David F. Dinges

Neurocognitive Consequences of Sleep Deprivation

Sleep deprivation is associated with considerable social, financial, and health-related costs, in large measure because it produces impaired cognitive performance due to increasing sleep propensity and instability of waking neurobehavioral functions. Cognitive functions particularly affected by sleep loss include psychomotor and cognitive speed, vigilant and executive attention, working memory, and higher cognitive abilities. Chronic sleep-restriction experiments--which model the kind of sleep loss experienced by many individuals with sleep fragmentation and premature sleep curtailment due to disorders and lifestyle--demonstrate that cognitive deficits accumulate to severe levels over time without full awareness by the affected individual. Functional neuroimaging has revealed that frequent and progressively longer cognitive lapses, which are a hallmark of sleep deprivation, involve distributed changes in brain regions including frontal and parietal control areas, secondary sensory processing areas, and thalamic areas. There are robust differences among individuals in the degree of their cognitive vulnerability to sleep loss that may involve differences in prefrontal and parietal cortices, and that may have a basis in genes regulating sleep homeostasis and circadian rhythms. Thus, cognitive deficits believed to be a function of the severity of clinical sleep disturbance may be a product of genetic alleles associated with differential cognitive vulnerability to sleep loss.

Microcomputer analyses of performance on a portable, simple visual RT task during sustained operations

The Institute of Pennsylvania Hospital and University of Pennsylvania, Philadelphia, Pennsylvania There is a need for brief, portable performance measures that are free of practice effects but that reliably show the impact of sleep loss on performance during sustained work. Reaction time (RT) tasks hold considerable promise in meeting this need, if the extensive number of responses they typically yield can be processed in ways that quickly provide the essential analyses. While testing the utility of a portable visual RT task during a sustained, quasi-continuous work schedule of 54 h, we developed a microcomputer software system that inputs, edits, transforms, analyzes, and reduces the data from the RT portable audiotapes, for each 10-min trial on the task. With relatively minor modifications, the software system can be used on a minimally configured microcomputer system that supports BASIC. The software is flexible and capable of retrieving distorted data, and it generates a variety of dependent variables reflecting intratrial optimum response capacity, lapsing, and response slowing.

An overview of sleepiness and accidents.

SUMMARY  This paper reviews the association between neurobiologically‐based sleepiness/fatigue and human‐error related accidents. It concludes that fatigue contributes to human error and accidents in technology‐rich, industrialized societies in terms of human, environmental and economic impacts. The cultural utilization of time as expressed in 24‐h work operations, combined with the widespread use of automation, will continue to escalate in the next century, further increasing the risks of fatigue‐related accidents, as more people conduct vigilance‐based activities at times other than the traditional daytime work hours. Fatigue management and prevention of fatigue‐related catastrophes need to become a sustained priority for government, industries, labour, and the public. Scientific data are urgently needed on the most likely areas in which sleepiness‐related performance failures contribute to accidents, and on the effectiveness of a wide range of potentially useful countermeasures.

Sleep deprivation and vigilant attention.

Sleep deprivation severely compromises the ability of human beings to respond to stimuli in a timely fashion. These deficits have been attributed in large part to failures of vigilant attention, which many theorists believe forms the bedrock of the other more complex components of cognition. One of the leading paradigms used as an assay of vigilant attention is the psychomotor vigilance test (PVT), a high signal‐load reaction‐time test that is extremely sensitive to sleep deprivation. Over the last twenty years, four dominant findings have emerged from the use of this paradigm. First, sleep deprivation results in an overall slowing of responses. Second, sleep deprivation increases the propensity of individuals to lapse for lengthy periods (>500 ms), as well as make errors of commission. Third, sleep deprivation enhances the time‐on‐task effect within each test bout. Finally, PVT results during extended periods of wakefulness reveal the presence of interacting circadian and homeostatic sleep drives. A theme that links these findings is the interplay of “top‐down” and “bottom‐up” attention in producing the unstable and unpredictable patterns of behavior that are the hallmark of the sleep‐deprived state.

A Meta-Analysis of the Impact of Short-Term Sleep Deprivation on Cognitive Variables

A substantial amount of research has been conducted in an effort to understand the impact of short-term (<48 hr) total sleep deprivation (SD) on outcomes in various cognitive domains. Despite this wealth of information, there has been disagreement on how these data should be interpreted, arising in part because the relative magnitude of effect sizes in these domains is not known. To address this question, we conducted a meta-analysis to discover the effects of short-term SD on both speed and accuracy measures in 6 cognitive categories: simple attention, complex attention, working memory, processing speed, short-term memory, and reasoning. Seventy articles containing 147 cognitive tests were found that met inclusion criteria for this study. Effect sizes ranged from small and nonsignificant (reasoning accuracy: g = -0.125, 95% CI [-0.27, 0.02]) to large (lapses in simple attention: g = -0.776, 95% CI [-0.96, -0.60], p < .001). Across cognitive domains, significant differences were observed for both speed and accuracy; however, there were no differences between speed and accuracy measures within each cognitive domain. Of several moderators tested, only time awake was a significant predictor of between-studies variability, and only for accuracy measures, suggesting that heterogeneity in test characteristics may account for a significant amount of the remaining between-studies variance. The theoretical implications of these findings for the study of SD and cognition are discussed.

Interfering with Theories of Sleep and Memory: Sleep, Declarative Memory, and Associative Interference

Mounting behavioral evidence in humans supports the claim that sleep leads to improvements in recently acquired, nondeclarative memories. Examples include motor-sequence learning; visual-discrimination learning; and perceptual learning of a synthetic language. In contrast, there are limited human data supporting a benefit of sleep for declarative (hippocampus-mediated) memory in humans (for review, see). This is particularly surprising given that animal models (e.g.,) and neuroimaging studies (e.g.,) predict that sleep facilitates hippocampus-based memory consolidation. We hypothesized that we could unmask the benefits of sleep by challenging the declarative memory system with competing information (interference). This is the first study to demonstrate that sleep protects declarative memories from subsequent associative interference, and it has important implications for understanding the neurobiology of memory consolidation.

Sleep Loss Reduces Diurnal Rhythm Amplitude of Leptin in Healthy Men

The aim of the current study was to investigate the effects of sleep loss on the diurnal rhythm of circulating leptin levels. An indwelling forearm catheter was used to sample blood at 90‐min intervals for a total of 120 h, which included 88 h of sustained sleeplessness, in 10 healthy men. The diurnal amplitude of leptin was reduced during total sleep deprivation and returned toward normal during the period of recovery sleep. This finding provides evidence that sleep influences the nocturnal leptin profile, and may have implications for the understanding of the role of sleep in metabolic regulation and the aetiologies of obesity and the night eating syndrome.

Lapsing during Sleep Deprivation Is Associated with Distributed Changes in Brain Activation

Lapses of attention manifest as delayed behavioral responses to salient stimuli. Although they can occur even after a normal nights sleep, they are longer in duration and more frequent after sleep deprivation (SD). To identify changes in task-associated brain activation associated with lapses during SD, we performed functional magnetic resonance imaging during a visual, selective attention task and analyzed the correct responses in a trial-by-trial manner modeling the effects of response time. Separately, we compared the fastest 10% and slowest 10% of correct responses in each state. Both analyses concurred in finding that SD-related lapses differ from lapses of equivalent duration after a normal nights sleep by (1) reduced ability of frontal and parietal control regions to raise activation in response to lapses, (2) dramatically reduced visual sensory cortex activation, and (3) reduced thalamic activation during lapses that contrasted with elevated thalamic activation during nonlapse periods. Despite these differences, the fastest responses after normal sleep and after SD elicited comparable frontoparietal activation, suggesting that performing a task while sleep deprived involves periods of apparently normal neural activation interleaved with periods of depressed cognitive control, visual perceptual functions, and arousal. These findings reveal for the first time some of the neural consequences of the interaction between efforts to maintain wakefulness and processes that initiate involuntary sleep in sleep-deprived persons.

The Neural Basis of Interindividual Variability in Inhibitory Efficiency after Sleep Deprivation

Sleep deprivation results in the loss of our ability to suppress a prepotent response. The extent of decline in this executive function varies across individuals. Here, we used functional magnetic resonance imaging to study the neural correlates of sleep deprivation-induced differences in inhibitory efficiency. Participants performed a go/no-go task after normal sleep and after 24 h of total sleep deprivation. Regardless of the extent of change in inhibitory efficiency, sleep deprivation lowered go/no-go sustained, task-related activation of the ventral and anterior prefrontal (PFC) regions bilaterally. However, individuals better able to maintain inhibitory efficiency after sleep deprivation could be distinguished by lower stop-related, phasic activation of the right ventral PFC during rested wakefulness. These persons also showed a larger rise in such activation both here and in the right insula after sleep deprivation relative to those whose inhibitory efficiency declined.

Home management of sickle cell-related pain in children and adolescents : natural history and impact on school attendance

&NA; Some children and adolescents with sickle cell disease experience frequent painful episodes. To gain information about the natural history of the pain and its impact on sleep and school attendance, we developed a home‐based diary system. Eighteen children and adolescents completed 4756 diary days, with an average compliance of 75%. Pain was reported on 30% of days and was managed at home nine‐tenths of the time. Girls reported more days with pain than did boys, and age was positively correlated with the length of the painful episodes. The pain affected school attendance and sleep. Patients were absent from school on 21% of 3186 school days, with half of the absenteeisms on days with reported pain. Of the pain‐associated absenteeisms, two‐thirds occurred when pain was managed at home, and one‐third when patients were hospitalized. The average consecutive number of school days missed was 2.7. These findings have implications for developmentally critical activities.