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睡眠剥夺影响风险决策的大尺度脑网络模型*
The Large-Scale Brain Network Model of Sleep Deprivation on Risky Decision Making
随着科技发展，睡眠不足问题日益普遍，这会显著损害个体的认知和情绪功能。风险决策在生活中无处不在，并受到睡眠不足的影响。近年来，越来越多研究开始探讨睡眠剥夺对风险决策的影响，但大多关注不同程度睡眠剥夺对特定脑区和单一脑网络激活水平的影响，忽略了大尺度脑网络的整体作用。研究比较了完全睡眠剥夺和部分睡眠剥夺对风险决策的影响，并分别从大尺度脑网络视角分析其作用机制。研究强调了中央执行网络、奖赏网络和凸显网络在这一过程中的执行控制、奖惩预期和风险评估作用，共同决定个体的决策表现。最后，本文讨论了未来研究可以从建立神经计算模型、探究动态影响等方面继续探究。
Sleep is a fundamental physiological phenomenon that is essential for physical health, cognitive ability and emotional regulation. However, with technological advances and the accelerated pace of life, sleep deprivation has become increasingly prevalent, significantly impairing the cognitive and emotional functioning of individuals. Risky decision making, as a type of uncertain decision making, refers to the process by which people weigh options that have multiple outcomes and the probability of each outcome occurring is known. People make risky decisions all the time in their daily lives and at work. Most studies have confirmed that sleep deprivation significantly affects an individual's risky decision making preferences.
The neural processes by which sleep deprivation affects risky decision-making involve three main large-scale brain networks: the central executive network, the reward network, and the salience network. Specifically, when individuals experience total sleep deprivation, the activation level of the central executive network is significantly reduced, i.e., the dorsolateral prefrontal activation level decreases and the individual's inhibitory control is severely impaired. The activation levels of the orbitofrontal cortex and the ventral medial prefrontal within the reward network decreased, but the activation level of the striatum was enhanced, and the brain regions interacted with each other to greatly weaken the individual's ability to resist immediate rewards and avoid impulsive behaviors. At the same time, decreased activation levels in the amygdala and the anterior insula within the salience network, but enhanced activation levels in the anterior cingulate cortex, lead individuals to make more irrational decisions. The same three large-scale brain networks are included when individuals with partial sleep deprivation make risky decisions. The difference is that partial sleep deprivation only significantly decreases activation levels in the dorsolateral prefrontal and enhances activation levels in the anterior insula. However, partial sleep deprivation reduces the functional connectivity of the dorsolateral prefrontal and striatum, the anterior insula, and the orbitofrontal cortex and amygdala, resulting in the inability of individuals to effectively inhibit high-risk behaviors and reduce decision-making performance.
Previous studies have mostly focused on the effects of different levels of sleep deprivation on the level of activation in specific brain regions and single brain networks, but ignored the overall role of large-scale brain networks. It has been found that the brain integrates and processes information in the form of brain networks, and multiple brain networks work together to ultimately change an individual's behavioral performance. Complete sleep deprivation affects an individual's risky decision-making performance by directly altering the activation levels of the central executive, reward, and salience networks. When an individual receives a reward or suffers a loss, the activation of the reward network or salience network is further enhanced, which in turn affects the central executive network and ultimately alters the individual's subsequent risky decision-making performance. The feedback mechanism for risky decision-making in partial sleep deprivation is impaired, making it difficult to effectively regulate individual decision-making behavior. As in the case of total sleep deprivation, the results of risky decision making in individuals with partial sleep deprivation were fed back to the reward and salience networks, which influenced the individual's future decision making.
Future research is suggested to further explore the following issues. Considering the development prospects of machine learning and deep learning technologies, future research should use these technologies to computationally model the rich brain network data to further deepen the understanding of brain function and structure. In addition, the dynamic effects of different degrees of sleep deprivation on risky decision making are further refined by carefully dividing sleep deprivation time. At the same time, the generalizability of the effects of sleep deprivation on decision making is explored.
完全睡眠剥夺 / 部分睡眠剥夺 / 风险决策 / 大尺度脑网络模型
total sleep deprivation / partial sleep deprivation / risk decision-making / large-scale brain network model
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邓尧, 王梦梦, 饶恒毅. (2022). 风险决策研究中的仿真气球冒险任务. 心理科学进展, 30(6), 1377-1392.
仿真气球冒险任务(The Balloon Analog Risk Task, BART)能在实验室环境下模拟真实世界的风险情境, 具有高生态性, 稳定性和可靠性等优点, 已经成为风险决策研究中最常用的实验范式之一。近年来, 研究者发展了多种BART变体范式, 对发展、健康以及精神病理等多领域的风险决策行为及其神经基础开展了广泛探索。BART任务中的风险决策加工与腹侧纹状体、前扣带皮层、脑岛、中脑及背外侧前额叶等脑区的激活相关。未来研究需要进一步完善BART任务在风险决策认知神经领域的信效度并扩展BART的应用情境。
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龚诗阳, 张义博, 高月涛. (2023). 睡眠剥夺与购物后悔:来自大规模个体层面数据的证据. 心理学报, 55(2), 286-302.
睡眠剥夺正在成为人们面临的一种普遍问题, 但是已有研究很少将睡眠剥夺与消费者行为联系起来。本文采用真实购物情境下的大规模消费者个体层面数据(N = 1625472), 通过建立计量经济学模型来研究睡眠剥夺与购物后悔的关系。结果表明, 睡眠剥夺显著地增加了消费者的购物后悔倾向, 具体在行为上表现为增加了商品的退货概率和加快了商品的退货速度。此外, 商品的价格正向调节了睡眠剥夺对购物后悔的影响, 而促销优惠金额的比例则负向调节了睡眠剥夺对购物后悔的影响。
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刘晓婷, 张丽锦, 张宁. (2019). 睡眠质量对冒险行为影响的证据及解析. 心理科学进展, 27(11), 1875-1886.
睡眠质量影响个体冒险行为已得到许多研究的验证和支持。睡眠缺失既影响大脑前额叶功能的完整性, 也影响杏仁核、纹状体等脑区的激活, 从而降低了个体对危险的知觉和对损失的敏感, 导致冒险意愿和冒险行为增加。已往相关研究多以成人群体为研究对象, 且忽略了个体特质与所处社会环境在睡眠质量与冒险行为关系中的交互影响。由于青少年期睡眠不足和高冒险行为普遍存在, 未来研究应对青少年睡眠质量与冒险行为的关系及其中的影响作用机制, 尤其是神经机制给予更多关注。
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Previous work suggests that sleep restriction (SR) reduces cognitive control and may increase negative implicit biases. Here we investigated whether SR might influence decision making on a social-evaluative task where individuals had to make judgments of threat based on facial photographs. Furthermore, we investigated the effect of changes in negative implicit biases as a result of sleep restriction on this decision-making task.Fourteen healthy adults underwent two 3-week counterbalanced in-laboratory stays (chronic SR and control sleep [CS] conditions). Participants completed the Arab Muslim Names implicit association test (a measure of implicit bias/attitudes toward Arab Muslims) and the Karolinska Airport Task (a measure of explicit decision making). The Karolinska Airport Task requires participants to judge the potential dangerousness of individuals based on facial photographs.After SR, participants were more likely to deem individuals with less positive and more negative facial features as dangerous than after CS. In addition, after SR, those participants showing higher negative implicit bias toward Arab Muslims tended to consider as more dangerous individuals with more quintessentially untrustworthy facial features (r = 0.76, P = .007), whereas this relationship was nonsignificant after CS (r = 0.33, P = .28).These findings show not only that SR may increase implicit biases against a particular minority group but that SR also modifies how individuals make explicit decisions about another's trustworthiness based on facial features. These findings may have important implications for many occupations where workers who are routinely restricted of sleep are also responsible for making judgments about other people's trustworthiness (eg, police, security, military personnel).Copyright © 2018 National Sleep Foundation. Published by Elsevier Inc. All rights reserved.
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The striatum is a critical component of the brain that controls motor, reward, and executive function. This ancient and phylogenetically conserved structure forms a central hub where rapid instinctive, reflexive movements and behaviors in response to sensory stimulation or the retrieval of emotional memory intersect with slower planned motor movements and rational behaviors. This review emphasizes two distinct pathways that begin in the thalamus and converge in the striatum to differentially affect movements, behaviors, and decision making. The convergence of excitatory glutamatergic activity from the thalamus and cortex, along with dopamine release in response to novel stimulation, provide the basis for motor learning, reward seeking, and habit formation. We outline how the rules derived through research on neural pathways may enhance the predictability of reflexive actions and rational responses studied in behavioral economics.
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Adequate sleep is essential for general healthy functioning. This paper reviews recent research on the effects of chronic sleep restriction on neurobehavioral and physiological functioning and discusses implications for health and lifestyle. Restricting sleep below an individual's optimal time in bed (TIB) can cause a range of neurobehavioral deficits, including lapses of attention, slowed working memory, reduced cognitive throughput, depressed mood, and perseveration of thought. Neurobehavioral deficits accumulate across days of partial sleep loss to levels equivalent to those found after 1 to 3 nights of total sleep loss. Recent experiments reveal that following days of chronic restriction of sleep duration below 7 hours per night, significant daytime cognitive dysfunction accumulates to levels comparable to that found after severe acute total sleep deprivation. Additionally, individual variability in neurobehavioral responses to sleep restriction appears to be stable, suggesting a trait-like (possibly genetic) differential vulnerability or compensatory changes in the neurobiological systems involved in cognition. A causal role for reduced sleep duration in adverse health outcomes remains unclear, but laboratory studies of healthy adults subjected to sleep restriction have found adverse effects on endocrine functions, metabolic and inflammatory responses, suggesting that sleep restriction produces physiological consequences that may be unhealthy.
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Following damage to the ventromedial prefrontal cortex, humans develop a defect in real-life decision-making, which contrasts with otherwise normal intellectual functions. Currently, there is no neuropsychological probe to detect in the laboratory, and the cognitive and neural mechanisms responsible for this defect have resisted explanation. Here, using a novel task which simulates real-life decision-making in the way it factors uncertainty of premises and outcomes, as well as reward and punishment, we find that prefrontal patients, unlike controls, are oblivious to the future consequences of their actions, and seem to be guided by immediate prospects only. This finding offers, for the first time, the possibility of detecting these patients' elusive impairment in the laboratory, measuring it, and investigating its possible causes.
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The somatic marker hypothesis provides a systems-level neuroanatomical and cognitive framework for decision making and the influence on it by emotion. The key idea of this hypothesis is that decision making is a process that is influenced by marker signals that arise in bioregulatory processes, including those that express themselves in emotions and feelings. This influence can occur at multiple levels of operation, some of which occur consciously and some of which occur non-consciously. Here we review studies that confirm various predictions from the hypothesis. The orbitofrontal cortex represents one critical structure in a neural system subserving decision making. Decision making is not mediated by the orbitofrontal cortex alone, but arises from large-scale systems that include other cortical and subcortical components. Such structures include the amygdala, the somatosensory/insular cortices and the peripheral nervous system. Here we focus only on the role of the orbitofrontal cortex in decision making and emotional processing, and the relationship between emotion, decision making and other cognitive functions of the frontal lobe, namely working memory.
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During insightful problem solving, the solution appears unexpectedly and is accompanied by the feeling of an AHA!. Research suggests that this affective component of insight can have consequences beyond the solution itself by motivating future behavior, such as risky (high reward and high uncertainty) decision making. Here, we investigate the behavioral and neural support for the motivational role of AHA in decision making involving monetary choices. The positive affect of the AHA! experience has been linked to internal reward. Reward in turn has been linked to dopaminergic signal transmission in the Nucleus Accumbens (NAcc) and risky decision making. Therefore, we hypothesized that insight activates reward-related brain areas, modulating risky decision making. We tested this hypothesis in two studies. First, in a pre-registered online study (Study 1), we demonstrated the behavioral effect of insight-related increase in risky decision making using a visual Mooney identification paradigm. Participants were more likely to choose the riskier monetary payout when they had previously solved the Mooney image with high compared to low accompanied AHA!. Second, in an fMRI study (Study 2), we measured the effects of insight on NAcc activity using a similar Mooney identification paradigm to the one of Study 1. Greater NAcc activity was found when participants solved the Mooney image with high vs low AHA!. Taken together, our results link insight to enhanced NAcc activity and a preference for high but uncertain rewards, suggesting that insight enhances reward-related brain areas possibly via dopaminergic signal transmission, promoting risky decision making.© 2023. Springer Nature Limited.
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Here we report preliminary findings from a small-sample functional magnetic resonance imaging (fMRI) study of healthy adolescents who completed a working memory task in the context of a chronic sleep restriction experiment. Findings were consistent with those previously obtained on acutely sleep-deprived adults. Our data suggest that, when asked to maintain attention and burdened by chronic sleep restriction, the adolescent brain responds via compensatory mechanisms that accentuate the typical activation patterns of attention-relevant brain regions. Specifically, it appeared that regions that are normally active during an attention-demanding working memory task in the well-rested brain became even more active to maintain performance after chronic sleep restriction. In contrast, regions in which activity is normally suppressed during such a task in the well-rested brain showed even greater suppression to maintain performance after chronic sleep restriction. Although limited by the small sample, study results provide important evidence of feasibility, as well as guidance for future research into the functional neurological effects of chronic sleep restriction in general, the effects of sleep restriction in children and adolescents, and the neuroscience of attention and its disorders in children.
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Rapid eye movement sleep (REMS) has been linked with spatial and emotional memory consolidation. However, establishing direct causality between neural activity during REMS and memory consolidation has proven difficult because of the transient nature of REMS and significant caveats associated with REMS deprivation techniques. In mice, we optogenetically silenced medial septum γ-aminobutyric acid-releasing (MS(GABA)) neurons, allowing for temporally precise attenuation of the memory-associated theta rhythm during REMS without disturbing sleeping behavior. REMS-specific optogenetic silencing of MS(GABA) neurons selectively during a REMS critical window after learning erased subsequent novel object place recognition and impaired fear-conditioned contextual memory. Silencing MS(GABA) neurons for similar durations outside REMS episodes had no effect on memory. These results demonstrate that MS(GABA) neuronal activity specifically during REMS is required for normal memory consolidation. Copyright © 2016, American Association for the Advancement of Science.
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Various neuropsychological studies have shown that decision-making deficits can occur in a wide range of patients with brain damage or dysfunctions. Decisions under ambiguity, as measured with the Iowa Gambling Task, primarily depend on the integrity of the ventromedial prefrontal cortex and the amygdala, as well as on further brain regions such as the somatosensory cortex. However, little is known about the specific role of these structures in decisions under risk measured with tasks that offer explicit rules for gains and losses and winning probabilities, for example, the Game of Dice Task. We aimed to investigate the potential role of the amygdala for decisions under risk. For this purpose, we examined three patients with Urbach-Wiethe disease--a rare syndrome associated with selective bilateral mineralisation of the amygdalae. Neuropsychological performance was assessed with the Iowa Gambling Task (decisions under ambiguity), the Game of Dice Task (decisions under risk), and an extensive neuropsychological test battery focussing on executive functions. Furthermore, previous studies found relationships between generating skin conductance responses and deciding advantageously in the Iowa Gambling Task. Accordingly, we recorded skin conductance responses during both decision tasks as a measure of emotional reactivity. Results indicate that patients with selective amygdala damage have lower scores in both decisions under ambiguity and decisions under risk. Decisions under risk are especially compromised in patients who also demonstrate deficits in executive functioning. In both gambling tasks, patients showed reduced skin conductance responses compared to healthy comparison subjects. The results suggest that deciding advantageously under risk conditions involves both the use of feedback from previous trials, as required by decisions under ambiguity, and in addition, executive functions.
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The anterior cingulate cortex (ACC) and the related medial wall play a critical role in recruiting cognitive control. Although ACC exhibits selective error and conflict responses, it has been unclear how these develop and become context-specific. With use of a modified stop-signal task, we show from integrated computational neural modeling and neuroimaging studies that ACC learns to predict error likelihood in a given context, even for trials in which there is no error or response conflict. These results support a more general error-likelihood theory of ACC function based on reinforcement learning, of which conflict and error detection are special cases.
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The Iowa Gambling Task (IGT) was created to assess real-world decision making in a laboratory setting and has been applied to various clinical populations (i.e., substance abuse, schizophrenia, pathological gamblers) outside those with orbitofrontal cortex damage, for whom it was originally developed. The current review provides a critical examination of lesion, functional neuroimaging, developmental, and clinical studies in order to examine the construct validity of the IGT. The preponderance of evidence provides support for the use of the IGT to detect decision making deficits in clinical populations, in the context of a more comprehensive evaluation. The review includes a discussion of three critical issues affecting the validity of the IGT, as it has recently become available as a clinical instrument: the lack of a concise definition as to what aspect of decision making the IGT measures, the lack of data regarding reliability of the IGT, and the influence of personality and state mood on IGT performance.
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A growing body of research has placed the ventral striatum at the center of a network of cerebral regions involved in anticipating rewards in healthy controls. However, little is known about the functional connectivity of the ventral striatum associated with reward anticipation in healthy controls. In addition, few studies have investigated reward anticipation in healthy humans with different levels of schizotypy. Here, we investigated reward anticipation in eighty-four healthy individuals (44 females) recruited based on their schizotypy scores. Participants performed a variant of the Monetary Incentive Delay Task while undergoing event-related fMRI.Participants showed the expected decrease in response times for highly rewarded trials compared to non-rewarded trials. Whole-brain activation analyses replicated previous results, including activity in the ventral and dorsal striatum. Whole-brain psycho-physiological interaction analyses of the left and right ventral striatum revealed increased connectivity during reward anticipation with widespread regions in frontal, parietal and occipital cortex as well as the cerebellum and midbrain. Finally, we found no association between schizotypal personality severity and neural activity and cortico-striatal functional connectivity. In line with the motivational, attentional, and motor functions of rewards, our data reveal multifaceted cortico-striatal networks taking part in reward anticipation in healthy individuals. The ventral striatum is connected to regions of the salience, attentional, motor and visual networks during reward anticipation and thereby in a position to orchestrate optimal goal-directed behavior.
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Functional magnetic resonance imaging (fMRI) research rarely reports gender differences in the neural correlates of risk decision making due to small sample sizes. In this functional near-infrared spectroscopy (fNIRS)-based imaging study of active and passive risk decision making, gender differences in oxygenated hemoglobin (HbO) concentration changes were investigated in the prefrontal cortex (PFC) of healthy adults. Forty adult participants (25-44 years; males=23) completed two sets of 15 balloon trials in active and passive decision making modes of the Balloon Analogue Risk Task (BART). In active mode, participants chose the number of balloon inflations, decided when to collect money, or risked accrued money if balloons exploded. BART is psychometrically well established and has predictive validity to real-world risk taking. The blocked experimental design and modification of BART for fNIRS were guided by a previous fMRI study that examined the neural correlates of risk decision making in young adults [Rao, H., Korczykowski, M., Pluta, J., Hoang, A., Detre, J.A., 2008. Neural correlates of voluntary and involuntary risk taking in the human brain: An fMRI study of the Balloon Analog Risk Task (BART). NeuroImage 42, 902-910]. Our findings were consistent with the previous fMRI study: no or little PFC activation during passive mode but strong PFC activation during active wins and losses among total sample. Active losses in females were associated with more significant bilateral activation in dorsal lateral prefrontal cortex (DLPFC) than males; no significant gender differences were found in DLPFC activation during active wins. Gender differences existed in direction and strength of correlations between BART behavioral and hemodynamic data. This study shows that use of fNIRS is a feasible, accessible, and less costly way to achieve adequate study power and investigate gender differences in neural correlates of risk decision making.Copyright © 2012 Elsevier Inc. All rights reserved.
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Background: Previous studies revealed that sleep deprivation (SD) impairs risk perception and leads to poor decision-making efficiency. However, how risk perception is related to brain regions’ communication after SD has not been elucidated. In this study, we investigated the neuropsychological mechanisms of SD-impaired risk perception. Methods: Nineteen healthy male adults were recruited and underwent resting-state functional magnetic resonance imaging during a state of rested wakefulness and after nearly 36 h of total SD. They then completed the balloon analog risk task, which was used to measure the risk perception ability of risky decision-making. Regional homogeneity (ReHo) and voxel-wise functional connectivity were used to investigate neurobiological changes caused by SD. Correlation analysis was used to investigate the relationship between changes in ReHo, function, and risk perception. Results: At the behavioral level, risk perception decreased after 36 h of SD. At the neural level, SD induced a significant increase in ReHo in the right postcentral gyrus and was positively correlated with risk perception changes. The functional connectivity between the right postcentral gyrus, left medial temporal gyrus, and right inferior temporal gyrus was enhanced. Critically, increased right postcentral gyrus and right inferior temporal gyrus connectivity positively correlated with changes in risk perception. Conclusions: SD impairs the risk perception associated with altered postcentral connectivity. The brain requires more energy to process and integrate sensory and perceptual information after SD, which may be one possible reason for decreased risk perception ability after SD.
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Idiopathic rapid eye movement sleep behavior disorder (iRBD) is a prodromal stage of synucleinopathies. Patients with synucleinopathies frequently display eye movement abnormalities. However, whether patients with iRBD have eye movement abnormalities remains unknown.The aim of this study was to assess eye movement abnormalities and related gray matter alterations and explore whether such abnormalities can serve as biomarkers to indicate phenoconversion to synucleinopathies in iRBD.Forty patients with iRBD with early disease progression and 35 healthy control subjects participated in a 15-minute ocular-tracking task that evaluated their control of eye movement abilities. They also underwent clinical assessments for olfactory function, nonmotor symptoms, and autonomic symptoms, all of which are biomarkers to predict phenoconversion to synucleinopathies in iRBD. A subgroup of the participants (20 patients with iRBD and 20 healthy control subjects) also participated in structural magnetic resonance imaging.The ocular-tracking ability in patients with iRBD was inferior to that of healthy control subjects in two aspects: pursuit initiation and steady-state tracking. Cortical thinning in the right visual area V4 in patients with iRBD is coupled with impaired pursuit initiation. Furthermore, prolonged pursuit initiation in patients with iRBD exhibits a trend of correlation with olfactory loss, the earliest biomarker that develops prior to other prodromal biomarkers.We found ocular-tracking abnormalities in patients with iRBD even early in their disease progression that have not been reported before. These abnormalities are coupled with atrophy of brain areas involved in the perception of object motion and might indicate phenoconversion to synucleinopathies in iRBD. © 2022 International Parkinson and Movement Disorder Society.© 2022 International Parkinson and Movement Disorder Society.
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External information can modify the subjective value of a tasted stimulus, but little is known about neural mechanisms underlying these behavioral modifications. This study used flavored drinks to produce variable degrees of discrepancy between expected and received flavor. During a learning session, 43 healthy young men learned 4 symbol-flavor associations. In a separate session, associations were presented again during an fMRI scan, but half of the trials introduced discrepancy with previously learned associations. Liking ratings of drinks were collected and were analyzed using a linear model to define the degree to which discrepant symbols affected liking ratings of the subjects during the fMRI session. Based on these results, a GLM analysis of fMRI data was conducted to determine neural correlates of observed behavior. Groups of subjects were composed based on their behavior in response to discrepant symbols, and comparison of brain activity between groups showed that activation in the PCC and the caudate nucleus was more potent in those subjects in which liking was not affected by discrepant symbols. These activations were not found in subjects who assimilated unexpected flavors to flavors preceeded by discrepant symbols. Instead, these subjects showed differences in the activity in the parietal operculum. The activity of reward network appears to be related to assimilation of received flavor to expected flavor in response to symbol-flavor discrepancy.Copyright © 2018 Elsevier Inc. All rights reserved.
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This study was designed to assess decision making and executive functions in patients with idiopathic REM sleep behavior disorder (iRBD). IRBD is often seen as an early sign of later evolving neurodegenerative disease, most importantly Parkinson disease (PD) and Lewy body dementia (DLB). It has been proposed that iRBD patients show a cognitive profile similar to patients with PD.All participants performed an extensive test battery tapping executive functions as well as the IOWA gambling task, which measures decision making under ambiguity.University hospital sleep disorders center.16 iRBD patients and 45 age- and education-matched controls.N.A.Compared with controls, iRBD patients showed disadvantageous decision making under ambiguity and did not learn by feedback over the task. IRBD patients' decision pattern was characterized by the lack of a consistent strategy, as indicated by frequent shifts between the single choices. A high proportion of iRBD patients (75%) showed random performance or worse even at the end of the task. No group differences were found in tasks assessing information sampling, flexibility and categorization, problem solving, and impulsivity.As suggested by the present investigation, iRBD patients may show difficulties in decision making under ambiguity in a stage when other cognitive functions are relatively well preserved. Whether this is driven by subgroups of patients prone to develop PD or DLB has to be assessed by follow-up investigations.
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Sleep is a complex and dynamic process for maintaining homeostasis, and a lack of sleep can disrupt whole-body functioning. No organ is as vulnerable to the loss of sleep as the brain. Accordingly, we examined a set of task-based functional magnetic resonance imaging (fMRI) data by using graph theory to assess brain topological changes in subjects in a state of chronic sleep restriction, and then identified diurnal variability in the graph-theoretic measures. Task-based fMRI data were collected in a 1.5T MR scanner from the same participants on two days: after a week of fully restorative sleep and after a week with 35% sleep curtailment. Each day included four scanning sessions throughout the day (at approximately 10:00 AM, 2:00 PM, 6:00 PM, and 10:00 PM). A modified spatial cueing task was applied to evaluate sustained attention. After sleep restriction, the characteristic path length significantly increased at all measurement times, and small-worldness significantly decreased. Assortativity, a measure of network fault tolerance, diminished over the course of the day in both conditions. Local graph measures were altered primarily across the limbic system (particularly in the hippocampus, parahippocampal gyrus, and amygdala), default mode network, and visual network.Copyright © 2019 Farahani, Fafrowicz, Karwowski, Douglas, Domagalik, Beldzik, Oginska and Marek.
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Sleep is imperative for brain health and well-being, and restorative sleep is associated with better cognitive functioning. Increasing evidence indicates that electrophysiological measures of sleep, especially slow wave activity (SWA), regulate the consolidation of motor and perceptual procedural memory. In contrast, the role of sleep EEG and SWA in modulating executive functions, including working memory (WM), has been far less characterized. Here, we investigated across-night changes in sleep EEG that may ameliorate WM performance. Participants (N = 25, M = 100%) underwent two consecutive nights with high-density EEG, along with N-back tasks, which were administered at three time points the day before and after the second night of sleep. Non-rapid eye movement sleep EEG power spectra, power topography, as well as several slow-wave parameters were computed and compared across nights. Improvers on the 1-back, but not non-improvers, showed a significant increase in SWA as well as in down slope and negative peak amplitude, in a fronto-parietal region, and these parameters increases predicted better WM performance. Overall, these findings show that slow-wave sleep has a beneficial effect on WM and that it can occur in the adult brain even after minimal training. This is especially relevant, when considering that WM and other executive function cognitive deficits are present in several neuropsychiatric disorders, and that slow-wave enhancing interventions can improve cognition, thus providing novel insights and treatment strategies for these patients.Copyright © 2019 Elsevier Inc. All rights reserved.
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Over the years, rapid eye movement (REM) sleep has been associated with general memory consolidation, specific consolidation of perceptual, procedural, emotional and fear memories, brain maturation and preparation of waking consciousness. More recently, some of these associations (e.g., general and procedural memory consolidation) have been shown to be unlikely, while others (e.g., brain maturation and consciousness) remain inconclusive. In this review, we argue that both behavioral and neurophysiological evidence supports a role of REM sleep for amygdala-related memory processing: the amygdala-hippocampus-medial prefrontal cortex network involved in emotional processing, fear memory and valence consolidation shows strongest activity during REM sleep, in contrast to the hippocampus-medial prefrontal cortex only network which is more active during non-REM sleep. However, more research is needed to fully understand the mechanisms. Copyright © 2015 Elsevier Inc. All rights reserved.
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| [42] |
Appropriate interpretation of pleasurable, rewarding experiences favors decisions that enhance survival. Conversely, dysfunctional affective brain processing can lead to life-threatening risk behaviors (e.g., addiction) and emotion imbalance (e.g., mood disorders). The state of sleep deprivation continues to be associated with maladaptive emotional regulation, leading to exaggerated neural and behavioral reactivity to negative, aversive experiences. However, such detrimental consequences are paradoxically aligned with the perplexing antidepressant benefit of sleep deprivation, elevating mood in a proportion of patients with major depression. Nevertheless, it remains unknown how sleep loss alters the dynamics of brain and behavioral reactivity to rewarding, positive emotional experiences. Using functional magnetic resonance imaging (fMRI), here we demonstrate that sleep deprivation amplifies reactivity throughout human mesolimbic reward brain networks in response to pleasure-evoking stimuli. In addition, this amplified reactivity was associated with enhanced connectivity in early primary visual processing pathways and extended limbic regions, yet with a reduction in coupling with medial frontal and orbitofrontal regions. These neural changes were accompanied by a biased increase in the number of emotional stimuli judged as pleasant in the sleep-deprived group, the extent of which exclusively correlated with activity in mesolimbic regions. Together, these data support a view that sleep deprivation not only is associated with enhanced reactivity toward negative stimuli, but imposes a bidirectional nature of affective imbalance, associated with amplified reward-relevant reactivity toward pleasure-evoking stimuli also. Such findings may offer a neural foundation on which to consider interactions between sleep loss and emotional reactivity in a variety of clinical mood disorders.
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| [43] |
Every day, individuals make dozens of choices between an alternative with higher overall value and a more tempting but ultimately inferior option. Optimal decision-making requires self-control. We propose two hypotheses about the neurobiology of self-control: (i) Goal-directed decisions have their basis in a common value signal encoded in ventromedial prefrontal cortex (vmPFC), and (ii) exercising self-control involves the modulation of this value signal by dorsolateral prefrontal cortex (DLPFC). We used functional magnetic resonance imaging to monitor brain activity while dieters engaged in real decisions about food consumption. Activity in vmPFC was correlated with goal values regardless of the amount of self-control. It incorporated both taste and health in self-controllers but only taste in non-self-controllers. Activity in DLPFC increased when subjects exercised self-control and correlated with activity in vmPFC.
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| [44] |
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| [45] |
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| [46] |
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| [47] |
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| [48] |
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| [49] |
Risk tolerance, the degree to which an individual is willing to tolerate risk in order to achieve a greater expected return, influences a variety of financial choices and health behaviors. Here we identify intrinsic neural markers for risk tolerance in a large (n = 108) multimodal imaging dataset of healthy young adults, which includes anatomical and resting-state functional MRI and diffusion tensor imaging. Using a data-driven approach, we found that higher risk tolerance was most strongly associated with greater global functional connectivity (node strength) of and greater gray matter volume in bilateral amygdala. Further, risk tolerance was positively associated with functional connectivity between amygdala and medial prefrontal cortex and negatively associated with structural connectivity between these regions. These findings show how the intrinsic functional and structural architecture of the amygdala, and amygdala-medial prefrontal pathways, which have previously been implicated in anxiety, are linked to individual differences in risk tolerance during economic decision making.Copyright © 2018 Elsevier Inc. All rights reserved.
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| [50] |
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| [51] |
Although not fully understood, sleep is accepted as a vital and organized sequence of events that follows a regular cyclic program each night to ensure the human body can perform at its optimum. A lack of sleep, or sleep deprivation (SD), is a widespread phenomenon that can induce adverse changes in cognitive performance. This review focused on the biological explanation as well as the research investigating the numerous effects that SD can have on cognition. A reduction in sleep does not occur independently of the effects on memory, attention, alertness, judgment, decision-making, and overall cognitive abilities in the brain, resulting in decreased function and impaired cognitive performance.Copyright: © Neurosciences.
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| [52] |
Individuals differ along a continuum of preference for diurnal activity level, known as Morningness-Eveningness. Individuals low in Morningness traits, i.e., preferring later awakening and bed times, have been shown to score higher on personality traits of impulsiveness and novelty-seeking. No studies have yet examined the association between Morningness-Eveningness and the related construct of risk-taking. Therefore, the present study examined (1) whether Morningness was correlated with self-reported and behavioral measures of risk-taking, and (2) whether one night of sleep deprivation would produce changes in risk-taking and sensation-seeking. 54 healthy adults were administered the Morningness-Eveningness Questionnaire at intake, and administered the Brief Sensation Seeking Scale, Evaluation of Risks Scale, and Balloon Analog Risk Task at rested baseline, again following 23 hr. of sleep deprivation, and finally after a 12-hr. period of recovery sleep. Lower Morningness scores were associated with higher self-reported total risk-taking propensity when rested (p<.05) and sleep deprived (p<.005), but correlations were not significant for sensation seeking or actual risk-taking behavior. Relative to baseline and postrecovery periods, sleep deprivation significantly reduced risk-taking propensity, including self-report indices of self-control, danger-seeking, energy level, and sensation-seeking, and behaviorally measured risk-taking. Chronotype did not interact with sleep condition for any of the dependent variables, although Evening Types scored higher on several indices of risk-propensity. Findings suggest that Morningness traits are inversely related to greater risk-taking propensity, while sleep deprivation significantly reduces self-reported and behaviorally demonstrated willingness to engage in high-risk and sensational activities under conditions of uncertainty, regardless of chronotype.
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| [53] |
Sleep deprivation reduces regional cerebral metabolism within the prefrontal cortex, the brain region most responsible for higher-order cognitive processes, including judgment and decision making. Accordingly, we hypothesized that two nights of sleep loss would impair decision making quality and lead to increased risk-taking behavior on the Iowa Gambling Task (IGT), which mimics real-world decision making under conditions of uncertainty. Thirty-four healthy participants completed the IGT at rested baseline and again following 49.5 h of sleep deprivation. At baseline, volunteers performed in a manner similar to that seen in most samples of healthy normal individuals, rapidly learning to avoid high-risk decks and selecting more frequently from advantageous low-risk decks as the game progressed. After sleep loss, however, volunteers showed a strikingly different pattern of performance. Relative to rested baseline, sleep-deprived individuals tended to choose more frequently from risky decks as the game progressed, a pattern similar to, though less severe than, previously published reports of patients with lesions to the ventromedial prefrontal cortex. Although risky decision making was not related to participant age when tested at rested baseline, age was negatively correlated with advantageous decision making on the IGT, when tested following sleep deprivation (i.e. older subjects made more risky choices). These findings suggest that cognitive functions known to be mediated by the ventromedial prefrontal cortex, including decision making under conditions of uncertainty, may be particularly vulnerable to sleep loss and that this vulnerability may become more pronounced with increased age.
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| [54] |
Sleep deprivation alters risk-related judgments, decision-making, and behavioral control. Stimulant medications are used to restore cognitive performance, but their effects on risk-taking and judgment in sleep-deprived subjects have not been explored.There were 54 healthy adults (29 men, 25 women; age range 18 to 36) who completed a test of cognitive ability and daily measures of risk-taking propensity, including the Brief Sensation Seeking Scale (BSSS), Evaluation of Risks (EVAR) scale, and the Balloon Analog RiskTask (BART). Following 44 h of continuous wakefulness, participants ingested caffeine 600 mg (N = 12), dextroamphetamine 20 mg (N = 16), modafinil 400 mg (N = 12), or a placebo (N = 14) in a double blind manner, and completed risk-taking measures 2 h later (i.e., 0535).Relative to rested baseline, the placebo group showed a decline in risk-taking as measured by the BSSS (16% decline), EVAR Danger Seeking (32% decline) and Energy (22% decline), and BART (32% decline), consistent with previous reports of the effects of sleep deprivation. Comparisons among drug conditions showed that dextroamphetamine restored risk-taking propensity and risky behavior to baseline levels, an effect that was significantly greater than placebo or caffeine for several indices of risk-taking, but which did not differ from modafinil. Cognitive ability was significantly correlated with changes on some risk-taking indices following stimulant administration.Stimulant medications, particularly dextroamphetamine, sustained risk-related attitudes and behavior during continuous wakefulness. The extent to which stimulants restore other aspects of judgment during sleep loss remains to be determined.
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| [55] |
Previous research suggests that sleep deprivation is associated with declines in metabolic activity within brain regions important for judgement and impulse control, yet previous studies have reported inconsistent findings regarding the effects of sleep loss and caffeine on risk-taking. In this study, 25 healthy adults (21 men, four women) completed the Balloon Analog Risk Task (BART) and Evaluation of Risks (EVAR) scale at regular intervals to examine behavioral and self-reported risk-taking propensity during 75 h of continuous sleep deprivation. Participants received either four double-blind administrations of 200 mg caffeine (n=12) or indistinguishable placebo (n=13) gum bi-hourly during each of the 3 nights of sleep deprivation. No significant effects of drug group or sleep deprivation were evident on the BART or EVAR when measured at 51 h of wakefulness. However, by 75 h, the placebo group showed a significant increase in risk-taking behavior on the cost-benefit ratio and total number of exploded balloons on the BART, whereas the caffeine group remained at baseline levels. On the EVAR, several factors of self-reported risk-taking propensity, including total risk, impulsivity and risk/thrill seeking, were reduced among subjects receiving caffeine across the 3 days of sleep deprivation, but remained at baseline levels for the placebo group. These results suggest that 3 nights of total sleep deprivation led to a significant increase in behavioral risk-taking but not self-reported perception of risk-propensity. Overnight caffeine prevented this increase in risky behavior.Published 2010. This article is a US Government work and is in the public domain in the USA.
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| [56] |
Sometimes when a choice is made, the outcome is not guaranteed and there is only a probability of its occurrence. Each individual's attitude to probability, sometimes called risk proneness or aversion, has been assumed to be static. Behavioral ecological studies, however, suggest such attitudes are dynamically modulated by the context an organism finds itself in; in some cases, it may be optimal to pursue actions with a low probability of success but which are associated with potentially large gains. We show that human subjects rapidly adapt their use of probability as a function of current resources, goals, and opportunities for further foraging. We demonstrate that dorsal anterior cingulate cortex (dACC) carries signals indexing the pressure to pursue unlikely choices and signals related to the taking of such choices. We show that dACC exerts this control over behavior when it, rather than ventromedial prefrontal cortex, interacts with posterior cingulate cortex. Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.
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| [57] |
How does a lack of sleep affect our brains? In contrast to the benefits of sleep, frameworks exploring the impact of sleep loss are relatively lacking. Importantly, the effects of sleep deprivation (SD) do not simply reflect the absence of sleep and the benefits attributed to it; rather, they reflect the consequences of several additional factors, including extended wakefulness. With a focus on neuroimaging studies, we review the consequences of SD on attention and working memory, positive and negative emotion, and hippocampal learning. We explore how this evidence informs our mechanistic understanding of the known changes in cognition and emotion associated with SD, and the insights it provides regarding clinical conditions associated with sleep disruption.
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| [58] |
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| [59] |
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| [60] |
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| [61] |
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| [62] |
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| [63] |
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| [64] |
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| [65] |
Attention is a cognitive domain that can be severely affected by sleep deprivation. Previous neuroimaging studies have used different attention paradigms and reported both increased and reduced brain activation after sleep deprivation. However, due to large variability in sleep deprivation protocols, task paradigms, experimental designs, characteristics of subject populations, and imaging techniques, there is no consensus regarding the effects of sleep loss on the attending brain. The aim of this meta-analysis was to identify brain activations that are commonly altered by acute total sleep deprivation across different attention tasks.Coordinate-based meta-analysis of neuroimaging studies of performance on attention tasks during experimental sleep deprivation.The current version of the activation likelihood estimation (ALE) approach was used for meta-analysis. The authors searched published articles and identified 11 sleep deprivation neuroimaging studies using different attention tasks with a total of 185 participants, equaling 81 foci for ALE analysis.The meta-analysis revealed significantly reduced brain activation in multiple regions following sleep deprivation compared to rested wakefulness, including bilateral intraparietal sulcus, bilateral insula, right prefrontal cortex, medial frontal cortex, and right parahippocampal gyrus. Increased activation was found only in bilateral thalamus after sleep deprivation compared to rested wakefulness.Acute total sleep deprivation decreases brain activation in the fronto-parietal attention network (prefrontal cortex and intraparietal sulcus) and in the salience network (insula and medial frontal cortex). Increased thalamic activation after sleep deprivation may reflect a complex interaction between the de-arousing effects of sleep loss and the arousing effects of task performance on thalamic activity.© 2015 Associated Professional Sleep Societies, LLC.
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| [66] |
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| [67] |
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| [68] |
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| [69] |
Chronic sleep restriction is highly prevalent in modern society and is, in its clinical form, insufficient sleep syndrome, one of the most prevalent diagnoses in clinical sleep laboratories, with substantial negative impact on health and community burden. It reflects every-day sleep loss better than acute sleep deprivation, but its effects and particularly the underlying mechanisms remain largely unknown for a variety of critical cognitive domains, as, for example, risky decision making.We assessed financial risk-taking behavior after 7 consecutive nights of sleep restriction and after 1 night of acute sleep deprivation compared to a regular sleep condition in a within-subject design. We further investigated potential underlying mechanisms of sleep-loss-induced changes in behavior by high-density electroencephalography recordings during restricted sleep.We show that chronic sleep restriction increases risk-seeking, whereas this was not observed after acute sleep deprivation. This increase was subjectively not noticed and was related to locally lower values of slow-wave energy during preceding sleep, an electrophysiological marker of sleep intensity and restoration, in electrodes over the right prefrontal cortex.This study provides, for the first time, evidence that insufficient sleep restoration over circumscribed cortical areas leads to aberrant behavior. In chronically sleep restricted subjects, low slow-wave sleep intensity over the right prefrontal cortex-which has been shown to be linked to risk behavior-may lead to increased and subjectively unnoticed risk-seeking. Ann Neurol 2017;82:409-418.© 2017 American Neurological Association.
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| [70] |
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| [71] |
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| [72] |
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| [73] |
Sleep deprivation (SD) has detrimental effects on cognition, but the affected psychological processes and underlying neural mechanisms are still essentially unclear. Here we combined functional magnetic resonance imaging and computational modeling to examine how SD alters neural representation of specific choice variables (subjective value and decision conflict) during reward-related decision making. Twenty-two human subjects underwent two functional neuroimaging sessions in counterbalanced order, once during rested wakefulness and once after 24 h of SD. Behaviorally, SD attenuated conflict-dependent slowing of response times, which was reflected in an attenuated conflict-induced decrease in drift rates in the drift diffusion model. Furthermore, SD increased overall choice stochasticity during risky choice. Model-based functional neuroimaging revealed attenuated parametric subjective value signals in the midbrain, parietal cortex, and ventromedial prefrontal cortex after SD. Conflict-related midbrain signals showed a similar downregulation. Findings are discussed with respect to changes in dopaminergic signaling associated with the sleep-deprived state.
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| [74] |
In everyday life, risky decision-making relies on multiple cognitive processes including sensitivity to reinforcers, exploration, learning, and forgetting. Neuroimaging evidence suggests that the dorsolateral prefrontal cortex (DLPFC) is involved in exploration and risky decision-making, but the nature of its computations and its causal role remain uncertain. We provide evidence for the role of the DLPFC in value-independent, directed exploration on the Iowa Gambling Task (IGT) and we describe a new computational model to account for the competition of directed exploration and exploitation in guiding decisions. Forty-two healthy human participants were included in a right DLPFC, left DLPFC or sham stimulation groups using continuous theta-burst stimulation (cTBS). Immediately after cTBS, the IGT was completed. Computational modelling was used to account for exploration and exploitation with different combinations with value-based and sensitivity to reinforcers for each group. Applying cTBS to the left and right DLPFC selectively decreased directed exploration on the IGT compared to sham stimulation. Model-based analyses further indicated that the right (but not the left) DLPFC stimulation increased sensitivity to reinforcers, leading to avoidance of risky choices and promoting advantageous choices during the task. Although these findings are based on small sample sizes per group, they nevertheless elucidate the causal role of the right DLPFC in governing the exploration-exploitation tradeoff during decision-making in uncertain and ambiguous contexts.Copyright © 2021 IBRO. Published by Elsevier Ltd. All rights reserved.
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| [75] |
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| [76] |
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| [77] |
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| [78] |
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| [79] |
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| [80] |
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| [81] |
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| [82] |
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| [83] |
Increasing effort has been devoted to understanding the neural mechanisms underlying decision making during risk, yet little is known about the effect of voluntary choice on risk taking. The Balloon Analog Risk Task (BART), in which subjects inflate a virtual balloon that can either grow larger or explode [Lejuez, C.W., Read, J.P., Kahler, C.W., Richards, J.B., Ramsey, S.E., Stuart, G.L., Strong, D.R., Brown, R.A., 2002. Evaluation of a behavioral measure of risk taking: the Balloon Analogue Risk Task BART. J. Exp. Psychol. Appl. 8, 75-84.], provides an ecologically valid model to assess human risk taking propensity and behaviour. In the present study, we modified this task for use during functional magnetic resonance imaging (fMRI) and administered it in both an active choice mode and a passive no-choice mode in order to examine the neural correlates of voluntary and involuntary risk taking in the human brain. Voluntary risk in the active choice task is associated with robust activation in mesolimbic-frontal regions, including the midbrain, ventral and dorsal striatum, anterior insula, dorsal lateral prefrontal cortex (DLPFC), and anterior cingulate/medial frontal cortex (ACC/MFC), in addition to activation in visual pathway regions. However, these mesolimbic-frontal activation patterns were not observed for involuntary risk in the passive no-choice task. Decision making was associated with neural activity in the right DLPFC. These findings demonstrate the utility of the modified BART paradigms for using during fMRI to assess risk taking in the human brain, and suggest that recruitment of the brain mesolimbic-frontal pathway during risk-taking is contingent upon the agency of the risk taker. The present paradigm may be extended to pathological populations to determine the specific neural components of their impaired risk behavior.
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| [84] |
Dendritic spines are the major sites of synaptic transmission in the central nervous system. Alterations in the strength of synaptic connections directly affect the neuronal communication, which is crucial for brain function as well as the processing and storage of information. Sleep and sleep loss bidirectionally alter structural plasticity, by affecting spine numbers and morphology, which ultimately can affect the functional output of the brain in terms of alertness, cognition, and mood. Experimental data from studies in rodents suggest that sleep deprivation may impact structural plasticity in different ways. One of the current views, referred to as the synaptic homeostasis hypothesis, suggests that wake promotes synaptic potentiation whereas sleep facilitates synaptic downscaling. On the other hand, several studies have now shown that sleep deprivation can reduce spine density and attenuate synaptic efficacy in the hippocampus. These data are the basis for the view that sleep promotes hippocampal structural plasticity critical for memory formation. Altogether, the impact of sleep and sleep loss may vary between regions of the brain. A better understanding of the role that sleep plays in regulating structural plasticity may ultimately lead to novel therapeutic approaches for brain disorders that are accompanied by sleep disturbances and sleep loss.Copyright © 2017 Elsevier Ltd. All rights reserved.
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| [85] |
There is nothing we spend as much time on in our lives as we do sleeping, which makes it even more surprising that we currently do not know why we need to sleep. Most of the research addressing this question is performed in rodents to allow for invasive, mechanistic approaches. However, in contrast to human sleep, we currently do not have shared and agreed upon standards on sleep states in rodents. In this article, we present an overview on sleep stages in humans and rodents and a historical perspective on the development of automatic sleep scoring systems in rodents. Further, we highlight specific issues in rodent sleep that also call into question some of the standards used in human sleep research.© 2022 The Authors. European Journal of Neuroscience published by Federation of European Neuroscience Societies and John Wiley & Sons Ltd.
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| [86] |
Patients sustaining lesions of the orbital prefrontal cortex (PFC) exhibit marked impairments in the performance of laboratory-based gambling, or risk-taking, tasks, suggesting that this part of the human PFC contributes to decision-making cognition. However, to date, little is known about the particular regions of the orbital cortex that participate in this function. In the present study, eight healthy volunteers were scanned, using H(2)(15)0 PET technology, while performing a novel computerized risk-taking task. The task involved predicting which of two mutually exclusive outcomes would occur, but critically, the larger reward (and penalty) was associated with choice of the least likely outcome, whereas the smallest reward (and penalty) was associated with choice of the most likely outcome. Resolving these "conflicting" decisions was associated with three distinct foci of regional cerebral blood flow increase within the right inferior and orbital PFC: laterally, in the anterior part of the middle frontal gyrus [Brodmann area 10 (BA 10)], medially, in the orbital gyrus (BA 11), and posteriorly, in the anterior portion of the inferior frontal gyrus (BA 47). By contrast, increases in the degree of conflict inherent in these decisions was associated with only limited changes in activity within orbital PFC and the anterior cingulate cortex. These results suggest that decision making recruits neural activity from multiple regions of the inferior PFC that receive information from a diverse set of cortical and limbic inputs, and that the contribution of the orbitofrontal regions may involve processing changes in reward-related information.
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| [87] |
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| [88] |
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| [89] |
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| [90] |
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| [91] |
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| [92] |
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| [93] |
The impact of sleep deprivation on working memory can only be reversed by recovery sleep (RS). However, there are limited electrophysiological studies on the effect of RS on the improvement in working memory after sleep deprivation, and the changes in the early components of event-related potentials (ERPs) before and after RS are still unclear. Therefore, this study aims to explore the effects of RS on the earlier ERP components related to object working memory following 36 h of total sleep deprivation (TSD). Twenty healthy male participants performed an object working memory task after 36 h of TSD and after 8 h of RS. Electroencephalogram data were recorded accordingly while the task was performed. Repeated ANOVA showed that P2 amplitudes related to object working memory decreased significantly after 8 h of RS compared to after a 36 h period of TSD, but there was no significant difference from baseline (BS), which indicates a trend of recovery to the baseline state. An 8 h RS can partially improve impaired object working memory caused by TSD. However, a longer period of RS is needed for the complete recovery of cognitive function after a long period of TSD.
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| [94] |
According to the dual systems perspective, risk taking peaks during adolescence because activation of an early-maturing socioemotional-incentive processing system amplifies adolescents' affinity for exciting, pleasurable, and novel activities at a time when a still immature cognitive control system is not yet strong enough to consistently restrain potentially hazardous impulses. We review evidence from both the psychological and neuroimaging literatures that has emerged since 2008, when this perspective was originally articulated. Although there are occasional exceptions to the general trends, studies show that, as predicted, psychological and neural manifestations of reward sensitivity increase between childhood and adolescence, peak sometime during the late teen years, and decline thereafter, whereas psychological and neural reflections of better cognitive control increase gradually and linearly throughout adolescence and into the early 20s. While some forms of real-world risky behavior peak at a later age than predicted, this likely reflects differential opportunities for risk-taking in late adolescence and young adulthood, rather than neurobiological differences that make this age group more reckless. Although it is admittedly an oversimplification, as a heuristic device, the dual systems model provides a far more accurate account of adolescent risk taking than prior models that have attributed adolescent recklessness to cognitive deficiencies. Copyright © 2016 The Authors. Published by Elsevier Ltd.. All rights reserved.
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| [95] |
Risk in the Iowa Gambling Task (IGT) is often understood in terms of intertemporal choices, i.e., preference for immediate outcomes in favor of delayed outcomes is considered risky decision making. According to behavioral economics, healthy decision makers are expected to refrain from choosing the short-sighted immediate gain because, over time (10 trials of the IGT), the immediate gains result in a long term loss (net loss). Instead decision makers are expected to maximize their gains by choosing options that, over time (10 trials), result in delayed or long term gains (net gain). However, task choices are sometimes made on the basis of the frequency of reward and punishment such that frequent rewards/infrequent punishments are favored over infrequent rewards/frequent punishments. The presence of these two attributes (intertemporality and frequency of reward) in IGT decision making may correspond to the emotion-cognition dichotomy and reflect a dual conception of risk. Decision making on the basis of the two attributes was tested under two conditions: delay in retest and sleep deprivation. An interaction between sleep deprivation and time delay was expected to attenuate the difference between the two attributes. Participants were 40 male university students. Analysis of the effects of IGT attribute type (intertemporal vs. frequency of reinforcement), sleep deprivation (sleep deprivation vs. no sleep deprivation), and test-retest gap (short vs. long delay) showed a significant within-subjects effect of IGT attribute type thus confirming the difference between the two attributes. Sleep deprivation had no effect on the attributes, but test-retest gap and the three-way interaction between attribute type, test-retest gap, and sleep deprivation were significantly different. Post-hoc tests revealed that sleep deprivation and short test-retest gap attenuated the difference between the two attributes. Furthermore, the results showed an expected trend of increase in intertemporal decision making at retest suggesting that intertemporal decision making benefited from repeated task exposure. The present findings add to understanding of the emotion-cognition dichotomy. Further, they show an important time-dependent effect of a universally experienced constraint (sleep deprivation) on decision making. It is concluded that risky decision making in the IGT is contingent on the attribute under consideration and is affected by factors such as time elapsed and constraint experienced before the retest.
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| [96] |
In humans, activity patterns in the ventromedial prefrontal cortex (vmPFC) have been found to be predictive of subsequent fear memory consolidation. Pioneering work in rodents has further shown that vmPFC-amygdala theta synchronization is correlated with fear memory consolidation. We aimed to evaluate whether vmPFC activity during fear conditioning is (1) correlated with fear expression the subsequent day and whether (2) this relationship is mediated by rapid eye movement (REM) sleep. We analyzed data from 17 young healthy subjects undergoing a fear conditioning task, followed by a fear extinction task 24 h later, both recorded with simultaneous skin conductance response (SCR) and functional magnetic resonance imaging measurements, with a polysomnographically recorded night sleep in between. Our results showed a correlation between vmPFC activity during fear conditioning and subsequent REM sleep amount, as well as between REM sleep amount and SCR to the conditioned stimulus 24 h later. Moreover, we observed a significant correlation between vmPFC activity during fear conditioning and SCR responses during extinction, which was no longer significant after controlling for REM sleep amount. vmPFC activity during fear conditioning was further correlated with sleep latency. Interestingly, hippocampus activity during fear conditioning was correlated with stage 2 and stage 4 sleep amount. Our results provide preliminary evidence that the relationship between REM sleep and fear conditioning and extinction observed in rodents can be modeled in healthy human subjects, highlighting an interrelated set of potentially relevant trait markers.
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| [97] |
It has been hypothesized that reward-seeking and impulsivity develop along different timetables and have different neural underpinnings, and that the difference in their timetables helps account for heightened risk-taking during adolescence. In order to test these propositions, age differences in reward-seeking and impulsivity were examined in a socioeconomically and ethnically diverse sample of 935 individuals between the ages of 10 and 30, using self-report and behavioral measures of each construct. Consistent with predictions, age differences in reward-seeking follow a curvilinear pattern, increasing between preadolescence and mid-adolescence, and declining thereafter. In contrast, age differences in impulsivity follow a linear pattern, with impulsivity declining steadily from age 10 on. Heightened vulnerability to risk-taking in middle adolescence may be due to the combination of relatively higher inclinations to seek rewards and still maturing capacities for self-control.(c) 2010 Wiley Periodicals, Inc.
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| [98] |
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| [99] |
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| [100] |
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| [101] |
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| [102] |
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| [103] |
The negative effects of sleep deprivation on alertness and cognitive performance suggest decreases in brain activity and function, primarily in the thalamus, a subcortical structure involved in alertness and attention, and in the prefrontal cortex, a region subserving alertness, attention, and higher-order cognitive processes. To test this hypothesis, 17 normal subjects were scanned for quantifiable brain activity changes during 85 h of sleep deprivation using positron emission tomography (PET) and (18)Fluorine-2-deoxyglucose ((18)FDG), a marker for regional cerebral metabolic rate for glucose (CMRglu) and neuronal synaptic activity. Subjects were scanned prior to and at 24-h intervals during the sleep deprivation period, for a total of four scans per subject. During each 30 min (18)FDG uptake, subjects performed a sleep deprivation-sensitive Serial Addition/Subtraction task. Polysomnographic monitoring confirmed that subjects were awake. Twenty-four hours of sleep deprivation, reported here, resulted in a significant decrease in global CMRglu, and significant decreases in absolute regional CMRglu in several cortical and subcortical structures. No areas of the brain evidenced a significant increase in absolute regional CMRglu. Significant decreases in relative regional CMRglu, reflecting regional brain reductions greater than the global decrease, occurred predominantly in the thalamus and prefrontal and posterior parietal cortices. Alertness and cognitive performance declined in association with these brain deactivations. This study provides evidence that short-term sleep deprivation produces global decreases in brain activity, with larger reductions in activity in the distributed cortico-thalamic network mediating attention and higher-order cognitive processes, and is complementary to studies demonstrating deactivation of these cortical regions during NREM and REM sleep.
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| [104] |
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| [105] |
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| [106] |
The brain is constantly bombarded by stimuli, and the relative salience of these inputs determines which are more likely to capture attention. A brain system known as the 'salience network', with key nodes in the insular cortices, has a central role in the detection of behaviourally relevant stimuli and the coordination of neural resources. Emerging evidence suggests that atypical engagement of specific subdivisions of the insula within the salience network is a feature of many neuropsychiatric disorders.
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| [107] |
The past decade has witnessed a proliferation of studies aimed at characterizing the human connectome. These projects map the brain regions comprising large-scale systems underlying cognition using non-invasive neuroimaging approaches and advanced analytic techniques adopted from network science. While the idea that the human brain is composed of multiple macro-scale functional networks has been gaining traction in cognitive neuroscience, the field has yet to reach consensus on several key issues regarding terminology. What constitutes a functional brain network? Are there "core" functional networks, and if so, what are their spatial topographies? What naming conventions, if universally adopted, will provide the most utility and facilitate communication amongst researchers? Can a taxonomy of functional brain networks be delineated? Here we survey the current landscape to identify six common macro-scale brain network naming schemes and conventions utilized in the literature, highlighting inconsistencies and points of confusion where appropriate. As a minimum recommendation upon which to build, we propose that a scheme incorporating anatomical terminology should provide the foundation for a taxonomy of functional brain networks. A logical starting point in this endeavor might delineate systems that we refer to here as "occipital", "pericentral", "dorsal frontoparietal", "lateral frontoparietal", "midcingulo-insular", and "medial frontoparietal" networks. We posit that as the field of network neuroscience matures, it will become increasingly imperative to arrive at a taxonomy such as that proposed here, that can be consistently referenced across research groups.
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| [108] |
The view that sleep is essential for survival is supported by the ubiquity of this behavior, the apparent existence of sleep-like states in the earliest animals, and the fact that severe sleep loss can be lethal. The cause of this lethality is unknown. Here we show, using flies and mice, that sleep deprivation leads to accumulation of reactive oxygen species (ROS) and consequent oxidative stress, specifically in the gut. ROS are not just correlates of sleep deprivation but drivers of death: their neutralization prevents oxidative stress and allows flies to have a normal lifespan with little to no sleep. The rescue can be achieved with oral antioxidant compounds or with gut-targeted transgenic expression of antioxidant enzymes. We conclude that death upon severe sleep restriction can be caused by oxidative stress, that the gut is central in this process, and that survival without sleep is possible when ROS accumulation is prevented. VIDEO ABSTRACT.Copyright © 2020 Elsevier Inc. All rights reserved.
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| [109] |
To inform the debate over whether human sleep can be chronically reduced without consequences, we conducted a dose-response chronic sleep restriction experiment in which waking neurobehavioral and sleep physiological functions were monitored and compared to those for total sleep deprivation.The chronic sleep restriction experiment involved randomization to one of three sleep doses (4 h, 6 h, or 8 h time in bed per night), which were maintained for 14 consecutive days. The total sleep deprivation experiment involved 3 nights without sleep (0 h time in bed). Each study also involved 3 baseline (pre-deprivation) days and 3 recovery days.Both experiments were conducted under standardized laboratory conditions with continuous behavioral, physiological and medical monitoring.A total of n = 48 healthy adults (ages 21-38) participated in the experiments.Noctumal sleep periods were restricted to 8 h, 6 h or 4 h per day for 14 days, or to 0 h for 3 days. All other sleep was prohibited.Chronic restriction of sleep periods to 4 h or 6 h per night over 14 consecutive days resulted in significant cumulative, dose-dependent deficits in cognitive performance on all tasks. Subjective sleepiness ratings showed an acute response to sleep restriction but only small further increases on subsequent days, and did not significantly differentiate the 6 h and 4 h conditions. Polysomnographic variables and delta power in the non-REM sleep EEG-a putative marker of sleep homeostasis--displayed an acute response to sleep restriction with negligible further changes across the 14 restricted nights. Comparison of chronic sleep restriction to total sleep deprivation showed that the latter resulted in disproportionately large waking neurobehavioral and sleep delta power responses relative to how much sleep was lost. A statistical model revealed that, regardless of the mode of sleep deprivation, lapses in behavioral alertness were near-linearly related to the cumulative duration of wakefulness in excess of 15.84 h (s.e. 0.73 h).Since chronic restriction of sleep to 6 h or less per night produced cognitive performance deficits equivalent to up to 2 nights of total sleep deprivation, it appears that even relatively moderate sleep restriction can seriously impair waking neurobehavioral functions in healthy adults. Sleepiness ratings suggest that subjects were largely unaware of these increasing cognitive deficits, which may explain why the impact of chronic sleep restriction on waking cognitive functions is often assumed to be benign. Physiological sleep responses to chronic restriction did not mirror waking neurobehavioral responses, but cumulative wakefulness in excess of a 15.84 h predicted performance lapses across all four experimental conditions. This suggests that sleep debt is perhaps best understood as resulting in additional wakefulness that has a neurobiological "cost" which accumulates over time.
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| [110] |
Adolescence is often described as a period of increased risk taking relative to both childhood and adulthood. This inflection in risky choice behavior has been attributed to a neurobiological imbalance between earlier developing motivational systems and later developing top-down control regions. Yet few studies have decomposed risky choice to investigate the underlying mechanisms or tracked their differential developmental trajectory. The current study uses a risk-return decomposition to more precisely assess the development of processes underlying risky choice and to link them more directly to specific neural mechanisms. This decomposition specifies the influence of changing risks (outcome variability) and changing returns (expected value) on the choices of children, adolescents, and adults in a dynamic risky choice task, the Columbia Card Task. Behaviorally, risk aversion increased across age groups, with adults uniformly risk averse and adolescents showing substantial individual differences in risk sensitivity, ranging from risk seeking to risk averse. Neurally, we observed an adolescent peak in risk-related activation in the anterior insula and dorsal medial PFC. Return sensitivity, on the other hand, increased monotonically across age groups and was associated with increased activation in the ventral medial PFC and posterior cingulate cortex with age. Our results implicate adolescence as a developmental phase of increased neural risk sensitivity. Importantly, this work shows that using a behaviorally validated decision-making framework allows a precise operationalization of key constructs underlying risky choice that inform the interpretation of results. Copyright © 2015 the authors 0270-6474/15/351549-12$15.00/0.
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| [111] |
Individuals with bipolar disorder (BD) exhibit deleterious decision making, negatively impacting their lives. Such aberrant decision making can be quantified using the Iowa Gambling Task (IGT), which requires choosing between advantageous and disadvantageous options based on different reward/punishment schedules. The mechanisms underlying this behavioral deficit are unknown, but may include the reduced dopamine transporter (DAT) functioning reported in BD patients. Using both human and mouse IGTs, we tested whether reduced DAT functioning would recreate patterns of deficient decision making of BD patients. We assessed the IGT performance of 16 BD subjects (7 female) and 17 healthy control (HC) subjects (12 female). We recorded standard IGT performance measures and novel post-reward and post-punishment decision-making strategies. We characterized a novel single-session mouse IGT using C57BL/6J mice (n = 44). The BD and HC IGT performances were compared with the effects of chronic (genetic knockdown (KD; n = 31) and wild-type (n = 28) mice) and acute (C57BL/6J mice (n = 89) treated with the DAT inhibitor GBR12909) reductions of DAT functioning in mice performing this novel IGT. BD patients exhibited impaired decision making compared with HC subjects. Both the good-performing DAT KD and GBR12909-treated mice exhibited poor decision making in the mouse IGT. The deficit of each population was driven by high-reward sensitivity. The single-session mouse IGT measures dynamic risk-based decision making similar to humans. Chronic and acute reductions of DAT functioning in mice impaired decision-making consistent with poor IGT performance of BD patients. Hyperdopaminergia caused by reduced DAT may impact poor decision making in BD patients, which should be confirmed in future studies.
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| [112] |
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| [113] |
Using a gambling task, we investigated how 24 hours of sleep deprivation modulates the neural response to the making of risky decisions with potentially loss-bearing outcomes.Two experiments involving sleep-deprived subjects were performed. In the first, neural responses to decision making and reward outcome were evaluated. A second control experiment evaluated responses to reward outcome only.Healthy right-handed adults participated in these experiments (26 [mean age 21.3 years] in Experiment 1 and 13 [mean age 21.7 years] in Experiment 2.)Following sleep deprivation, choices involving higher relative risk elicited greater activation in the right nucleus accumbens, signifying an elevated expectation of the higher reward once the riskier choice was made. Concurrently, activation for losses in the insular and orbitofrontal cortices was reduced, denoting a diminished response to losses. This latter finding of reduced insular activation to losses was also true when volunteers were merely shown the results of the computer's decision, that is, without having to make their own choice.These results suggest that sleep deprivation poses a dual threat to competent decision making by modulating activation in nucleus accumbens and insula, brain regions associated with risky decision making and emotional processing.
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| [114] |
Genetic factors, externalizing personality traits such as impulsivity, and brain processing of salient stimuli all can affect individual risk for alcoholism. One of very few confirmed genetic association findings differentiating alcoholics from non-alcoholics is with variants in the inhibitory γ-amino butyric acid α2 receptor subunit (GABRA2) gene. Here we report the association of two of these GABRA2 variants with measures of alcohol symptoms, impulsivity and with insula cortex activation during anticipation of reward or loss using functional magnetic resonance imaging (fMRI). In a sample of 173 families (449 subjects), 129 of whom had at least one member diagnosed with alcohol dependence or abuse, carriers for the G allele in two single-nucleotide polymorphisms (SNPs) and haplotypes were more likely to have alcohol dependence symptoms (rs279858, P=0.01; rs279826, P=0.05; haplotype, P=0.02) and higher NEO Personality Inventory-Revised (NEO-PI-R) Impulsiveness scores (rs279858, P=0.016; rs279826, P=0.012; haplotype, P=0.032) with a stronger effect in women (rs279858, P=0.011; rs279826, P=0.002; haplotype, P=0.006), all P-values are corrected for family history and age. A subset of offspring from these families (n=44, 20 females), genotyped for GABRA2, participated in an fMRI study using a monetary incentive delay task. Increased insula activation during reward (r(2)=0.4; P=0.026) and loss (r(2)=0.38; P=0.039) anticipation was correlated with NEO-PI-R Impulsiveness and further associated with the GG genotype for both SNPs (P's<0.04). Our results suggest that GABRA2 genetic variation is associated with Impulsiveness through variation of insula activity responses, here evidenced during anticipatory responses.
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| [115] |
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| [116] |
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| [117] |
To better understand the sometimes catastrophic effects of sleep loss on naturalistic decision making, we investigated effects of sleep deprivation on decision making in a reversal learning paradigm requiring acquisition and updating of information based on outcome feedback.Subjects were randomized to a sleep deprivation or control condition, with performance testing at baseline, after 2 nights of total sleep deprivation (or rested control), and following 2 nights of recovery sleep. Subjects performed a decision task involving initial learning of go and no go response sets followed by unannounced reversal of contingencies, requiring use of outcome feedback for decisions. A working memory scanning task and psychomotor vigilance test were also administered.Six consecutive days and nights in a controlled laboratory environment with continuous behavioral monitoring.Twenty-six subjects (22-40 y of age; 10 women).Thirteen subjects were randomized to a 62-h total sleep deprivation condition; the others were controls.Unlike controls, sleep deprived subjects had difficulty with initial learning of go and no go stimuli sets and had profound impairment adapting to reversal. Skin conductance responses to outcome feedback were diminished, indicating blunted affective reactions to feedback accompanying sleep deprivation. Working memory scanning performance was not significantly affected by sleep deprivation. And although sleep deprived subjects showed expected attentional lapses, these could not account for impairments in reversal learning decision making.Sleep deprivation is particularly problematic for decision making involving uncertainty and unexpected change. Blunted reactions to feedback while sleep deprived underlie failures to adapt to uncertainty and changing contingencies. Thus, an error may register, but with diminished effect because of reduced affective valence of the feedback or because the feedback is not cognitively bound with the choice. This has important implications for understanding and managing sleep loss-induced cognitive impairment in emergency response, disaster management, military operations, and other dynamic real-world settings with uncertain outcomes and imperfect information.© 2015 Associated Professional Sleep Societies, LLC.
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| [118] |
Slow-wave activity (SWA), and its coupling with other sleep features, reorganizes cortical circuitry, supporting cognition. This raises the question: can cognition be improved through SWA enhancement? SWA enhancement techniques range from behavioral interventions (such as exercise), which have high feasibility but low specificity, to laboratory-based techniques (such as transcranial stimulation), which have high specificity but are less feasible for widespread use. In this review we describe the pathways through which SWA is enhanced. Pathways encompass enhanced neural activity, increased energy metabolism, and endocrine signaling during wakefulness; also direct enhancement during sleep. We evaluate the robustness and practicality of SWA-enhancement techniques, discuss approaches for determining a causal role of SWA on cognition, and present questions to clarify the mechanisms of SWA-dependent cognitive improvements.Copyright © 2018 Elsevier Ltd. All rights reserved.
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| [119] |
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| [120] |
Sleep loss is common problem with a wide range of consequences. One possible consequence of sleep loss may be risk-taking behavior (RTB). The present review examined the empirical literature on the relationship between sleep loss and RTB. We found 23 studies that met inclusion criteria. Overall, sleep loss was positively associated with RTB, and there was evidence that changes in sleep loss are causally related to changes in RTB. One possible mediator of the relationship between sleep loss and RTB was reduced functioning of the ventromedial prefrontal cortex (VMPFC). Possible moderators of this relationship included type of RTB measure and general versus specific RTB. We discussed limitations and recommendations for future research in this area.
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| [121] |
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| [122] |
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| [123] |
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| [124] |
Background: Patients with obstructive sleep apnea syndrome (OSAS) have cognitive dysfunction in many aspects, however, these patients’ decision-making function remains unclear. In this study, the Game of Dice Task (GDT) was used to investigate the function of decision making in patients with OSAS. Methods: 30 participants with moderate to severe OSAS and 27 participants with no or mild OSAS diagnosed by sleep breathing monitor were selected from June 2021 to March 2022. Risky decision making was tested through the GDT with known risk probability. General demographic information and background cognitive functions, such as the overall cognitive functioning and executive functioning, were tested to establish baseline data. Results: There were no significant differences in gender, age, and years of education between the two groups. During the GDT, the moderate to severe OSAS group opted for the safety option at a statistically significant lower rate when compared to the no or mild OSAS group (7.53 ± 4.43 vs. 10.26 ± 4.26, p = 0.022). The moderate to severe OSAS group utilized the higher risk option than the group with no or mild OSAS (10.47 ± 4.43 vs. 7.74 ± 4.26, p = 0.022). The utilization rate of negative feedback in the moderate and severe OSAS group was lower than that in the no or mild OSAS group (7.50, 52.50 vs. 28.57, 100.00, p = 0.001). At the end of the GDT, the moderate and severe OSAS group was more likely to have negative total assets than the patients with no or mild OSAS (−1846.67 ± 2587.20 vs. 300.00 ± 1509.97, p < 0.001). Multiple linear regression analysis shows that there is a negative correlation between the selection of risk options and negative feedback utilization in the GDT. Conclusion: Patients with moderate and severe OSAS displayed impaired decision-making throughout the study. Impaired decision-making is related to executive processes and may be caused by diminished prefrontal cortex functioning. However, the functions of memory, attention, language, abstraction, and orientation are relatively retained.
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