Sleep deprivation changes frequency-specific functional organization of the resting human brain.

Previous resting-state functional magnetic resonance imaging (rs-fMRI) studies have widely explored the temporal connection changes in the human brain following long-term sleep deprivation (SD). However, the frequency-specific topological properties of sleep-deprived functional networks remain virtually unclear. In this study, thirty-seven healthy male subjects underwent resting-state fMRI during rested wakefulness (RW) and after 36 hours of SD, and we examined frequency-specific spectral connection changes (0.01-0.08 Hz, interval = 0.01 Hz) caused by SD. First, we conducted a multivariate pattern analysis combining linear SVM classifiers with a robust feature selection algorithm, and the results revealed that accuracies of 74.29%-84.29% could be achieved in the classification between RW and SD states in leave-one-out cross-validation at different frequency bands, moreover, the spectral connection at the lowest and highest frequency bands exhibited higher discriminative power. Connection involving the cingulo-opercular network increased most, while connection involving the default-mode network decreased most following SD. Then we performed a graph-theoretic analysis and observed reduced low-frequency modularity and high-frequency global efficiency in the SD state. Moreover, hub regions, which were primarily situated in the cerebellum and the cingulo-opercular network after SD, exhibited high discriminative power in the aforementioned classification consistently. The findings may indicate the frequency-dependent effects of SD on the functional network topology and its efficiency of information exchange, providing new insights into the impact of SD on the human brain.

Effects of sleep deprivation on language-related brain functional connectivity: differences by gender and age.

Sleep deprivation (SD) negatively affects many cognitive functions, such as language performance. However, what remains unclear is whether and how SD affects the language-related brain network based on gender and age differences. The current study of 86 healthy adults used resting-state functional magnetic resonance imaging (rs-fMRI) to measure language-related functional connectivity after full sleep or partial SD. Gender and age differences in functional connectivity were assessed across four linguistic aspects: phonetics, morphology, semantics, and syntax. The results showed that SD can affect the connectivity status of language-related brain networks, especially syntax-related networks. Furthermore, the influence of SD on the functional connectivity in language-related networks differed between male and female groups, and between younger and older groups. Specifically, there were gender differences in the temporal association cortex and age differences in the parietal association cortex, during full sleep versus partial SD. These findings highlight changes in the brain's functional connectivity in response to SD as a potential source of gender and age differences in brain function.

Altered neuronal response to visual food stimuli in adolescents undergoing chronic sleep restriction.

STUDY OBJECTIVES: Poor sleep in adolescents can increase the risk of obesity, possibly due to changes in dietary patterns. Prior neuroimaging evidence, mostly in adults, suggests that lacking sleep results in increased response to food cues in reward-processing brain regions. Needed is a clarification of the mechanisms by which food reward processing is altered by the kind of chronic sleep restriction (SR) typically experienced by adolescents. This study aimed to elucidate the impact of sleep duration on response to visual food stimuli in healthy adolescents using functional neuroimaging, hypothesizing increased reward processing response after SR compared to a well-rested condition. METHODS: Thirty-nine healthy adolescents, 14-17 years old, completed a 3-week protocol: (1) sleep phase stabilization; (2) SR (~6.5 h nightly); and (3) healthy sleep (HS) duration (~9 h nightly). Participants underwent functional MRI while performing a visual food paradigm. Contrasts of food versus nonfood responses were compared within-subject between conditions of SR and HS. RESULTS: Under SR, there was a greater response to food stimuli compared to HS in a voxel cluster including the left ventral tegmental area and substantia nigra. No change in food appeal rating due to the sleep manipulation was detected. CONCLUSIONS: Outcomes of this study suggest that SR, as commonly experienced by healthy adolescents, results in the elevated dopaminergic drive of the reward network that may augment motivation to seek food in the context of individual food appeal and inhibitory profiles. Countermeasures that reduce food salience could include promoting consistent HS habits.

White matter structural topologic efficiency predicts individual resistance to sleep deprivation.

BACKGROUND: Sleep deprivation (SD) is commonplace in modern society and there are large individual differences in the vulnerability to SD. We aim to identify the structural network differences based on diffusion tensor imaging (DTI) that contribute to the individual different vulnerability to SD. METHODS: The number of psychomotor vigilance task (PVT) lapses was used to classify 49 healthy subjects on the basis of whether they were vulnerable or resistant to SD. DTI and graph theory approaches were used to investigate the topologic organization differences of the brain structural connectome between SD-vulnerable and -resistant individuals. We measured the level of global efficiency and clustering in rich club and non-rich club organizations. RESULTS: We demonstrated that participants vulnerable to SD had less global efficiency, network strength, and local efficiency but longer shortest path length compared with participants resistant to SD. Lower efficiency was mainly distributed in the right insula, bilateral thalamus, bilateral frontal, temporal, and temporal lobes. Furthermore, a disrupted subnetwork was observed that consisted of widespread connections. Moreover, the vulnerable group showed significantly decreased strength of the rich club compared with the resistant group. The strength of rich club connectivity was found to be correlated negatively with PVT performance (r = -0.395, p = 0.005). We further tested the reliability of the results. CONCLUSION: The findings revealed that individual differences in resistance to SD are related to disrupted topologic efficiency connectome pattern, and our study may provide potential connectome-based biomarkers for the early detection of the vulnerable degree to SD.

The restoration ability of a short nap after sleep deprivation on the brain cognitive function: A dynamic functional connectivity analysis.

AIMS: The brain function impairment induced by sleep deprivation (SD) is temporary and can be fully reversed with sufficient sleep. However, in many cases, long-duration recovery sleep is not feasible. Thus, this study aimed to investigate whether a short nap after SD is sufficient to restore brain function. METHODS: The data of 38 subjects, including resting state functional magnetic resonance imaging data collected at three timepoints (before SD, after 30 h of SD, and after a short nap following SD) and psychomotor vigilance task (PVT) data, were collected. Dynamic functional connectivity (DFC) analysis was used to evaluate changes in brain states among three timepoints, and four DFC states were distinguished across the three timepoints. RESULTS: Before SD, state 2 (a resting-like FC matrix) was dominant (48.26%). However, after 30 h SD, the proportion of state 2 dramatically decreased, and state 3 (still resting-like, but FCs were weakened) became dominant (40.92%). The increased proportion of state 3 positively correlated with a larger PVT "lapse" time. After a nap, the proportions of states 2 and 3 significantly increased and decreased, respectively, and the change in proportion of state 2 negatively correlated with the change in PVT "lapse" time. CONCLUSIONS: Taken together, the results indicated that, after a nap, the cognitive function impairment caused by SD may be reversed to some extent. Additionally, DFC differed among timepoints, which was also associated with the extent of cognitive function impairment after SD (state 3) and the extent of recovery therefrom after a nap (state 2).

Age-Related Subcortical Brain Morphology Changes Following Three Hours of Sleep Deprivation.

Sleep deprivation (SD) disrupted subcortical regions involved in emotion and attention. However, the age-related changes on subcortical brain morphology in processing of emotion and attention following SD remains unclear. Eighty participants consisting of 43 young people and 37 old people were included in this study. The volumetric analysis and vertex-wise shape analysis were employed to assess age-dependent structural abnormalities after SD. By volumetric analysis, we found significant main effect of deprivation with local atrophy in right amygdala. Shape analysis also showed the significant main effect of age in all subcortical structures. Moreover, the significant correlations between volume changes of bilateral amygdala and left thalamus after SD and scales scores refer to emotion processing and attention were observed in old adults. These findings indicated that SD altered gray matter volume and surface morphology of subcortical regions in old adults and suggested disrupted subcortical regions were associated with emotion and attention in old adults.

Altered Functional Connectivity in Working Memory Network After Acute Sleep Deprivation.

Acute sleep deprivation (SD) has a detrimental effect on working memory (WM). However, prior functional magnetic resonance imaging (fMRI) studies have failed to reach consistent results on brain functions underlying WM decline after acute SD. Thus, we aimed to identify convergent patterns of abnormal brain functions due to WM decline after acute SD. A coordinate-based activation likelihood estimation (ALE) meta-analysis of task-state fMRI studies testing the effects of acute SD on WM was performed to construct WM network. Then 26 healthy subjects with regular sleep performed the n-back task and underwent resting-state fMRI scanning before and after 24 h of SD. The functional connectivity (FC) among these brain regions and correlations with WM performance were calculated. The ALE results displayed that SD subjects performing WM-related tasks had consistent hypoactivation in the occipital lobe, left middle occipital gyrus, parietal lobe, precuneus, inferior parietal lobule, right sub-gyral, right cuneus, right limbic lobe, and right posterior cingulate. Consistent hyperactivation was showed in the left cerebrum, including the lingual gyrus, posterior lobe, cuneus, temporal lobe, and fusiform gyrus. These identified brain regions as the seeds to construct WM network. The increased FC between the left declive and right sub-gyral, left cuneus and left lingual gyrus, and left cuneus and right post cingulate were found. Furthermore, the impaired WM performance negatively correlated with increased FC. Taken together, our findings highlight that the altered FC in WM network may be the underlying mechanisms of WM decline after acute SD.

Cognitive impairment after sleep deprivation: The role of precuneus related connectivity on the intra-individual variability changes.

OBJECTIVE: Intra-individual variability (IIV) in cognitive performance is thought to reflect the efficiency with which attentional resources are allocated in different circumstances requiring cognitive control. IIV in cognitive performance is associated with the strength of the negative correlation between task-positive network and default mode network (DMN) activity. In this study, we investigated the impact of sleep deprivation (SD) on functional connectivity (FC) between the DMN and psychomotor vigilance task-related network (PVT-RN), and its relationship with IIV in cognitive performance. METHODS: Two analyses, network-level independent component analysis (NL-ICA) and region-level (RL)-ICA, were employed to compare the coefficient of variation (CV) of the PVT between normal sleep and SD conditions across 67 healthy participants. RESULTS: After SD, in NL-ICA, the FC between the PVT-RN and DMN was positively correlated with the CV of the PVT, as well as the changes therein, compared with normal sleep. Using a mask derived from the DMN and PVT-RN, the RL-ICA revealed that 12 edges/connections between DMN and PVT independent components were associated with the CV of the PVT, with nine of these connections involving the precuneus. CONCLUSIONS: These findings suggest that the precuneus may play a crucial role in the interactions of various brain functions during the PVT, with the connections between the precuneus and frontoparietal and somatosensory networks being significantly altered after SD. Moreover, following SD, weakened negative FC between the precuneus and bilateral inferior parietal lobule may disrupt the balance between cognitive and executive control functions, leading to a decline in cognitive performance.

Human brain solute transport quantified by glymphatic MRI-informed biophysics during sleep and sleep deprivation.

Whether you are reading, running or sleeping, your brain and its fluid environment continuously interacts to distribute nutrients and clear metabolic waste. Yet, the precise mechanisms for solute transport within the human brain have remained hard to quantify using imaging techniques alone. From multi-modal human brain MRI data sets in sleeping and sleep-deprived subjects, we identify and quantify CSF tracer transport parameters using forward and inverse subject-specific computational modelling. Our findings support the notion that extracellular diffusion alone is not sufficient as a brain-wide tracer transport mechanism. Instead, we show that human MRI observations align well with transport by either by an effective diffusion coefficent 3.5[Formula: see text] that of extracellular diffusion in combination with local clearance rates corresponding to a tracer half-life of up to 5 h, or by extracellular diffusion augmented by advection with brain-wide average flow speeds on the order of 1-9 [Formula: see text]m/min. Reduced advection fully explains reduced tracer clearance after sleep-deprivation, supporting the role of sleep and sleep deprivation on human brain clearance.

Is Short Sleep Bad for the Brain? Brain Structure and Cognitive Function in Short Sleepers.

Many sleep less than recommended without experiencing daytime sleepiness. According to prevailing views, short sleep increases risk of lower brain health and cognitive function. Chronic mild sleep deprivation could cause undetected sleep debt, negatively affecting cognitive function and brain health. However, it is possible that some have less sleep need and are more resistant to negative effects of sleep loss. We investigated this using a cross-sectional and longitudinal sample of 47,029 participants of both sexes (20-89 years) from the Lifebrain consortium, Human Connectome project (HCP) and UK Biobank (UKB), with measures of self-reported sleep, including 51,295 MRIs of the brain and cognitive tests. A total of 740 participants who reported to sleep <6 h did not experience daytime sleepiness or sleep problems/disturbances interfering with falling or staying asleep. These short sleepers showed significantly larger regional brain volumes than both short sleepers with daytime sleepiness and sleep problems (n = 1742) and participants sleeping the recommended 7-8 h (n = 3886). However, both groups of short sleepers showed slightly lower general cognitive function (GCA), 0.16 and 0.19 SDs, respectively. Analyses using accelerometer-estimated sleep duration confirmed the findings, and the associations remained after controlling for body mass index, depression symptoms, income, and education. The results suggest that some people can cope with less sleep without obvious negative associations with brain morphometry and that sleepiness and sleep problems may be more related to brain structural differences than duration. However, the slightly lower performance on tests of general cognitive abilities warrants closer examination in natural settings.SIGNIFICANCE STATEMENT Short habitual sleep is prevalent, with unknown consequences for brain health and cognitive performance. Here, we show that daytime sleepiness and sleep problems are more strongly related to regional brain volumes than sleep duration. However, participants sleeping ≤6 h had slightly lower scores on tests of general cognitive function (GCA). This indicates that sleep need is individual and that sleep duration per se is very weakly if at all related brain health, while daytime sleepiness and sleep problems may show somewhat stronger associations. The association between habitual short sleep and lower scores on tests of general cognitive abilities must be further scrutinized in natural settings.

Enhanced amygdala-cingulate connectivity associates with better mood in both healthy and depressive individuals after sleep deprivation.

Sleep loss robustly disrupts mood and emotion regulation in healthy individuals but can have a transient antidepressant effect in a subset of patients with depression. The neural mechanisms underlying this paradoxical effect remain unclear. Previous studies suggest that the amygdala and dorsal nexus (DN) play key roles in depressive mood regulation. Here, we used functional MRI to examine associations between amygdala- and DN-related resting-state connectivity alterations and mood changes after one night of total sleep deprivation (TSD) in both healthy adults and patients with major depressive disorder using strictly controlled in-laboratory studies. Behavioral data showed that TSD increased negative mood in healthy participants but reduced depressive symptoms in 43% of patients. Imaging data showed that TSD enhanced both amygdala- and DN-related connectivity in healthy participants. Moreover, enhanced amygdala connectivity to the anterior cingulate cortex (ACC) after TSD associated with better mood in healthy participants and antidepressant effects in depressed patients. These findings support the key role of the amygdala-cingulate circuit in mood regulation in both healthy and depressed populations and suggest that rapid antidepressant treatment may target the enhancement of amygdala-ACC connectivity.

Acute sleep deprivation: impairment of biventricular function assesed by speckle tracking echocardiography in healthy subjects.

OBJECTIVES: Sleep deprivation (SD) has been found to be associated with an increased incidence of adverse cardiovascular disease (CVD) events. The aim of this study was to investigate whether or not acute SD has a pathological effect on the geometry and the systolic and diastolic functions of the right and left heart chambers by standard transthoracic echocardiography (TTE) and speckle tracking echocardiography (STE) in healthy individuals with acute SD. METHODS: Nurses with no history of acute or chronic diseases underwent TTE and STE after working a night shift, a sleepless period of 24 h and 7 days of normal sleep after the night shift. Measurements of TTE and STE taken in the rested state were compared with those taken after 24 h of sleep deprivation. RESULTS: The study included 52 nurses (38 women, 73%). The mean age of the study population was 27.9 ± 7.4 years and mean BMI was 24.1 ± 4.8. Left atrial reservoir (51.5 ± 13.5 vs. 45.4 ± 10; p = 0.004), conduit (- 37.3 ± 11.3 vs. - 33.6 ± 7.9; p = 0.01), left ventricular global longitudinal strain (LVGLS, - 22.6 ± 2.4 vs. - 21.3 ± 2.4; p = 0.001), right ventricular global longitudinal strain (RVGLS, - 25.3 ± 3.7 vs. - 23.5 ± 3.9; p = 0.005) and right ventricular free wall longitudinal strain (RVFWSL, - 29.1 ± 4.2 vs. - 27 ± 4.5; p = 0.001) were impaired significantly after SD. CONCLUSION: This study is the first to investigate the negative effects of acute sleep deprivation on LV and RV strain in healthy adults using echocardiography. The findings showed that acute sleep deprivation leads to deterioration in function of both ventricles and left atrium. Speckle tracking echocardiography demonstrated subclinical diminished heart function.

Dissociable brainstem functional connectivity changes correlate with objective and subjective vigilance decline after total sleep deprivation in healthy male subjects.

The maintenance of vigilance relies on the activation of the cerebral cortex by the arousal system centered on the brainstem. Previous studies have suggested that both objective and subjective vigilance are susceptible to sleep deprivation. This study aims to explore the alterations in brainstem arousal system functional connectivity (FC) and its involvement in these two types of vigilance decline following total sleep deprivation (TSD). Thirty-seven healthy male subjects underwent two counterbalanced resting-state fMRI scans, once in rested wakefulness (RW) and once after 36 h of TSD. The pontine tegmental area and caudal midbrain (PTA-cMidbrain), the core regions of the brainstem arousal system, were chosen as the seeds for FC analysis. The difference in PTA-cMidbrain FC between RW and TSD conditions was then investigated, as well as its associations with objective vigilance measured by psychomotor vigilance task (PVT) and subjective vigilance measured by Stanford Sleepiness Scale. The sleep-deprived subjects showed increased PTA-cMidbrain FC with the thalamus and cerebellum and decreased PTA-cMidbrain FC with the occipital, parietal, and sensorimotor regions. TSD-induced increases in PVT reaction time were negatively correlated with altered PTA-cMidbrain FC in the dorsolateral prefrontal cortex, extrastriate visual cortex, and precuneus. TSD-induced increases in subjective sleepiness were positively correlated with altered PTA-cMidbrain FC in default mode regions including the medial prefrontal cortex and precuneus. Our results suggest that different brainstem FC patterns underlie the objective and subjective vigilance declines induced by TSD.

Total Sleep Deprivation Increases Brain Age Prediction Reversibly in Multisite Samples of Young Healthy Adults.

Sleep loss pervasively affects the human brain at multiple levels. Age-related changes in several sleep characteristics indicate that reduced sleep quality is a frequent characteristic of aging. Conversely, sleep disruption may accelerate the aging process, yet it is not known what will happen to the age status of the brain if we can manipulate sleep conditions. To tackle this question, we used an approach of brain age to investigate whether sleep loss would cause age-related changes in the brain. We included MRI data of 134 healthy volunteers (mean chronological age of 25.3 between the age of 19 and 39 years, 42 females/92 males) from five datasets with different sleep conditions. Across three datasets with the condition of total sleep deprivation (>24 h of prolonged wakefulness), we consistently observed that total sleep deprivation increased brain age by 1-2 years regarding the group mean difference with the baseline. Interestingly, after one night of recovery sleep, brain age was not different from baseline. We also demonstrated the associations between the change in brain age after total sleep deprivation and the sleep variables measured during the recovery night. By contrast, brain age was not significantly changed by either acute (3 h time-in-bed for one night) or chronic partial sleep restriction (5 h time-in-bed for five continuous nights). Together, the convergent findings indicate that acute total sleep loss changes brain morphology in an aging-like direction in young participants and that these changes are reversible by recovery sleep.SIGNIFICANCE STATEMENT Sleep is fundamental for humans to maintain normal physical and psychological functions. Experimental sleep deprivation is a variable-controlling approach to engaging the brain among different sleep conditions for investigating the responses of the brain to sleep loss. Here, we quantified the response of the brain to sleep deprivation by using the change of brain age predictable with brain morphologic features. In three independent datasets, we consistently found increased brain age after total sleep deprivation, which was associated with the change in sleep variables. Moreover, no significant change in brain age was found after partial sleep deprivation in another two datasets. Our study provides new evidence to explain the brainwide effect of sleep loss in an aging-like direction.

Sleep deprivation altered encoding of basolateral amygdala on fear acquisition.

Sleep deprivation (SD) may lead to the development of fear- and anxiety-related emotional disorders. However, the neural mechanisms underlying the effects of SD on fear acquisition are unclear. Here, we tested whether and how SD influences the behavioral and neural manifestations of fear acquisition. We found that subjective fear ratings and objective fear indices (skin conductance response [SCR]) in the SD group were greater than those in the control group during fear acquisition, suggesting that SD facilitated fear acquisition (nSD = 18 and ncontrol = 23 for self-reported rating analysis; nSD = 10 and ncontrol = 10 for SCR analysis). Neuroimaging data showed that the SD group exhibited stronger activity in the left basolateral amygdala (BLA) and left superficial amygdala (SFA). Moreover, the left BLA activity, which positively correlated with the objective fear indices, significantly mediated the effect of SD on fear acquisition. Together, the present findings indicate that SD facilitates fear acquisition by augmenting threat-specific encoding in the BLA, which may be a potential biomarker of the risk of developing fear-related disorders under traumatic and distressing situations.

Functional Connectivity Alterations During Sleep Deprivation: Investigating Key Brain Regions and Networks.

BACKGROUND: Sleep deprivation (SD) has emerged as a significant public health concern because of its adverse effects on cognition and behavior. However, the influence of circadian rhythms on SD and brain activities has been less studied. This study employed functional magnetic resonance imaging (fMRI) and functional connectivity density (FCD) metrics to investigate the interaction between sleep pressure and circadian rhythms during SD. METHODS: Thirty-six volunteers with good sleep habits underwent a sleep deprivation trial. Sleepiness was assessed using the Stanford Sleepiness Scale (SSS) at multiple time points, and fMRI scans were conducted to derive global and local FCD (gFCD and iFCD) values. This study focused on specific brain regions and networks, including the thalamus, the frontoparietal network (FPN), and the default mode network (DMN). RESULTS: Analysis indicated significant changes in gFCD and iFCD values in several key brain regions. A strong correlation was found between sleepiness and both gFCD and iFCD values in certain areas, such as the left superior temporal gyrus and left thalamus. The gFCD values in these regions showed a gradual increase across sessions, while iFCD values in the right superior frontal gyrus decreased. CONCLUSIONS: This study revealed that SD leads to enhanced functional activities in the DMN and thalamus and decreased activity in the FPN. These changes in brain activity were significantly correlated with increases in sleepiness, as measured by the SSS. Our findings underscore the importance of understanding the neural underpinnings of SD and could guide future clinical interventions aimed at mitigating its effects.

Amide Proton Transfer-Weighted Imaging Detects Hippocampal Proteostasis Disturbance Induced by Sleep Deprivation at 7.0 T MRI.

Sleep deprivation leads to hippocampal injury. Proteostasis disturbance is an important mechanism linking sleep deprivation and hippocampal injury. However, identifying noninvasive imaging biomarkers for hippocampal proteostasis disturbance remains challenging. Amide proton transfer-weighted (APTw) imaging is a chemical exchange saturation transfer technique based on the amide protons in proteins and peptides. We aimed to explore the ability of APTw imaging in detecting sleep deprivation-induced hippocampal proteostasis disturbance and its biological significance, as well as its biological basis. In vitro, the feasibility of APTw imaging in detecting changes of the protein state was evaluated, demonstrating that APTw imaging can detect alterations in the protein concentration, conformation, and aggregation state. In vivo, the hippocampal APTw signal declined with increased sleep deprivation time and was significantly lower in sleep-deprived rats than that in normal rats. This signal was positively correlated with the number of surviving neurons counted in Nissl staining and negatively correlated with the expression of glucose-regulated protein 78 evaluated in immunohistochemistry. Differentially expressed proteins in proteostasis network pathways were identified in the hippocampi of normal rats and sleep-deprived rats via mass spectrometry proteomics analysis, providing the biological basis for the change of the hippocampal APTw signal in sleep-deprived rats. These findings demonstrate that APTw imaging can detect hippocampal proteostasis disturbance induced by sleep deprivation and reflect the extent of neuronal injury and endoplasmic reticulum stress.

Preoperative Acute Sleep Deprivation Causes Postoperative Pain Hypersensitivity and Abnormal Cerebral Function.

Preoperative sleep loss can amplify post-operative mechanical hyperalgesia. However, the underlying mechanisms are still largely unknown. In the current study, rats were randomly allocated to a control group and an acute sleep deprivation (ASD) group which experienced 6 h ASD before surgery. Then the variations in cerebral function and activity were investigated with multi-modal techniques, such as nuclear magnetic resonance, functional magnetic resonance imaging, c-Fos immunofluorescence, and electrophysiology. The results indicated that ASD induced hyperalgesia, and the metabolic kinetics were remarkably decreased in the striatum and midbrain. The functional connectivity (FC) between the nucleus accumbens (NAc, a subregion of the ventral striatum) and the ventrolateral periaqueductal gray (vLPAG) was significantly reduced, and the c-Fos expression in the NAc and the vLPAG was suppressed. Furthermore, the electrophysiological recordings demonstrated that both the neuronal activity in the NAc and the vLPAG, and the coherence of the NAc-vLPAG were suppressed in both resting and task states. This study showed that neuronal activity in the NAc and the vLPAG were weakened and the FC between the NAc and the vLPAG was also suppressed in rats with ASD-induced hyperalgesia. This study highlights the importance of preoperative sleep management for surgical patients.

Altered effective connectivity of thalamus with vigilance impairments after sleep deprivation.

The thalamus is an essential gating hub to relay brainstem ascending arousal signals to attention-related networks, including the frontal-parietal attention network and default mode network, which plays an important role in attentional maintenance. Research has proved that sleep loss leads to impairment of attentional performance by affecting neural connectivity between thalamic and attention-related cortical regions. However, the effective connectivity between thalamic and cortical areas in the resting state remains unclear after sleep deprivation. The present study aimed to investigate the effect of sleep deprivation on the effective connectivity between thalamic and cortical areas, and explored whether the alteration of the effective connectivity can predict vigilance impairment after sleep deprivation. We implemented resting-state functional magnetic resonance imaging with 31 participants under both normally-rested and sleep-deprivation conditions. The Granger causality analysis was used to investigate the alteration of effective connectivity between thalamic and cortical areas, and the psychomotor vigilance task was used to measure vigilance. Correlation analysis investigated the relationship between the alteration in effective connectivity and vigilance performance. Sleep deprivation significantly decreased the effective connectivity from the thalamus to the nodes in the default mode network, and significantly increased in the effective connectivity from the thalamus to the nodes in the frontal-parietal attention network. Critically, increased thalamus-parietal effective connectivity was correlated with decreased lapses. The findings indicated sleep deprivation induced a robust alteration of the communication from the sub-cortical to cortical regions. The alteration of thalamus-parietal effective connectivity was anti-correlated with sustained attentional impairment after sleep deprivation.

Abnormal dynamic functional connectivity after sleep deprivation from temporal variability perspective.

Sleep deprivation (SD) is very common in modern society and regarded as a potential causal mechanism of several clinical disorders. Previous neuroimaging studies have explored the neural mechanisms of SD using magnetic resonance imaging (MRI) from static (comparing two MRI sessions [one after SD and one after resting wakefulness]) and dynamic (using repeated MRI during one night of SD) perspectives. Recent SD researches have focused on the dynamic functional brain organization during the resting-state scan. Our present study adopted a novel metric (temporal variability), which has been successfully applied to many clinical diseases, to examine the dynamic functional connectivity after SD in 55 normal young subjects. We found that sleep-deprived subjects showed increased regional-level temporal variability in large-scale brain regions, and decreased regional-level temporal variability in several thalamus subregions. After SD, participants exhibited enhanced intra-network temporal variability in the default mode network (DMN) and increased inter-network temporal variability in numerous subnetwork pairs. Furthermore, we found that the inter-network temporal variability between visual network and DMN was negative related with the slowest 10% respond speed (ß = -.42, p = 5.57 × 10-4 ) of the psychomotor vigilance test after SD following the stepwise regression analysis. In conclusion, our findings suggested that sleep-deprived subjects showed abnormal dynamic brain functional configuration, which provides new insights into the neural underpinnings of SD and contributes to our understanding of the pathophysiology of clinical disorders.