Artificial neural network detects changes in electro-encephalogram power spectrum of different sleep-wake states in an animal model of heat stress

An effective application is presented of a back-propagation artificial neural network (ANN) in differentiating electro-encephalogram (EEG) power spectra of stressed and normal rats in three sleep-wakefulness stages. The rats were divided into three groups, one subjected to acute heat stress, one subjected to chronic heat stress and one a handling control group. The polygraphic sleep recordings were performed by simultaneous recording of cortical EEG, electro-oculogram (EOG) and electromyogram (EMG) on paper and in digital form on a computer hard disk. The preprocessed EEG signals (after removal of DC components and reduction of base-line movement) were fragmented into 2s artifact-free epochs for the calculation of power spectra. The slow-wave sleep (SWS), rapid eye movement (REM) sleep and awake (AWA) states were analysed separately. The power spectrum data for all three sleep-wake states in the three groups of rats were tested by a back-propagation ANN. The network contained 60 nodes in the input layer, weighted from power spectrum data from 0 to 30 Hz, 18 nodes in the hidden layer and an output node. The ANN was found effective in differentiating the EEG power spectra from stressed to normal spectral patterns following acute (92% in SWS, 85.5% in REM sleep, 91% in AWA state) as well as chronic heat exposure (95.5% in SWS, 93.8% in REM sleep, 98.5% in AWA state).     

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.     

Systematic Trends Across the Night in Human Sleep Cycles

The durations of successive sleep cycles, defined according to NREM (stage 2) or REM onsets, were objected to trend analysis in three groups of normal subjects and in a group of elderly patients with chronic brain syndrome (CBS). NREM sleep cycles showed consistent curvilinear trends for all groups except that the trend in children was distinguished by a lengthy first NREM cycle. REM steep cycles showed quite similar curvilinear trends for the three normal age groups with the middle two cycles being longer than the first and fourth. In the CBS patients, REM sleep cycles did not show a significant trend across the night. Real-time cycles (i.e., with time awake included) manifested trends quite similar to those excluding waking. The trends in sleep cycle durations are normative characteristics of sleep which may not be apparent on a single night. A more constant cycle was found in the CBS elderly and may indicate brain pathology. Sleep cycle trends, along with such other temporal characteristics as the decline in stage 4, may provide clues to the metabolic processes which underlie the sleep EEG. They also provide a more exact basis for investigation of hypothesized biorhythm correlates of NREM-REM cycles.     

Spectral analysis of all-night human sleep EEG in narcoleptic patients and normal subjects

To investigate the pathophysiology of narcoleptic patients' sleep in detail, we analysed and compared the whole-night polysomnograms of narcoleptic patients and normal human subjects. Eight drug-naive narcoleptic patients and eight age-matched normal volunteers underwent polysomnography (PSG) on two consecutive nights. In addition to conventional visual scoring of the polysomnograms, rapid eye movement (REM)-density and electroencephalograph (EEG) power spectra analyses were also performed. Sleep onset REM periods and fragmented nocturnal sleep were observed as expected in our narcoleptic patients. In the narcoleptic patients, REM period duration across the night did not show the significant increasing trend that is usually observed in normal subjects. In all narcoleptic patient REM periods, eye movement densities were significantly increased. The power spectra of narcoleptic REM sleep significantly increased between 0.3 and 0.9 Hz and decreased between 1.0 and 5.4 Hz. Further analysis revealed that non-rapid eye movement (NREM) period duration and the declining trend of delta power density in the narcoleptic patients were not significantly different from the normal subjects. Compared with normal subjects, the power spectra of narcoleptic NREM sleep increased in the 1.0-1.4 Hz and 11.0-11.9 Hz frequency bands, and decreased in a 24.0-26.9 Hz frequency band. Thus, increased EEG delta and decreased beta power densities were commonly observed in both the NREM and REM sleep of the narcoleptic patients, although the decrease in beta power during REM sleep was not statistically significant. Our visual analysis revealed fragmented nocturnal sleep and increased phasic REM components in the narcoleptic patients, which suggest the disturbance of sleep maintenance mechanism(s) and excessive effects of the mechanism(s) underlying eye movement activities during REM sleep in narcolepsy. Spectral analysis revealed significant increases in delta components and decreases in beta components, which suggest decreased activity in central arousal mechanisms. These characteristics lead us to hypothesize that two countervailing mechanisms underlie narcoleptic sleep pathology.     

Beneficial effects of regular exercise on sleep in old F344 rats

With aging there is a significant decline in the normal architecture of sleep and a reduction in the diurnal amplitude of core body temperature. Regular moderate exercise has been shown to have a positive impact in the elderly and here we investigate whether sleep–wake patterning can also be improved. Young (3 months) and old (22 months) F344 rats were exercised once a day for 50 min at night onset over an 8-week period. Thereafter, polysomnographic recordings were obtained immediately after exercise. To determine the lasting consequences of exercise, sleep was also recorded 2 days and 2 weeks after exercise had ended. Old rats that were exercised had a significant weight loss, were awake more during the last third of their active period, had less sleep fragmentation and the amplitude of the diurnal rhythm of core body temperature was significantly increased. Old exercised rats also had an overall increase in the amplitude of EEG power (0.5–16 Hz) during wake and theta EEG power during REM sleep. In young rats regular exercise increased EEG delta power (0.5–4 Hz) during NREM sleep. Our data indicate regular exercise in old rats improves sleep architecture, EEG power and diurnal rhythm of temperature.     

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.     

NREM sleep EEG frequency spectral correlates of sleep complaints in primary insomnia subtypes

STUDY OBJECTIVES: To determine whether the frequency spectrum of the sleep EEG is a physiologic correlate of 1) the degree to which individuals with persistent primary insomnia (PPI) underestimate their sleep time compared with the traditionally scored polysomnogram (PSG) and 2) the sleep complaints in PPI subjects who have relatively long traditionally scored PSG sleep times and relatively greater underestimation of sleep time. DESIGN: We compared EEG frequency spectra from REM and NREM sleep in PPI subjects subtyped as subjective insomnia sufferers (those with relatively long total sleep time and relative underestimation of sleep time compared with PSG), and objective insomnia sufferers (those with relatively short PSG total sleep time) with EEG frequency spectra in normals. We also studied the correlation between these indices and the degree of underestimation of sleep. Further, we determined the degree to which sleep EEG indexes related to sleep complaints. SETTING: Duke University Medical Center Sleep Laboratory. PARTICIPANTS: Normal (N=20), subjective insomnia (N=12), and objective insomnia (N=18) subjects. INTERVENTIONS: N/A MEASUREMENTS AND RESULTS: Lower delta and greater alpha, sigma, and beta NREM EEG activity were found in the patients with subjective insomnia but not those with objective insomnia, compared with the normal subjects. These results were robust to changes in the subtyping criteria. No effects were found for REM spectral indexes. Less delta non- REM EEG activity predicted greater deviation between subjective and PSG estimates of sleep time across all subjects. For the subjective insomnia subjects, diminished low-frequency and elevated higher frequency non- REM EEG activity was associated with their sleep complaints. CONCLUSIONS: NREM EEG frequency spectral indexes appear to be physiologic correlates of sleep complaints in patients with subjective insomnia and may reflect heightened arousal during sleep.     

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.     

Enhanced slow-wave activity within NREM sleep in the cortical and subcortical EEG of the cat after sleep deprivation.

Electroencephalograms (EEGs) of the cortex and of seven subcortical structures were recorded during two baseline days and during a recovery day following a 12-hour period of sleep deprivation (SD) in eight cats. The EEGs were analyzed by visual scoring and by spectral analysis. The following subcortical structures were studied: hippocampus, amygdala, hypothalamus, nucleus centralis lateralis of the thalamus, septum, nucleus caudatus and substantia nigra. The EEGs of all brain structures exhibited sleep state-dependent changes. In general, slow-wave activity (SWA, 0.5-4.0 Hz) during nonrapid eye movement (NREM) sleep exceeded that of REM sleep. The power spectra (0.5-24.5 Hz) in NREM, as well as the relationship between the power spectra of NREM and REM sleep, differed between the recording sites. Moreover, the rate of increase of SWA in the course of an NREM episode and the rate of decrease of SWA at the transition from NREM to REM sleep differed between the brain structures. During the first 12 hours following SD, the duration of NREM increased due to a prolongation of the NREM episodes. REM increased by a rise in the number of REM episodes. During the same period, the NREM EEG power density in the delta and theta frequencies was enhanced in all brain structures. Furthermore, in all structures the enhancement of SWA was most pronounced at the beginning of the recovery period and gradually declined thereafter. SD also induced a rise in the rate of increase of SWA in the NREM episodes in all recording sites. This indicates that the enhancement of EEG power density was not only due to prolongation of the NREM episodes. The EEG activity during REM was barely affected by the SD. It is concluded that, in all brain structures studied, the EEG during NREM is characterized by high levels of SWA. Furthermore, in each brain structure, SWA within NREM sleep is enhanced after a prolonged vigil. These data may indicate that SWA reflects a recovery process in cortical and subcortical structures.     

Quantitative electroencephalography during rapid eye movement (REM) and non‐REM sleep in combat‐exposed veterans with and without post‐traumatic stress disorder

Sleep disturbances are a hallmark feature of post‐traumatic stress disorder (PTSD), and associated with poor clinical outcomes. Few studies have examined sleep quantitative electroencephalography (qEEG), a technique able to detect subtle differences that polysomnography does not capture. We hypothesized that greater high‐frequency qEEG would reflect ‘hyperarousal’ in combat veterans with PTSD (n = 16) compared to veterans without PTSD (n = 13). EEG power in traditional EEG frequency bands was computed for artifact‐free sleep epochs across an entire night. Correlations were performed between qEEG and ratings of PTSD symptoms and combat exposure. The groups did not differ significantly in whole‐night qEEG measures for either rapid eye movement (REM) or non‐REM (NREM) sleep. Non‐significant medium effect sizes suggest less REM beta (opposite to our hypothesis), less REM and NREM sigma and more NREM gamma in combat veterans with PTSD. Positive correlations were found between combat exposure and NREM beta (PTSD group only), and REM and NREM sigma (non‐PTSD group only). Results did not support global hyperarousal in PTSD as indexed by increased beta qEEG activity. The correlation of sigma activity with combat exposure in those without PTSD and the non‐significant trend towards less sigma activity during both REM and NREM sleep in combat veterans with PTSD suggests that differential information processing during sleep may characterize combat‐exposed military veterans with and without PTSD.     

Polygraphic findings in young infants with Joubert's syndrome

SUMMARY  In three young infants with Joubert's syndrome polygraphic recordings were carried out in the awake state and during REM and NREM sleep in order to characterize the respiratory disorder associated with this condition.
In all three states disturbed respiration parameters were found in variable amounts. The highest breath rate occurred in the awake state followed by REM and NREM sleep. The highest incidence of apnoea and periodic breathing was observed in NREM sleep, followed by REM sleep and the awake state.     

Sleep and EEG spectra in the rabbit under baseline conditions and following sleep deprivation

The 24-hr sleep-wake distribution and power spectra of the electroencephalogram were determined in rabbits that had been implanted with cortical and hippocampal electrodes. A diurnal preference for sleep was observed. The spectral power density in nonrapid eye movement sleep (NREM sleep) of the cortex showed a decreasing trend in most frequencies within the 12-hr light period. In the 12-hr dim period no clear trend was present. Most hippocampal EEG frequencies decreased in NREM sleep in the first two hours of the light period, and thereafter stayed on a constant level. Sleep deprivation elicited the following changes: a prolonged increase of NREM sleep and a short increase of REM sleep; in the cortex, an increase of slow-wave activity (SWA; power density in the 0.25-2.0 Hz frequency band) in NREM sleep, which declined in the course of recovery; an enhancement of slow-wave (1.25-3 Hz) and theta (6.25-7 Hz) activity in REM sleep. The hippocampus showed an increase in NREM sleep power density in almost all frequencies. In REM sleep the hippocampus exhibited an increase in power density in the 6.25-7 Hz and 12.25-13 Hz bands, whereas in the 7.25-8 Hz band the values were below baseline. The results show that SWA in NREM sleep and theta activity in REM sleep are enhanced by sleep deprivation, as has been observed in other mammalian species. The EEG changes in the hippocampus resembled those in the cortex.     

Effects of sleep restriction on the sleep electroencephalogram of adolescents

Study ObjectivesThis report describes findings from an ongoing longitudinal study of the effects of varied sleep durations on wake and sleep electroencephalogram (EEG) and daytime function in adolescents. Here, we focus on the effects of age and time in bed (TIB) on total sleep time (TST) and nonrapid eye movement (NREM) and rapid eye movement (REM) EEG.MethodsWe studied 77 participants (41 male) ranging in age from 9.9 to 16.2 years over the 3 years of this study. Each year, participants adhered to each of three different sleep schedules: four consecutive nights of 7, 8.5, or 10 h TIB.ResultsAltering TIB successfully modified TST, which averaged 406, 472 and 530 min on the fourth night of 7, 8.5, and 10 h TIB, respectively. As predicted by homeostatic models, shorter sleep durations produced higher delta power in both NREM and REM although these effects were small. Restricted sleep more substantially reduced alpha power in both NREM and REM sleep. In NREM but not REM sleep, sleep restriction strongly reduced both the all-night accumulation of sigma EEG activity (11–15 Hz energy) and the rate of sigma production (11–15 Hz power).ConclusionsThe EEG changes in response to TIB reduction are evidence of insufficient sleep recovery. The decrease in sigma activity presumably reflects depressed sleep spindle activity and suggests a manner by which sleep restriction reduces waking cognitive function in adolescents. Our results thus far demonstrate that relatively modest TIB manipulations provide a useful tool for investigating adolescent sleep biology.     

Temporal evolution of coherence and power in the human sleep electroencephalogram

Coherence analysis of the human sleep electroencephalogram (EEG) was used to investigate relations between brain regions. In all-night EEG recordings from eight young subjects, the temporal evolution of power and coherence spectra within and between cerebral hemispheres was investigated from bipolar derivations along the antero-posterior axis. Distinct peaks in the power and coherence spectra were present in NREM sleep but not in REM sleep. They were situated in the frequency range of sleep spindles (13–14 Hz), alpha band (9–10 Hz) and low delta band (1–2 Hz). Whereas the peaks coincided in the power and coherence spectra, a dissociation of their temporal evolution was observed. In the low delta band, only power but not coherence showed a decline across successive NREM sleep episodes. Moreover, power increased gradually in the first part of a NREM sleep episode, whereas coherence showed a rapid rise. The results indicate that the intrahemispheric and interhemispheric coherence of EEG activity attains readily a high level in NREM sleep and is largely independent of the signal amplitude.     

Are microarousals preceded by electroencephalographic slow wave synchronization precursors of confusional awakenings?

The number of microarousals preceded by electroencephalographic (EEG) slow wave synchronization (MAS) and the number not preceded by EEG slow wave synchronization (K-complexes and/or delta groups) (MA) were analyzed during the first night of sleep in nine young patients with somnambulism and/or sleep terrors and in eight age- and sex-matched controls. While MAs peaked in REM ad intermediate sleep, MASs appeared as a phenomenon of NREM sleep, peaking in stage 2. The number of MASs was significantly greater in all stages of NREM sleep in the patient group, but number and distribution of MAs did not differ between the two groups. In the patient group, the MASs occurred in slow wave sleep (stages 3-4 of each sleep cycle); in controls, MASs occurred infrequently. MASs were frequently associated with automatic chewing movements. The higher frequency of microarousals in the patient group did not result in an increase in time awake during the night. The increase in number of microarousals supports Broughton's hypothesis of the presence of some "arousal disorder" in somnambulism and/or sleep terrors. MASs may be predictive markers of ensuing confusional awakenings.     

Effects of eszopiclone and zolpidem on sleep and waking states in the adult guinea pig

STUDY OBJECTIVE: The present study was designed to compare and contrast the effects of eszopiclone and zolpidem on the states of sleep and wakefulness in chronically instrumented, unanesthetized adult guinea pigs. DESIGN: Adult guinea pigs were implanted with electrodes to record sleep and waking states and to perform a frequency analysis of the EEG. Eszopiclone (1 and 3 mg/kg) and zolpidem (1 and 3 mg/kg) were administered intraperitoneally. MEASUREMENTS AND RESULTS: The administration of eszopiclone (1 and 3 mg/kg) resulted in a significant dose-dependent increase in NREM sleep. Zolpidem produced a significant increase in NREM sleep, but only at a dose of 3 mg/kg. The following changes in NREM and REM sleep, as well as in the power spectra, were all significant when the effects of 1 and 3 mg/kg of eszopiclone were compared with responses induced with 1 and 3 mg/kg of zolpidem, respectively: The increase in NREM sleep produced by eszopiclone was greater than that following the administration of zolpidem. The mean latency to NREM sleep following the administration of eszopiclone was significantly shorter than zolpidem. Eszopiclone significantly increased the latency to REM sleep. The mean duration of episodes of NREM sleep was increased by eszopiclone, but not by zolpidem. The EEG power increased in the delta band and decreased in the theta band during NREM sleep following the administration of eszopiclone. No significant changes occurred in any of the frequency bands analyzed following zolpidem administration. CONCLUSIONS: The differences in the effects of eszopiclone and zolpidem on sleep and waking states and the power spectra of the EEG likely reflect the fact that eszopiclone and zolpidem bind to different subunits of the GABAA receptor complex.     

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.     

Effects of pinealectomy on baseline sleep and response to sleep deprivation

STUDY OBJECTIVES: We have previously reported that older (24 mo.) Fischer rats manifest a diminished post-sleep deprivation increase in NREM and REM sleep. In order to examine whether this decline reflects an age-related change in pineal function, we are now reporting on baseline and recovery sleep parameters in pinealectomized 3-, 12-, and 24-month old rats following 24 hours of sleep deprivation using the disk-over-water method. DESIGN: Three independent age groups; within each group there were sequential measures of sleep under baseline conditions and during recovery from sleep deprivation. SETTING: The Sleep Research Laboratory at the University of Chicago PARTICIPANTS: 56 male Fisher (F344) rats INTERVENTIONS: 24 hours of total sleep deprivation using the disk-over-water method MEASUREMENTS: Sleep staging of EEG and EMG, and power spectral analysis of the EEG RESULTS: Pinealectomized (pinex) rats did not differ from sham-operated (sham) rats in total sleep, REM sleep, super-modal high-amplitude NREM sleep (HS2), a measure of NREM EEG delta power, or circadian rhythm amplitude. In the pinex rats, there was a modest (2.5%) age-independent increase in NREM sleep (p<0.02). The pinex rats of all ages failed to manifest the increase in NREM sleep during recovery seen in the sham-operated animals (p<0.04). CONCLUSIONS: We found no evidence that altered pineal function is responsible for age-related changes in baseline sleep in the rat. These data also suggest that, independent of age, normal pineal function may be relevant to the ability to generate increased NREM sleep in response to prior sleep deprivation.     

Rapid tryptophan depletion reverses phenelzine-induced suppression of REM sleep

Treatment with the monoamine oxidase inhibitor phenelzine completely suppressed rapid eye movement (REM) sleep in five depressed patients. Hypothesizing that increased serotonergic neurotransmission eliminated REM sleep, we administered a tryptophan-free amino acid drink (TFD) known to reduce plasma tryptophan and brain levels of serotonin. The TFD reversed the REM sleep suppression, while the control drink (TFD plus tryptophan) had virtually no effect on sleep. Neither TFD nor control drink affected mood, total sleep time, sleep efficiency or the all-night electroencephalogram power spectra in non-rapid eye movement (NREM) sleep. We report the first non-disruptive, double-blind method for studying human subjects overnight with and without REM sleep. It opens up a novel strategy for investigating the functions of REM sleep, and the roles of serotonin and REM sleep in the regulation of NREM sleep and mood.