Assessing functioning of the prefrontal cortical subregions with auditory evoked potentials in sleep-wake cycle

Our previously observations showed that the amplitude of cortical evoked potentials to irrelevant auditory stimulus (probe) recorded from several different cerebral areas was differentially modulated by brain states. At present study, we simultaneously recorded auditory evoked potentials (AEPs) from the dorsolateral prefrontal cortex (DLPFC) and the ventromedial prefrontal cortex (VMPFC) in the freely moving rhesus monkey to investigate state-dependent changes of the AEPs in the two subregions of prefrontal cortex. AEPs obtained during passive wakefulness (PW), active wakefulness (AW), slow wave sleep (SWS) and rapid-eye-movement sleep (REM) were compared. Results showed that AEPs from two subregions of prefrontal cortex were modulated by brain states. Moreover, a significantly greater increase of the peak-to-peak amplitude (PPA) of N1-P1 complexes appears in the DLPFC during PW compared to that during AW. During REM, the PPA of N1-P1 complexes presents a contrary change in the two subregions with significant difference: a significant increase in the DLPFC and a slight decrease in the VMPFC compared to that during AW. These results indicate that the modulation of brain states on AEPs from two subregions of the prefrontal cortex investigated is also not uniform, which suggests that different subregions of the prefrontal cortex have differential functional contributions during sleep-wake cycle.     

Corticospinal excitability and sleep: a motor threshold assessment by transcranial magnetic stimulation after awakenings from REM and NREM sleep

Transcranial magnetic stimulation (TMS) is a recently established technique in the neurosciences that allows the non-invasive assessment, among other parameters, of the excitability of motor cortex. Up to now, its application to sleep research has been very scarce and because of technical problems it provided contrasting results. In fact delivering one single suprathreshold magnetic stimulus easily awakes subjects, or lightens their sleep. For this reason, in the present study we assessed motor thresholds (MTs) upon rapid eye movement (REM) and non-rapid eye movement (NREM) sleep awakenings, both in the first and in the last part of the night. Taking into account that a full re-establishment of wake regional brain activity patterns upon awakening from sleep needs up to 20-30 min, it is possible to make inferences about the neurophysiological characteristics of the different sleep stages by analyzing the variables of interest immediately after provoked awakenings. Ten female volunteers slept in the lab for four consecutive nights. During the first night the MTs were collected, following a standardized procedure: 5 min before lights off, upon stage 2 awakening (second NREM period), upon REM sleep awakening (second REM period), upon the final morning awakening (always from stage 2). Results showed that MTs increased linearly from presleep wakefulness to REM sleep awakenings, and from the latter to stage 2 awakenings. There was also a time-of-night effect on MTs upon awakening from stage 2, indicating that MTs decreased from the first to the second part of the night. The increase in corticospinal excitability across the night, which parallels the fulfillment of sleep need, is consistent with the linear decrease of auditory arousal thresholds during the night. The maximal reduction of corticospinal excitability during early NREM sleep can be related to the hyperpolarization of thalamocortical neurons, and is in line with the decreased metabolic activity of motor cortices during this sleep stage. On the contrary, the increase of MTs upon REM sleep awakenings should reflect peripheral factors. We conclude that our findings legitimate the introduction of the TMS technique as a new proper tool in sleep research.     

Voluntary oculomotor performance upon awakening after total sleep deprivation

The potential impact of sleep inertia on measures of voluntary oculomotor control have been surprisingly neglected. The present study examined the effects of 40 hours of sleep deprivation on saccadic (SAC) and smooth pursuit (SP) performance, attentional/visual search performance (Letter Cancellation Task, LCT) and subjective sleepiness (Sleepiness Visual Analog Scale, SVAS) recorded immediately after awakening. Standard polysomnography of nine normal subjects was recorded for 3 nights (1 adaptation, AD; 1 baseline, BSL; 1 recovery, REC); BSL and REC were separated by a period of 40 h of continuous wakefulness, during which subjects were tested every two hours. Within 30 s of each morning awakening, a test battery (SAC, SP, LCT, SVAS) was administered to subjects in bed. For data analysis, mean performance obtained during the day preceding the sleep deprivation night was considered as "Diurnal Baseline" and compared to performance upon awakening from nocturnal sleep. As a consequence of sleep deprivation, SWS percentage was doubled during REC. Saccade latency increased and velocity decreased significantly upon awakening from REC as compared to the other three conditions (Diurnal baseline, AD awakening, BSL awakening); accuracy was unaffected. As regards SP, phase did not show any impairment upon awakening, while velocity gain upon awakening from REC was significantly lower as compared to the other conditions. Finally, number of hits on LCT upon awakening from REC was significantly lower and subjective sleepiness higher as compared to Diurnal Baseline. It is concluded that 40 h of sleep deprivation significantly impaired performance to SAC and SP tasks recorded upon awakening from recovery sleep. This performance worsening is limited to the measures of speed, while both SAC accuracy and SP phase do not show a significant decrease upon awakening. Since saccadic velocity has recently been found to negatively correlate with simulator vehicle crash rates, it is suggested that the adverse effects of sleep deprivation on sleep inertia magnitude should be avoided by any personnel who may have to perform critical tasks involving high oculomotor control immediately after awakening.     

Changes in the waking EEG as a consequence of sleep and sleep deprivation.

Electroencephalographic (EEG) activity was monopolarly recorded during resting wakefulness in 10 volunteers under the following conditions: at night before going to sleep, at night before total sleep deprivation, in the morning after waking, in the morning after sleep deprivation and at night after having slept during the day. Absolute and relative power and inter- and intrahemispheric correlation were established. After diurnal and nocturnal sleep as compared to sleep deprivation, we obtained the following significant results: interhemispheric correlations were higher; intrahemispheric correlations were lower; absolute power of alpha 2, beta 1 and beta 2 was lower; and relative power of alpha 2 and beta 2 was lower. EEG changes as a consequence of sleep or lack of sleep are dependent on prior sleep and/or wakefulness and not on circadian phase. EEG activity during wakefulness is a sensitive parameter and a useful tool to assess the consequences of sleep on brain functional organization.     

Reduction of transcallosal inhibition upon awakening from REM sleep in humans as assessed by transcranial magnetic stimulation

STUDY OBJECTIVES: The aim of the study is to assess, in humans, transcallosal inhibition upon awakening from rapid eye movement (REM) and non-REM sleep, by paired-pulse transcranial magnetic stimulation (TMS). DESIGN: During the daytime, a baseline session of motor evoked potentials (MEPs) was recorded. During the nighttime, the TMS sessions were administered just before sleep onset and upon awakenings from REM and stage 2 sleep, both in the early and final part of night. SETTING: The sleep research laboratory at the University of Rome "La Sapienza." PARTICIPANTS: Ten right-handed subjects participated in the experiment for 4 consecutive sleep-recording nights. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: During the daytime, a robust transcallosal inhibition was found; the MEP amplitude reduction ranged from 35% to 40%. During the nighttime, a decrease of transcallosal inhibition from right-to-left motor cortex, as compared to that from left-to-right motor cortex, was observed. The direct assessment of MEP changes, as a function of sleep stage and of the time of night, pointed to a drop of transcallosal inhibition after awakening from REM sleep. Therefore, the inhibitory activity of transcallosal fibers observed after non-REM awakening almost disappeared after REM sleep awakenings. CONCLUSIONS: The drastic drop of transcallosal inhibition after awakenings from REM sleep represents the first evidence in humans of a change of interhemispheric connectivity mediated by the corpus callosum during this sleep stage and may open new avenues for a better understanding of some aspects of sleep mechanisms (ie, dreaming function and dream mentation).     

Caffeine eliminates psychomotor vigilance deficits from sleep inertia.

STUDY OBJECTIVES: This study sought to establish the effects of caffeine on sleep inertia, which is the ubiquitous phenomenon of cognitive performance impairment, grogginess and tendency to return to sleep immediately after awakening. DESIGN: 28 normal adult volunteers were administered sustained low-dose caffeine or placebo (randomized double-blind) during the last 66 hours of an 88-hour period of extended wakefulness that included seven 2-hour naps during which polysomnographical recordings were made. Every 2 hours of wakefulness, and immediately after abrupt awakening from the naps, psychomotor vigilance performance was tested. SETTING: N/A. PARTICIPANTS: N/A. Interventions: N/A. MEASUREMENTS AND RESULTS: In the placebo condition, sleep inertia was manifested as significantly impaired psychomotor vigilance upon awakening from the naps. This impairment was absent in the caffeine condition. Caffeine had only modest effects on nap sleep. CONCLUSIONS: Caffeine was efficacious in overcoming sleep inertia. This suggests a reason for the popularity of caffeine-containing beverages after awakening. Caffeine's main mechanism of action on the central nervous system is antagonism of adenosine receptors. Thus, increased adenosine in the brain upon awakening may be the cause of sleep inertia.     

Cardiac autonomic nervous system activity during presleep wakefulness and Stage 2 NREM sleep

Previous research has found that cardiac parasympathetic nervous system (PNS) activity increases and cardiac sympathetic nervous system (SNS) activity decreases during night-time sleep. This study aimed to examine in greater detail the time course of these changes in cardiac autonomic nervous system (ANS) activity. In the week prior to the experimental night, nine subjects maintained a constant sleep-wake schedule and experienced an adaptation night. Each subject's experimental night consisted of 2 h of presleep wakefulness, followed by a night of sleep, commencing at each subject's normal sleep onset time. One hundred and twenty beat blocks of presleep wakefulness and stable Stage 2 non-rapid eye movement (NREM) sleep across the night were selected. SNS activity was assessed using pre-ejection period, the amplitude of the T-wave in the ECG and the 0.1 Hz peak from the spectral analysis of the ECG. PNS activity was assessed using respiratory sinus arrhythmia (spectral analysis). Heart rate and respiratory rate were also measured. The results indicated a progressive decrease in SNS activity throughout sleep and a rise in PNS activity during the first half of the normal sleep period. The changes in PNS activity were similar, while the changes in SNS activity were altered, compared with a previous study in which stage of sleep was not controlled. This indicates a likely sleep stage influence on SNS activity, but not on cardiac PNS activity. These results are consistent with the concept of a primarily circadian, but not sleep, influence on PNS activity, and primarily a sleep, but not circadian, influence on SNS activity.     

Sleep, dreaming, and adaptation to a stressful intellectual activity

Sixteen male subjects slept in the laboratory for 4 consecutive nights. Night 1 was an adaptation night and night 2 was a baseline night of uninterrupted sleep. On nights 3 and 4 subjects were asked to complete "intelligence" tests prior to sleep. One half of the subjects attempted to complete difficult versions of "intelligence" tests without knowing that they could not be completed in te time allotted. The other subjects were given easier versions of the same tests that they were able to complete in the time allotted. Night 3 was a night of uninterrupted sleep and night 4 involved REM period awakenings for the purpose of dream collection. Stressful manipulation consisted of telling the subjects before the administration of either set of tests that an average university student should complete most of the items within the allotted time. On night 3 both groups showed a significant increase in sleep latency and a significant decrease in REM density compared to the baseline night. On night 4 subjects in the difficult condition experienced significantly more anxiety in their dreams and somewhat higher levels of incorporation of the presleep material than subjects in the easy condition. Our findings suggest that following a stressful experience uninterrupted sleep has more short term adaptive value than a procedure which enhances dream recall and that subjects who incorporate elements from a presleep stressful event into their remembered dreams show less adaptation on awakening than subjects who do not.     

The effects of slow-wave sleep (SWS) deprivation and time of night on behavioral performance upon awakening

The aim of the present study is to evaluate the effects of selective SWS deprivation on the motor and sensory motor performance impairment immediately after awakening from nocturnal sleep at different times of the night. Ten normal males slept for 6 consecutive nights in the laboratory: one adaptation, two baseline, two selective SWS deprivation, and one recovery night. During the last 4 nights performance was assessed four times: (a) before sleep, as a baseline measure; (b) within 30 s from the first nighttime awakening, after 2 h of sleep; (c) within 30 s from the second nighttime awakening, after 5 h of sleep; (d) within 30 s from the final morning awakening. After each awakening, following a 3-min cognitive test, a simple Auditory Reaction Time task (ART, about 5 min) and a Finger Tapping Task (FTT, 3 min) were administered. Median of Reaction Times (RT) and of Intertapping Intervals (ITI), 10% fastest RT, 10% slowest RT, and number of misses were considered as dependent variables. The selective SWS deprivation was very effective: SWS percentage during both the deprivation nights was close to zero. This strong manipulation of SWS amount interacted with time-of-night factors in influencing sleep inertia. The SWS deprivation procedure caused a worsening of behavioral performance during the deprivation nights. as well as upon the final awakening of the recovery night. Behavioral performance slowing upon awakening is accounted for by: (1) a general decrement in overall response speed (median of RT); (2) an "optimum response shift", i.e., a decrease in speed of the fastest responses; (3) an increase of lapsing, with more marked response delays resulting in a further decrease in response speed in the "lapse domain". Finally, our results do not support the existence of a circadian rhythm of sleep inertia linked to body temperature rhythm.     

Renin as a biological marker of the NREM-REM sleep cycle: effect of REM sleep suppression

SUMMARY  We have previously described that, in normal man, the nocturnal oscillations of plasma renin activity (PRA) exactly reflect the rapid eye movement (REM)–non(N)REM sleep cycles, with increasing PRA levels during NREM sleep and decreasing levels during REM sleep. This study was carried out to determine whether REM sleep suppression affects nocturnal renin profiles and to define which sleep stage is essential for renin release.
In a first experimental series, REM sleep was suppressed by using clomipramine, a tricyclic antidepressant. Seven healthy young men were studied once during a night when a placebo was given and once during a night following a single dose of 50 mg clomipramine. Blood was collected every 10 min from 23.00 hours to 07.00 hours. PRA was measured by radio-immunoassay and the nocturnal profiles were analysed using the pulse detection program ULTRA. Clomipramine suppressed REM sleep in all subjects but one, but did not affect the number of SWS episodes nor their duration. Similar PRA profiles were observed in both experimental conditions. Neither the mean levels, nor the number and the amplitude of the oscillations were modified and the normal relationship between slow wave sleep and increasing PRA levels was preserved.
In a second experimental series, REM sleep was prevented by rapidly awakening the subjects as soon as they fell into REM sleep. The four subjects studied attempted several times to go into REM sleep, but only when PRA levels were decreasing. The interruption of REM sleep by short waking periods did not disturb PRA for which the oscillations remained unaffected. Again, the relationship between SWS and increasing PRA levels was preserved.
These results provide evidence that mechanisms increasing slow-wave activity are principally involved in increasing PRA levels and that replacing REM sleep by waking periods and light sleep does not modify nocturnal PRA oscillations.     

Sleep and respiratory stimulus specific dampening of cortical responsiveness in OSAS

The application of inspiratory occlusion stimuli produces cortical responses called respiratory-related evoked potentials (RREPs). During wakefulness the RREP waveform consists of early P1 and Nf components, an N1 and a P300. During non-REM sleep the predominant component is an N550, best seen in the averages of elicited K-complexes. Obstructive sleep apnea syndrome (OSAS) patients have been previously shown to have a normal wake RREP but to have a reduced amplitude N550 and a smaller proportion of elicited K-complexes than controls. The present study tested the hypothesis that this reflects a sleep-specific dampening peculiar to inspiratory effort-related stimuli, by assessing both respiratory and auditory evoked potentials (AEPs) during wakefulness and non-REM sleep in OSAS patients and controls. Auditory tones were presented in an oddball sequence during wakefulness and as a monotonous series during stage 2 sleep. Inspiratory occlusions, delivered for 500 msec via an nCPAP mask were also presented during wakefulness and stage 2 sleep, every three to five breaths. Data were collected from ten OSAS patients and ten controls. There were no significant differences in the amplitudes of the auditory N1 and P3 or the respiratory P1, Nf, N1 or P3 components during wakefulness. The amplitude of the auditory N550 and the proportion of elicited K-complexes did not differ between groups for auditory stimuli presented during stage 2 sleep. The respiratory N550 and K-complex elicitation rate were both significantly reduced in the OSAS group, despite there being no differences in the mask occlusion pressure response to the occlusion. The results confirm a blunted cortical response to inspiratory occlusions that is specific to sleep. The absence of significant group differences in the responses to auditory stimuli highlight that the sleep-related differences seen in OSAS patients are specific to the processing of inspiratory effort related stimuli.     

Training subjective insomniacs to accurately perceive sleep onset.

Subjective insomniacs overestimate sleep latency at the beginning of their nocturnal sleep period. It was hypothesized that subjective insomniacs could be trained to accurately estimate sleep latency by learning to differentiate wakefulness from sleep. Ten subjective insomniacs were randomly assigned to one of two groups. Group 1 subjects participated in both a control and a training week; group 2 subjects participated only during a training week. Each week consisted of a baseline lab night, a training lab night (treatment or control), a home (unmonitored night) and a recovery lab night. During training, subjects were taught to use sleep markers (A, B or C) to help them more accurately estimate sleep latency and were given feedback about the accuracy of their estimates. Marker A corresponded to an electroencephalographic level of wakefulness; marker B corresponded to the initial sleep spindle; marker C corresponded to 5 minutes of continuous sleep after the first sleep spindle. In the control condition, subjects had no feedback and were not taught to use markers to help them judge sleep from wakefulness. Total sleep time and percent stage 3 sleep increased, and objective sleep latency decreased on recovery nights. After training, subjective sleep latency, correctness of estimates of sleep versus wakefulness and perceived ability to fall asleep significantly improved. This study helps to establish that subjective insomniacs can learn to more accurately estimate sleep from wakefulness with the use of sleep-wake markers.     

NOCTURNAL EEG-GSR PROFILES: THE INFLUENCE OF PRESLEEP STATES

The number of nocturnal galvanic skin responses-(GSRs) varied widely between the electroencephalograph (EEG) stages of sleep as well as from night to night and from person to person. As others have found, non-specific GSRs occurred much more frequently during stage IV than other EEG stages, and were rare in stage REM. However, night-to-night variation and individual differences were related to the presleep state of the person. In general, electrodermal activity increased in all EEG stages as daytime stress increased, being especially great on nights preceding important school examinations. The nocturnal EEG profile was also related to the presleep state, the percentage of stage IV decreasing as daytime stress increased. The percentage of stage REM showed no systematic relation to stress. The occurrence of GSR “storms” during slow-wave sleep is consistent with the notion of release of cortical or other inhibitory influences during this state, but another mechanism is needed to explain the fact that presleep stress increases the frequency of GSRs in all stages of sleep, while simultaneously decreasing the percentage of slow-wave sleep.     

Nocturnal cardiac autonomic profile in young primary insomniacs and good sleepers

We investigated cardiac vagal and sympathetic activity in 13 young primary insomniacs (PI; 24.4 ± 1.6 years) and 14 good sleepers (GS; 23.3 ± 2.5 years) during nocturnal sleep. Pre-ejection period (PEP; inversely related to beta-adrenergic sympathetic activity), interval between consecutive R-waves (RR), and vagal-related indices of time- and frequency-domain heart rate variability were computed during pre-sleep wakefulness and undisturbed arousal-free sleep stages (N2, SWS, REM) as well as across the whole night irrespective of the presence of disruptive sleep events (e.g. sleep arousals/awakenings) and/or sleep stage transitions. Groups exhibited a similar vagal activity throughout each undisturbed sleep stage as well as considering the whole night, with a higher modulation during sleep compared to prior wakefulness. However, PEP was constantly shorter (higher sympathetic activity) during pre-sleep wakefulness and each sleep stage in PI compared to GS. Moreover, pre-sleep RR intervals were positively associated with sleep efficiency and negatively associated with wake after sleep onset in PI. Altogether our findings indicated a dysfunctional sympathetic activity but a normal parasympathetic modulation before and during sleep in young adults with insomnia.     

Propriospinal myoclonus at the sleep-wake transition: a new type of parasomnia.

STUDY OBJECTIVES: To describe the clinical, neurophysiological, and polysomnographic characteristics of propriospinal myoclonus (PSM) at the sleep-wake transition. DESIGN: Patients referred for insomnia due to myoclonic activity arising during relaxed wakefulness preceding sleep, or complaining of muscular jerks also during intrasleep wakefulness and upon awakening in the morning were considered. SETTING: All patients underwent EEG-EMG recordings during wakefulness and night sleep. Back-averaging of the EEG activity preceding the jerks was performed. Somatosensory evoked potentials (SEPs), transcranial magnetic stimulation (TMS) and spinal and cranial MRI were also done. PARTICIPANTS: Four patients were studied all affected with involuntary jerks arising when falling asleep, and one with jerks also during sleep and upon awakening in the morning. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Polysomnographic investigations revealed jerks arising during the sleep-wake transition period. Myoclonic activity was neurophysiologically documented to be of the propriospinal type. SEPs, TMS and MRI were normal CONCLUSIONS: PSM may have a peculiar relationship with the state of vigilance and represent a sleep-wake transition disorder. In this regard we consider PSM a new type of parasomnia.     

Selective slow-wave sleep deprivation and time-of-night effects on cognitive performance upon awakening

We evaluated the effects of selective slow-wave sleep (SWS) deprivation and time-of-night factors on cognitive performance upon awakening. Ten normal men slept for 6 consecutive nights in the laboratory: 1 adaptation, 2 baseline, 2 selective SWS deprivation, and 1 recovery night. Cognitive performance was assessed by means of a Descending Subtraction Task after 2, 5, and 7.5 h of sleep. There was an almost complete selective SWS suppression during both deprivation nights, and a significant SWS rebound during the recovery sleep. Regarding cognitive performance, a progressive linear decrease of sleep inertia upon successive awakenings was found during all experimental nights except for the recovery night. In addition, a significant decrease of sleep inertia was observed upon the morning awakening of the second deprivation night for the measure of performance speed, and a significant increase of sleep inertia upon the morning awakening of the recovery night for the measure of performance accuracy. The results show that cognitive performance upon awakening is adversely affected by sleep depth and that, during the sleep-wake transition, cognitive performance accuracy is more impaired than performance speed.     

Auditory Evoked Potential in Stage 2 and REM Sleep During a 30-Day Exposure to Tone Pulses

Ten subjects were exposed to 3.5K Hz tone pulses of 660 msec duration, presented 24-hr-per-day for 30 days. The interstimulus interval was 22 sec. There were 10 days each at 80, 85, and 90 dB in that order. The average evoked potential (AEP) at C₃ referenced to linked mastoids was obtained from contiguous stage 2 and REM sleep segments on the first, second, and last recorded nights of tone-pulse exposure. The AEP was consistently larger in stage 2 than in REM sleep. In both stage 2 and REM sleep, AEP amplitude on the second recorded night bore no consistent relationship to first or last recorded night AEPs. Only the N2–P3 amplitude yielded consistent decreases, with 9 of 10 subjects in both stage 2 and REM sleep having smaller N2–P3 amplitudes on the last than on the first recorded night. There were no changes in latency of any component. During sleep there is little, if any, habituation of the auditory AEP during long-duration exposures to nonmeaningful stimuli, and certainly no extinction of the AEP under these conditions.     

How accurately does wrist actigraphy identify the states of sleep and wakefulness?

STUDY OBJECTIVES: Because sleep and wakefulness differ from each other by the amount of body movement, it has been claimed that the two states can be accurately distinguished by wrist actigraphy. Our objective was to test this claim in lengthy polysomnographic (psg) and actigraphic (acf) samples that included night and day components. DESIGN: Fourteen healthy young (21-35 years) and old (70-72 years) men and women lived in a laboratory without temporal cues for 7 days. Each subject continuously wore sleep-recording electrodes as well as 2 wrist-movement recorders. Act measurements were converted to predictions of sleep and wakefulness by simple-threshold and multiple-regression methods. Psg served as the gold standard for calculation of predictive values (PV, the probability that an act prediction is correct by psg criteria). SETTING: N/A. PARTICIPANTS: N/A. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: The 7-day act recordings showed clear circadian cycles of high and low activity that respectively corresponded to subjective days, when subjects were wakeful, and subjective nights when they slept. Lower act levels corresponded to deeper states of psg sleep. Logistic regression on a 20-minute moving average of act gave the highest overall PV's. Nevertheless, the mean PV for sleep (PVS) was only 62.2% in complete, day + night samples. PVS was 86.6% in night samples. Act successfully predicted wakefulness during subjective nights (PVW = 89.6) and accurately measured circadian period length and the extent of sleep-wake consolidation, but it overestimated sleep rate and sleep efficiency. Act systematically decreased before sleep onset and increased before awakening, but reliable transitions among joint psg/act states (the Markov-1 property) were not demonstrated. CONCLUSIONS: Low PV's and overestimation of sleep currently disqualify actigraphy as an accurate sleep-wake indicator. Actigraphy may, however, by useful for measuring circadian period and sleep-wake consolidation and has face validity as a measure of rest/activity.     

Asymmetrical auditory probe evoked potentials during REM and NREM sleep

Two experiments were conducted to evaluate interhemispheric differences in late auditory evoked potentials (AEPs) during rapid-eye-movement (REM), Stage 2, and Stage 4 sleep. In the first study, 1,000-Hz stimuli [80 db (SPL)] were presented binaurally at a rate of 1/1.1 s. Analyses of variance were computed on the absolute difference in the amplitude of right and left evoked responses. N1 AEPs were significantly more asymmetrical in Stage 4 sleep compared to either REM or Stage 2 sleep. A second study was conducted with a wider topographical electrode distribution. This study used both a long and a short interstimulus interval with 500-Hz 80-db SPL tone pips. The absolute difference in the amplitude of right and left AEPs was compared across sleep stage. Asymmetries were larger in Stage 4 sleep than in either REM or Stage 2. Examination of these data indicated relative hemispheric balance in REM and Stage 2 sleep with largest asymmetries in Stage 4. The results do not support the view that REM and non-REM sleep stages are associated with differential activation of the two cerebral hemispheres. Rather, they suggest that the sleep cycle is characterized by variations in the degree of asymmetry. Asymmetries in Stage 4 sleep were not consistently in favor of the left hemisphere.     

Studies of Spontaneous Electro dermal Responses in Sleep

A series of studies on spontaneous electro dermal responses (storming) in normal human stage 3–4 sleep J5 reported. It was found that: (a) storming rates during sleep are positively correlated with spontaneous response rates during wakefulness, (b) more storming is demonstrated by subjects who remain awake during a baseline recording at the start of the night, (c) there is a negative correlation between storming rate and amount of stage 3–4 sleep, (d) storming rates decrease from night 1 to night 2, (e) stunners differ from non-stormers on several MMPI measures of anxiety and ego-strength, and (f) dream reports are given more often on awakenings from storming than non-storming stage 3–4 sleep. The results are compared to other studies of storming, and the conclusion is made that storming is related to presleep variables and is not a simple byproduct of a release of cortical inhibitory mechanisms. If one function of storming is to reduce the amount of stage 3–4 sleep, this might have survival value in the presence of environmental threat.