Neurocognitive Consequences of Sleep Deprivation

TLDR

Sleep deprivation impairs cognitive performance, affecting psychomotor speed, attention, working memory, and higher cognition due to increased sleep propensity and instability of waking functions. Chronic sleep‑restriction experiments demonstrate that cognitive deficits accumulate progressively over time, often without the individual’s awareness. Functional neuroimaging shows that frequent cognitive lapses during sleep deprivation involve distributed changes in frontal, parietal, sensory, and thalamic regions, and that individual differences in vulnerability are linked to prefrontal/parietal cortex and genes regulating sleep homeostasis and circadian rhythms.

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.