An approach to estimate EEG power spectrum as an index of heat stress using backpropagation artificial neural network

A method has been presented for an effective application of backpropagation artificial neural network (ANN) in establishment of electro-encephalogram (EEG) power spectra as an index of stress in hot environment. The power spectrum data for slow wave sleep (SWS), rapid eye movement (REM) sleep and awake (AWA) states in three groups of rats (acute heat stress, chronic heat stress and the normal) were tested by an ANN, containing 60 nodes in input layer, weighted from power spectrum data from 0 to 30 Hz, 18 nodes in hidden layer and an output node. The target output values for this network were determined with another five-layered neural network (with the structure of 3-12-1-12-3). The input and output of this network was assigned with the three well-established heat stress indices (body temperature, body weight and plasma corticosterone). The most important feature for acute stress, chronic stress and normal conditions were extracted from the third layer single neuron and used for the target value for the three-layered neural network. The ANN was found effective in recognising the EEG power spectra with an average of 96.67% for acute heat stress, 97.17% for chronic heat stress and 98.5% for normal subjects.     

Electro-encephalogram disturbances in different sleep-wake states following exposure to high environmental heat

In this study, cerebral electrical activity or electro-encephalogram (EEG) was studied following exposure to high environmental heat, in three different age groups of freely moving rats. Each age group was subdivided into three groups: the acute heat stress group, subjected to a single exposure of 4h at 38°C in the biological oxygen demand incubator; the chronic heat stress group, exposed for 21 days, for 1 h each day, at 38°C in the incubator; and the handling control group. The polygraphic sleep-wake recordings involved simultaneous recordings of cortical EEG, electrooculogram (EOG), and electromyogram (EMG), on paper and in digital form on computer hard disk, just after the heat exposure for the acute stressed rats and on the 22nd day for the chronic stressed rats. The power spectrum was calculated for 2s epochs of the EEG signals. Quantitative analyses of EEG (qEEG) showed that, in all three age groups, changes in higher-frequency components (β₂) were significant in all sleep-wake states following both acute and chronic heat stress conditions. The power of β₂ activity in all three age groups after acute heat exposure was significantly decreased during slow wave sleep (SWS) (p<0.05) and rapid eye movement sleep (p<0.05), whereas the reverse was observed in the awake state (p<0.05). Following chronic heat exposure, β₂ activity was found to increase in all three sleep-wake stages in all groups of rats (p<0.01 for SWS in the weaning group and p<0.05 for other data). Thus the study demonstrated that the cortical EEG is sensitive to environmental heat, and alterations in EEG frequencies in different states of mental consciousness due to high heat can be differentiated efficiently by EEG power spectrum analysis.     

Neural Network-Based Evaluation of Chronic Non-Thermal Effects of Modulated 2450 MHz Microwave Radiation on Electroencephalogram

The effects of chronic exposure (2 h daily for 21 days) of 1 kHz square wave-modulated 2450 MHz microwave radiation (non-thermal) on sleep-EEG, open field behavior, and thyroid hormones (T₃, T₄, and TSH) have been analyzed in an animal model. Results revealed significant changes in these pathophysiological parameters (p < 0.05 or better), except body temperature, grooming behavior, and TSH levels. The sleep-EEG power spectrum data for slow wave sleep (SWS), rapid eye movement (REM) sleep, and awake (AWA) states in two experimental groups of rats (microwave exposed and the control) were tested by an artificial neural network (ANN), containing 60 nodes in input layer, weighted from power spectrum data from 0 to 30 Hz, 18 nodes in hidden layer and an output node. The target output values for this network were determined with another five-layered neural network (with the structure of 6-14-1-14-6). The input and output of this network was assigned with the six confirmed pathophysiological changes. The most important feature for chronic exposure of 2450 MHz microwave exposure and for control subjects was extracted from the third layer single neuron and used as the target value for the three-layered ANN. The network was found effective in recognizing the EEG power spectra with an average of 71.93% for microwave exposure and 93.13% for control subjects, respectively. However, the lower percentage of pattern identification agreement in the microwave-exposed group in comparison to the control group suggest only mild effects of microwave exposure with this experimental setup.     

Sleep-wake study in an animal model of acute and chronic heat stress

The study of the variations in different parameters of sleep-wake states following exposure to high environmental heat in three different age groups of freely moving rats have been presented in this paper. Each age group of rats was subdivided in three group (i) acute heat stress--subjected to a single exposure for 4 h in the BOD (Biological Oxygen Demand) incubator at 38 degrees C; (ii) chronic heat stress--exposed for 21 days daily for 1 h in the incubator at 38 degrees C, and (iii) handling control groups. The polygraphic, analog as well as digital sleep-wake recordings were performed just after the heat exposure from acute stressed rats and on 22nd day from chronic stressed rats. The results of this study revealed that acute exposure to high environmental heat increases sleep efficiency with significant increase in SWS (slow wave sleep) decrease in AWA (awake) time in all three age groups of rats. The increase in SWS and the sleep efficiency in these groups of rats at the cost of decreased time of AWA, indicates the involvement of the hypothalamus in thermoregulatory mechanism to conserve the energy of the body following sudden exposure to high heat. However, the reverse results were observed in the chronic stressed groups of rats, which have occurred mostly owing to the adaptations of the brain functions due to repetitive exposure to environmental heat. In consequence, the present study exhibits that the sleep is highly susceptible to the environmental heat and it is sensitive to the intensity, duration and the mode of exposure.     

A neural network confirms that physical exercise reverses EEG changes in depressed rats

The use of an artificial neural network (ANN) system to differentiate the EEG power density spectra in depressed from normal rats was tried. The beneficial effects of chronic physical exercise in reducing the effects of stress and therefore depression was also to be tested in animals by the same method. In this study, rats were divided into 4 groups, subjected to (i) chronic stress (D group); (ii) chronic exercise by treadmill running (EO group); (iii) exercise with stress (ES group) and (iv) handling (C group). The prefrontal cortical EEG, EMG and EOG were recorded simultaneously on paper and the digitized EEG signals were also stored in the hard-disk of a PC-AT through an ADC. After filtering the digitize signals, the EEG power spectra were calculated by an FFT routine. Three successive 4 s artefact-free epochs were averaged. The REM and NREM sleep periods as well as the awake period signals were analyzed separately. The FFT values from each of the 3 states, in the 4 groups of animals were tested by an ANN with 30 first layer neurons and a 2nd layer of a majority-vote-taker. The ANN could distinguish the depressed from the normal rats' EEG very well in REM (99%) sleep, NREM (95%) sleep and awake (81%) states. In most of the cases it identified the exercised rats' EEG as normal.     

Brief skin temperature changes towards thermoneutrality trigger REM sleep in rats

When rats were in slow-wave sleep (SWS) at an environmental temperature (23°C) below their thermoneutral zone (27–31°C), brief skin warming by either radiant heating, or forced air convection resulted in REM sleep on 79–80% of the trials. During control nonwarmed SWS bouts, the animals went into REM sleep on only 22–24% of the trials. When the environmental temperature was above thermoneutrality, 34°C, lowering skin temperature by convective cooling resulted in REM sleep entry 68% of the time, compared to 21% for noncooled, control trials. Skin warming and cooling at 29°C decreased the percent occurrence of REM sleep to 22% and 9% respectively, for at this thermoneutral temperature 46% of the control SWS bouts ended in REM sleep. Thus, peripheral temperature changes towards thermoneutrality trigger REM sleep in mildly thermally stressed rats.     

Increased EEG spectral power density during sleep following short-term sleep deprivation in pigeons (Columba livia): evidence for avian sleep homeostasis

Birds provide a unique opportunity to evaluate current theories for the function of sleep. Like mammalian sleep, avian sleep is composed of two states, slow-wave sleep (SWS) and rapid eye-movement (REM) sleep that apparently evolved independently in mammals and birds. Despite this resemblance, however, it has been unclear whether avian SWS shows a compensatory response to sleep loss (i.e., homeostatic regulation), a fundamental aspect of mammalian sleep potentially linked to the function of SWS. Here, we prevented pigeons (Columba livia) from taking their normal naps during the last 8 h of the day. Although time spent in SWS did not change significantly following short-term sleep deprivation, electroencephalogram (EEG) slow-wave activity (SWA; i.e., 0.78-2.34 Hz power density) during SWS increased significantly during the first 3 h of the recovery night when compared with the undisturbed night, and progressively declined thereafter in a manner comparable to that observed in similarly sleep-deprived mammals. SWA was also elevated during REM sleep on the recovery night, a response that might reflect increased SWS pressure and the concomitant 'spill-over' of SWS-related EEG activity into short episodes of REM sleep. As in rodents, power density during SWS also increased in higher frequencies (9-25 Hz) in response to short-term sleep deprivation. Finally, time spent in REM sleep increased following sleep deprivation. The mammalian-like increase in EEG spectral power density across both low and high frequencies, and the increase in time spent in REM sleep following sleep deprivation suggest that some aspects of avian and mammalian sleep are regulated in a similar manner.     

Interhemispheric asymmetry of human sleep EEG in response to selective slow-wave sleep deprivation

Recent evidence suggests that the human sleep electroencephalogram (EEG) shows regional differences over both the sagittal and coronal planes. In the present study, in a group of 10 right-handers, the authors investigated the presence of hemispheric asymmetries in the homeostatic regulation of human sleep EEG power during and after selective slow-wave sleep (SWS) deprivation. The SWS deprivation was slightly more effective over the right hemisphere, but the left hemisphere showed a markedly larger increase of EEG power in the 1.00-24.75 Hz range during recovery-night non-REM sleep, and a larger increase of EEG power during both deprivation-night and recovery-night REM sleep. These results support the greater need for sleep recuperative processes of the left hemisphere, suggesting that local sleep regulation processes may also act during REM sleep.     

Slow-wave sleep: do young adult men and women age differently?

The differential effects of ageing on polysomnographic and EEG spectral characteristics of sleep were explored in men and women between the ages of 20 and 40. Men and women in their twenties were found to have similar percentages of slow-wave sleep (SWS) (% Stage 3 and 4) and mean EEG slow wave activity (quantified by spectral analysis). Significant reductions in the percentage of SWS and mean slow wave activity over the night occurred in men during their thirties but not in the women. This suggests that gender difference in SWS may emerge between age 30 and 40 in young adults. Men in this sample were also found to have significant increases in Stage 2 sleep, and decreases in REM sleep time, REM activity, REM density and REM intensity. No significant effects of age were found for women in any visually scored sleep variables. Both men and women had age related reductions in spectral power in the spindle frequencies. Taken together, these findings suggest that the sleep of men and women over age 20–40 may age differently.     

Relationship between spike-wave discharges and vigilance levels in rats with spontaneous petit mal-like epilepsy

The relationship between states of vigilance and spike and wave discharges (SWD) was examined during 12 hours in 4 Wistar rats from a strain bred for spontaneous generalized non-convulsant seizures. On the basis of cortical and hippocampal EEG and EMG activity, wakefulness (W), slow wave sleep (SWS) and paradoxical sleep (REM) were distinguished. Of the SWD 86% occurred during quiet W, 14% during the first minutes of SWS. No SWD occurred during active wakefulness and they were exceptional during REM. These results show that the states of quiet W and transitional states favour the SWD in rats with petit mal-like epilepsy, as in human petit mal.     

Electroencephalogram asymmetry and spectral power during sleep in the northern fur seal

The fur seal (Callorhinus ursinus), a member of the Pinniped family, displays a highly expressed electroencephalogram (EEG) asymmetry during slow wave sleep (SWS), which is comparable with the unihemispheric sleep in cetaceans. In this study, we investigated the EEG asymmetry in the fur seal using spectral analysis. Four young (2-3 years old) seals were implanted with EEG electrodes for polygraphic sleep recording. In each animal, EEG spectral power in the frequency range of 1.2-16 Hz was computed in symmetrical cortical recordings over two consecutive nights. The degree of EEG asymmetry was measured by using the asymmetry index [AI = (L - R)/(L + R), where L and R are the spectral powers in the left and right hemispheres, respectively]. In fur seals, EEG asymmetry, as measured by the percent of 20-s epochs with absolute AI > 0.3 and >0.6, was expressed in the entire frequency range (1.2-16 Hz). The asymmetry was significantly greater during SWS (25.6-44.2% of all SWS epochs had an absolute AI > 0.3 and 2.1-12.2% of all epochs had AI > 0.6) than during quiet waking (11.0-20.3% and 0-1.9% of all waking epochs, respectively) and REM sleep (4.2-8.9% of all REM sleep epochs and no epochs, respectively). EEG asymmetry was recorded during both low- and high-voltage SWS, and was maximal in the range of 1.2-4 and 12-16 Hz. As shown in this study, the degree of EEG asymmetry and the frequency range in which it is expressed during SWS in fur seals are profoundly different from those of terrestrial mammals and birds.     

不同行为状态下大鼠脑电时频变化特性的直方图分析

结合应用多分辨率小波分解方法和直方图参数统计方法 ,分析大鼠脑电信号 (Electroencephalogram,EEG)在不同行为状态下的非稳态时频动态变化特性。利用埋植电极记录自由活动大鼠在清醒期、慢波睡眠期和快动眼睡眠期的皮层 EEG,应用小波变换将 EEG分解成 δ、θ、α和 β四个分量 ,求各分量功率对数值直方图和功率百分比值直方图的均值、方差、偏斜度和峭度。结果表明 :EEG功率对数值的分布比较接近正态分布 ,而多数功率百分比值的分布与正态分布差别显著。单因素方差分析结果显示这些直方图统计参数在不同行为状态之间和不同分解分量之间具有显著差别。 EEG在不同时期的某些特征波 (例如 :慢波睡眠期的 δ波、清醒期和快动眼睡眠期的 θ波等 )使功率对数值分布具有较大的偏斜度值和峭度值。由此可见 ,EEG小波分解分量的直方图参数是一种新的描述EEG动态时频变化特性的定量分析指标     

Electroencephalogram and cardiovascular responses to noise during daytime sleep in shiftworkers

Summary Intermittent noise occurring during sleep has been found to induce heart rate, peripheral vasomotor and electroencephalogram (EEG) changes. This study analysed these responses during the daytime and night-time sleep of shiftworkers doing a three shift system, to determine the influence of the inversion of the sleep-wake cycle on the sensitivity to noise. A group of 14 shiftworkers [aged 37 (SD 5) years] underwent an habituation daytime sleep, two experimental daytime sleeps and a night-time sleep. Traffic noises were presented during sleep [truck, 71 dB(A); motorbike, 67 dB(A); and car, 64 dB(A)] at a rate of nine each hour. The EEG measurements of sleep, electrocardiogram and finger pulse amplitude were recorded continuously. The results were expressed by computing the percentage of observed cardiac response (%HRR) and vasoconstrictive response (%FPR), magnitude of heart rate variation (heart rate response; HRR), percentage of reduction of the digital blood flow (finger pulse response, FPR), cardiac cost (CC = % HRR x HRR) and vasomotor cost (VC = % FPR x FPR). The results showed that, compared to night-time sleep, there was change in the structure of daytime sleep, that is an increase in slow wave sleep (SWS), especially stage 4 sleep decrease of stage 2 and rapid eye movement (REM) sleep latencies, and an earlier SWS and REM sleep barycentric point. During daytime sleep the % FPR was significantly smaller in SWS than in stage 2 or REM sleep. Large differences were observed in % HRR, HRR and CC between daytime sleep stages (SWS less than stage 2 less than REM sleep). These differences were not observed during night-time sleep. Moreover, compared to night-time sleep, CC was increased during daytime REM sleep and decreased during daytime SWS. The inversion of the sleep-wake cycle in shiftworkers, did not influence the overall cardiovascular reactivity to noise. This was explained by a compensatory effect due to an increase in this reactivity during daytime REM sleep and its decrease in daytime SWS. The second reason is due to an increase in the percentage of stage 4 sleep during daytime sleep (less disturbed by noise than other sleep stages). This increased percentage of stage 4 sleep was probably a consequence of the partial sleep deprivation occurring after a week working on nightshift.     

Sleep and EEG spectra in rats recorded via telemetry during surgical recovery

STUDY OBJECTIVE: To determine sleep and EEG spectra in rats during surgical recovery. DESIGN: Sleep, activity, and EEG spectral power were examined in rats via telemetry on days 1, 2, 3, 7, 14, and 15 after implantation surgery. RESULTS: NREM sleep and total sleep were increased on days 1 and 2 compared to later days. REM sleep was decreased on days 2 and 3 compared to days 14 and 15, and activity was decreased on days 1 and 2 compared to later days. EEG power (0.5-5 Hz for NREM and wakefulness, and 5.5-10 Hz for REM and wakefulness) was increased on days 1-3 compared to days 7, 14, and 15. CONCLUSION: The results are discussed in terms of their implications for post-surgery stabilization of sleep and potential relevance for sleep after injury.     

Circadian variation of EEG power spectra in NREM and REM sleep in humans: Dissociation from body temperature

In humans, EEG power spectra in REM and NREM sleep, as well as characteristics of sleep spindles such as their duration, amplitude, frequency and incidence, vary with circadian phase. Recently it has been hypothesized that circadian variations in EEG spectra in humans are caused by variations in brain or body temperature and may not represent phenomena relevant to sleep regulatory processes. To test this directly, a further analysis of EEG power spectra - collected in a forced desynchrony protocol in which sleep episodes were scheduled to a 28-h period while the rhythms of body temperature and plasma melatonin were oscillating at their near 24-h period - was carried out. EEG power spectra were computed for NREM and REM sleep occurring between 90-120 and 270-300 degrees of the circadian melatonin rhythm, i.e. just after the clearance of melatonin from plasma in the 'morning' and just after the 'evening' increase in melatonin secretion. Average body temperatures during scheduled sleep at these two circadian phases were identical (36.72 degrees C). Despite identical body temperatures, the power spectra in NREM sleep were very different at these two circadian phases. EEG activity in the low frequency spindle range was significantly and markedly enhanced after the evening increase in plasma melatonin as compared to the morning phase. For REM sleep, significant differences in power spectra during these two circadian phases, in particular in the alpha range, were also observed. The results confirm that EEG power spectra in NREM and REM sleep vary with circadian phase, suggesting that the direct contribution of temperature to the circadian variation in EEG power spectra is absent or only minor, and are at variance with the hypothesis that circadian variations in EEG power spectra are caused by variations in temperature.     

Are antibiotic effects on sleep behavior in the rat due to modulation of gut bacteria?

The sleep-inducing substance Factor S (FS) is unique among candidate sleep molecules because of its bacterial origin. FS is derived from the bacterial cell wall and accumulates in the brain and body fluids of sleep-deprived animals including man. Exogenous administration of FS and related muramyl peptides results in an increase in slow-wave sleep (SWS). To test the possibility that gastrointestinal bacteria are a source of FS, rats were placed on an antibiotic regimen (neomycin and metronidazole in drinking water) and sleep measures taken after one week. There was a significant reduction in SWS in the first three hours of the lights-on period as well as an increase in sleep latency. No other sleep parameters, including Rapid Eye Movement (REM) sleep measures, were affected, suggesting that there was a specific SWS effect due to bacterial reduction. Possible toxic effects of the antibiotic treatment were unlikely factors in SWS reduction due to the stability of other sleep measures such as number of episodes of SWS and REM, total sleep time and REM latency. Oral administration of live E. coli to rats did not affect any sleep measures. It appears that FS may be specifically involved in the early sleep period where it promotes sleep onset and SWS generation.     

The diurnal distribution of sleep propensity: experimental data about the interaction of the propensities for slow-wave sleep and REM sleep

The aim of the present study was to assess the diurnal variation of sleep propensity by evaluating the temporal distribution of sleep onset latency (SOL) and REM- and slow-wave sleep (SWS) parameters in systematically scheduled daytime naps for 12 young males. To reduce the effect of prior SWS on subsequent REM sleep, a double-nap technique was used, i.e. two adjacent naps A and B, which were separated by a 10-min break. Nap duration was adjusted in such a way that nap A allowed 30 min of sleep and nap B one complete NREM–REM cycle. EEG slow wave activity (SWA, power density from 0.5–4 Hz) was estimated from nap A and REM sleep parameters from nap B. The time span between 08.00 hours and 24.00 hours was covered by nine double-naps at 2 h intervals. The order of the nap sessions was systematically varied within and across subjects. For each subject, the time between successive double-nap recordings was at least three days. SOL was shortest in the time interval 12.00 hours to 16.00 hours and significantly longer between 20.00 hours and 24.00 hours. REM sleep duration and the percentage of sleep onset REM episodes decreased continuously from 08.00 hours to the interval 18.00–20.00 hours and increased thereafter, with a time course inversely related to the one of body temperature, which was also measured continuously. SWA showed a steady, threefold increase from 08.00 hours to 24.00 hours. The study offers new data on the diurnal variation of sleep propensity which seems to be a composite function of the drives for SWS and REM sleep.     

The dynamics of the first sleep cycle.

Eight subjects participated in an experiment in which sleep stages and electroencephalographic (EEG) power density during the first sleep cycles (and where such appeared, also second cycles) were studied in a design involving 8, 4, 2 or 0 hr of progressively postponed night-time sleep. Each of these four manipulations was followed by a day-time sleep beginning at 1100 hr. No significant changes in the duration of the first sleep cycle appeared. As the prior sleep loss increased both SWE (slow-wave energy; accumulated EEG delta power density) and SWA (slow-wave activity; EEG delta power per minute) increased during the 1100-hr sleeps. This was observed for the entire cycles, the nonrapid eye movement (NREM) periods, and the SWS periods, respectively. SWS latency decreased and SWS duration increased, respectively, markedly with prior waking. Also, for the progressively postponed sleeps (started at 2300 hr, 0300 hr, 0500 hr and 1100 hr) there were changes, but not as clear. After 28 hr of continuous waking there was a marked increase of SWA during SWS. Also, at this level there was a spill over of SWA to the second cycle. It is suggested that there might be a limit to the amount and intensity of SWS that can be accommodated in the first sleep cycle and that this limit is reached before the appearance of REM sleep.     

Comparison of MK-801 and sleep deprivation effects on NREM, REM, and waking spectra in the rat.

In previous studies, we showed that blockade of the cation channel gated by NMDA glutamate receptors with ketamine or MK-801 massively stimulates NREM delta. We now test whether this NREM delta stimulation is physiological by comparing the EEG response following MK-801 to the EEG response following sleep deprivation (SD). Our previous studies measured only NREM 1-4 Hz EEG with period-amplitude analysis (PAA). Here we extended the analysis of MK-801 effects on sleep EEG by applying power spectral analysis (PSA) to examine delta and higher frequency spectra (.2-100 Hz) in NREM and by including REM and waking spectra. The changes in EEG spectra following MK-801 and SD were remarkably similar. Both SD and MK-801 produced their largest changes in NREM delta and REM 10-20 Hz power. There were some differences in the high frequency EEG, but the overall similarity of the PSA spectra in all three vigilance states after MK-801 and SD supports the possibility that MK-801 stimulated physiologic sleep, perhaps by increasing the need for homeostatic recovery from the metabolic effects of NMDA channel blockade.     

Effects of the selective 5-HT1B agonist, CGS 12066B, on sleep/waking stages and EEG power spectrum in rats

SUMMARY  Sleep/waking stages and EEG power spectra were studied in rats for 8 h following intraperitoneal administration of CGS 12066B, a selective 5-HT_1B agonist. Waking was increased and rapid eye movement (REM) sleep decreased in a dose-dependent manner. Total slow-wave sleep (TSWS) was reduced, but only in the first 2 h period. The latencies to REM sleep and stable sleep were increased dose-dependently. The drug also induced profound behavioural changes that may account for some of the sleep/waking changes. EEG power densities in waking and TSWS were reduced dose-dependently from 7 to 20 Hz after CGS 12066B, suggesting a tendency towards general deactivation. The increase in waking together with a general deactivation suggest complex effects of CGS 12066B on the sleep/waking axis.