Sex hormones play a role in vulnerability to sleep loss on emotion processing tasks.

The central aim of this study was to investigate hormones as a predictor of individual vulnerability or resiliency on emotion processing tasks following one night of sleep restriction. The restriction group was instructed to sleep 3 a.m.-7 a.m. (13 men, 13 women in follicular phase, 10 women in luteal phase of menstrual cycle), and a control group slept 11 p.m.-7 a.m. (12 men, 12 follicular women, 12 luteal women). Sleep from home was verified with actigraphy. Saliva samples were collected on the evening prior to restriction, and in the morning and afternoon following restriction, to measure testosterone, estradiol, and progesterone. In the laboratory, event-related potentials (ERPs) were recorded during presentation of images and faces to index neural processing of emotional stimuli. Compared to controls, sleep-restricted participants had a larger amplitude Late Positive Potential (LPP) ERP to positive vs neutral images, reflecting greater motivated attention towards positive stimuli. Sleep-restricted participants were also less accurate categorizing sad faces and exhibited a larger N170 to sad faces, reflecting greater neural reactivity. Sleep-restricted luteal women were less accurate categorizing all images compared to control luteal women, and progesterone was related to several outcomes. Morning testosterone in men was lower in the sleep-restricted group compared to controls; lower testosterone was associated with lower accuracy to positive images, a greater difference between positive vs neutral LPP amplitude, and lower accuracy to sad and fearful faces. In summary, women higher in progesterone and men lower in testosterone were more vulnerable to the effects of sleep restriction on emotion processing tasks. This study highlights a role for sex and sex hormones in understanding individual differences in vulnerability to sleep loss.

Impact of total sleep deprivation on behavioural neural processing of emotionally expressive faces.

Sleep deprivation impacts subjective mood states, but very little research has examined the impact on processing emotional information. In the current study, we investigated the impact of total sleep deprivation on neural responses to emotional facial expressions as well as the accuracy and speed with which these faces were categorized. Forty-nine participants completed two tasks in which they were asked to categorize emotional facial expressions as Happy, Sad, Angry, or Fearful. They were shown the 'full' expression of the emotions in one task and more subtle expressions in a second task in which expressions were 'morphed' with neutral faces so that the intensity of emotion varied. It was expected that sleep deprivation would lead to greater reactivity (indexed by larger amplitude N170 event-related potentials), particularly for negative and more subtle facial expressions. In the full face task, sleep-deprived (SD) participants were significantly less accurate than controls (C) at identifying Sad faces and slower to identify all emotional expressions. P1 was smaller and N170 was larger for the SD compared to C group, but for all emotions, indicating generalized impairment in low-level visual processing. In the more difficult morphed face task, SD participants were less accurate than C participants for Sad faces; as well, the group difference in reaction time was greatest for Sad faces. For the SD group, N170 increased in amplitude with increasing perceptual difficulty for the Fearful and Angry faces, but decreased in amplitude with increasing difficulty for Sad faces. These data illustrate that sleep deprivation led to greater neural reactivity for the threat-related negative emotions as they became more subtle; however, there was a failure to engage these perceptual resources for the processing of Sad faces. Sleep loss preferentially impacted the processing of Sad faces; this has widespread implications for sleep-deprived groups.

Sleep spindles and learning potential.

The number of sleep spindles remains relatively stable within individuals from night to night. However, there is little explanation for the large interindividual differences in spindles. The authors investigated the relationship between spindles and intelligence quotient (IQ) in 3 separate studies. The number of spindles and sigma power were positively correlated with performance IQ (PIQ), but not verbal IQ (VIQ). The perceptual/analytical skills measured by the PIQ Picture Completion subscale accounted for most of the interindividual differences in spindles. Furthermore, there was a relationship between the rapid eye movements (REMs) of REM sleep and VIQ in individuals with higher IQ scores. A similar pattern was observed between spindles and PIQ. It was hypothesized that high-IQ individuals have more spindles that can support more complex cortical networks underlying perceptual/analytical abilities.

Neurophysiological evidence for the detection of external stimuli during sleep.

STUDY OBJECTIVES: A cognitive evoked potential, labelled "P300," is elicited when an observer attends to and detects an infrequently delivered "target" stimulus. It is not typically present if the target is ignored or undetected. P300 is therefore thought to reflect some aspect of consciousness of the stimulus. There has been much controversy concerning whether P300 can be recorded in sleep, a state in which information processing of external events is presumably reduced. The present study investigated the effects of both pitch and intensity stimuli on information processing, in order to determine whether a more salient stimulus might elicit a P300 in sleep that is comparable to the waking P300. DESIGN: A true P300 will have a parietal maximum peak following a rare stimulus, and its amplitude will vary inversely with the probability of stimulus delivery. Participants were thus randomly assigned to one of three probability groups, in which the deviant was presented on 20%, 10%, or 5% of trials. SETTING: Data were collected in the Human Neurophysiology Laboratory at the University of Ottawa. PARTICIPANTS: Twenty-four young adults. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: During wakefulness, a parietal P300 was apparent following both pitch and intensity deviants when participants were asked to detect deviant stimuli. A P300 was also apparent following the intensity deviant when participants were instructed to ignore the stimuli. During non-REM sleep, no P300 could be identified. In REM sleep, very rare (p=.05) loud deviants elicited a parietal P300. This P300 was attenuated relative to the waking ignore condition. Moreover, the frontal dispersion of the peak was absent. CONCLUSIONS: These data provide evidence that participants are conscious (parietal P300) of very rare and intrusive stimuli during REM sleep, although the frontal aspects associated with this consciousness may be absent.

Exposure to pulsed high-frequency electromagnetic field during waking affects human sleep EEG.

The aim of the study was to investigate whether the electromagnetic field (EMF) emitted by digital radiotelephone handsets affects brain physiology. Healthy, young male subjects were exposed for 30 min to EMF (900 MHz; spatial peak specific absorption rate 1 W/kg) during the waking period preceding sleep. Compared with the control condition with sham exposure, spectral power of the EEG in non-rapid eye movement sleep was increased. The maximum rise occurred in the 9.75-11.25 Hz and 12.5-13.25 Hz band during the initial part of sleep. These changes correspond to those obtained in a previous study where EMF was intermittently applied during sleep. Unilateral exposure induced no hemispheric asymmetry of EEG power. The present results demonstrate that exposure during waking modifies the EEG during subsequent sleep. Thus the changes of brain function induced by pulsed high-frequency EMF outlast the exposure period.

The role of the spindle in human information processing of high-intensity stimuli during sleep.

Sleep spindles are 12-14 Hz oscillations in EEG, which are thought to inhibit or 'gate' information processing. Event-related potentials may be employed to probe the extent of information processing during sleep. Previous research indicates that event-related potentials elicited by moderate intensity stimuli show increased positivity (or further removal of negativity) when stimuli are presented concurrent with spindles. However, the effectiveness of spindles to inhibit the processing of much louder stimuli remains unknown. The purpose of the present study was to investigate the extent of this gating, by using a range of stimuli including those that are loud and intrusive. Eight good sleepers were recorded during a single night. Auditory stimuli were delivered randomly at 0, 60, 80 or 100 dB SPL. Trials were sorted off-line by sleep stage, stimulus intensity and spindle characteristic (i.e. spindle absent, spindle present). During the sleep-onset period, the often-reported changes in event-related potentials were observed - N1 decreased and P2 increased in amplitude. In Stage 2 sleep, P2 was affected by the presence of spindles, particularly when stimulus intensity was loud. Its amplitude was greatest when spindles occurred following the onset of the stimulus. Scalp-recorded spindles might, therefore, be a consequence of the prior thalamic inhibition of information processing, especially when confronted by loud, intrusive external stimuli.

The effects of varying stimulus intensity on P300 during REM sleep.

Event-related potentials (ERPs) are often used to measure the extent of information processing during sleep. Previous studies have indicated that a late positive wave, P300, can be elicited during REM sleep if stimuli are very rare and/or very loud. The present study examined the role of stimulus intensity in eliciting a P300 during REM sleep. Eight subjects were presented with auditory tone pips with an intensity of either 0, 60, 80 or 100 dB SPL. Stimuli were delivered at random with equal probability. Trials were sorted by stage of sleep, stimulus intensity, and presence or absence of rapid eye movements in REM sleep. During the waking state, when subjects read a book, the loud 100 dB stimulus elicited short (P3a) and long latency (P300) positive waves (peaking at 293 and 373 ms respectively). In stage of 2 non-REM sleep, N1 decreased to baseline level while P2 increased in amplitude compared to the waking state. A P300 could not be observed in stage 2 sleep regardless of the level of stimulus intensity. During REM sleep, a late P300 (latency 363 ms) was elicited by the 100 dB stimulus. The earlier positive peak (i.e. P3a) was not apparent. The P300 was reduced in amplitude compared to the waking state. Its amplitude did not differ between phasic and tonic states of REM sleep. A late parietal negative slow wave (SW) was also apparent during REM. Although the SW was larger during phasic compared to tonic REM, the difference was not significant. These data suggest that stimuli which are sufficiently intrusive to elicit a P300 in the waking state continue to do so in REM sleep.

P300 to high intensity stimuli during REM sleep.

OBJECTIVES: The P300 component of the auditory event-related potential (ERP) is a large amplitude positive wave peaking at approximately 300 ms following detection of a rare significant stimulus. Although P300 is typically only evoked when the subject attends to the stimulus, it may also be elicited in an awake, inattentive subject if the stimulus is sufficiently intrusive. We therefore employed an oddball task to determine if high intensity stimuli would elicit the P300 during sleep. METHODS: A loud 90 dB SPL tone pip was presented infrequently (P = 0.05) in a train of lower intensity 70 dB SPL standard stimuli. A multiple channel EEG was recorded from 8 good sleepers during a single night. RESULTS: A large amplitude parieto-central P300, peaking at 321 ms, was apparent in REM sleep to the loud deviant stimulus. In stage two non-REM sleep, a later positive wave, peaking at 446 ms, was apparent even after K-Complexes were removed from the average. This non-REM P450 was however maximum over occipito-parietal areas of the scalp. CONCLUSION: The presence of a P300 in REM sleep following a loud, rare stimulus indicates that sensory discrimination capabilities remain intact during this state. This may be associated with either pre- or conscious processing of relevant stimuli.

Scalp topography of the auditory evoked K-complex in stage 2 and slow wave sleep.

During NREM sleep a very large amplitude wave-form, known as the K-complex, may be elicited upon presentation of an external stimulus. The present study compared the scalp distribution of a prominent negative wave peaking at about 550 ms and a later positive wave peaking between 900 and 1300 ms in stage 2 and slow wave sleep (SWS). Nine subjects spent a single night in the laboratory. They were presented with an 80 dB SPL 2000 Hz auditory tone pip every 15 s. The EEG was recorded from 29 electrode sites and referenced to the nose. A K-complex was elicited on 34% of trials in stage 2 and on 46% of trials in SWS. A negative wave peaking at 330 ms was larger on trials in which the K-complex was elicited than on trials in which it was not. The large amplitude N550 was readily observable on trials in which the K-complex was elicited but could not be observed on trials in which it was not. The N550 was bilaterally symmetrical and was maximum over fronto-central areas of the scalp in both stage 2 and SWS. It inverted in polarity at the mastoid and inferior parietal regions. The scalp distribution of N550 significantly differed between stage 2 and SWS. It showed a sharper decline in amplitude over parietal and posterior-inferior areas of the scalp in stage 2 compared to SWS. A later P900 was maximum over centro-frontal areas of the scalp and was also bilaterally symmetrical. It showed a significantly sharper decline in amplitude over widespread inferior areas during SWS. Because the scalp maps of the N550 and P900 are different in stage 2 and SWS, their intracranial sources must also be different.