Enhanced brain small‐worldness after sleep deprivation: a compensatory effect

Sleep deprivation has a variable impact on extrinsic activities during multiple cognitive tasks, especially on mood and emotion processing. There is also a trait‐like individual vulnerability or compensatory effect in cognition. Previous studies have elucidated the altered functional connectivity after sleep deprivation. However, it remains unclear whether the small‐world properties of resting‐state network are sensitive to sleep deprivation. A small‐world network is a type of graph that combines a high local connectivity as well as a few long‐range connections, which ensures a higher information‐processing efficiency at a low cost. The complex network of the brain can be described as a small‐world network, in which a node is a brain region and an edge is present when there is a functional correlation between two nodes. Here, we investigated the topological properties of the human brain networks of 22 healthy subjects under sufficient sleep and sleep‐deprived conditions. Specifically, small‐worldness is utilized to quantify the small‐world property, by comparing the clustering coefficient and path length of a given network to an equivalent random network with same degree distribution. After sufficient sleep, the brain networks showed the property of small‐worldness. Compared with the resting state under sufficient sleep, the small‐world property was significantly enhanced in the sleep deprivation condition, suggesting a possible compensatory adaptation of the human brain. Specifically, the altered measurements were correlated with the neuroticism of subjects, indicating that individuals with low‐levels of neuroticism are more resilient to sleep deprivation.     

Effects of Prolonged Sleep Deprivation, With and Without Chronic Physical Exercise, on Mood and Performance

The effects of physical exercise and sleep deprivation on mood and cognitive performance were studied in 12 healthy young male volunteers deprived of sleep on two occasions. During the first 60-hr period without sleep, half of the subjects walked on a treadmill at 25–30% of their maximum aerobic capacity (Exercise condition) for 1 out of every 3 hrs while the remaining 6 subjects remained physically inactive (No Exercise condition) during that same hour. Eight weeks later the same 12 subjects underwent an identical sleep-deprivation protocol except that those who were previously inactive exercised, while those who previously exercised remained inactive. Throughout the sleep deprivation periods, subjects in both conditions completed subjective assessments of fatigue, sleepiness and mood every 3 hrs, performed an auditory vigilance task every 6 hrs, and completed a cognitive test battery every 12 hrs. The results revealed clear decrements in mood and performance as a function of sleep loss. However, with the exception of somewhat more long reaction times in the Exercise condition, exercise neither increased nor decreased the impairment induced by sleep deprivation.     

Sleep, Performance and Mood After the Energy-Expenditure Equivalent of 40 Hours of Sleep Deprivation

Twelve Marine subjects marched approximately 20 miles to expend as much energy in one 16-hr day as is expended during 40 hrs of relatively inactive sleep deprivation. At the end of the march, performance on addition, vigilance, choice reaction time, tapping, short-term memory, symbol substitution, and three mood scales was decremented significantly. Those decrements closely approximated decrements reported in the literature following 40 hrs of sleep deprivation. However, recovery sleep stages and arousal thresholds were essentially unchanged as compared to baseline and were significantly different from those predicted after 40 hrs of sleep loss. It was concluded that while changes in performance were probably linked to total energy consumption, the commonly measured sleep variables were not.     

Hypothesis for the pathophysiology of delirium: role of baseline brain network connectivity and changes in inhibitory tone

Normal brain function is facilitated by a highly organized and interconnected structure allowing complex integration of sensory information and motor responses. The acute confusional state of delirium is characterized by a fluctuating disturbance in consciousness, arousal level and cognition-memory; as such, delirium represents a failure in the integration and appropriate processing of information. The pathogenesis of this cognitive disintegration is unclear; herein a hypothesis is proposed that delirium results from an acute breakdown in network connectivity within the brain. The hypothesis predicts that the extent to which the network connectivity breaks down is dependent on two factors: (i) the baseline connectivity within the brain and (ii) the level of inhibitory tone. Baseline connectivity is the connectivity of neural networks within the brain before the precipitating insult provoking delirium. Many non-modifiable risk factors for delirium influence baseline connectivity such as age, cognitive impairment, dementia and depression. Precipitant events that provoke delirium (modifiable risk factors) are hypothesized to further, and acutely, breakdown network connectivity by increasing inhibitory tone within the brain. Modifiable risk factors include inflammation, metabolic abnormalities, sleep deprivation and medication such as benzodiazepines. An important role for GABAergic neurotransmission is implicated in increasing the inhibitory tone to produce delirium. This theory accounts for the various forms of delirium, hypoactive, hyperactive and mixed. The form of delirium that ensues will depend upon how and which networks breakdown (dependent on both the individual’s baseline network connectivity and the degree change in inhibitory tone produced).     

Sleep loss impairs short and novel language tasks having a prefrontal focus

Most cognitive tests administered during sleep loss are well rehearsed to remove practice effects. This can introduce tedium and a loss of novelty, which may be the key to the test's subsequent sensitivity to sleep loss, and why it may need only a few minutes administration before sleep loss effects are apparent. There is little evidence to show that any of these tests are actually affected by sleep loss if given de novo, without practice, but using a non-sleep deprived control group. Although the sleep deprivation literature advocates that short, novel and stimulating tests would not be expected to be sensitive to sleep loss, recent sleep loss findings using neuropsychological tests focussing on the prefrontal cortex, indicate that such tests may challenge this maxim. Twenty healthy young adults were randomly assigned to two groups: nil sleep deprivation (control), and 36h continuous sleep deprivation (SD). Two, novel, interesting and short (6 min) language tests, known (by brain imaging) to have predominantly a PFC focus, were given, once, towards the end of SD: (i) the Haylings test – which measures the capacity to inhibit strong associations in favour of novel responses, and (ii) a variant of the word fluency test – innovation in a verb-to-noun association. Subjects were exhorted to do their best. Compared with control subjects both tasks were significantly impaired by SD. As a check on the effects on the Haylings test, a repeat study was undertaken with 30 more subjects randomly divided as before. The outcome was similar. Linguistically, sleep loss appears to interfere with novel responses and the ability to suppress routine answers.     

Altered cerebrocerebellar functional connectivity in patients with obstructive sleep apnea and its association with cognitive function

Study ObjectivesPrevious functional MRI studies have reported altered brain networks in patients with obstructive sleep apnea (OSA). However, the extent and pattern of abnormal connectivity were inconsistent across studies, and cerebrocerebellar connections have been rarely assessed. We investigated functional network changes in cerebral and cerebellar cortices of OSA patients.MethodsResting-state functional MRI, polysomnography, and neuropsychological (NP) test data were acquired from 74 OSA patients (age: 45.8 ± 10.7 years) and 33 healthy subjects (39.6 ± 9.3 years). Connectivity matrices were extracted by computing correlation coefficients from various regions of interest, and Fisher r-to-z transformations. In the functional connections that showed significant group differences, linear regression was conducted to examine the association between connectivity and clinical characteristics.ResultsPatients with OSA showed reduced functional connectivity (FC) in cerebrocerebellar connections linking different functional networks, and greater FC in cortical between-network connections in prefrontal regions involving the default mode network (DMN) and the control network. For OSA group, we found no correlation between FC and sleep parameters including lowest SaO₂ and arousal index in the connections where significant associations were observed in healthy subjects. FC changes in DMN areas were related to reduced verbal fluency in OSA. Lower local efficiency and lower clustering coefficient of the salience network in the left cerebellum were also observed in OSA.ConclusionsOSA affects mainly the cerebrocerebellar pathway. The disruption of function in these connections are related to sleep fragmentation and hypoxia during sleep. These abnormal network functions, especially DMN, are suggested to participate in cognitive decline of OSA.     

Less effective executive functioning after one night's sleep deprivation

The prefrontal cortex (PFC) is affected negatively by sleep deprivation (SD) and executive functioning is largely dependent on activity in the PFC. Earlier studies have focused on subsystems of executive functioning, and tests of executive functioning have shown both low reliability and low validity. In the present study, 11 healthy volunteers were sleep deprived and compared with 11 healthy controls in a study on effects of one night's SD on integrative executive functioning. Following SD, the performance of subjects on an ecologically valid test, the modified Six Elements Test, was significantly impaired. There were no group differences on psychomotor vigilance, verbal or visuo-spatial working memory. This extends previous knowledge of performance effects of SD, and may be of special importance for individuals with cognitive work tasks.     

Sleep Stage Physiology, Mood, and Vigilance Responses to Total Sleep Deprivation in Healthy 80-Year-Olds and 20-Year-Olds

Little is known about sleep and the effects of total sleep loss in the 'old old' (i.e., 80-year-olds). We investigated sleep, mood, and performance responses to acute sleep deprivation in healthy 80-year-olds (n = 10) and 20-year-olds (n = 14). The protocol consisted of three nights of baseline sleep, one night of total sleep deprivation, and two nights of recovery sleep. Mood and vigilance were tested using visual analog scales and a Mackworth clock procedure in the morning and evening of each study day. Daytime sleepiness was measured by five naps on the days following the third and sixth nights. Old subjects had lower sleep efficiency and less delta sleep than young subjects. However, sleep continuity and delta sleep were enhanced in both groups on the first recovery night, indicating that sleep changes in old subjects are at least partially reversible by this procedure. Surprisingly, young subjects had shorter daytime sleep latencies than the old, suggesting a greater unmet sleep need in the former group. Mood and performance were disturbed by sleep loss in both groups, but to a greater extent among the young. This suggests that acute total sleep loss is a more disruptive procedure for the young than for the old.     

Associations between insomnia symptoms and functional connectivity in the UK Biobank cohort (n = 29,423)

An increasing number of studies harness resting-state fMRI functional connectivity analysis to investigate the neurobiological mechanisms of insomnia. The results to date are inconsistent and the detection of minor and widely distributed alterations in functional connectivity requires large sample sizes. The present study investigated associations between insomnia symptoms and resting-state functional connectivity at the whole-brain level in the largest sample to date. This cross-sectional analysis used resting-state imaging data from the UK Biobank, a large scale, population-based biomedical database. The analysis included 29,423 participants (age: 63.1 ± 7.5 years, 54.3% female), comprising 9210 with frequent insomnia symptoms and 20,213 controls without. Linear models were adjusted for relevant clinical, imaging, and socio-demographic variables. The Akaike information criterion was used for model selection. Multiple comparisons were corrected using the false discovery rate with a significance level of q < 0.05. Frequent insomnia symptoms were associated with increased connectivity within the default mode network and frontoparietal network, increased negative connectivity between the default mode network and the frontoparietal network, and decreased connectivity between the salience network and a node of the default mode network. Furthermore, frequent insomnia symptoms were associated with altered functional connectivity between nodes comprising sensory areas and the cerebellum. These functional alterations of brain networks may underlie dysfunctional affective and cognitive processing in insomnia and contribute to subjectively and objectively impaired sleep. However, it must be noted that the item that was used to assess frequent insomnia symptoms in this study did not assess all the characteristics of clinically diagnosed insomnia.     

Sleep deprivation selectively disrupts top–down adaptation to cognitive conflict in the Stroop test

Sleep deprivation is known to exert detrimental effects on various cognitive domains, including attention, vigilance and working memory. Seemingly at odds with these findings, prior studies repeatedly failed to evidence an impact of prior sleep deprivation on cognitive interference in the Stroop test, a hallmark paradigm in the study of cognitive control abilities. The present study investigated further the effect of sleep deprivation on cognitive control using an adapted version of the Stroop test that allows to segregate top–down (attentional reconfiguration on incongruent items) and bottom–up (facilitated processing after repetitions in responses and/or features of stimuli) components of performance. Participants underwent a regular night of sleep or a night of total sleep deprivation before cognitive testing. Results disclosed that sleep deprivation selectively impairs top–down adaptation mechanisms: cognitive control no longer increased upon detection of response conflict at the preceding trial. In parallel, bottom–up abilities were found unaffected by sleep deprivation: beneficial effects of stimulus and response repetitions persisted. Changes in vigilance states due to sleep deprivation selectively impact on cognitive control in the Stroop test by affecting top–down, but not bottom–up, mechanisms that guide adaptive behaviours.     

急性睡眠剥夺时程对青年男性军人脑认知功能的影响

目的:研究急性睡眠剥夺(SD)不同时程对脑认知功能的影响。方法:76例军医大学男性健康志愿者学员,接受48小时持续睡眠剥夺,全程进行脑电监测,每12小时进行事件相关电位、记忆分离加工检测。结果:1记忆测试:睡眠剥夺后外显记忆成绩(F=65.5732,P=0.0001)、内隐记忆成绩(F=44.3333,P=0.0001)均较基线出现显著性差异;2事件相关电位(ERP):睡眠剥夺后ERP潜伏期(F=61.0453~244.0524,P=0.0001)及波幅(F=10.5511~23.9379,P=0.0001)较基线出现显著性差异;3脑电非线性动力学分析:睡眠剥夺后关联维度(F=133.9194,P=0.0001)、近似熵(F=11.4091,P=0.0001)均较基线出现显著性差异。结论:急性睡眠剥夺将会阻碍脑认知信息加工过程,促使外显及内隐记忆消退,使得脑神经元信息网络呈现更复杂的混沌模式,上述效应随SD时程不同而程度各异。     

睡眠剥夺对认知功能影响的研究进展

为了充分探究睡眠对认知的作用机制，睡眠剥夺是一个有效的途径。目前有多种手段研究睡眠剥夺如何影响认知功能，包括认知心理学评价、脑成像方法、脑电生理的变化等。所研究的方面覆盖认知科学的多个领域，目前国内外均有学者致力于此研究，并已经取得了初步的成果，但是存在多种影响因素，尚未得到统一的结论。我们从睡眠剥夺引起认知功能下降的机制出发，综述了通过脑成像方法研究神经生理学变化以及脑电生理方法评价认知功能下降的研究进展，并分析研究的影响因素和目前关注的发展方向。     

Gray matter deficits and resting-state abnormalities in abstinent heroin-dependent individuals

Previous neuroimaging studies have demonstrated both structural and functional damages in heroin-dependent individuals. However, few studies investigated gray matter deficits and abnormal resting-state networks together in heroin-dependent individuals. In the present study, voxel-based morphometry (VBM) was used to identify brain regions with gray matter density reduction. Resting-state fMRI connectivity analysis was employed to assess potential functional abnormalities during resting-state. All clinical significances were investigated by examining their association with duration of heroin use. Compared with healthy subjects, heroin-dependent individuals showed significant reduction in gray matter density in the right dorsolateral prefrontal cortex (DLPFC) and a decrease in resting-state functional connectivity between the right DLPFC and left inferior parietal lobe (IPL). The gray matter density of the right DLPFC and its resting-state functional connectivity with the left IPL both showed significantly negative correlation with duration of heroin use, which were likely to be related to the functional impairments in decision-making and cognitive control exhibited by heroin-dependent individuals. Our findings demonstrated that long heroin dependence impairs the right DLPFC in heroin-dependent individuals, including structural deficits and resting-state functional impairments.     

Combining spatial and temporal information to explore resting-state networks changes in abstinent heroin-dependent individuals

Majority of previous heroin fMRI studies focused on abnormal brain function in heroin-dependent individuals. However, few fMRI studies focused on the resting-state abnormalities in heroin-dependent individuals and assessed the relationship between the resting-state functional connectivity changes and duration of heroin use. In the present study, discrete cosine transform (DCT) was employed to explore spatial distribution of low frequency BOLD oscillations in heroin-dependent individuals and healthy subjects during resting-state; meanwhile resting-state functional connectivity analysis was used to investigate the temporal signatures of overlapping brain regions obtained in DCT analysis among these two groups. Main finding of the present study is that the default mode network (DMN) and rostral anterior cingulate cortex (rACC) network of heroin-dependent individuals were changed compared with healthy subjects. More importantly, these changes negatively correlated with duration of heroin use. These resting-state functional abnormalites in heroin-dependent individuals provided evidence for abnormal functional organization in heroin-dependent individuals, such as functional impairments in decision-making and inhibitory control.     

Cerebral and blood correlates of reduced functional connectivity in mild cognitive impairment

Growing evidence suggests that decreased functional connectivity in cortical networks precedes clinical stages of Alzheimer’s disease (AD), although our knowledge about cerebral and biological correlates of this phenomenon is limited. To shed light on this issue, we have investigated whether resting-state oscillatory connectivity patterns in healthy older (HO) and amnestic mild cognitive impairment (aMCI) subjects are related to anatomical grey matter (GM) and functional (2-[18F]fluoro-2-deoxy-d-glucose (FDG)-PET) changes of neuroelectric sources of alpha rhythms, and/or to changes in plasma amyloid-beta (Aβ) and serum lipid levels, blood markers tied to AD pathogenesis and aging-related cognitive decline. We found that aMCI subjects showed decreased levels of cortical connectivity, reduced FDG-PET intake of the precuneus, and GM atrophy of the thalamus, together with higher levels of Aβ and apolipoprotein B (ApoB) compared to HO. Interestingly, levels of high-density lipoprotein (HDL) cholesterol were positively correlated with the strength of neural-phase coupling in aMCI subjects, and increased triglycerides accompanied bilateral GM loss in the precuneus of aMCI subjects. Together, these findings provide peripheral blood correlates of reduced resting-state cortical connectivity in aMCI, supported by anatomo-functional changes in cerebral sources of alpha rhythms. This framework constitutes an integrated approach to assess functional changes in cortical networks through neuroimaging and peripheral blood markers during early stages of neurodegeneration.     

Relationships between affect, vigilance, and sleepiness following sleep deprivation

This pilot study examined the relationships between the effects of sleep deprivation on subjective and objective measures of sleepiness and affect, and psychomotor vigilance performance. Following an adaptation night in the laboratory, healthy young adults were randomly assigned to either a night of total sleep deprivation (SD group; n = 15) or to a night of normal sleep (non-SD group; n = 14) under controlled laboratory conditions. The following day, subjective reports of mood and sleepiness, objective sleepiness (Multiple Sleep Latency Test and spontaneous oscillations in pupil diameter, PUI), affective reactivity/regulation (pupil dilation responses to emotional pictures), and psychomotor vigilance performance (PVT) were measured. Sleep deprivation had a significant impact on all three domains (affect, sleepiness, and vigilance), with significant group differences for eight of the nine outcome measures. Exploratory factor analyses performed across the entire sample and within the SD group alone revealed that the outcomes clustered on three orthogonal dimensions reflecting the method of measurement: physiological measures of sleepiness and affective reactivity/regulation, subjective measures of sleepiness and mood, and vigilance performance. Sleepiness and affective responses to sleep deprivation were associated (although separately for objective and subjective measures). PVT performance was also independent of the sleepiness and affect outcomes. These findings suggest that objective and subjective measures represent distinct entities that should not be assumed to be equivalent. By including affective outcomes in experimental sleep deprivation research, the impact of sleep loss on affective function and their relationship to other neurobehavioral domains can be assessed.     

Performance and Mood Following Variations in the Length and Timing of Sleep

The relative effects of extended sleep, sleep deprivation, and shifts of accustomed sleep time on subsequent performance and mood were studied. Ten regular 2400–0800 sleepers worked on E-paced addition and vigilance tasks, and completed an adjective check list to rate their mood following 2100-0800 extended, 2100-0500 advanced-shift, 2400-0800 habitual, 0300-0800 deprivation, and 0300-1100 delayed-shift conditions of sleep. Accuracy and speed of response on the vigilance task were significantly poorer, and negative affect was significantly greater after the conditions of shifted sleep and altered sleep duration than after the habitual sleep condition. Changes in the mood and performance measures were unrelated to prior sleep length or any specific alterations in the electrophysiological patterns of sleep.     

Sleep difficulties are associated with increased symptoms of psychopathology

Sleep problems often co-occur with psychopathological conditions and affective dysregulation. Individuals with mood disorders have significantly higher rates of sleep disturbances than healthy individuals, and among those with mood disorders, sleep problems are associated with lower rates of remission and response to treatment. Sleep disruption may itself be a risk factor for various forms of psychopathology, as experimental sleep deprivation has been found to lead to increased affective, cognitive, and somatic symptoms within healthy volunteers. However, little is known about the relationship between recurring sleep complaints in a naturalistic environment and symptoms of psychopathology among healthy individuals. In the present study, 49 healthy adults (21 males and 28 females) reported sleep quality and completed the Personality Assessment Inventory, a standardized self-report assessment of symptoms of psychopathology. Consistent with prior published findings during total sleep deprivation, individuals endorsing self-reported naturally occurring sleep problems showed higher scores on scales measuring somatic complaints, anxiety, and depression. Furthermore, the reported frequency of sleep disturbance was closely linked with the severity of self-reported symptoms. While causal directionality cannot be inferred, these findings support the notion that sleep and emotional functioning are closely linked.     

Age, Sleep Deprivation, and Performance

Men 18–22 and 40–49 yrs old were repeatedly given a battery of monitoring, persistence, and cognitive tasks over an extended period of sleep deprivation. The older subjects, who generally exhibited superior performance, were also more affected by the acute deprivation of sleep.     

脑静息功能连接自发波动的可变性分析

静息脑功能连接的动态性被认为能够反映大尺度功能脑网络的基本性质,近年来受到越来越多的关注。过去很少有研究分析静息脑连接自发波动的空间分布特点。采用远程功能连接度结合滑动窗口方法,分析一组大样本(n=396)年轻成年人脑静息功能连接低频自发波动的可变性。首先采用36 s滑动窗,计算全脑动态连接时间序列;然后在每个窗口内,以半径为14 mm的球形邻域计算每个体素的远程连接度;最后引入低频振荡幅值(ALFF)指标,评估各体素连接度波动的大小。研究结果表明: 默认网络具有最小的波动性(ALFF=402.3±79.9),暗示该网络在稳定脑自发神经活动中起主要作用。与之对比,感觉运动网络相关连接波动呈现出最大的可变性(ALFF=551.2±74.7),可能与被试在无任务状态下不定期感知外界环境有关。首次揭示静息态认知网络与感觉运动网络在静息功能连接波动性方面存在显著差异(双样本t检验: t=-6.38, P<0.000 1),有助于进一步理解无任务状态下脑功能的动态组织方式, 并为研究神经心理疾病提供新的方法。