Twenty-four hours of total sleep deprivation selectively impairs attentional networks

Performance decrements after sleep loss have been extensively studied and are usually attributed to generic attentional deficits. This claim, however, is based on the view of attention as a unitary construct, despite evidence that it should be considered a multidimensional cognitive ability. The aim of the present study was to evaluate the impact of one night of sleep deprivation on the efficiency of three attentional networks, defined by Posner and Raichle (1994) in anatomical and functional terms, as alerting, orienting, and executive control. Thirty participants performed the Attention Network Test at 9:00 a.m. following two different sleep conditions: baseline (a normal night of sleep) and deprivation (24 hrs of wakefulness). Results showed an overall slowing in reaction times and a significant decrease in accuracy after sleep deprivation. Sleep deprivation selectively affected the three attentional networks, given that only executive control efficacy significantly decreased after sleep deprivation. By contrast, phasic alerting and orienting showed no differences in the two sleep conditions. Thus, performance deficits following sleep deprivation do not reflect global attentional deficits.     

Sleep deprivation affects multiple distinct cognitive processes

Sleep deprivation adversely affects the ability to perform cognitive tasks, but theories range from predicting an overall decline in cognitive functioning (because of reduced stability in attentional networks) to claiming specific deficits in executive functions. In the present study, we measured the effects of sleep deprivation on a two-choice numerosity discrimination task. A diffusion model was used to decompose accuracy and response time distributions in order to produce estimates of distinct components of cognitive processing. The model assumes that, over time, noisy evidence from the task stimulus is accumulated to one of two decision criteria and that parameters governing this process can be extracted and interpreted in terms of distinct cognitive processes. The results showed that sleep deprivation affects multiple components of cognitive processing, ranging from stimulus processing to peripheral nondecision processes. Thus, sleep deprivation appears to have wide-ranging effects: Reduced attentional arousal and impaired central processing combine to produce an overall decline in cognitive functioning.     

Acute inhibition of calcineurin restores associative learning and memory in Tg2576 APP transgenic mice

Misfolded amyloid beta peptide (Abeta) is a pathological hallmark of Alzheimer's disease (AD), a neurodegenerative illness characterized by cognitive deficits and neuronal loss. Transgenic mouse models of Abeta over-production indicate that Abeta-induced cognitive deficits occur in the absence of overt neuronal death, suggesting that while extensive neuronal death may be associated with later stages of the human disease, subtle physiological changes may underlie initial cognitive deficits. Therefore, identifying signaling elements involved in those Abeta-induced cognitive impairments that occur prior to loss of neurons may reveal new potential pharmacological targets. Here, we report that the enzymatic activity of calcineurin, a key protein phosphatase involved in phosphorylation-dependent kinase activity crucial for synaptic plasticity and memory function, is upregulated in the CNS of the Tg2576 animal model for Abeta over-production. Furthermore, acute treatment of Tg2576 mice with the calcineurin inhibitor FK506 (10mg/kg i.p.) improves memory function. These results indicate that calcineurin may mediate some of the cognitive effects of excess Abeta such that inhibition of calcineurin shall be further explored as a potential treatment to reverse cognitive impairments in AD.     

Personality as a predictor of the objective and subjective impact of sleep deprivation

Although, impairments following sleep deprivation have been clearly demonstrated in the literature, researchers have found a wide range of individual variation in response to sleep deprivation. The relationship between personality and the subjective and objective impact of sleep deprivation was examined using the Epworth Sleepiness Scale, Stanford Sleepiness Scale, Sleep Hygiene Index, Profile of Mood States, an oddball reaction time test, a multi-task cognitive performance battery (SynWin), and the NEO Personality Inventory Revised. Subjects (14 males, 14 females, mean age 20.5) were sleep deprived for 28–35 h and during this time were allowed access to self-reported typical amounts of tobacco, caffeine, and food. Post sleep deprivation: (a) higher neuroticism scores were related to participants feeling sleepier, experiencing more mood disturbance, and performing inferiorly on a behavioral task; (b) subjects scoring as introverts showed more compromised behavioral performance compared to extraverts. The authors suggest that potential moderating variables of the relationship between personality and sleep deprivation such as stimulant use, food intake, and socialization warrant further investigation.     

Stress‐related exhaustion disorder – clinical manifestation of burnout? A review of assessment methods,sleep impairments,cognitive disturbances,and neuro‐biological and physiological changes in clinical burnout

The aim of this paper was to provide an overview of the literature on clinically significant burnout, focusing on its assessment, associations with sleep disturbances, cognitive impairments, as well as neurobiological and physiological correlates. Fifty‐nine English language articles and six book chapters were included. The results indicate that exhaustion disorder (ED), as described in the Swedish version of the International Classification of Diseases, seems to be the most valid clinical equivalent of burnout. The data supports the notion that sleep impairments are causative and maintaining factors for this condition. Patients with clinical burnout/ED suffer from cognitive impairments in the areas of memory and executive functioning. The studies on neuro‐biological mechanisms have reported functional uncoupling of networks relating the limbic system to the pre‐frontal cortex, and decreased volumes of structures within the basal ganglia. Although there is a growing body of literature on the physiological correlates of clinical burnout/ED, there is to date no biomarker for this condition. More studies on the role of sleep disturbances, cognitive impairments, and neurobiological and physiological correlates in clinical burnout/ED are warranted.     

Sleep deprivation and sustained attention performance: integrating mathematical and cognitive modeling

A long history of research has revealed many neurophysiological changes and concomitant behavioral impacts of sleep deprivation, sleep restriction, and circadian rhythms. Little research, however, has been conducted in the area of computational cognitive modeling to understand the information processing mechanisms through which neurobehavioral factors operate to produce degradations in human performance. Our approach to understanding this relationship is to link predictions of overall cognitive functioning, or alertness, from existing biomathematical models to information processing parameters in a cognitive architecture, leveraging the strengths from each to develop a more comprehensive explanation. The integration of these methodologies is used to account for changes in human performance on a sustained attention task across 88 h of total sleep deprivation. The integrated model captures changes due to time awake and circadian rhythms, and it also provides an account for underlying changes in the cognitive processes that give rise to those effects. The results show the potential for developing mechanistic accounts of how fatigue impacts cognition, and they illustrate the increased explanatory power that is possible by combining theoretical insights from multiple methodologies.     

Lack of degradation in visuospatial perception of line orientation after one night of sleep loss

Sleep deprivation impairs a variety of cognitive abilities including vigilance, attention, and executive function. Although sleep loss has been shown to impair tasks requiring visual attention and spatial perception, it is not clear whether these deficits are exclusively a function of reduced attention and vigilance or if there are also alterations in visuospatial perception. Visuospatial perception and sustained vigilance performance were therefore examined in 54 healthy volunteers at rested baseline and again after one night of sleep deprivation using the Judgment of Line Orientation Test and a computerized test of psychomotor vigilance. Whereas psychomotor vigilance declined significantly from baseline to sleep-deprived testing, scores on the Judgment of Line Orientation did not change significantly. Results suggest that documented performance deficits associated with sleep loss are unlikely to be the result of dysfunction within systems of the brain responsible for simple visuospatial perception and processing of line angles.     

Computational cognitive modeling of the temporal dynamics of fatigue from sleep loss

Computational models have become common tools in psychology. They provide quantitative instantiations of theories that seek to explain the functioning of the human mind. In this paper, we focus on identifying deep theoretical similarities between two very different models. Both models are concerned with how fatigue from sleep loss impacts cognitive processing. The first is based on the diffusion model and posits that fatigue decreases the drift rate of the diffusion process. The second is based on the Adaptive Control of Thought – Rational (ACT-R) cognitive architecture and posits that fatigue decreases the utility of candidate actions leading to microlapses in cognitive processing. A biomathematical model of fatigue is used to control drift rate in the first account and utility in the second. We investigated the predicted response time distributions of these two integrated computational cognitive models for performance on a psychomotor vigilance test under conditions of total sleep deprivation, simulated shift work, and sustained sleep restriction. The models generated equivalent predictions of response time distributions with excellent goodness-of-fit to the human data. More importantly, although the accounts involve different modeling approaches and levels of abstraction, they represent the effects of fatigue in a functionally equivalent way: in both, fatigue decreases the signal-to-noise ratio in decision processes and decreases response inhibition. This convergence suggests that sleep loss impairs psychomotor vigilance performance through degradation of the quality of cognitive processing, which provides a foundation for systematic investigation of the effects of sleep loss on other aspects of cognition. Our findings illustrate the value of treating different modeling formalisms as vehicles for discovery.     

睡眠不足对人际交互的影响及其认知神经机制

睡眠不足会对人的认知、情感和人际交互产生诸多影响。这种影响在社会情绪层面表现为个体情绪共情和认知共情的减少,易激惹性与愤怒情绪的增加;在社会行为层面则表现为亲社会行为的减少和攻击行为的增加。在睡眠不足状态下,情绪系统和认知系统功能连接的减弱可能是这些变化的潜在机制。未来应结合生态效度较高的睡眠操作手段,系统考察睡眠不足如何导致各种高级社会情绪的改变,以及这些社会情绪的变化如何导致社会行为的变化。     

Cognitive dysfunction in depression: neurocircuitry and new therapeutic strategies

Major depressive disorder (MDD) is a disabling medical condition associated with significant morbidity, mortality and public health costs. However, neurocircuitry abnormalities underlying depression remain incompletely understood and consequently current treatment options are unfortunately limited in efficacy. Recent research has begun to focus specifically on cognitive aspects of depression and potential neurobiological correlates. Two fundamental types of cognitive dysfunction observed in MDD are cognitive biases, which include distorted information processing or attentional allocation toward negative stimuli, and cognitive deficits, which include impairments in attention, short-term memory and executive functioning. In this article, we present a selective review of current research findings in these domains and examine neuroimaging research that is beginning to characterize the neurocircuitry underlying these biases and deficits. We propose that deficient cognitive functioning, attention biases and the sustained negative affect characteristic of MDD can be understood as arising in part from dysfunctional prefrontal-subcortical circuitry and related disturbances in the cognitive control of emotion. Finally, we highlight potential new pharmacological and non-pharmacological therapeutic strategies for MDD based on an evolving mechanistic understanding of the disorder.     

The effects of sleep deprivation on the attentional functions and vigilance

The study of sleep deprivation is a fruitful area of research to increase our knowledge of cognitive functions and their neural basis. In the current work, 26 healthy young adults participated in a sleep deprivation study, in which the Attentional Networks Test for Interactions and Vigilance (ANTI-V) was performed at 10a.m. after a night of normal sleep and again at 10 a.m. after 25.5-27.5 h of total sleep deprivation. The ANTI-V is an experimental task that provides measures of alerting, orienting and executive control attentional functions. Compared with previous versions, the ANTI-V includes a vigilance task, more reliable auditory alerting signals, non-predictive peripheral orienting cues, and also a neutral no-cue condition allowing the analysis of reorienting costs and orienting benefits. Thus, new evidence to evaluate the influence of sleep deprivation on attentional functioning is provided. Results revealed differences in both tonic and phasic alertness after sleep deprivation. Vigilance performance was deteriorated, while a warning tone was more helpful to increase participants' alertness, resulting in slightly faster RT and, in particular, fewer errors. The reorienting costs of having an invalid spatial cue were reduced after sleep loss. No sleep deprivation effect on the executive control measure was found in this study. Finally, since no control group was used, particular precautions were taken to reduce the influence of potential practice effects.     

The impact of cognitive interference on performance during prolonged sleep loss

Summary A study was conducted on the effects of off-task cognitions on performance during sleep deprivation. Subjects answered the Thought Occurrence Questionnaire, assessing their proneness to engage in off-task cognitions, and were deprived of sleep for 72 hours, during which they performed a variety of tasks including visual discrimination and three versions of a logical reasoning task in which cognitive load was varied systematically. In addition, every day subjects answered the Cognitive Interference Questionnaire, which taps off-task cognitions during the experiment. Results indicated that subjects who habitually engage in off-task cognitions performed worse during 72 hours of sleep loss than subjects who do not engage in such distracting activities. In addition, it was found that the engagement in off-task cognitions increased during the 72 hours of sleep loss and such an engagement was related to deficits in performance accuracy. The mechanisms of off-task cognitions and sleep loss underlying these effects are discussed.     

An Integrated Sleep and Reward Processing Model of Major Depressive Disorder

Major depressive disorder with comorbid sleep disturbance has been associated with negative outcomes, including lower rates of treatment response and a greater likelihood of depressive relapse compared to those without sleep disturbance. However, little, if any, research has been conducted to understand why such negative treatment outcomes occur when sleep disturbance is present. In this conceptual review, we argue that the relationship of sleep disturbance and negative treatment outcomes may be mediated by alterations in neural reward processing in individuals with blunted trait-level reward responsivity. We first briefly characterize sleep disturbance in depression, discuss the nature of reward processing impairments in depression, and summarize the sleep/reward relationship in healthy human subjects. We then introduce a novel Integrated Sleep and Reward model of the course and maintenance of major depressive disorder and present preliminary evidence of sleep and reward interaction in unipolar depression. Finally, we discuss limitations of the model and offer testable hypotheses and directions for future research.     

Specifying the Neuropsychology of Affective Disorders: Clinical,Demographic and Neurobiological Factors

Neuropsychological research in patients with affective disorders shows heterogeneous results with regard to the severity and profile of cognitive impairments. In this paper we hypothesize that the investigation of clinical (subtypes, comorbidity, traumatization, personality, severity, diurnal swings, course, duration, age of onset, biased processing, rumination, motivation, experience of failure, sleep, suicidal tendencies, computer attitudes), demographic (age, education, gender) and neurobiological factors (structural and functional brain changes, glucocorticoids, medication, ECT) that are related to cognitive performance has specified the understanding of severity and profile of neuropsychological impairments. We reviewed the literature pertaining to clinical, demographic and neurobiological factors following Pubmed and PsychInfo databases using different combinations of general key-terms including “Affective Disorder,” “Depression,” “Mania,” “Neuropsychological,” “Neurobiological,” “Moderator,” and “Review” as well as more specific demographic, clinical and neurobiological search terms. Findings from the literature show that the consideration of these factors has improved knowledge about the severity of neuropsychological impairments in patients with affective disorders whereas the neuropsychological profile is still poorly understood. Despite limited understanding, however, the existent results provide promising suggestions for the development of treatment programs.     

Sleep disruption explains age-related prospective memory deficits: implications for cognitive aging and intervention

The high prevalence of sleep disruption among older adults may have implications for cognitive aging, particularly for higher-order aspects of cognition. One domain where sleep disruption may contribute to age-related deficits is prospective memory—the ability to remember to perform deferred actions at the appropriate time in the future. Community-dwelling older adults (55–93 years, N = 133) undertook assessment of sleep using actigraphy and participated in a laboratory-based prospective memory task. After controlling for education, sleep disruption (longer awakenings) was associated with poorer prospective memory. Additionally, longer awakenings mediated the relationship between older age and poorer prospective memory. Other metrics of sleep disruption, including sleep efficiency and wake after sleep onset, were not related to prospective memory, suggesting that examining the features of individual wake episodes rather than total wake time may help clarify relationships between sleep and cognition. The mediating role of awakening length was partially a function of greater depression and poorer executive function (shifting) but not retrospective memory. This study is among the first to examine the association between objectively measured sleep and prospective memory in older adults. Furthermore, this study is novel in suggesting sleep disruption might contribute to age-related prospective memory deficits; perhaps, with implications for cognitive aging more broadly. Our results suggest that there may be opportunities to prevent prospective memory decline by treating sleep problems.     

Aged rats are impaired on an attentional set-shifting task sensitive to medial frontal cortex damage in young rats

Normal aging is associated with disruption of neural systems that subserve different aspects of cognitive function, particularly in the hippocampus and frontal cortex. Abnormalities in hippocampal function have been well investigated in rodent models of aging, but studies of frontal cortex function in aged rodents are few. We tested young (4–5 mo old) and aged (27–28 mo old) male Long-Evans rats on an attentional set-shifting task modified slightly from previous publication. After training on two problems in which the reward was consistently associated with the same stimulus dimension, and a reversal of one problem, a new problem was presented in which the reward was consistently associated with the previously irrelevant stimulus dimension (extradimensional shift [EDS]). Aged rats as a group were significantly impaired on the EDS, although some individual aged rats performed as well as young rats on this phase. In addition, some aged rats were impaired on the reversal, although a group effect did not reach significance in this phase. Impairment in neither reversal nor EDS was associated with impairments in spatial learning in the Morris water maze. Young rats with neurotoxic lesions of medial frontal cortex are also selectively impaired on the EDS. These results indicate that normal aging in rats is associated with impaired medial frontal cortex function. Furthermore, age-related declines in frontal cortex function are independent of those in hippocampal function. These results provide a possible basis for correlating age-related changes in neurobiological markers in frontal cortex with cognitive decline.     

Motor, Emotional, and Cognitive Empathy in Children and Adolescents with Autism Spectrum Disorder and Conduct Disorder

It is unclear which aspects of empathy are shared and which are uniquely affected in autism spectrum disorder (ASD) and conduct disorder (CD) as are the neurobiological correlates of these empathy impairments. The aim of this systematic review is to describe the overlap and specificity of motor, emotional, and cognitive aspects of empathy in children and adolescents with ASD or CD. Motor and cognitive empathy impairments are found in both ASD and CD, yet the specificity seems to differ. In ASD facial mimicry and emotion recognition may be impaired for all basic emotions, whereas in CD this is only the case for negative emotions. Emotional empathy and the role of attention to the eyes therein need further investigation. We hypothesize that impaired motor and cognitive empathy in both disorders are a consequence of lack of attention to the eyes. However, we hypothesize major differences in emotional empathy deficits between ASD and CD, probably due to emotional autonomic and amygdala hyper-responsivity in ASD versus hypo-responsivity in CD, both resulting in lack of attention to the eyes.     

Cognitive functions and corticostriatal circuits: insights from Huntington's disease

The basic mechanisms of information processing by corticostriatal circuits are currently a matter of intense debate amongst cognitive scientists. Huntington's disease, an autosomal-dominant neurogenetic disorder characterized clinically by a triad of motor, cognitive, and affective disturbance, is associated with neuronal loss within corticostriatal circuits, and as such provides a valuable model for understanding the role of these circuits in normal behaviour, and their disruption in disease. We review findings from our studies of the breakdown of cognition in Huntington's disease, with a particular emphasis on executive functions and visual recognition memory. We show that Huntington's disease patients exhibit a neuropsychological profile that shows a discernible pattern of progression with advancing disease, and appears to result from a breakdown in the mechanisms of response selection. These findings are consistent with recent computational models that suggest that corticostriatal circuits compute the patterns of sensory input and response output which are of behavioural significance within a particular environmental context.     

Absorbed in sleep: Dissociative absorption as a predictor of sleepiness following sleep deprivation in two high-functioning samples

In recent years, a labile sleep-wake cycle has been implicated as a cause for dissociative experiences, and studies show that dissociation is elevated following sleep deprivation. Dissociative individuals may find it harder to regulate sleepiness in the face of sleep disruption. Although there is significant variability in reactions to sleep deprivation, research on trait predictors is scarce. The present study examined the ability of trait dissociation to prospectively predict sleepiness following sleep loss and recovery sleep. Two high-functioning samples, namely, Remotely Piloted Aircraft officers (N = 29) and Air Force jet pilots (N = 57) completed state and trait questionnaires assessing sleep and dissociation before and after full or partial sleep loss. Dissociative absorption was a consistent predictor of an increase in sleepiness following sleep loss and following recovery sleep, controlling for baseline sleepiness levels. We discuss the findings in light of a difficulty to regulate and monitor consciousness states.     

Training the brain: practical applications of neural plasticity from the intersection of cognitive neuroscience, developmental psychology, and prevention science

Prior researchers have shown that the brain has a remarkable ability for adapting to environmental changes. The positive effects of such neural plasticity include enhanced functioning in specific cognitive domains and shifts in cortical representation following naturally occurring cases of sensory deprivation; however, maladaptive changes in brain function and development owing to early developmental adversity and stress have also been well documented. Researchers examining enriched rearing environments in animals have revealed the potential for inducing positive brain plasticity effects and have helped to popularize methods for training the brain to reverse early brain deficits or to boost normal cognitive functioning. In this article, two classes of empirically based methods of brain training in children are reviewed and critiqued: laboratory-based, mental process training paradigms and ecological interventions based upon neurocognitive conceptual models. Given the susceptibility of executive function disruption, special attention is paid to training programs that emphasize executive function enhancement. In addition, a third approach to brain training, aimed at tapping into compensatory processes, is postulated. Study results showing the effectiveness of this strategy in the field of neurorehabilitation and in terms of naturally occurring compensatory processing in human aging lend credence to the potential of this approach. (PsycINFO Database Record (c) 2012 APA, all rights reserved).