Sleep Deprivation Condition Research Articles

Sleep deprivation impairs binding of information with its context.

Binding information to its context in long-term memory is critical for many tasks, including memory tasks and decision making. Failure to associate information to its context could be an important aspect of sleep deprivation effects on cognition, but little is known about binding problems from being sleep-deprived at the time of encoding. We studied how sleep deprivation affects binding using a well-established paradigm testing the ability to remember auditorily presented words (items) and their speakers (source context). In a laboratory study, 68 healthy young adults were randomly assigned to total sleep deprivation or a well-rested control condition. Participants completed an affective item and source memory task twice: once after 7-hour awake during baseline and again 24 hours later, after nearly 31 hours awake in the total sleep deprivation condition or 7 hours awake in the control condition. Participants listened to negative, positive, and neutral words presented by a male or female speaker and were immediately tested for recognition of the words and their respective speakers. Recognition of items declined during sleep deprivation, but even when items were recognized accurately, recognition of their associated sources also declined. Negative items were less bound with their sources than positive or neutral items, but sleep deprivation did not significantly affect this pattern. Our findings indicate that learning while sleep-deprived disrupts the binding of information to its context independent of item valence. Such binding failures may contribute to sleep deprivation effects on tasks requiring the ability to bind new information together in memory.

Sleep contributes to preference for novel food odours in Drosophila melanogaster

The importance of sleep in maintaining cognitive functions such as learning and memory has been reported in both vertebrates and invertebrates. Previous studies demonstrated that sleep deprivation impaired the olfactory memory retention of fruit flies as described in the classical conditioning paradigm. Here, we show that sleep deprivation leads to a preference for the odours of the rearing environment in Drosophila melanogaster. Flies whose sleep had been disturbed with periodic rotation stimuli during night-time preferred apple cider vinegar (ACV) to broth, while this preference was lower in flies without sleep deprivation and those rotated during daytime. Experiments using single odours showed an increase in responses to ACV due to sleep deprivation. These results suggest that sleep functions in food odour preference. Flies grown on medium supplemented with ACV showed greater preference for ACV, and those grown with broth supplementation showed a greater preference for broth under sleep-deprived conditions. These results suggest that flies with night-time sleep deprivation become attached to the environment on which they have developed, and that sleep contributes to preference for novel food odours. This study offers an approach to investigating the interaction between sleep and neural disorders concerning cognitive deficits towards novel stimuli.

Sleep deprivation reduces vagal tone during an inspiratory endurance task in humans.

Sleep deprivation alters inspiratory endurance by reducing inspiratory motor output. Vagal tone is involved in exercise endurance. This study aimed to investigate the effect of sleep deprivation on vagal tone adaptation in healthy subjects performing an inspiratory effort. Vagal tone was assessed using Heart Rate Variability normalized units of frequency domain component HF (high frequency) before, at the start, and the end of an inspiratory loading trial performed until exhaustion by 16 volunteers after one night of sleep deprivation and one night of normal sleep, where sleep deprivation reduced the inspiratory endurance by half compared to the normal sleep condition (30 min vs 60 min). At rest, heart rate was similar in sleep deprivation and normal sleep conditions. In normal sleep condition, heart rate increased during inspiratory loading task; this increase was greater in sleep deprivation condition. In normal sleep condition, vagal tone increased at the beginning of the trial. This vagal tone increase was absent in sleep deprivation condition. Sleep deprivation abolished vagal tone response to inspiratory load, possibly contributing to a higher heart rate during the trial and to a reduced inspiratory endurance. NCT02725190.

Post-Training Sleep Modulates Topographical Relearning-Dependent Resting State Activity.

Continuation of experience-dependent neural activity during offline sleep and wakefulness episodes is a critical component of memory consolidation. Using functional magnetic resonance imaging (fMRI), offline consolidation effects have been evidenced probing behavioural and neurophysiological changes during memory retrieval, i.e., in the context of task practice. Resting state fMRI (rsfMRI) further allows investigating the offline evolution of recently learned information without the confounds of online task-related effects. We used rsfMRI to investigate sleep-related changes in seed-based resting functional connectivity (FC) and amplitude of low frequency fluctuations (ALFF) after spatial navigation learning and relearning. On Day 1, offline resting state activity was measured immediately before and after topographical learning in a virtual town. On Day 4, it was measured again before and after relearning in an extended version of the town. Navigation-related activity was also recorded during target retrieval, i.e., online. Participants spent the first post-training night under regular sleep (RS) or sleep deprivation (SD) conditions. Results evidence FC and ALFF changes in task-related neural networks, indicating the continuation of navigation-related activity in the resting state. Although post-training sleep did not modulate behavioural performance, connectivity analyses evidenced increased FC after post-training SD between navigation-related brain structures during relearning in the extended environment. These results suggest that memory traces were less efficiently consolidated after post-learning SD, eventually resulting in the use of compensatory brain resources to link previously stored spatial elements with the newly presented information.

Disruption of Circadian Transcriptome in Lung by Acute Sleep Deprivation.

Inadequate sleep prevails in modern society and it impairs the circadian transcriptome. However, to what extent acute sleep deprivation (SD) has impact on the circadian rhythms of peripheral tissues is not clear. Here, we show that in mouse lung, a 10-h acute sleep deprivation can alter the circadian expression of approximately 3,000 genes. We found that circadian rhythm disappears in genes related to metabolism and signaling pathways regulating protein phosphorylation after acute sleep deprivation, while the core circadian regulators do not change much in rhythmicity. Importantly, the strong positive correlation between mean expression and amplitude (E-A correlation) of cycling genes has been validated in both control and sleep deprivation conditions, supporting the energetic cost optimization model of circadian gene expression. Thus, we reveal that acute sleep deprivation leads to a profound change in the circadian gene transcription that influences the biological functions in lung.

The impact of the wake maintenance zone on attentional capacity, physiological drowsiness, and subjective task demands during sleep deprivation.

We aimed to investigate the impact of the Wake Maintenance Zone (WMZ) on measures of drowsiness, attention, and subjective performance under rested and sleep deprived conditions. We studied 23 healthy young adults (18 males; mean age=25.41±5.73years) during 40hr of total sleep deprivation under constant routine conditions. Participants completed assessments of physiological drowsiness (EEG-scored slow eye movements and microsleeps), sustained attention (PVT), and subjective task demands every two hours, and four-hourly ocular motor assessment of inhibitory control (inhibition of reflexive saccades on an anti-saccade task). Tests were analyzed relative to dim light melatonin onset (DLMO); the WMZ was defined as the 3hr prior to DLMO, and the preceding 3hr window was deemed the pre-WMZ. The WMZ did not mitigate the adverse impact of ~37hr sleep deprivation on drowsiness, sustained attention, response inhibition, and self-rated concentration and difficulty, relative to rested WMZ performance (~13hr of wakefulness). Compared to the pre-WMZ, though, the WMZ improved measures of sustained attention, and subjective concentration and task difficulty, during sleep deprivation. Cumulatively, these results expand on previous work by characterizing the beneficial effects of the WMZ on operationally-relevant indices of drowsiness, inhibitory attention control, and self-rated concentration and task difficulty relative to the pre-WMZ during sleep deprivation. These results may inform scheduling safety-critical tasks at more optimal circadian times to improve workplace performance and safety.

Altered frontal connectivity after sleep deprivation predicts sustained attentional impairment: A resting-state functional magnetic resonance imaging study.

A series of studies have shown that sleep loss impairs one's capability for sustained attention. However, the underlying neurobiological mechanism linking sleep loss with sustained attention has not been elucidated. The present study aimed to investigate the effect of sleep deprivation on the resting-state brain and explored whether the magnitude of vigilance impairment after acute sleep deprivation can be predicted by measures of spontaneous fluctuations and functional connectivity. We implemented resting-state functional magnetic resonance imaging with 42 participants under both normal sleep and 24-hr sleep-deprivation conditions. The amplitude of low-frequency fluctuations (ALFF) and functional connectivity was used to investigate the neurobiological change caused by sleep deprivation, and the psychomotor vigilance task (PVT) was used to measure sustained attention in each state. Correlation analysis was used to investigate the relationship between the change in ALFF/functional connectivity and vigilance performance. Sleep deprivation induced significant reductions in ALFF in default mode network nodes and frontal-parietal network nodes, while inducing significant increments of ALFF in the bilateral thalamus, motor cortex, and visual cortex. The increased ALFF in the visual cortex was correlated with increased PVT lapses. Critically, decreased frontal-thalamus connectivity was correlated with increased PVT lapses, while increased frontal-visual connectivity was correlated with increased PVT lapses. The findings indicated that acute sleep deprivation induced a robust alteration in the resting brain, and sustained attentional impairment after sleep deprivation could be predicted by altered frontal connectivity with crucial neural nodes of stimulus input, such as the thalamus and visual cortex.

Alteration of fear behaviors in sleep-deprived adolescent rats: increased fear expression and delayed fear extinction

ABSTRACT Disruption of sleep due to acute or chronic stress can lead to changes in emotional memory processing. Sleep disturbances are highly prevalent in post-traumatic stress disorder (PTSD), but still, the contribution of sleep deprivation on the susceptibility to PTSD has received little attention. To determine whether rapid eye movement sleep deprivation (SD) alters the development of fear expression or fear-associated memory impairment in adolescent rats, we performed animal emotional behavior tests using an SD animal model with the flowerpot technique. SD rats showed an increase in locomotor activity frequency and a decrease in sucrose consumption compared to control rats. An increase in freezing behavior during shock trials was observed in SD rats. Noticeably, it was observed that when applying the SD condition after fear stimuli exposure, fear extinction was delayed more in SD rats than in control rats. Overall, these results indicate that SD in adolescent rats leads to increased locomotor activity and anhedonic behavior, as well as increased fear expression and delayed fear extinction, suggesting that SD would lead to increased severity of PTSD-like phenotype.

Sleep Deprivation and Sleep-Onset Insomnia are Associated with Blunted Physiological Reactivity to Stressors.

Military operations often involve intense exposure to stressors combined with acute sleep deprivation, while military personnel also experience high prevalence of chronic sleep deficiency from insomnia and other sleep disorders. However, the impact of acute and chronic sleep deficiency on physiologic stressor responses is poorly understood. In a controlled laboratory study with normal sleepers and individuals with chronic sleep-onset insomnia, we measured responses to an acute stressor administered in a sleep deprivation condition or a control condition. Twenty-two adults (aged 22-40 years; 16 females)-11 healthy normal sleepers and 11 individuals with sleep-onset insomnia-completed a 5-day (4-night) in-laboratory study. After an adaptation day and a baseline day, subjects were assigned to a 38-hour total sleep deprivation (TSD) condition or a control condition; the study ended with a recovery day. At 8:00 PM after 36 hours awake in the sleep deprivation condition or 12 hours awake in the control condition, subjects underwent a Maastricht Acute Stress Test (MAST). Salivary cortisol was measured immediately before the MAST at 8:00 PM, every 15 minutes after the MAST from 8:15 PM until 9:15 PM, and 30 minutes later at 9:45 PM. Baseline salivary cortisol was collected in the evening of the baseline day. Additionally, before and immediately upon completion of the MAST, self-report ratings of affect and pain were collected. The MAST elicited a stressor response in both normal sleepers and individuals with sleep-onset insomnia, regardless of the condition, as evidenced by increases in negative affect and pain ratings. Relative to baseline, cortisol levels increased immediately following the MAST, peaked 30 minutes later, and then gradually returned to pre-MAST levels. At the cortisol peak, there was a significant difference across groups and conditions, reflecting a pronounced blunting of the cortisol response in the normal sleepers in the TSD condition and the sleep-onset insomnia group in both the TSD and control conditions. Blunted stressor reactivity as a result of sleep deficiency, whether acute or chronic, may reflect reduced resiliency attributable to allostatic load and may put warfighters at increased risk in high-stakes, rapid response scenarios.

An Adaptive EEG Feature Extraction Method Based on Stacked Denoising Autoencoder for Mental Fatigue Connectivity.

Mental fatigue is a common psychobiological state elected by prolonged cognitive activities. Although, the performance and the disadvantage of the mental fatigue have been well known, its connectivity among the multiareas of the brain has not been thoroughly studied yet. This is important for the clarification of the mental fatigue mechanism. However, the common method of connectivity analysis based on EEG cannot get rid of the interference from strong noise. In this paper, an adaptive feature extraction model based on stacked denoising autoencoder has been proposed. The signal to noise ratio of the extracted feature has been analyzed. Compared with principal component analysis, the proposed method can significantly improve the signal to noise ratio and suppress the noise interference. The proposed method has been applied on the analysis of mental fatigue connectivity. The causal connectivity among the frontal, motor, parietal, and visual areas under the awake, fatigue, and sleep deprivation conditions has been analyzed, and different patterns of connectivity between conditions have been revealed. The connectivity direction under awake condition and sleep deprivation condition is opposite. Moreover, there is a complex and bidirectional connectivity relationship, from the anterior areas to the posterior areas and from the posterior areas to the anterior areas, under fatigue condition. These results imply that there are different brain patterns on the three conditions. This study provides an effective method for EEG analysis. It may be favorable to disclose the underlying mechanism of mental fatigue by connectivity analysis.

Evidence of sleep duration and weekend sleep recovery impact on suicidal ideation in adolescents with allergic rhinitis.

Sleep problems are common in allergic rhinitis (AR) and are a modifiable risk factor for suicidal ideation. However, the effect of sleep duration and weekend catch-up sleep (WCUS)-sleep time on weekends that exceeds sleep time on weekdays-on suicidal ideation for adolescents with AR is unknown. The objective of this study was to explore whether sleep duration and WCUS have an impact on suicidal ideation among adolescents with AR. From the annual Korean Youth Risk Behavior Web-Based Surveys (completed from 2013-2017), data were obtained from a stratified, multistage, clustered sample. Using self-reported questionnaires, students provided doctor-diagnosed AR and sleep time. Among 134,417 and 262,653 adolescents with and without AR, respectively, those with AR compared with those without AR had more sleep dissatisfaction (46.6% vs 40.8%), slept less (sleep duration: 6.71 ± 1.37 hours vs 7.01 ± 1.48 hours), and had longer WCUS (3.46 ± 0.11 hours vs 2.11 ± 0.14 hours). After adjustment, the odds ratio of patients with sleep dissatisfaction was a 1.22 (95% confidence interval, 1.17-1.28) times higher risk of suicidal ideation than in those with sleep satisfaction. For average sleep duration (defining 7-8 hours as the reference), the odds ratio of short sleep (≤ 5 hours) was 1.45 (95% confidence interval, 1.32-1.53). Notably, long WCUS (≥ 2 hours) was significantly associated with decreased suicidal ideation (odds ratio, 0.85; 95% confidence interval, 0.81-0.92). Although further research is needed to clarify this association, under the condition of sleep deprivation, WCUS at a certain extent may be associated with a low risk for suicidal ideation in adolescents with AR. Kim CW, Jeong SC, Hwang SW, Jo SH, Kim SH. Evidence of sleep duration and weekend sleep recovery impact on suicidal ideation in adolescents with allergic rhinitis. J Clin Sleep Med. 2021;17(8):1521-1532.

The effect of situation awareness on driving performance in young sleep-deprived drivers

This study aims to investigate how situation awareness (SA) when driving in sleep-deprived condition mediates the effect of sleep deprivation and driving performance in young drivers. Fifteen male students (mean age 21.1 ± 0.8 years) underwent two 45-min driving simulation sessions in random counterbalanced order: one in the morning after approximately seven hours sleep (normal-sleep condition) and another one in the morning after 24 h sleep deprivation (sleep-deprived condition). SA was measured using quantitative analysis of situation awareness (QASA). Driving performance was measured in terms of the number of collisions. Here we find that SA and driving performance decrement when driving in sleep-deprived condition. Compared to normal-sleep condition, driving in sleep-deprived condition impaired SA (p = 0.024) and driving performance (p = 0.006). The mediation analysis shows that the decrement of driving performance is predicted by sleep deprivation (p = 0.021) and SA (p = 0.041). These results indicate that SA partially mediates the effect of sleep deprivation on driving performance. SA decrement in sleep-deprived condition impairs driving performance that can pose a danger to safety-critical action during driving in young drivers.

Sleeping Sickness Disrupts the Sleep-Regulating Adenosine System.

Patients with sleeping sickness, caused by the parasite Trypanosoma brucei, have disruptions in both sleep timing and sleep architecture. However, the underlying cause of these sleep disturbances is not well understood. Here, we assessed the sleep architecture of male mice infected with T. brucei and found that infected mice had drastically altered sleep patterns. Interestingly, T. brucei-infected mice also had a reduced homeostatic sleep response to sleep deprivation, a response modulated by the adenosine system. We found that infected mice had a reduced electrophysiological response to an adenosine receptor antagonist and increased adenosine receptor gene expression. Although the mechanism by which T. brucei infection causes these changes remains to be determined, our findings suggest that the symptoms of sleeping sickness may be because of alterations in homeostatic adenosine signaling.SIGNIFICANCE STATEMENT Sleeping sickness is a fatal disease that disrupts the circadian clock, causes disordered temperature regulation, and induces sleep disturbance. To examine the neurologic effects of infection in the absence of other symptoms, in this study, we used a mouse model of sleeping sickness in which the acute infection was treated but brain infection remained. Using this model, we evaluated the effects of the sleeping sickness parasite, Trypanosoma brucei, on sleep patterns in mice, under both normal and sleep-deprived conditions. Our findings suggest that signaling of adenosine, a neuromodulator involved in mediating homeostatic sleep drive, may be reduced in infected mice.

Abstract P017: Increased Sodium Excretion And Urinary Output During Acute Human Sleep Deprivation

Introduction: Insufficient sleep contributes to an increased risk (e.g. ~60%) of hypertension. While BP is influenced by renal regulation of sodium and water, the underlying mechanism involved the modulation of renin-angiotensin-aldosterone-system (RAAS) by sleep deprivation is unknown. This project investigated the RAAS regulation of water and salt balance (e.g. urine output, sodium excretion) during prolonged sleep deprivation in humans. Methods: Twenty-six subjects (35±1 yrs; 9 women) completed a highly controlled 7-day in hospital study. They were randomly assigned to an 88-h total sleep deprivation (TSD; N=17) condition or an 8-h/night sleep control (SC; N=9) condition. Twenty-four-hour urinary output was collected from baseline (Day 2) to recovery (Day 7). Water and sodium intake were controlled and data were collected. The 24-h sodium excretion value (mmol) was calculated by multiplying the concentrations of sodium in the urine by the urinary volume. Frequent blood samples were collected throughout the experimental period in this study. Results: There was a significant interaction effect of TSD on sodium excretion and urinary output (condition x day, p<0.05). Both TSD and SC groups showed continuous increases in sodium excretion during experimental period compared to baseline (p<0.05). The increases in TSD were significantly higher compared to SC (condition x day, p<0.05). In addition, there was a dose dependent effect of TSD on sodium excretion (i.e. p<0.05 for 48-h TSD compared to 24-h TSD). Diet and fluid intake were controlled and there was no interaction effect for TSD on 24-h water intake or oral sodium intake (condition x day, p>0.05). Urinary output significantly increased from baseline, to 24-h and 72-h (p<0.05) during TSD, but remained at baseline levels throughout days in SC group. Preliminary plasma renin activity analyses (assays ongoing) showed a decreasing statistical trend during TSD compared to baseline (p=0.058). Conclusion: Prolonged TSD significantly increases sodium excretion and urinary output from the body compared to control group, despite similar water and sodium intake levels between two groups. In addition, the increases of sodium excretion are also dose dependent during TSD.

The influence of acute partial sleep deprivation on liking, choosing and consuming high- and low-energy foods

A wealth of cross-sectional studies found a link between sleep deprivation and food-related outcomes like energy intake and BMI. Recent experimental studies suggest that this link is causal. However, the mechanisms through which sleep deprivation influences intake remain unclear. Here, we tested two prevailing hypotheses: that sleep deprivation leads to 1) increased food reward sensitivity and 2) decreased food-related self-control.In a within-subject study (n = 60 normal-weight females), we compared outcome measures under normal sleep and partial sleep deprivation conditions. Our outcome measures were 1) proxies for food reward sensitivity – liking of high and low energy foods, 2) binary food choices ranging in level of self-control conflict, and 3) intake of high and low energy foods. Eye-movements during food choice were measured with an eye-tracker to gain insights in implicit food choice processes.Food reward sensitivity outcomes showed a lower liking of low energy foods after partial sleep deprivation. More high energy foods were chosen after partial sleep deprivation independent of the level of self-control conflict. Intake of high energy foods was higher in the partial sleep deprivation condition. Lastly, the number of gaze switches between high and low energy foods, an implicit measure of conflict in choice, was lower in the high-conflict trials after sleep deprivation than after a normal night sleep.To conclude, the increased intake of high energy foods after sleep deprivation may be driven by a decreased liking of low energy foods, rather than an increased liking of high energy foods. Further, sleep deprivation may affect self-control conflict detection as indicated by a lower number of gaze switches between food options.

The association between REM sleep and decision-making: Supporting evidences

Studies suggest that REM sleep is important for the maintenance of prefrontal cortex functioning. Therefore, reducing REM sleep may have an impact on cognitive functions such as impulse control and decision-making processes. This study examined the association between impulsiveness and sensation seeking personality traits, REM sleep and performance on a decision-making computer task following a habitual night of sleep and a partial sleep deprivation (PSD) condition with advanced wake-up time. Eighteen young adults participated in two experimental conditions: a control (habitual bedtime and wake time) and a 50% PSD with an advanced wake time. Impulsiveness and sensation seeking personality traits were measured with a personality inventory (NEO-PI-3), sleep was assessed using standard polysomnography and the Iowa Gambling Task (IGT) was completed at noon following each sleep condition. Results showed that when sleep deprived, participants choose more often to play riskier decks of cards during the last half of the IGT. Results also showed that REM sleep duration and REM sleep deprivation were associated with riskier decisions on the IGT. Moreover, impulsiveness was associated with riskier decisions after a normal night of sleep. These findings suggest that REM sleep duration and impulsiveness are important factors to consider while investigating decision-making processes under conditions of uncertainty and risk.

Electroencephalographic Markers of Idiopathic Hypersomnia: Where We are and Where We are Going

Idiopathic hypersomnia is a poorly defined nosological entity and has important phenotype heterogeneity. Moreover, diagnosing idiopathic hypersomnia is challenging as patients can report significant symptoms but may not meet diagnostic criteria on standard objective tests. Advanced analyses of electroencephalographic (EEG) activity could provide objective markers of idiopathic hypersomnia and explain part of its pathophysiology and heterogeneity. In fact, the EEG signal recorded during wakefulness and sleep not only captures sleep macroarchitecture but also homeostatic sleep process efficiency, strength of neural synchrony during sleep, sleep consolidation, and changes in cognitive processes. In this review, we will present current and potential markers of idiopathic hypersomnia, with a focus on sleep propensity. We will also discuss EEG changes occurring in sleep deprivation conditions and recovery nights, as well as those observed in other central hypersomnolence conditions, namely narcolepsy type-1 and type-2. Among EEG markers studied in sleep deprivation and narcolepsy are those derived from sleep macroarchitecture (sleep consolidation, sleep stage proportion, sleep-stage transitions, sleep onset in rapid-eye movement sleep) and microarchitecture (slow-wave activity, spindles), spectral analysis of the waking electroencephalographic signal, and cognitive event–related potentials. To date, no clear objective EEG markers of idiopathic hypersomnia exist, as studies were generally performed on small samples, used heterogeneous protocols (including changes of diagnostic criteria that occurred over time), and most of them focused on more traditional macroarchitecture sleep analyses. Based on studies of sleep deprivation and narcolepsy, further studies are needed to understand the EEG signal in idiopathic hypersomnia. Future studies should take advantage of the richness and the complexity of the EEG signal and verify whether subgroups of hypersomniac patients exist.

Interpersonal brain synchronization with instructor compensates for learner's sleep deprivation in interactive learning

Recent advances shifted the focus on single-brain functioning toward two-brain communication during learning interactions, following the demonstration that interpersonal brain synchronization (IBS) can track instructor-learner information exchange. Here, we investigated (i) whether sleep deprivation (SD) that potentially impacts both social interactions and learning abilities modulates IBS, and (ii) conversely whether and to what extent IBS might compensate for SD-related learning deficits. Instructors (always with regular sleep, RS) were asked to teach numerical reasoning strategies to learners (either SD or RS), during which the activity of both brains was simultaneously recorded using functional near-infrared spectroscopy (fNIRS). SD learners initially performed below their baseline level, worse than RS learners, but learning improvement was comparable between RS and SD conditions after learning with the instructor. IBS within the instructor-learner dyads was higher in the SD (vs. RS) condition in the left inferior frontal cortex. In addition, clustered IBS (estimated by nonnegative matrix factorization) was correlated with performance improvement. Finally, Granger Causality analyses revealed biased causality with higher instructor-to-learner than learner-to-instructor directionality in brain signal processing. Together, these results indicate that SD-related learning deficits can to some extent be compensated via interactions with an instructor, as reflected by increased IBS and preserved learning ability. It suggests an essential role of the instructor in driving synchrony between teaching and SD learning brains during interactions.

0208 The Effect of Mastication on Psychomotor Vigilance Performance

Abstract Introduction Sustained attention is important for optimal neurobehavioral performance, but many biological and environment factors (e.g., circadian rhythm, distraction) may cause sustained attention deficits. Mastication (chewing) has been suggested to provide a countermeasure to sustained attention deficits. To investigate this, we conducted a randomized, within-subjects, cross-over study of sustained attention with a mastication condition and a control condition. Methods N=58 adults (ages 18–45; 38 females) completed a 5h in-laboratory study. Subjects entered the laboratory at 09:00. Following training on performance tasks, they had a 1h break before beginning the first of two test bouts at 11:00. Each test bout was 40min long and included subjective rating scales, the Sustained Attention to Response Task, and the Psychomotor Vigilance Test (PVT). Here we focus on PVT lapses of attention (RT > 500 ms), false starts, and mean reaction time (RT) as measures of sustained attention. In between test bouts, subjects had a 1h break inside the laboratory. During one of the two test bouts, subjects were instructed to chew a piece of gum at a steady, comfortable rate. Mastication activity was verified via electromyography (EMG). Half of the sample was assigned to the mastication condition during the first test bout, the other half during the second test bout. Results Controlling for order of conditions, there were no significant differences between conditions for PVT lapses (F1,56=0.40, P=0.54) or false starts (F1,56=0.10, P=0.80). Mean RT was higher in the mastication condition by 8.9±2.5ms (F1,56 =12.68, P<0.001). Conclusion Using this test paradigm, we were unable to detect any significant improvement in PVT performance, although mastication resulted in a very small increase in mean RT. However, subjects were not sleep-deprived, distracted, or otherwise perturbed. A follow-up study under conditions of sleep deprivation and/or with longer task duration may provide further insight into the countermeasure potential of mastication. Support Mars Wrigley Confectionery, U.S., LLC

0297 Relationship Between Sleepiness Symptoms Questionnaire Ratings and Psychomotor Vigilance Performance in a Total Sleep Deprivation Study

Abstract Introduction While measuring the neurobehavioral consequences of sleepiness is arguably best done with performance tasks providing objective assessments of impairment, this often proves challenging in real-world operational settings. Self-report instruments measuring subjective sleepiness provide a practical alternative, but field studies generally fail to show high correlation between objective and subjective assessments of impairment. The Sleepiness Symptoms Questionnaire (SSQ) is a self-report instrument developed to address this issue by asking about observable symptoms of sleepiness and (motor vehicle driving) performance impairment. In a laboratory sleep deprivation study, we compared SSQ sleepiness ratings to performance impairment on a 10min psychomotor vigilance test (PVT). Methods N=12 healthy normal sleepers (ages 21-39y, 6 females) participated in a 4-day in-laboratory study. After a baseline day (9h time in bed; 22:00-07:00), subjects underwent 38h total sleep deprivation (TSD) followed by a recovery day (9h time in bed; 22:00-07:00). As part of neurobehavioral testing throughout the experiment, subjects completed the SSQ and PVT back to back at 6.5h, 14.5h, 22.5h, and 30.5h TSD, and 6.5h after recovery sleep. Data from one subject were incomplete and discarded prior to analysis. Results As TSD progressed, the SSQ sleepiness ratings and the number of lapses (RTs>500ms) on the PVT were elevated, with sleepiness and performance impairment peaking at 22.5h TSD. Both measures returned to baseline levels after recovery sleep. Mixed-effects analysis of covariance showed moderate correlation between SSQ ratings and PVT lapses (r=0.44, F1,43=24.1, p<0.001). Conclusion Self-reported sleepiness on the SSQ reflected the expected homeostatic and circadian changes in sleep pressure during TSD and following recovery sleep, as did PVT performance impairment. The moderate correlation between subjective ratings on the SSQ, with its emphasis on observable sleepiness symptoms, and objective impairment on the PVT suggests that the SSQ may be a reasonably reliable instrument for measuring sleepiness under conditions of acute sleep deprivation. Support Jazz Pharmaceuticals