Neurocognitive consequences of sleep deprivation

Abstract

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.

Thieme Medical Publishers.

Figures

Figure 1

Functional magnetic resonance imaging (fMRI) responses from three cortical areas during a visual, global/local selective attention task performed by N = 24 healthy young adults when not sleep deprived (RW, in blue) and when sleep deprived (SD, in red) for one night. The graphs display differential neural responses in the medial frontal cortex (top), bilateral intraparietal sulcus (middle), and bilateral inferior occipital cortices (bottom), in association with the fastest 10% reaction times (RT) (left column) and the slowest 10% RTs (right column). A threshold of p < 0.001 was used to detect task-related activation. For both RW and SD states, slower responses were associated with higher peak fMRI signals in the medial frontal cortex and bilateral intraparietal sulcus (all p < 0.005). When comparing SD with RW, peak signal for the slowest 10% of trials was significantly lower in the parietal and occipital regions (right middle and bottom), but not in the medial frontal cortex (right top). SD also attenuated task-related thalamic activation (not shown). Peak signal in the occipital region after SD was significantly lower than RW even for the fastest 10% of trials (left bottom). However, there was no difference between RW and SD states in the frontal or parietal peak fMRI signals for the fastest responses across states (left top and middle). The shaded time points indicate those contrasted to assess significant state effects. The inset shows the mean peak signal associated with the time points under consideration. Error bars represent SEM. Significant differences between peak signals associated with a lapse and the average response for each state are marked with an asterisk. *p < 0.01, **p < 0.001. (Reprinted from Chee et al, with permission from The Journal of Neuroscience.)

Figure 2

A graphic comparison of performance on a behavioral alertness test following 14 days of partial sleep restriction or 3 days of total sleep deprivation, as a function of cumulative sleep debt (panel A) or cumulative excess wakefulness (panel B). Alertness was measured by lapses on the Psychomotor Vigilance Test (PVT). Cumulative sleep debt was determined by summating the difference between a statistically derived average sleep time of 8.16 hour/night and the actual hours of sleep each night (panel A). Cumulative excess wakefulness was determined by summating the difference between a statistically derived average daily wake time of 15.84 hour/day and the actual hours of wake each day (panel B). Each point represents the average time/day for each subject across 14 days of partial sleep restriction or 3 days of total sleep deprivation. Data from three partial sleep restriction groups (8 hours = diamond, 6 hours = square, and 4 hours = open circle) and one total sleep deprivation group (at days 1, 2, and 3 of total sleep deprivation = solid square) are shown. Panel A illustrates a difference (nonlinear relationship) between behavioral performance in the partial sleep restriction and total sleep deprivation groups as a function of cumulative sleep debt. Panel B demonstrates a similarity (linear relationship) between behavioral performance in the partial sleep restriction and total sleep deprivation groups as a function of cumulative excess wakefulness. The difference in analysis between panel A and panel B affects only the total sleep deprivation condition because subjects who receive 0 hours of sleep per day build up a statistically estimated average sleep debt of 8.16 hours per day, but extend their wakefulness by 24 hours per day. Thus, panel B shows a monotonic, near-proportional relationship between cumulative excess wakefulness and neurobehavioral performance deficits. (Reprinted with permission from Van Dongen et al.)