Topographic electroencephalogram changes associated with psychomotor vigilance task performance after sleep deprivation

ObjectivesThe psychomotor vigilance task (PVT) is a widely used method for the assessment of vigilance after sleep deprivation (SDEP). However, the neural basis of PVT performance during SDEP has not been fully understood. In particular, no studies have investigated the possible relation between EEG topographical changes after sleep loss and PVT performance. The aim of the present study is to assess the EEG topographic correlates of PVT performance after SDEP.MethodsDuring 40 h of SDEP, 16 healthy male subjects were evaluated in four sessions performed at the same time (11:00 a.m. and 11:00 p.m.) of the first and second day with: (a) subjective sleepiness recordings by means of the Karolinska Sleepiness Scale (KSS); (b) EEG recordings (5 min eyes-open condition); and (c) PVT.ResultsSDEP induced a slowing of PVT reaction times (RTs), higher level of subjective sleepiness and an increase of delta, theta, alpha and beta 1 EEG activity. Only slowest PVT RTs were influenced by circadian factors, with longer RTs in the morning. Both fastest PVT RTs and KSS scores were positively correlated with post-SDEP changes in EEG theta activity, mainly in centro-posterior areas, but not with other EEG frequencies. KSS scores and PVT measures were also positively correlated.ConclusionsThese findings suggest that SDEP differently affects PVT variables, and that an increase in theta activity may be the principal EEG basis of the post-SDEP slowing of fastest PVT RTs. Similar neural mechanisms seem to underlie both performance deterioration to PVT and the increase of subjective sleepiness.     

EEG and behavioural correlates of mild sleep deprivation and vigilance

ObjectiveThe current study investigated the behavioral, cognitive, and electrophysiological impact of mild (only a few hours) and acute (one night) sleep loss via simultaneously recorded behavioural and physiological measures of vigilance.MethodsParticipants (N = 23) came into the lab for two testing days where their brain activity and vigilance were recorded and assessed. The night before the testing session, participants either slept from 12am to 9am (Normally Rested), or from 1am to 6am (Sleep Restriction).ResultsVigilance was reduced and sleepiness was increased in the Sleep Restricted vs. Normally Rested condition, and this was exacerbated over the course of performing the vigilance task. As well, sleep restriction resulted in more intense alpha bursts. Lastly, EEG spectral power differed in Sleep Restricted vs. Normally Rested conditions as sleep onset progressed, particularly for frequencies reflecting arousal (e.g., delta, alpha, beta).ConclusionsThe findings of this study suggest that only one night of mild sleep loss significantly increases sleepiness and, importantly, reduces vigilance. In addition, this sleep loss has a clear impact on the physiology of the brain in ways that reflect reduced arousal.SignificanceUnderstanding the neural correlates and cognitive processes associated with loss of sleep may lead to important advancements in identifying and preventing deleterious or potentially dangerous, sleep-related lapses in vigilance.     

Body core temperature and depression during total sleep deprivation in depressives

Endogenously depressed patients were subjected to a total sleep deprivation (TSD) schedule of sleep-TSD-sleep-TSD. They were simultaneously treated with the antidepressant drug clomipramine. Self- and observer-rated depression was measured daily. Continuously measured rectal temperature (RT) data were available for the second TSD. It was found that a higher nocturnal minimum RT during this TSD was associated with a positive clinical response.     

Cardiac autonomic changes after 40 hours of total sleep deprivation in women

ObjectivesThe effect of total sleep deprivation on heart rate variability (HRV) in groups of postmenopausal women on oral hormone therapy (HT) (on-HT, n = 10, 64.2 (1.4) years), postmenopausal women without HT (off-HT, n = 10, 64.6 (1.4) years) and young women (n = 11, 23.1 (0.5) years) was studied using a prospective case–control setup.MethodsPolysomnography was performed over an adaptation night, a baseline night, and a recovery night after 40 h of total sleep deprivation. Time and frequency domain and nonlinear HRV from overnight electrocardiogram recordings were compared between groups during baseline and recovery nights. Further, the changes in HRV from baseline to recovery were analysed and compared between groups. Finally, correlations of HRV to percentages of sleep stages and measures of sleep fragmentation were analysed during baseline and recovery.ResultsYoung women had higher HRV than older women; the most marked difference was between young and on-HT postmenopausal women. Sleep deprivation induced a decrease in frequency domain HRV in young and in off-HT women, an increase in α2 in off-HT women, and an increase in mean heart rate in on-HT women. The sleep deprivation effect was mainly uncorrelated to changes in sleep parameters.ConclusionsAcute total sleep deprivation has a deleterious effect on the autonomic nervous system in young women, but an even more pronounced effect in postmenopausal women. Hormone therapy use in late postmenopause does not give protection against these changes. These harmful effects may partly explain the increased cardiovascular morbidity and overall mortality associated with sleep loss.     

Sleep deprivation and hormone therapy in postmenopausal women

BACKGROUND AND PURPOSE: Sleep complaints increase after menopause, but literature on the effect of postmenopausal hormone therapy (HT) on sleep is controversial. The purpose of this study was to determine the effect of ageing and HT on sleep quality, assessed using polysomnography, and on the accuracy of the subjective estimation of sleep quality in women before and after sleep deprivation. PATIENTS AND METHODS: Twenty postmenopausal women (aged 58-72 years) were recruited: 10 HT-users and 10 non-HT-users. Eleven young women (aged 20-26 years) served as controls. Polysomnography and subjective sleep quality were measured on four consecutive nights: adaptation, baseline, 40-h sleep deprivation and recovery. RESULTS: Although the postmenopausal women slept worse than the controls at baseline, and in particular during the recovery night, their recovery response to sleep deprivation was well preserved. At baseline, HT-users had a shorter latency to rapid eye movement (REM) (P=0.043), with fewer awakenings from slow wave sleep (SWS) (P=0.029) but more from REM (P=0.033) than non-HT-users. During recovery, the HT-users had more stage 2 sleep (P=0.048) and less slow wave activity (SWA) in the first non-rapid eye movement (NREM) sleep episode (P=0.021) than the non-HT-users. The poor correlation between subjective and objective sleep quality at baseline became significant during recovery. CONCLUSIONS: Although sleep in postmenopausal women was worse than in young controls, the recovery response following sleep deprivation was relatively well preserved. HT offered no significant advantage to sleep at baseline and slightly weakened the recovery response to prolonged wakefulness.     

Cognitive deterioration and changes of P300 during total sleep deprivation

The study was conducted to evaluate the cognitive deteriorations induced by sleep deprivation with the computerized neurocognitive tests and the P300 event-related potential. Thirty healthy college students (22 men, eight women) participated in the present study. Subjects remained awake for 38 h under continuous surveillance. In the morning and the evening of the two study days, the computerized neurocognitive tests and the P300 were performed. In vigilance test and reaction unit test, there were significant cognitive impairments during sleep deprivation. However, in the cognitrone test there was significant functional improvement, which might be due to the practice effect. The P300 latency was significantly prolonged and the amplitudes decreased during sleep deprivation. The cognitive impairment during 38 h of sleep deprivation was mainly in terms of vigilance and reaction time. In contrast, higher complex cognitive function such as fine perceptual analyses, visual discrimination and working memory might be not affected by 38 h of total sleep deprivation. The changes of P300 were significantly correlated with the results of vigilance and reaction unit tests but not with the cognitrone test. Taken together, these results suggest that the P300 changes that occur during sleep deprivation are a reflection of the decrement in vigilance, which prolongs reaction time.     

Baseline odor identification ability predicts degradation of psychomotor vigilance during 77 hours of sleep deprivation

Scores on the University of Pennsylvania Smell Identification Test, a measure of the functional integrity of the orbitofrontal cortex, were used to predict the vulnerability to cognitive declines during 77 hr of sleep deprivation. Twenty-one healthy volunteers completed the Smell Identification Test at rested baseline followed by repeated psychomotor vigilance testing throughout each night. Participants with better smell identification abilities sustained faster speeds and fewer lapses on the second and third nights of sleep deprivation than participants with lower scores. Individual differences in trait-like functioning of the orbitofrontal cortex are predictive of the ability to sustain alertness and vigilance during continuous wakefulness.     

全部睡眠剥夺对健康男性青年情绪的影响

目的 探讨长时间睡眠剥夺（SD）对情绪的影响。方法 挑选身体健康男性青年志愿者30名,剥夺全部睡眠52h。采用情绪状态问卷、贝克焦虑问卷、考虑自评量表、状态焦虑问卷和自评抑郁量表,分别在SD前（基础值）、SD期间（1次／6h,共8次）及一夜恢复性睡眠后评定受试者的情绪状态。结果 与基础值比较,随SD时间的延长,疲惫－惰性、焦虑、抑郁、困惑-迷茫等消极情绪的因子分逐渐增加（P＜0．05－0．001）,并与SD时间呈正相关;而有力－好动积极情绪因子分逐渐下降（P＜0．001）,与SD时间呈负相关（r＝－0．846,P＜0．001）。一夜恢复性睡眠后,疲惫－惰性和有力－好动因子分与基础值的差异仍有显著性（P＜0．05－0．01）,余均恢复到基础水平。结论 长时间的SD可导致情绪逐渐恶化。;一夜的恢复性睡眠对情绪的改善有一定效果。     

全部睡眠剥夺对健康男性青年脑电功率谱的影响

目的 探讨全部睡眠剥夺对健康男性青年脑电功率谱的影响。方法 选身体健康男性青年（１９￣２２岁）自愿受试者２０名,剥夺全部睡眠５０ｈ,定时记录脑电图共８次（间隔６ｈ）,分析各脑区各频段脑电功率。结果 睡眠剥夺５０ｈ后所有脑区（双侧枕区除外）的δ频段（Ｐ〈０．０５￣Ｐ〈０．００１）、θ频段（Ｐ〈０．０１￣Ｐ〈０．００１）功率升高,α２频段功率降低（Ｐ〈０．００１）,并与睡眠剥夺时间呈线性相关（Ｐ〈０．０１￣Ｐ〈０．００１）。例如,Ｆ３区δ、θ和α２频段脑电功率在睡眠剥夺前后分别为３．７８、４．１７;３．６５、４．３４;４．６４和３．９１ｌｎ（μＶ＾２）。脑电功率出现显著变化的时间由早以晚依次为α２频段、θ频段和δ频段。额前区、中央区、顶区和颞中区的改变较早,左半球比右半球早。脑电功率具有显著的随时间变化现象。快波频     

The effects of 40 hours of total sleep deprivation on inflammatory markers in healthy young adults

Inflammatory cytokines are released in response to stress, tissue damage, and infection. Acutely, this response is adaptive; however, chronic elevation of inflammatory proteins can contribute to health problems including cardiovascular, endocrine, mood, and sleep disorders. Few studies have examined how sleep deprivation acutely affects inflammatory markers, which was the aim of the current study. Nineteen healthy men and women aged 28.05+/-8.56 (mean+/-SD) were totally sleep deprived for 40 h under constant routine conditions. Pro-inflammatory markers: intracellular adhesion molecule-1 (ICAM-1), E-selectin, vascular adhesion molecule-1 (VCAM-1), c-reactive protein (CRP), interleukin-6 (IL-6), and interleukin-1beta (IL-1beta), and the anti-inflammatory cytokine interleukin-1 receptor antagonist (IL-1ra) were assayed in plasma. Daytime levels during baseline (hours 1-15 of scheduled wakefulness) were compared to daytime levels during sleep deprivation (hours 25-39 of scheduled wakefulness), thus controlling for circadian phase within an individual. Repeated measures ANOVA with planned comparisons showed that 40 h of total sleep deprivation induced a significant increase in E-selectin, ICAM-1, IL-1beta, and IL-1ra, a significant decrease in CRP and IL-6, and no significant change in VCAM-1. Alterations in circulating levels of pro- and anti-inflammatory cytokines and cell adhesion molecules during sleep deprivation were consistent with both increased and decreased inflammation. These findings suggest that one night of sleep loss triggers a stress response that includes stimulation of both pro- and anti-inflammatory proteins in the healthy young subjects tested under our experimental conditions.     

Abnormal brain response of chronic schizophrenia patients despite normal performance during a visual vigilance task

Deficits of attention are common among individuals with schizophrenia (SZ) and are related both to genetic liability to the disorder and to functional outcome among patients. To explore the brain systems underlying these attentional abnormalities, we compared the response of nine patients with chronic SZ or schizoaffective disorder to that of 10 matched healthy individuals performing a simple visual vigilance task during functional magnetic resonance imaging. The two groups performed equivalently on the task. When the blood oxygen level dependent (BOLD) signal during identification of a target letter among similar-looking letters was compared to the response during fixation trials, both groups showed multiple clusters of significant brain response in widespread cortical regions. Compared with healthy participants, SZ patients showed a diminished response in the inferior frontal cortex and an abnormally enhanced response in right postcentral gyrus, right medial temporal lobe and left cerebellum. The results suggest that abnormalities of functional brain response to attentional tasks can be observed among patients with SZ even when behavioral performance is unimpaired, and provide further evidence that brain systems related to attention are likely to be involved in the pathophysiology of the disorder.     

Response to total sleep deprivation and clomipramine in endogenous depression

In 44 endogenously depressed patients, response to total sleep deprivation (TSD) was investigated as a function of several biographical and clinical variables. All patients were subjected to a schedule of sleep-TSD-sleep-TSD. Antidepressant drug treatment (clomipramine) was started on the day before the first TSD. Sex, age, educational status, number of previous hospitalizations and duration of the current depressive episode were not related to the response to either the first or the second TSD. Likewise, no significant differences were found in the responses of unipolar and bipolar patients. In contrast, diurnal variation appeared to be positively correlated with response to TSD. Depressives with psychotic features reacted more favourably than non-psychotic depressives.     

Auditory evoked potentials and total sleep deprivation in depressed patients

Cortical auditory evoked potentials (latencies N1 and P2, N1-P2 amplitude, and amplitude/stimulus intensity function) were studied before and after 1 night's total sleep deprivation in 20 drug-free depressed inpatients. Responders to sleep deprivation showed an augmenting pattern on the non-dominant hemisphere and a reducing pattern on the dominant hemisphere. The interhemispheric difference in auditory cortex was also apparent in the group of patients who failed to respond to sleep deprivation, but with values pointing in the opposite direction. The augmenting pattern shown by responders in the nondominant hemisphere may be a predictor of therapeutic response to sleep deprivation and to subsequent treatment with drugs influencing serotonergic pathways.     

Abnormal brain response of chronic schizophrenia patients despite normal performance during a visual vigilance task

Deficits of attention are common among individuals with schizophrenia (SZ) and are related both to genetic liability to the disorder and to functional outcome among patients. To explore the brain systems underlying these attentional abnormalities, we compared the response of nine patients with chronic SZ or schizoaffective disorder to that of 10 matched healthy individuals performing a simple visual vigilance task during functional magnetic resonance imaging. The two groups performed equivalently on the task. When the blood oxygen level dependent (BOLD) signal during identification of a target letter among similar-looking letters was compared to the response during fixation trials, both groups showed multiple clusters of significant brain response in widespread cortical regions. Compared with healthy participants, SZ patients showed a diminished response in the inferior frontal cortex and an abnormally enhanced response in right postcentral gyrus, right medial temporal lobe and left cerebellum. The results suggest that abnormalities of functional brain response to attentional tasks can be observed among patients with SZ even when behavioral performance is unimpaired, and provide further evidence that brain systems related to attention are likely to be involved in the pathophysiology of the disorder.     

Caffeine challenge in insomniac patients after total sleep deprivation

BACKGROUND AND PURPOSE: This study compared the effects of caffeine in patients with primary insomnia and normal volunteers. The main goal was to determine the differences in sensitivity to caffeine between the groups. We investigated the effects on daytime sleep of placebo or caffeine after a night of total sleep deprivation (SD). We hypothesized that insomniacs would be more affected by caffeine, which would suggest a change in adenosine receptor (number or sensitivity) in primary insomniacs. PATIENTS AND METHODS: Six primary insomnia patients (Diagnostic and Statistical Manual of Mental Disorders (DSM-IV)) and six normal volunteers with no sleep complaints participated in a double-blind study with caffeine or placebo administered under a cross-over design with each subject serving as his or her own control. The participants did not have a history of drinking coffee or caffeinated beverages. Data from all-night polysomnography and multiple sleep latency test (MSLT) were collected in the sleep research laboratory of National Institute of Medical Sciences and Nutrition Salvador Zubirán. RESULTS: During the baseline night, patients with insomnia had significantly less delta sleep and less total sleep time than the normal volunteers. Mean sleep latency under basal MSLT did not differ between the groups. However, insomnia patients had significantly less total sleep during each nap compared to normal volunteers. After one night of total SD and under caffeine administration, the insomniacs had significantly longer sleep latency and less total sleep time in MSLT compared to normal volunteers. After SD, healthy volunteers reduced sleep latencies in MSLT with or without caffeine. CONCLUSIONS: Patients with insomnia had a higher sensitivity to the diurnal awakening effect of caffeine even after one night of SD. This suggests that changes in the adenosine receptors could, in part, be responsible for the hyperarousal state that has been reported in primary insomnia.     

Temporal order of sleepiness, performance and physiological indices during 19-h sleep deprivation

Nineteen-hour variation of subjective sleepiness, performance and physiological indices were assessed during sleep deprivation. Longitudinal data of each index had its characteristic curve through which the values changed from day level to night level. A comparison of the time when each curve crossed its mid-range (50% value of its range) showed that those of subjective sleepiness and heart rate were significantly earlier than those of tracking error and coefficient of variation of R-R interval (CV(R-R)), P<0.01. That of rectal temperature was located at between 1:00 and 4:00 am. These temporal relationships were reproducible under two lighting conditions. These results will be useful in considering the occurrence of human errors by night-time workers in the early morning.