Effects of Sleep Deprivation on Performance during a Change Signal Task with Adaptive Dynamics.

Augmented cognition, which refers to real-time modifications to a human-system interface to improve performance and includes dynamic task environments with automated adaptations, can serve to protect against performance impairment under challenging work conditions. However, the effectiveness of augmented cognition as a countermeasure for performance impairment due to sleep loss is unknown. Here, in a controlled laboratory study, an adaptive version of a Change Signal task was administered repeatedly to healthy adults randomized to 62 h of total sleep deprivation (TSD) or a rested control condition. In the computerized task, a left- or right-facing arrow was presented to start each trial. In a subset of trials, a second arrow facing the opposite direction was presented after a delay. Subjects were to respond within 1000 ms of the trial start by pressing the arrow key corresponding to the single arrow (Go trials) or to the second arrow when present (Change trials). The Change Signal Delay (CSD)-i.e., the delay between the appearance of the first and second arrows-was shortened following incorrect responses and lengthened following correct responses so that subsequent Change trials became easier or harder, respectively. The task featured two distinct CSD dynamics, which produced relatively stable low and high error rates when subjects were rested (Low and High Error Likelihood trials, respectively). During TSD, the High Error Likelihood trials produced the same, relatively high error rate, but the Low Error Likelihood trials produced a higher error rate than in the rested condition. Thus, sleep loss altered the effectiveness of the adaptive dynamics in the Change Signal task. A principal component analysis revealed that while subjects varied in their performance of the task along a single dominant dimension when rested, a second inter-individual differences dimension emerged during TSD. These findings suggest a need for further investigation of the interaction between augmented cognition approaches and sleep deprivation in order to determine whether and how augmented cognition can be relied upon as a countermeasure to performance impairment in operational settings with sleep loss.

Paradoxical effects from stimulus density manipulation provide new insight into the impact of sleep deprivation on PVT performance.

Study Objectives: The psychomotor vigilance test (PVT), a 10-min one-choice reaction time task with random response-stimulus intervals (RSIs) between 2 and 10 s, is highly sensitive to behavioral alertness deficits due to sleep loss. To investigate what drives the performance deficits, we conducted an in-laboratory total sleep deprivation (TSD) study and compared performance on the PVT to performance on a 10-min high-density PVT (HD-PVT) with increased stimulus density and truncated RSI range between 2 and 5 s. We hypothesized that the HD-PVT would show greater impairments from TSD than the standard PVT. Methods: n = 86 healthy adults were randomized (2:1 ratio) to 38 h of TSD (n = 56) or corresponding well-rested control (n = 30). The HD-PVT was administered when subjects had been awake for 34 h (TSD group) or 10 h (control group). Performance on the HD-PVT was compared to performance on the standard PVTs administered 1 h earlier and 1 h later. Results: The HD-PVT yielded approximately 60% more trials than the standard PVT. The HD-PVT had faster mean response times (RTs) and equivalent lapses (RTs > 500 ms) compared to the standard PVT, with no differences between the TSD effects on mean RT and lapses between tasks. Further, the HD-PVT had a dampened time-on-task effect in both the TSD and control conditions. Conclusions: Contrary to expectation, the HD-PVT did not show greater performance impairment during TSD, indicating that stimulus density and RSI range are not primary drivers of the PVT's responsiveness to sleep loss.

Enhancing learning and retention through the distribution of practice repetitions across multiple sessions.

The acquisition and retention of knowledge is affected by a multitude of factors including amount of practice, elapsed time since practice occurred, and the temporal distribution of practice. The third factor, temporal distribution of practice, is at the heart of research on the spacing effect. This research has consistently shown that separating practice repetitions by a delay slows acquisition but enhances retention. The current study addresses an empirical gap in the spacing effects literature. Namely, how does the allocation of a fixed number of practice repetitions among multiple sessions impact learning and retention? To address this question, we examined participants' acquisition and retention of declarative knowledge given different study schedules in which the number of practice repetitions increased, decreased, or remained constant across multiple acquisition sessions. The primary result was that retention depended strongly on the total number of sessions in which an item appeared, but not on how practice repetitions were distributed among those sessions. This outcome was consistent with predictions from a computational cognitive model of skill acquisition and retention called the Predictive Performance Equation (PPE). The success of the model in accounting for the patterns of performance across a large set of study schedules suggests that it can be used to tame the complexity of the design space and to identify schedules to enhance knowledge acquisition and retention.

Pain Catastrophizing Mediates the Relationship Between Pain Intensity and Sleep Disturbances in U.S. Veterans With Chronic Pain.

INTRODUCTION: Veterans with chronic pain frequently report comorbid disruptions in sleep and psychological dysfunction. The purpose of this study was to investigate whether psychological function variables mediate the sleep-pain relationship. Knowledge regarding such contributing factors can inform the development and optimization of treatments for sleep disturbances and pain. MATERIALS AND METHODS: In an IRB-approved, registered clinical trial, we collected objective sleep data from U.S. military Veterans with chronic pain (N = 184, ages 23-81) using wrist actigraphy for 7 days and self-reported survey data assessing sleep quality, pain intensity, and psychological function (depression, anxiety, post-traumatic stress disorder, and pain catastrophizing). We investigated the associations between objectively measured and self-reported sleep quality and self-reported pain intensity. In addition, using parallel mediation analyses, we examined whether psychological function variables mediated these associations. RESULTS: Actigraphy showed suboptimal sleep duration (less than 7 hours) and sleep fragmentation for most participants. Self-reported poor sleep quality and pain intensity were significantly correlated. Pain catastrophizing was found to mediate the association between self-reported sleep quality and pain intensity. CONCLUSIONS: Sleep disturbances in this sample of Veterans with chronic pain included insufficient sleep, fragmented sleep, and perceived poor sleep quality. Analyses suggest that poor perceived sleep quality and pain intensity are mediated via pain catastrophizing. The finding highlights the potential importance of pain catastrophizing in Veterans with chronic pain. Future longitudinal research is needed to determine the extent to which treatments that reduce pain catastrophizing might also improve both sleep and pain outcomes.

Working around the Clock: Is a Person's Endogenous Circadian Timing for Optimal Neurobehavioral Functioning Inherently Task-Dependent?

Neurobehavioral task performance is modulated by the circadian and homeostatic processes of sleep/wake regulation. Biomathematical modeling of the temporal dynamics of these processes and their interaction allows for prospective prediction of performance impairment in shift-workers and provides a basis for fatigue risk management in 24/7 operations. It has been reported, however, that the impact of the circadian rhythm-and in particular its timing-is inherently task-dependent, which would have profound implications for our understanding of the temporal dynamics of neurobehavioral functioning and the accuracy of biomathematical model predictions. We investigated this issue in a laboratory study designed to unambiguously dissociate the influences of the circadian and homeostatic processes on neurobehavioral performance, as measured during a constant routine protocol preceded by three days on either a simulated night shift or a simulated day shift schedule. Neurobehavioral functions were measured every 2 h using three functionally distinct assays: a digit symbol substitution test, a psychomotor vigilance test, and the Karolinska Sleepiness Scale. After dissociating the circadian and homeostatic influences and accounting for inter-individual variability, peak circadian performance occurred in the late biological afternoon (in the "wake maintenance zone") for all three neurobehavioral assays. Our results are incongruent with the idea of inherent task-dependent differences in the endogenous circadian impact on performance. Rather, our results suggest that neurobehavioral functions are under top-down circadian control, consistent with the way they are accounted for in extant biomathematical models.

Trait Interindividual Differences in the Magnitude of Subjective Sleepiness from Sleep Inertia.

In shift work settings and on-call operations, workers may be at risk of sleep inertia when called to action immediately after awakening from sleep. However, individuals may differ substantially in their susceptibility to sleep inertia. We investigated this using data from a laboratory study in which 20 healthy young adults were each exposed to 36 h of total sleep deprivation, preceded by a baseline sleep period and followed by a recovery sleep period, on three separate occasions. In the week prior to each laboratory session and on the corresponding baseline night in the laboratory, participants either extended their sleep period to 12 h/day or restricted it to 6 h/day. During periods of wakefulness in the laboratory, starting right after scheduled awakening, participants completed neurobehavioral tests every 2 h. Testing included the Karolinska Sleepiness Scale to measure subjective sleepiness, for which the data were analyzed with nonlinear mixed-effects regression to quantify sleep inertia. This revealed considerable interindividual differences in the magnitude of sleep inertia, which were highly stable within individuals after both baseline and recovery sleep periods, regardless of study condition. Our results demonstrate that interindividual differences in subjective sleepiness due to sleep inertia are substantial and constitute a trait.

Reversal learning deficits during sleep deprivation: investigating the role of information acquisition failures.

Besides degrading vigilant attention, total sleep deprivation (TSD) impairs reversal learning performance and blunts affective reactions to feedback. Whether these effects are downstream consequences of information acquisition failures from degraded vigilant attention, or distinct from degraded vigilant attention, is unclear. In well-rested individuals we simulated information acquisition failures by masking a portion of trial information in a go/no-go reversal learning task with four conditions: stimulus masking, feedback masking, alternating stimulus/feedback masking, and no-masking control. No condition reproduced the previously documented pattern of TSD effects, suggesting that information acquisition failures cannot fully account for impaired reversal learning and blunted affective reactions during TSD.

DRD2 C957T genotype modulates the time-on-task effect during total sleep deprivation.

Total sleep deprivation (TSD) and time-on-task (TOT), especially in combination, increase cognitive instability and cause performance impairment. There are large inter-individual differences in TSD and TOT effects which, in part, have a genetic basis. Here, we show that the dopamine receptor D2 C957T genetic polymorphism predicts the magnitude of the TOT effect on a psychomotor vigilance test (PVT) during 38 h of TSD. This finding indicates that dopamine availability in the striatum, where the dopamine receptor D2 is most prevalent, influences the TOT effect, suggesting a role for dopaminergic pathways in sustained attention deficits during sleep loss.

Speed/accuracy trade-off in the effects of acute total sleep deprivation on a sustained attention and response inhibition task.

Total sleep deprivation (TSD) is known to impair sustained attention. However, previously reported effects of TSD on response inhibition are mixed. We administered a "stop-signal" variation of the psychomotor vigilance test, which included 25% of trials requiring withholding of a response to assess response inhibition alongside sustained attention. Participants completed the task at baseline and after 34.5 h of wakefulness. Accuracy was not reduced during TSD. However, response times were significantly slower. A speed/accuracy trade-off allowed participants to effectively withhold responses on inhibition trials and conferred resilience of inhibitory control during TSD under conditions of relatively low time pressure.

New insights into the cognitive effects of sleep deprivation by decomposition of a cognitive throughput task.

STUDY OBJECTIVES: A cognitive throughput task known as the Digit Symbol Substitution Test (DSST) (or Symbol Digit Modalities Test) has been used as an assay of general cognitive slowing during sleep deprivation. Here, the effects of total sleep deprivation (TSD) on specific cognitive processes involved in DSST performance, including visual search, spatial memory, paired-associate learning, and motor response, were investigated through targeted task manipulations. METHODS: A total of 12 DSST variants, designed to manipulate the use of specific cognitive processes, were implemented in two laboratory-based TSD studies with N = 59 and N = 26 subjects, respectively. In each study, the Psychomotor Vigilance Test (PVT) was administered alongside the DSST variants. RESULTS: TSD reduced cognitive throughput on all DSST variants, with response time distributions exhibiting rightward skewing. All DSST variants showed practice effects, which were however minimized by inclusion of a pause between trials. Importantly, TSD-induced impairment on the DSST variants was not uniform, with a principal component analysis revealing three factors. Diffusion model decomposition of cognitive processes revealed that inter-individual differences during TSD on a two-alternative forced choice DSST variant were different from those on the PVT. CONCLUSIONS: While reduced cognitive throughput has been interpreted to reflect general cognitive slowing, such TSD-induced impairment appears to reflect cognitive instability, like on the PVT, rather than general slowing. Further, comparisons between task variants revealed not one, but three distinct underlying processes impacted by sleep deprivation. Moreover, the practice effect on the task was found to be independent of the TSD effect and minimized by a task pacing manipulation.

Sleep deprivation, vigilant attention, and brain function: a review.

Vigilant attention is a major component of a wide range of cognitive performance tasks. Vigilant attention is impaired by sleep deprivation and restored after rest breaks and (more enduringly) after sleep. The temporal dynamics of vigilant attention deficits across hours and days are driven by physiologic, sleep regulatory processes-a sleep homeostatic process and a circadian process. There is also evidence of a slower, allostatic process, which modulates the sleep homeostatic setpoint across days and weeks and is responsible for cumulative deficits in vigilant attention across consecutive days of sleep restriction. There are large inter-individual differences in vulnerability to sleep loss, and these inter-individual differences constitute a pronounced human phenotype. However, this phenotype is multi-dimensional; vulnerability in terms of vigilant attention impairment can be dissociated from vulnerability in terms of other cognitive processes such as attentional control. The vigilance decrement, or time-on-task effect-a decline in performance across the duration of a vigilant attention task-is characterized by progressively increasing response variability, which is exacerbated by sleep loss. This variability, while crucial to understanding the impact of sleep deprivation on performance in safety-critical tasks, is not well explained by top-down regulatory mechanisms, such as the homeostatic and circadian processes. A bottom-up, neuronal pathway-dependent mechanism involving use-dependent, local sleep may be the main driver of response variability. This bottom-up mechanism may also explain the dissociation between cognitive processes with regard to trait vulnerability to sleep loss.

Working Time Society consensus statements: Prescriptive rule sets and risk management-based approaches for the management of fatigue-related risk in working time arrangements.

Traditionally, working time arrangements to limit fatigue-related risk have taken a prescriptive approach, which sets maximum shift durations in order to prevent excessive buildup of fatigue (and the associated increased risk) within shifts and sets minimum break durations to allow adequate time for rest and recovery within and/or between shifts. Prescriptive rule sets can be successful when, from a fatigue-related risk standpoint, they classify safe work hours as permitted and unsafe work hours as not permitted. However, prescriptive rule sets ignore important aspects of the biological factors (such as the interaction between circadian and homeostatic processes) that drive fatigue, which are critical modulators of the relationship between work hours and fatigue-related risk. As such, in around-the-clock operations when people must work outside of normal daytime hours, the relationship between regulatory compliance and safety tends to break down, and thus these rule sets become less effective. To address this issue, risk management-based approaches have been designed to regulate the procedures associated with managing fatigue-related risk. These risk management-based approaches are suitable for nighttime operations and a variety of other non-standard work schedules, and can be tailored to the particular job or industry. Although the purpose of these fatigue risk management approaches is to curb fatigue risk, fatigue risk cannot be measured directly. Thus, the goal is not on regulating fatigue risk per se, but rather to put in place procedures that serve to address fatigue before, during, and after potential fatigue-related incidents. Examples include predictive mathematical modeling of fatigue for work scheduling, proactive fatigue monitoring in the workplace, and reactive post-incident follow-up. With different risks and different needs across industries, there is no "one size fits all" approach to managing fatigue-related risk. However, hybrid strategies combining prescriptive rule sets and risk management-based approaches can create the flexibility necessary to reduce fatigue-related risk based on the specific needs of different work environments while maintaining appropriate regulatory oversight.

Sleep Deprivation Diminishes Attentional Control Effectiveness and Impairs Flexible Adaptation to Changing Conditions.

Insufficient sleep is a global public health problem resulting in catastrophic accidents, increased mortality, and hundreds of billions of dollars in lost productivity. Yet the effect of sleep deprivation (SD) on decision making and performance is often underestimated by fatigued individuals and is only beginning to be understood by scientists. The deleterious impact of SD is frequently attributed to lapses in vigilant attention, but this account fails to explain many SD-related problems, such as loss of situational awareness and perseveration. Using a laboratory study protocol, we show that SD individuals can maintain information in the focus of attention and anticipate likely correct responses, but their use of such a top-down attentional strategy is less effective at preventing errors caused by competing responses. Moreover, when the task environment requires flexibility, performance under SD suffers dramatically. The impairment in flexible shifting of attentional control we observed is distinct from lapses in vigilant attention, as corroborated by the specificity of the influence of a genetic biomarker, the dopaminergic polymorphism DRD2 C957T. Reduced effectiveness of top-down attentional control under SD, especially when conditions require flexibility, helps to explain maladaptive performance that is not readily explained by lapses in vigilant attention.

Shift Work: Disrupted Circadian Rhythms and Sleep-Implications for Health and Well-Being.

PURPOSE OF REVIEW: Our 24/7 society is dependent on shift work, despite mounting evidence for negative health outcomes from sleep displacement due to shift work. This paper reviews short- and long-term health consequences of sleep displacement and circadian misalignment due to shift work. RECENT FINDINGS: We focus on four broad health domains: metabolic health; risk of cancer; cardiovascular health; and mental health. Circadian misalignment affects these domains by inducing sleep deficiency, sympathovagal and hormonal imbalance, inflammation, impaired glucose metabolism, and dysregulated cell cycles. This leads to a range of medical conditions, including obesity, metabolic syndrome, type II diabetes, gastrointestinal dysfunction, compromised immune function, cardiovascular disease, excessive sleepiness, mood and social disorders, and increased cancer risk. SUMMARY: Interactions of biological disturbances with behavioral and societal factors shape the effects of shift work on health and well-being. Research is needed to better understand the underlying mechanisms and drive the development of countermeasures.

3-minute smartphone-based and tablet-based psychomotor vigilance tests for the assessment of reduced alertness due to sleep deprivation.

The psychomotor vigilance test (PVT) is widely used to measure reduced alertness due to sleep loss. Here, two newly developed, 3-min versions of the psychomotor vigilance test, one smartphone-based and the other tablet-based, were validated against a conventional 10-min laptop-based PVT. Sixteen healthy participants (ages 22-40; seven males, nine females) completed a laboratory study, which included a practice and a baseline day, a 38-h total sleep deprivation (TSD) period, and a recovery day, during which they performed the three different versions of the PVT every 3 h. For each version of the PVT, the number of lapses, mean response time (RT), and number of false starts showed statistically significant changes across the sleep deprivation and recovery days. The number of lapses on the laptop was significantly correlated with the numbers of lapses on the smartphone and tablet. The mean RTs were generally faster on the smartphone and tablet than on the laptop. All three versions of the PVT exhibited a time-on-task effect in RTs, modulated by time awake and time of day. False starts were relatively rare on all three PVTs. For the number of lapses, the effect sizes across 38 h of TSD were large for the laptop PVT and medium for the smartphone and tablet PVTs. These results indicate that the 3-min smartphone and tablet PVTs are valid instruments for measuring reduced alertness due to sleep deprivation and restored alertness following recovery sleep. The results also indicate that the loss of sensitivity on the 3-min PVTs may be mitigated by modifying the threshold defining lapses.

P2X7 receptors in body temperature, locomotor activity, and brain mRNA and lncRNA responses to sleep deprivation.

The ionotropic purine type 2X7 receptor (P2X7R) is a nonspecific cation channel implicated in sleep regulation and brain cytokine release. Many endogenous rhythms covary with sleep, including locomotor activity and core body temperature. Furthermore, brain-hypothalamic cytokines and purines play a role in the regulation of these physiological parameters as well as sleep. We hypothesized that these parameters are also affected by the absence of the P2X7 receptor. Herein, we determine spontaneous expression of body temperature and locomotor activity in wild-type (WT) and P2X7R knockout (KO) mice and how they are affected by sleep deprivation (SD). We also compare hypothalamic, hippocampal, and cortical cytokine- and purine-related receptor and enzyme mRNA expressions before and after SD in WT and P2X7RKO mice. Next, in a hypothesis-generating survey of hypothalamic long noncoding (lnc) RNAs, we compare lncRNA expression levels between strains and after SD. During baseline conditions, P2X7RKO mice had attenuated temperature rhythms compared with WT mice, although locomotor activity patterns were similar in both strains. After 6 h of SD, body temperature and locomotion were enhanced to a greater extent in P2X7RKO mice than in WT mice during the initial 2-3 h after SD. Baseline mRNA levels of cortical TNF-α and P2X4R were higher in the KO mice than WT mice. In response to SD, the KO mice failed to increase hypothalamic adenosine deaminase and P2X4R mRNAs. Further, hypothalamic lncRNA expressions varied by strain, and with SD. Current data are consistent with a role for the P2X7R in thermoregulation and lncRNA involvement in purinergic signaling.