http://download.neurosky.com/docs/papers/bcq/Klimesch_1999_EEG_alpha_and_theta_oscillations_reflect_cognitive_and_memory_performance.pdf

EEG alpha and theta oscillations reflect cognitive and memory performance: a review and analysis

Sleep deprivation severely compromises the ability of human beings to respond to stimuli in a timely fashion. These deficits have been attributed in large part to failures of vigilant attention, which many theorists believe forms the bedrock of the other more complex components of cognition. One of the leading paradigms used as an assay of vigilant attention is the psychomotor vigilance test (PVT), a high signal-load reaction-time test that is extremely sensitive to sleep deprivation. Over the last twenty years, four dominant findings have emerged from the use of this paradigm. First, sleep deprivation results in an overall slowing of responses. Second, sleep deprivation increases the propensity of individuals to lapse for lengthy periods (>500ms), as well as make errors of commission. Third, sleep deprivation enhances the time-on-task effect within each test bout. Finally, PVT results during extended periods of wakefulness reveal the presence of interacting circadian and homeostatic sleep drives. A theme that links these findings is the interplay of “top-down” and “bottom-up” attention in producing the unstable and unpredictable patterns of behavior that are the hallmark of the sleep-deprived state.

Sleep Deprivation and Vigilant Attention

Vigilance, alertness, or sustained attention: physiological basis and measurement.

The brain is not only immunologically active of its own accord, but also has complex peripheral immune interactions. Given the central role of cytokines in neuroimmmunoendocrine processes, it is hypothesized that these molecules influence cognition via diverse mechanisms. Peripheral cytokines penetrate the blood-brain barrier directly via active transport mechanisms or indirectly via vagal nerve stimulation. Peripheral administration of certain cytokines as biological response modifiers produces adverse cognitive effects in animals and humans. There is abundant evidence that inflammatory mechanisms within the central nervous system (CNS) contribute to cognitive impairment via cytokine-mediated interactions between neurons and glial cells. Cytokines mediate cellular mechanisms subserving cognition (e.g., cholinergic and dopaminergic pathways) and can modulate neuronal and glial cell function to facilitate neuronal regeneration or neurodegeneration. As such, there is a growing appreciation of the role of cytokine-mediated inflammatory processes in neurodegenerative diseases such as Alzheimer's disease and vascular dementia. Consistent with their involvement as mediators of bidirectional communication between the CNS and the peripheral immune system, cytokines play a key role in the hypothalamic-pituitary-adrenal axis activation seen in stress and depression. In addition, complex cognitive systems such as those that underlie religious beliefs, can modulate the effects of stress on the immune system. Indirect means by which peripheral or central cytokine dysregulation could affect cognition include impaired sleep regulation, micronutrient deficiency induced by appetite suppression, and an array of endocrine interactions. Given the multiple levels at which cytokines are capable of influencing cognition it is plausible that peripheral cytokine dysregulation with advancing age interacts with cognitive aging.

Cytokines and cognition--the case for a head-to-toe inflammatory paradigm.

The aim of this study was to compare the effects of total sleep deprivation (TSD), rapid eye movement (REM) sleep and slow wave sleep (SWS) interruption and sleep recovery on mechanical and thermal pain sensitivity in healthy adults. Nine healthy male volunteers (age 26--43 years) were randomly assigned in this double blind and crossover study to undergo either REM sleep or SWS interruption. Periods of 6 consecutive laboratory nights separated by at least 2 weeks were designed as follows: N1 Adaptation night; N2 Baseline night; N3 Total sleep deprivation (40 h); N4 and N5 SWS or REM sleep interruption; N6 Recovery. Sleep was recorded and scored using standard methods. Tolerance thresholds to mechanical and thermal pain were assessed using an electronic pressure dolorimeter and a thermode operating on a Peltier principle. Relative to baseline levels, TSD decreased significantly mechanical pain thresholds (-8%). Both REM sleep and SWS interruption tended to decrease mechanical pain thresholds. Recovery sleep, after SWS interruption produced a significant increase in mechanical pain thresholds (+ 15%). Recovery sleep after REM sleep interruption did not significantly increase mechanical pain thresholds. No significant differences in thermal pain thresholds were detected between and within periods. In conclusion this experimental study in healthy adult volunteers has demonstrated an hyperalgesic effect related to 40 h TSD and an analgesic effect related to SWS recovery. The analgesic effect of SWS recovery is apparently greater than the analgesia induced by level I (World Health Organization) analgesic compounds in mechanical pain experiments in healthy volunteers.

https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.1365-2869.2001.00240.x

The effects of total sleep deprivation, selective sleep interruption and sleep recovery on pain tolerance thresholds in healthy subjects.

Nine paid volunteers were sleep deprived over a period of 40 hours. Every 2 hours during total sleep deprivation (TSD) and after recovery sleep, oral temperature (OT), reaction time (RT) in a vigilance task and electroencephalogram (EEG) with eyes open and closed (C3, C4, T3 and T4) were recorded. Ten artifact-free samples from each condition were Fourier transformed. Absolute power was calculated for six bands. Analyses of variance with deprivation and time of day as factors showed the following significant results : 1) TSD induced an increase in RT, of theta power in all derivations, of beta power in both centrals and a decrease of alpha power with eyes closed ; OT was not affected. 2) All bands showed a peak of power at 1800 hours, 2 hours in advance of the OT acrophase at 2000 hours. All variables recovered baseline values after 1 night of sleep. Significant linear correlations of hours of wakefulness with EEG and RT, and of EEG power with OT and RT, were observed. The present findings show a linear increase in EEG power and RT with TSD, and a diurnal oscillation of EEG power, which is independent of TSD.

Effect of total sleep deprivation on reaction time and waking EEG activity in man

Nine young adult male (23-30 years old) paid volunteers were subjected to total sleep deprivation (TSD), after two consecutive nights in the laboratory, for 40 hours (from 0800 hours on the first day to 2400 hours on the following day). Oral temperature (OT), reaction time (RT) in a visual vigilance task, and electroencephalogram (EEG ; C3, C4, T3, and T4) while performing the task were recorded every 2 hours during TSD and after recovery sleep. One second of EEG, before target and non-target stimuli for every subject and condition was visually inspected, and artifact-free epochs were Fourier transformed. Absolute power (AP) was calculated for 4-20 Hz (full band) and for theta, alpha1, alpha2, and beta1. Analyses of variance (ANOVAs), with TSD and time-of-day as factors, showed the following significant results : TSD induced an increase in RT and AP of the full band at C3 and C4, of all bands at C3, of theta at T3, and of beta1 at T4 (p < 0.009 for all comparisons). No time-of-day effects nor interactions were found. OT was not affected by TSD. All variables returned to baseline values after recovery sleep. RT and EEG power showed a linear increase with accumulating hours of wakefulness. The increment in RT also correlated with the increase in EEG power. The results demonstrate that the increment in RT is associated with the increase in AP, particularly in the left central cortex ; that the EEG may be used to identify sleepiness ; and that EEG during task performance is more sensitive to TSD than during relaxed wakefulness.

Time course of reaction time and EEG while performing a vigilance task during total sleep deprivation.

12 sessions of EEG activity, one every second day, were recorded at F3, F4, C3, C4, P3, P4, O1 and O2 in 9 women with regular menstrual cycles. The following significant oscillations were observed: 1) absolute power was lower during periovulatory period; 2) absolute power of delta theta and alpha1 was higher during premenstrual period whereas absolute power of alpha2, betal and beta2 was higher during menstruation; 3) relative power of low alpha frequencies was lower and that of high frequencies was higher during premenstrual period; 4) interhemispheric correlation between frontals was higher during ovulation and between occipitals was higher during premenstrual phase; 5) no significant power asymmetries were observed. The present findings suggest higher activation of centro-parietal regions during menstruation and lower activation of frontal regions during premenstrual phase.

EEG oscillations during menstrual cycle.

Eight adult males were subjected to 40 hours of total sleep deprivation (TSD). Reaction time in a visual task and electroncephalographam (C 3 ) were evaluated every 2 hours. One second of EEG before the stimuli was Fourier-transformed, and 750 ms after target and nontarget stimuli were averaged and visual event-related potentials (ERP) were obtained. Factorial analysis identified time windows that showed significant amplitude reduction and longer latencies with TSD: (1) 140 to 288 ms (P180-N242-P281); (2) 288 to 413 ms and 601 to 749 ms (N382; P718) and; (3) 531 to 601 ms (N500). Effect was strongest for N382 and P718, the amplitudes of which dropped to 20% of original size. The entire waveform recovered initial amplitudes and latencies after recovery sleep except for P718 latency. Waveforms within similar time intervals have been associated with attentional gating, sensory discrimination, target selection, uncertainty and decision processes. Amplitudes of the visual ERP were inversely correlated with hours of TSD, reaction time, and absolute power of the prestimulus EEG. Present results clearly show changes in fundamental neurophysiologic mechanisms as a result of TSD, indicating variability and reduction of the alertness mechanisms and changes in thalamocortical gating affecting attention, discrimination and decision-making.

/pdf/amplitude-reduction-in-visual-event-related-potentials-as-a-4oew9l48kj.pdf

Amplitude reduction in visual event-related potentials as a function of sleep deprivation.

Inter- (INTERr) and intrahemispheric (INTRAr) electroencephalographic (EEG) correlations were assessed in eight young male adults during wakefulness with eyes closed before going to sleep, and during stage 2, stage 4 and paradoxical sleep (PS) on the second night spent at the laboratory. Pearson product-moment correlations were calculated between EEG signals of every pair of electrodes (C3, C4, F3, F4, T3, T4) for six bands and for every 0.5 Hz from 1.5 to 15 Hz. Previous results of higher INTERr during sleep compared to during wakefulness were confirmed for the delta and theta bands during stage 2 sleep and PS and for sleep spindles during stage 2 sleep. The present results extend these findings to INTERr between F3 and F4 and during stage 4 sleep. INTRAr of 1.5-6.5 and 11-15 Hz was significantly higher during stages 2 and 4, whereas during PS INTRAr did not change. These data show that cortical changes during sleep are also observed in functional differentiation between cortical sites. Inter- and intrahemispheric differentiation is attenuated during stage 2 and 4 sleep, whereas during PS only inter-hemispheric differentiation is attenuated but intrahemispheric differentiation maintains similar levels of wakefulness. The attenuation of cortical differentiation may be of relevance for the understanding of mental activity changes during sleep.

M. A. Guevara

Papers

Effect of total sleep deprivation on reaction time and waking EEG activity in man

Time course of reaction time and EEG while performing a vigilance task during total sleep deprivation.

EEG oscillations during menstrual cycle.

Amplitude reduction in visual event-related potentials as a function of sleep deprivation.

Inter- and intrahemispheric EEG correlation during sleep and wakefulness.