Neurocognitive Consequences of Sleep Deprivation

被引:1713
作者
Goel, Namni [1 ]
Rao, Hengyi [1 ]
Durmer, Jeffrey S. [2 ]
Dinges, David F. [1 ]
机构
[1] Univ Penn, Sch Med, Div Sleep & Chronobiol, Dept Psychiat, Philadelphia, PA 19104 USA
[2] Fus Sleep, Sleep Med Program, Suwanee, GA USA
基金
美国国家卫生研究院;
关键词
Neurobehavioral performance; sleep restriction; attention and executive function; functional neuroimaging; prefrontal cortex; thalamus; sensory processing areas; genetics; RESTLESS LEGS SYNDROME; LIMB MOVEMENT-DISORDER; CIRCADIAN CLOCK GENES; BOLD FMRI STATISTICS; CEREBRAL-BLOOD-FLOW; HUMAN PER3 GENE; WORKING-MEMORY; INDIVIDUAL-DIFFERENCES; INTERINDIVIDUAL DIFFERENCES; LENGTH POLYMORPHISM;
D O I
10.1055/s-0029-1237117
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
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.
引用
收藏
页码:320 / 339
页数:20
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