001), and shared attention (P < 0.05). HT users performed better than nonusers in the visual episodic memory test (P < 0.05) and in one of three subtests of shared attention (cancellation P = 0.040). Otherwise hormone therapy did not influence the results. CONCLUSIONS: In postmenopausal women, sleep deprivation impaired visual functions and attention. However, this effect was not prolonged because after one rebound night the performance was improved, compared with baseline. Hormone therapy did not modify the cognitive performance during sleep deprivation.     

Effects of Sleep Deprivation on Dissociated Components of Executive Functioning

Study Objectives:

We studied the effects of sleep deprivation on executive functions using a task battery which included a modified Sternberg task, a probed recall task, and a phonemic verbal fluency task. These tasks were selected because they allow dissociation of some important executive processes from non-executive components of cognition.

Design:

Subjects were randomized to a total sleep deprivation condition or a control condition. Performance on the executive functions task battery was assessed at baseline, after 51 h of total sleep deprivation (or no sleep deprivation in the control group), and following 2 nights of recovery sleep, at fixed time of day (11:00). Performance was also measured repeatedly throughout the experiment on a control task battery, for which the effects of total sleep deprivation had been documented in previously published studies.

Setting:

Six consecutive days and nights in a controlled laboratory environment with continuous behavioral monitoring.

Participants:

Twenty-three healthy adults (age range 22–38 y; 11 women). Twelve subjects were randomized to the sleep deprivation condition; the others were controls.

Results:

Performance on the control task battery was considerably degraded during sleep deprivation. Overall performance on the modified Sternberg task also showed impairment during sleep deprivation, as compared to baseline and recovery and compared to controls. However, two dissociated components of executive functioning on this task—working memory scanning efficiency and resistance to proactive interference—were maintained at levels equivalent to baseline. On the probed recall task, resistance to proactive interference was also preserved. Executive aspects of performance on the phonemic verbal fluency task showed improvement during sleep deprivation, as did overall performance on this task.

Conclusion:

Sleep deprivation affected distinct components of cognitive processing differentially. Dissociated non-executive components of cognition in executive functions tasks were degraded by sleep deprivation, as was control task performance. However, the executive functions of working memory scanning efficiency and resistance to proactive interference were not significantly affected by sleep deprivation, nor were dissociated executive processes of phonemic verbal fluency performance. These results challenge the prevailing view that executive functions are especially vulnerable to sleep loss. Our findings also question the idea that impairment due to sleep deprivation is generic to cognitive processes subserved by attention.

Citation:

Tucker AM; Whitney P; Belenky G; Hinson JM; Van Dongen HPA. Effects of sleep deprivation on dissociated components of executive functioning. SLEEP 2010;33(1):47-57.     

Emotional working memory during sustained wakefulness

In the present study we investigated whether one night of sleep deprivation can affect working memory (WM) performance with emotional stimuli. Twenty‐five subjects were tested after one night of sleep deprivation and after one night of undisturbed sleep at home. As a second aim of the study, to evaluate the cumulative effects of sleep loss and of time‐of‐day changes on emotional WM ability, the subjects were tested every 4 h, from 22:00 to 10:00 hours, in four testing sessions during the sleep deprivation period (deprivation sessions: D1, D2, D3 and D4). Subjects performed the following test battery: Psychomotor Vigilance Task, 0‐back task, 2‐back task and an ‘emotional 2‐back task’ with neutral, positive and negative emotional pictures selected from the International Affective Picture System. Results showed lower accuracy in the emotional WM task when the participants were sleep‐deprived relative to when they had slept, suggesting the crucial role of sleep for preserving WM ability. In addition, the accuracy for the negative pictures remains stable during the sessions performed from 22:00 to 06:00 hours (D1, D2 and D3), while it drops at the D4 session, when the participants had accumulated the longest sleep debt. It is suggested that, during sleep loss, attentional and WM mechanisms may be sustained by the higher arousing characteristics of the emotional (negative) stimuli.     

The effects of one night of sleep deprivation on known-risk and ambiguous-risk decisions

Sleep deprivation has been shown to alter decision-making abilities. The majority of research has utilized fairly complex tasks with the goal of emulating 'real-life' scenarios. Here, we use a Lottery Choice Task (LCT) which assesses risk and ambiguity preference for both decisions involving potential gains and those involving potential losses. We hypothesized that one night of sleep deprivation would make subjects more risk seeking in both gains and losses. Both a control group and an experimental group took the LCT on two consecutive days, with an intervening night of either sleep or sleep deprivation. The control group demonstrated that there was no effect of repeated administration of the LCT. For the experimental group, results showed significant interactions of night (normal sleep versus total sleep deprivation, TSD) by frame (gains versus losses), which demonstrate that following as little as 23 h of TSD, the prototypical response to decisions involving risk is altered. Following TSD, subjects were willing to take more risk than they ordinarily would when they were considering a gain, but less risk than they ordinarily would when they were considering a loss. For ambiguity preferences, there seems to be no direct effect of TSD. These findings suggest that, overall, risk preference is moderated by TSD, but whether an individual is willing to take more or less risk than when well-rested depends on whether the decision is framed in terms of gains or losses.     

Behavioral and genetic effects promoted by sleep deprivation in rats submitted to pilocarpine-induced status epilepticus

The interaction between sleep deprivation and epilepsy has been well described in electrophysiological studies, but the mechanisms underlying this association remain unclear. The present study evaluated the effects of sleep deprivation on locomotor activity and genetic damage in the brains of rats treated with saline or pilocarpine-induced status epilepticus (SE). After 50 days of pilocarpine or saline treatment, both groups were assigned randomly to total sleep deprivation (TSD) for 6 h, paradoxical sleep deprivation (PSD) for 24 h, or be kept in their home cages. Locomotor activity was assessed with the open field test followed by resection of brain for quantification of genetic damage by the single cell gel electrophoresis (comet) assay. Status epilepticus induced significant hyperactivity in the open field test and caused genetic damage in the brain. Sleep deprivation procedures (TSD and PSD) did not affect locomotor activity in epileptic or healthy rats, but resulted in significant DNA damage in brain cells. Although PSD had this effect in both vehicle and epileptic groups, TSD caused DNA damage only in epileptic rats. In conclusion, our results revealed that, despite a lack of behavioral effects of sleep deprivation, TSD and PSD induced genetic damage in rats submitted to pilocarpine-induced SE.     

White Matter Differences Predict Cognitive Vulnerability to Sleep Deprivation

Objectives:

In other disciplines, white matter (WM) differences have been linked to cognitive impairments. This study sets out to clarify whether similar microstructural differences in WM tracts predict a person''s cognitive vulnerability to the effects of total sleep deprivation (TSD).

Design:

Participants completed a simple visual-motor task both before and after 24 h of TSD. Using a median split on the percent change in accuracy from pre-TSD to post-TSD, participants were separated into susceptibility groups. A diffusion tensor MR imaging (DTI) scan was acquired from each participant, and fractional anisotropy (FA) was calculated, examined across the brain, and compared between susceptibility groups.

Setting:

University of Texas at Austin.

Participants:

Thirty-two West Point cadets (9 females, 23 males) between 19 and 25 years of age.

Results:

Participant susceptibility to TSD was correlated with lower FA values in multiple regions of white matter, including the genu of corpus callosum and ascending and longitudinal white matter pathways. Significantly higher FA values in those less vulnerable to TSD, indicating increased neural connectivity and WM organization, may moderate the cognitive effects of sleep deprivation.

Conclusions:

Differences in distributed WM pathways reflect, and may contribute to, a person''s ability to function effectively when sleep deprived. The widespread nature of this effect supports previous views that TSD has a global effect on brain functioning.

Citation:

Rocklage M; Williams V; Pacheco J; Schnyer DM. TitleTitleTitle. SLEEP 2009;32(8):1100-1103.     

Disruptive effects of rapid eye movement sleep deprivation on long-term memory

The fact that sleep is associated with very active endogenous neural (chemical and electrical) processes, suggests that these processes may be involved in the maintenance of long-term memory storage. The present experiments were designed to examine the hypothesis that rapid eye movement (REM) sleep deprivation will produce impairment of long-term memory. Mice deprived of REM sleep for 3, 5 or 7 continuous days, during the interval between a one-trial inhibitory avoidance training experience and a subsequent retention test, displayed a temporary retrograde amnesia when tested 30 min or three hr following termination of REM deprivation. The mice did not recover from the amnesia if electroconvulsive shock was administered immediately following the interval of REM sleep deprivation. In a further study, the generality of these findings was obtained by depriving mice of REM sleep during the interval between a discrimination training experiment in a black-white T-maze and the subsequent retention test.     

Real‐time individualization of the unified model of performance

Existing mathematical models for predicting neurobehavioural performance are not suited for mobile computing platforms because they cannot adapt model parameters automatically in real time to reflect individual differences in the effects of sleep loss. We used an extended Kalman filter to develop a computationally efficient algorithm that continually adapts the parameters of the recently developed Unified Model of Performance (UMP) to an individual. The algorithm accomplishes this in real time as new performance data for the individual become available. We assessed the algorithm's performance by simulating real‐time model individualization for 18 subjects subjected to 64 h of total sleep deprivation (TSD) and 7 days of chronic sleep restriction (CSR) with 3 h of time in bed per night, using psychomotor vigilance task (PVT) data collected every 2 h during wakefulness. This UMP individualization process produced parameter estimates that progressively approached the solution produced by a post‐hoc fitting of model parameters using all data. The minimum number of PVT measurements needed to individualize the model parameters depended upon the type of sleep‐loss challenge, with ~30 required for TSD and ~70 for CSR. However, model individualization depended upon the overall duration of data collection, yielding increasingly accurate model parameters with greater number of days. Interestingly, reducing the PVT sampling frequency by a factor of two did not notably hamper model individualization. The proposed algorithm facilitates real‐time learning of an individual's trait‐like responses to sleep loss and enables the development of individualized performance prediction models for use in a mobile computing platform.     

Total sleep deprivation augments balloon angioplasty-induced neointimal hyperplasia in rats

Sleep deprivation has been shown to be associated with an increase in inflammation that is also involved in the development of neointimal hyperplasia (or restenosis). The purpose of this study was to investigate whether total sleep deprivation (TSD) would worsen neointimal formation by balloon injury. Sixteen rats were randomly allocated into the following four groups: group 1, balloon angioplasty alone; group 2, TSD prior to angioplasty; group 3, angioplasty before TSD; and group 4, TSD before and after angioplasty. Total sleep deprivation was induced by the disc-over-water method, and balloon angioplasty was performed in the carotid artery. Histopathological analysis and assay of cytokines were applied to evaluate the effects of TSD in this study. Total sleep deprivation significantly increased the ratio of postinjury neointima-to-media area in groups 2, 3 and 4 (all P < 0.01) compared with group 1. Additionally, in all groups with TSD administration the serum level of interleukin 10 was also markedly decreased on day 3 after angioplasty injury (P < 0.05 or P < 0.01). Our findings suggest that perioperative TSD can significantly augment neointimal hyperplasia of the carotid artery in rats, which may be partly caused by a TSD-induced effect in suppressing the serum level of the anti-inflammatory cytokine, interleukin 10.     

Modafinil activates cortical and subcortical sites in the sleep-deprived state

SUBJECT OBJECTIVES: To assess the effect of the wake-promoting drug modafinil on working memory and brain activation in the executive network, following a single night of sleep deprivation. DESIGN: Randomized, placebo-controlled, 4-arm, double-blind evaluation of a single 200-mg dose of modafinil on working memory (1-, 2-, and 3-back)-related functional brain activation and performance following overnight sleep deprivation. SETTING: General Clinical Research Center, Biomedical Imaging Center. SUBJECTS: Eight medication-free men, aged 21 to 35 years. Interventions: Overnight sleep deprivation, single-dose 200-mg modafinil, functional magnetic resonance imaging MEASUREMENTS AND RESULTS: Brain activation patterns and regional signal intensity based on the blood-oxygen level-dependent signal were assessed. The following reaction times were used as measures of performance: (1) attention in the scanner before functional scanning, (2) "back" responses during the active-task block, and (3) attention during the baseline task block. Contrast of activation maps among conditions revealed sleep-deprivation and drug effects, and their interactions. Performance in the deprived state was enhanced by modafinil only at an intermediate (2-back) level of task difficulty and was associated with the recruitment of increased cortical activation volumes. Strong and consistent individual differences in performance were noted on the working memory tasks. CONCLUSIONS: Modafinil effectively counters the adverse effects of overnight sleep deprivation on working memory but only when task difficulty is moderate, recruiting extensive areas in the executive network to do so. Interindividual differences in working-memory performance are stable trait characteristics.     

The effect of a REM sleep deprivation procedure on different aspects of memory function in humans

Previous studies have suggested that memory is dependent on the occurrence of REM sleep. Research has mainly focused on two distinct types of memory function, declarative and procedural, and it seems that the latter may more directly depend on REM sleep. Memory consolidation has been more investigated than acquisition, maintenance, and recall, despite the fact that sleep may affect flow of information into/from storage. Moreover, tests have often been limited to stimuli within only one modality (usually visual or verbal). This study aimed to clarify the role of REM sleep in memory by investigating aspects of memory function, processing, and modality in the same experimental setting. Tests of acquisition and consolidation of multiple aspects of memory function within the visual and verbal modalities were administrated to subjects before and after REM sleep deprivation. Results show that test performance was not affected by REM sleep deprivation.     

Relations between depressed mood and vocal parameters before, during and after sleep deprivation: a circadian rhythm study

The mechanism underlying improvement after total sleep deprivation (TSD) was studied in 14 major depressed patients. The suggestions that (1) circadian processes and/or (2) dimensions of arousal may play a role in the response to TSD were investigated. Diurnal variation of depressed mood and of mood- and arousal-related vocal parameters was studied in relation to the effect of TSD on depressed mood and vocal parameters. During 3 baseline days, during TSD and 2 days after TSD vocal parameters and depressed mood were assessed 6 and 3 times daily respectively. The mean fundamental frequency (frequency of vocal fold vibration, F0) (presumably reflecting aspects of arousal) as well as the range of the F0 (proposed to reflect sadness) showed a clear circadian pattern with a peak at about 4.00 p.m. TSD affected the circadian organization of the mean F0 and advanced the peak of the curve. After one night of subsequent sleep this effect disappeared. In addition, improvement after TSD coincided with an increase of the mean F0. The diurnal variation of mood before TSD predicted the mood response to TSD, whereas diurnal variation of vocal parameters did not. Moreover, circadian changes in vocal parameters were not related to changes in depressed mood. These findings suggest that the diurnal variations in mood and vocal parameters are regulated by different mechanisms. Data support the presumption that circadian as well as arousal processes are involved in the mood response to TSD. Circadian changes in vocal parameters due to TSD are not likely to reflect changes in the biological clock.     

Assessing the effect of verbal working memory load on visuo-spatial exogenous orienting

The aim of this study was to assess whether or not loading verbal working memory (WM) affects the exogenous orienting of visuo-spatial attention. Visuo-spatial exogenous orienting was measured under low/high WM load conditions by means of an orthogonal spatial cuing paradigm. Participants had to discriminate the elevation (up versus down) of a visual target preceded by a peripheral spatially-nonpredictive visual cue presented on either the left or right. This elevation discrimination task was carried out in-between a verbal WM test, in which a sequence of six digits (to be remembered for report at the end of the trial) was presented either in numerically ascending or random order (i.e., low and high load conditions, respectively). Participants made significantly more recall errors in the high load than in the low load condition, demonstrating that the verbal WM load manipulation had been effective. However, WM load did not interact with visuo-spatial exogenous orienting (i.e., comparable cuing effects were reported in both load conditions). These results are consistent with the view that peripheral visual onsets automatically capture spatial attention, regardless any concurrent increase of verbal WM load.     

Effects of total sleep deprivation on components of top-down attentional control using a flexible attentional control task

Sleep deprivation consistently decreases vigilant attention, which can lead to difficulty in performing a variety of cognitive tasks. However, sleep-deprived individuals may be able to compensate for degraded vigilant attention by means of top-down attentional control. We employed a novel task to measure the degree to which individuals overcome impairments in vigilant attention by using top-down attentional control, the Flexible Attentional Control Task (FACT). The FACT is a two-choice task that has trials with valid, invalid, and neutral cues, along with an unexpected switch in the probability of cue validity about halfway in the task. The task provides indices that isolate performance components reflecting vigilant attention and top-down attentional control. Twelve healthy young adults completed an in-laboratory study. After a baseline day, the subjects underwent 39 hours of total sleep deprivation (TSD), followed by a recovery day. The FACT was administered at 03:00, 11:00, and 19:00 during sleep deprivation (TSD condition) and at 11:00 and 19:00 after baseline sleep and at 11:00 after recovery sleep (rested condition). When rested, the subjects demonstrated both facilitation and interference effects on cued trials. While sleep deprived, the subjects showed vigilant attention deficits on neutral cue trials, and an impaired ability to reduce these deficits by using predictive contextual cues. Our results indicate that the FACT can dissociate vigilant attention from top-down attentional control. Furthermore, they show that during sleep deprivation, contextual cues help individuals to compensate partially for impairments in vigilant attention, but the effectiveness of top-down attentional control is diminished.     

The neural basis of the psychomotor vigilance task

STUDY OBJECTIVE: To identify brain regions underlying the fastest and slowest reaction times on the Psychomotor Vigilance task (PVT) under well-rested conditions, as well as brain regions related to particularly poor performance after sleep deprivation. DESIGN: Subjects took the PVT twice while undergoing functional magnetic resonance imaging: once 12 hours after waking from a normal night of sleep and once after 36 hours of total sleep deprivation (TSD). Session order was counterbalanced. SETTING: UCSD J. Christian Gillin Laboratory for Sleep and Chronobiology (the sleep core of the General Clinical Research Center) and UCSD Magnetic Resonance Institute. PATIENTS OR PARTICIPANTS: Twenty right-handed healthy adults (8 women; age = 27.4 +/- 6.7 years; education = 15.6 +/- 1.5 years). MEASUREMENTS AND RESULTS: After a normal night of sleep, optimal performance was related to greater cerebral responses within a cortical sustained attention network and the cortical and subcortical motor systems. Slow reaction times, particularly after TSD, were associated with greater activity in the "default mode network" consisting of frontal and posterior midline regions. CONCLUSIONS: Optimal performance on the PVT appears to rely on activation both within the sustained attention system and within the motor system. Poor performance following TSD may result from a disengagement from the task and related inattention, and brain regions responsible for this localize within midline structures shown to be involved in the brain's "default mode." Finally, particularly poor performance after TSD may elicit a subsequent attentional recovery that manifests as greater activation within the same regions normally responsible for fast reaction times.     

Early morning executive functioning during sleep deprivation is compromised by a PERIOD3 polymorphism

STUDY OBJECTIVES: To contrast the effects of total sleep deprivation (TSD) on executive and non-executive function in volunteers homozygous for either the short or long variant of a variable number tandem repeat polymorphism in PERIODS, which is a genetic marker for susceptibility to the negative effect of sleep loss on waking performance. DESIGN: Following two laboratory nights of baseline sleep, both groups underwent an approximately 40-hour constant routine, performing brief tests of executive, memory, attention, and motor function every 2 hours. SETTING: Clinical Research Centre. PARTICIPANTS: Fourteen PER3(4/4) (homozygotes for shorter variant of the gene) and 10 PER3(5/5) (homozygotes for longer variant) healthy, young adults (mean 25.0 +/- 1.0 years). INTERVENTIONS: Total sleep deprivation (approximately 40 hours) following baseline sleep. MEASUREMENTS AND RESULTS: Hormonal assays established that melatonin levels, which reflect circadian phase, reached their midpoint around 04:00 in both genotypes. Cognitive performance deteriorated across the night, and was similar for both genotypes throughout, except 2-4 h after the midpoint of the melatonin rhythm. Only at this time-point and only on tests of executive function (e.g., 3-back, paced visual serial addition task) did PER3(5/5) participants perform reliably worse. Covariance analyses controlling for genotype dependent differences in homeostatic sleep pressure derived from principal component analysis of baseline sleep latency, slow wave sleep and wake after sleep onset largely removed these early morning differences in executive function. CONCLUSIONS: This PER3 polymorphism differentially influences the effects of sleep deprivation on executive and non-executive function in the early morning. These effects appear to be mediated through homeostatic sleep pressure.     

Effect of total sleep deprivation on the dimensional complexity of the waking EEG

STUDY OBJECTIVES: Sleep deprivation can affect the waking EEG that may reflect information processing of the brain. We examined the effect of total sleep deprivation (TSD) on nonlinear dynamics of the waking EEG. DESIGN: Paired-group design. SETTING: A sleep disorders laboratory in a hospital. PARTICIPANTS: Twenty healthy male volunteers. INTERVENTIONS: Waking EEG data were recorded from subjects with eyes closed after (a) an 8-hour night's sleep and (b) TSD for 24 hours. The dimensional complexity (D2), as a nonlinear measure of complexity, of the EEG after a full night sleep were compared with those of the EEG after TSD. MEASUREMENTS AND RESULTS: The sleep-deprived states had lower D2 values at three channels (P4, O2, and C3) than normal states. CONCLUSIONS: TSD results in the decrease of complexity in the brain, which may imply sub-optimal information processing of the cerebral cortex. We suggest that the investigation of the relation between nonlinear dynamics of the waking EEG induced by TSD and cognitive performance may offer fruitful clues for understanding the role of sleep and the effects of sleep deprivation on brain function.