Effect of a presleep optokinetic stimulation on rapid eye movements during REM sleep

Some evidence supports the view point that phasic motor events of REM sleep show a complementary relation with the corresponding wake motor activities: (a) an inverse relationship between waking saccades and REM sleep eye movements (REMs) has been found with respect to frequency, amplitude, and direction; (b) an increase of middle-ear muscle activity (MEMA) in the 2 h before sleep causes a complementary decrease of MEMA during REM sleep. The present study evaluated this relation with respect to the optokinetic (OKN) system, assessing the role of automatically induced eye movements in affecting direction and frequency of REMs during sleep. Ten subjects were recorded following standard rules in 3 consecutive nights (one adaptation, one baseline, one experimental). In the experimental night subjects underwent 2 h presleep OKN stimulation at 15 degrees /s. The actual mean number of quick phases of nystagmus induced by the OKN stimulation was 12461.4 +/- 1.7 quick phases/s). No significant effect was found with regard to direction or frequency of REMs; the hypothesis that differences in REM direction and frequency could be modulated by the rank order of REM episodes (i.e., as a function of time elapsed from presleep stimulation) also failed to show any effect of a complementary relation between OKN and REMs. The results suggest that the complementary relation between wake and sleep eye movements is specific for the saccadic system, allowing us to exclude a peripheral mechanism, that is, an effect due to fatigue of extraocular muscles.     

Sleep deprivation and phasic activity of REM sleep: independence of middle-ear muscle activity from rapid eye movements

In the recovery nights after total and partial sleep deprivation there is a reduction of rapid eye movements during REM sleep as compared to baseline nights; recent evidence provided by a selective SWS deprivation study also shows that the highest percentage of variance of this reduction is explained by SWS rebound. The present study assesses whether the reduction of rapid eye movements (REMs) during the recovery night after total sleep deprivation is paralleled by a decrease of middle-ear muscle activity (MEMA), another phasic muscle activity of REM sleep. Standard polysomnography, MEMA and REMs of nine subjects were recorded for three nights (one adaptation, one baseline, one recovery); baseline and recovery night were separated by a period of 40 hours of continuous wake. Results show that, in the recovery night, sleep deprivation was effective in determining an increase of SWS amount and of the sleep efficiency index, and a decrease of stage 1, stage 2, intra-sleep wake, and NREM latencies, without affecting REM duration and latency. However, MEMA frequency during REM sleep did not diminish during these nights as compared to baseline ones, while there was a clear effect of REM frequency reduction. Results indicate an independence of phasic events of REM sleep, suggesting that the inverse relation between recovery sleep after sleep deprivation and REM frequency is not paralleled by a concomitant variation in MEMA frequency.     

Modification of EEG asymmetry induced by auditory biofeedback loop during REM sleep in man

Several studies have emphasized the relationship between (1) rapid eye movement sleep (REM sleep) and learning, and (2) between REM sleep and asymmetry in EEG activity. Since we have shown that obtaining operant conditioned responses via auditory biofeedback during REM sleep is feasible, we demonstrate here that REM contingent auditory stimulations (white noise stimulation or interruption of a continuous white noise stimulation) lead to differential changes in phasic and tonic components of REM sleep. Whereas during baseline nights a relative right activation is found in the medium bands of EEG frequencies, our procedure seems to induce a systematic interhemispheric change during experimental nights. A new approach to the information processing hypothesis during REM sleep is proposed in terms of functional lateralized modifications of the EEG.     

Middle-ear muscle activity (MEMA) and its association with motor activity in the extremities and head in sleep.

Middle-ear muscle activity (MEMA) in sleep was simultaneously recorded from both ears using extratympanic manometry. Head movement, speech movements, ankle flexion and wrist movement were monitored by electromyographic recording using surface electrodes at the back of the neck, second laryngeal notch, anterior tibialis and forearm muscle. Motor events recorded from these electrode placements were examined for correlation with MEMA to test the hypothesis that the middle-ear muscles are activated in conjunction with other motor activities, aside from eye movements, by a central motor command system. Phi coefficients were calculated for each subject; all were positive, thus indicating an association between MEMA and other noneye movement motor events. These results suggest that there is a central phasic motor system responsible for MEMA and associated phasic motor activity in sleep.     

Enhanced synchronization of gamma activity between frontal lobes during REM sleep as a function of REM sleep deprivation in man

Studies have shown that synchrony or temporal coupling of gamma activity is involved in processing and integrating information in the brain. Comparing rapid eye movement (REM) sleep to waking and non-REM (NREM) sleep, interhemispheric temporal coupling is higher, but lower between the frontal and posterior association areas of the same hemisphere. However, the homeostatic response of REM sleep temporal coupling after selective REM sleep deprivation (REMD) has not been studied. This study proposed exploring the effect of one night of selective REMD on the temporal coupling of cortical gamma activity during recovery REM sleep. Two groups of healthy subjects were subjected to either REMD by awakening them at each REM sleep onset, or to NREM sleep interruptions. Subjects slept four consecutive nights in the laboratory: first for adaptation, second as baseline, third for sleep manipulation, and fourth for recovery. Interhemispheric and intrahemispheric EEG correlations were analyzed during tonic REM (no eye movements) for the first three REM sleep episodes during baseline sleep, and recovery sleep after one night of selective REMD. Temporal coupling between frontal lobes showed a significant homeostatic rebound that increased during recovery REM sleep relative to baseline and controls. Results showed a rebound in temporal coupling between the two frontal lobes after REM sleep deprivation, indicating that the enhanced gamma temporal coupling that occurs normally during REM sleep has functional consequences. Conclusion: results suggest that synchronized activity during REM sleep may play an important role in integrating and reprocessing information.     

The relationship between frequency of rapid eye movements in REM sleep and SWS rebound

Previous studies have shown a decrease in rapid eye movement (REM) frequency during desynchronized sleep in recovery nights following total or partial sleep deprivation. This effect has been ascribed to an increase in sleep need or sleep depth consequent to sleep length manipulations. The aims of this study were to assess REM frequency variations in the recovery night after two consecutive nights of selective slow-wave sleep (SWS) deprivation, and to evaluate the relationships between REM frequency and SWS amount and auditory arousal thresholds (AAT), as an independent index of sleep depth. Ten normal males slept for six consecutive nights in the laboratory: one adaptation, two baseline, two selective SWS deprivation and one recovery night. SWS deprivation allowed us to set the SWS amount during both deprivation nights close to zero, without any shortening of total sleep time. In the ensuing recovery night a significant SWS rebound was found, accompanied by an increase in AAT. In addition, REM frequency decreased significantly compared with baseline. This effect cannot be attributed to a variation in prior sleep duration, since there was no sleep loss during the selective SWS deprivation nights. Stepwise regression also showed that the decrease in REM frequency is not correlated with the increase in AAT, the traditional index of sleep depth, but is correlated with SWS rebound.     

Isolated sleep paralysis elicited by sleep interruption.

We elicited isolated sleep paralysis (ISP) from normal subjects by a nocturnal sleep interruption schedule. On four experimental nights, 16 subjects had their sleep interrupted for 60 minutes by forced awakening at the time when 40 minutes of nonrapid eye movement (NREM) sleep had elapsed from the termination of rapid eye movement (REM) sleep in the first or third sleep cycle. This schedule produced a sleep onset REM period (SOREMP) after the interruption at a high rate of 71.9%. We succeeded in eliciting six episodes of ISP in the sleep interruptions performed (9.4%). All episodes of ISP except one occurred from SOREMP, indicating a close correlation between ISP and SOREMP. We recorded verbal reports about ISP experiences and recorded the polysomnogram (PSG) during ISP. All of the subjects with ISP experienced inability to move and were simultaneously aware of lying in the laboratory. All but one reported auditory/visual hallucinations and unpleasant emotions. PSG recordings during ISP were characterized by a REM/W stage dissociated state, i.e. abundant alpha electroencephalographs and persistence of muscle atonia shown by the tonic electromyogram. Judging from the PSG recordings, ISP differs from other dissociated states such as lucid dreaming, nocturnal panic attacks and REM sleep behavior disorders. We compare some of the sleep variables between ISP and non-ISP nights. We also discuss the similarities and differences between ISP and sleep paralysis in narcolepsy.     

Human amygdala activation during rapid eye movements of rapid eye movement sleep: an intracranial study

The amygdaloid complex plays a crucial role in processing emotional signals and in the formation of emotional memories. Neuroimaging studies have shown human amygdala activation during rapid eye movement sleep (REM). Stereotactically implanted electrodes for presurgical evaluation in epileptic patients provide a unique opportunity to directly record amygdala activity. The present study analysed amygdala activity associated with REM sleep eye movements on the millisecond scale. We propose that phasic activation associated with rapid eye movements may provide the amygdala with endogenous excitation during REM sleep. Standard polysomnography and stereo‐electroencephalograph (SEEG) were recorded simultaneously during spontaneous sleep in the left amygdala of four patients. Time–frequency analysis and absolute power of gamma activity were obtained for 250 ms time windows preceding and following eye movement onset in REM sleep, and in spontaneous waking eye movements in the dark. Absolute power of the 44–48 Hz band increased significantly during the 250 ms time window after REM sleep rapid eye movements onset, but not during waking eye movements. Transient activation of the amygdala provides physiological support for the proposed participation of the amygdala in emotional expression, in the emotional content of dreams and for the reactivation and consolidation of emotional memories during REM sleep, as well as for next‐day emotional regulation, and its possible role in the bidirectional interaction between REM sleep and such sleep disorders as nightmares, anxiety and post‐traumatic sleep disorder. These results provide unique, direct evidence of increased activation of the human amygdala time‐locked to REM sleep rapid eye movements.     

Biperiden administration during REM sleep deprivation diminished the frequency of REM sleep attempts.

Sixteen subjects were assigned to a group using either placebo or biperiden, with eight subjects in each group. Both groups were studied for one acclimatization night, one baseline night, four nights of rapid eye movement (REM) sleep deprivation and two recovery nights. All the subjects received either placebo or 4 mg biperiden 1 hour before sleep during the four nights of REM sleep deprivation. During the baseline and the recovery nights both groups received placebo capsules. The results showed that REM sleep time during the REM sleep deprivation was reduced by 70-75% below the baseline night in both groups. The number of attempts to enter REM sleep was significantly reduced by biperiden as compared to placebo for each of the four REM sleep deprivation nights. Because the total sleep time in the biperiden group was reduced, the number of REM sleep attempts was corrected by the total sleep time. The adjusted number of REM sleep attempts was also significantly reduced in the biperiden group. REM sleep latency showed a reduction in the placebo group, whereas in the biperiden group REM sleep latency was unchanged throughout the deprivation nights. In the recovery night REM sleep time was increased in both groups, with no differences between the groups. The REM sleep latency showed a reduction in the first recovery night in both groups that persisted through the second recovery night. The above findings support the role of biperiden as a REM sleep suppressive drug.     

Spontaneous eyelid movements during human sleep: a possible ponto‐geniculo‐occipital analogue?

The aim of the present study was to investigate whether eye lid movements (ELMs) were temporally related to the activity of other skeletal musculature and to proposed analogues of ponto-geniculo-occipital (PGO) waves during human sleep. Electroencephalogram (EEG), laryngeal-masseter electromyogram (EMG), electrooculgram (EOG), peri-orbital integrated potentials (PIPs), middle ear muscle activity (MEMA), ankle flexion (AF) and respiration (RESP) were monitored with ELMs during one night's sleep. Results showed that ELMs always occurred during full arousal and movement time. The ELMs that occurred during sleep were most prominent during rapid eye movement (REM) sleep, occurred at higher frequency just before REM, and were observed synchronously with other PGO analogues, supporting the notion that ELMs may be an indicator of PGO activity in humans. Of the ELMs observed during sleep, 16% showed changes in EOG, PIP, MEMA, AF and RESP simultaneously, suggesting generalized muscle activation. This coactivation of muscle activity suggested that the relationship between the muscular measures and PGO activity might be an indirect one, possibly mediated by alerting mechanisms, previously shown to be related to PGO waves in animals. Such an interpretation is consistent with the use of ELM as a widely accepted measure of the eye-blink startle response in awake human subjects.     

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.     

Psychological correlates of electrodermal activity during REM sleep

Eight subjects each spent 2 nights in the sleep laboratory during which electrodermal activity (EDA) was recorded in addition to standard sleep monitoring. On the experimental night, following an adaptation night, subjects were awakened four times from REM sleep: in the presence of phasic EDA and eye movements; in the presence of phasic EDA without eye movements; in the presence of eye movements without phasic EDA; and in the absence of both eye movements and phasic EDA. Detailed mentation reports were obtained, coded, and rated on scales of emotionality and bizarreness. EDA was found to be associated with bizarre mentation. Implications for the study of nocturnal phasic activity in general and for the study of EDA are discussed. An improved circuit for the long-term recording of EDA is described in sufficient detail to allow its duplication.     

Sleep deprivation suppresses the increase of rapid eye movement density across sleep cycles

We investigated the association between rapid eye movement (REM) density (REMd) and electroencephalogram (EEG) activity during non‐rapid eye movement (NREM) and REM sleep, within the re‐assessment, in a large sample of normal subjects, of the reduction of oculomotor activity in REM sleep after total sleep deprivation (SD). Coherently with the hypothesis of a role of homeostatic sleep pressure in influencing REMd, a negative correlation between changes in REMd and slow‐wave activity (SWA) was expected. A further aim of the study was to evaluate if the decreased REMd after SD affects ultradian changes across sleep periods. Fifty normal subjects (29 male and 21 female; mean age = 24.3 ± 2.2 years) were studied for four consecutive days and nights. Sleep recordings were scheduled in the first (adaptation), second (baseline) and fourth night (recovery). After awakening from baseline sleep, a protocol of 40 h SD started at 10:00 hours. Polysomnographic measures, REMd and quantitative EEG activity during NREM and REM sleep of baseline and recovery nights were compared. We found a clear reduction of REMd in the recovery after SD, due to the lack of REMd changes across cycles. Oculomotor changes positively correlated with a decreased power in a specific range of fast sigma activity (14.75–15.25 Hz) in NREM, but not with SWA. REMd changes were also related to EEG power in the 12.75–13.00 Hz range in REM sleep. The present results confirm the oculomotor depression after SD, clarifying that it is explained by the lack of changes in REMd across sleep cycles. The depression of REMd can not simply be related to homeostatic mechanisms, as REMd changes were associated with EEG power changes in a specific range of spindle frequency activity, but not with SWA.     

Experimentally induced arousals during sleep: a cross-modality matching paradigm

Micro-arousals occur spontaneously or in response to exogenous and endogenous sensory input during sleep. The function of micro-arousals remains unclear, for example, whether it reflects a disturbance or a preparatory response to environmental changes. The goal of this study was to assess arousal responsiveness when two types of sensory stimulations were used: auditory (AD) alone and the addition of a vibrotactile (VT) sensation. Ten normal sleepers participated in three nights of polygraphic recordings. The first night was for habituation and to rule out sleep disorders, and the second to collect baseline sleep data. During the third night, AD and VT + AD stimuli, with three levels of intensities for auditory and vibratory signals, were randomly given to induce arousal responses in sleep stages 2, 3 and 4 and rapid eye movement (REM). The frequency of the arousal responses increased with stimulus intensity for all sleep stages and was lowest in stages 3 and 4. In non-REM (NREM) sleep, combined VT + AD stimulation induced more frequent and more intense arousal responses than AD alone. In REM sleep, more frequent micro-arousals rather than awakenings were triggered by combined stimulations. In stage 2, the response rate of total induced K-complexes did not differ between both types of stimulations while more K-complexes followed by arousals were evoked by the combined VT + AD stimulation than by the AD alone. The induced arousals were associated with an increase in heart rate in all sleep stages. An increase in suprahyoid muscle tone was observed in NREM sleep only, REM being not associated with a rise in muscle tone following experimental stimulation. Most leg and body movements occurred in response to induced awakenings. These results suggest that the cross-modality sensory stimuli triggered more arousal responses in comparison with single-modality stimuli. In an attempt to wake a sleeping subject, the addition of a tactile stimulation, such as shaking the shoulder, is an effective strategy that increases the arousal probability.     

An inexpensive alternative for recording middle ear muscle activity (MEMA) during sleep.

In past studies of middle ear muscle activity (MEMA) in sleep, one of two methods of recording has been used: an acoustic impedance bridge (AIB) or a miniaturized pressure transducer (MPT). A low-cost and less fragile piezoresistive pressure transducer was tested to determine its practicality in recording MEMA during sleep in humans. A specialized ear mold accommodating both types of pressure transducer was custom-fitted for six subjects. The sleep of each subject was analyzed epoch by epoch for one night to determine comparability of the two transducers. In no case did either transducer indicate a MEMA without confirmation by the other. It is recommended that this type of transducer would be practical for researchers interested in recording MEMA in sleep.     

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.     

Phasic events of REM sleep: phenomenology of middle ear muscle activity and periorbital integrated potentials in the same normal population.

Both periorbital integrated potentials (PIPs) and middle ear muscle activity (MEMAs) were recorded in a sample of normal male veterans. Activity measures were constructed for each REM period and for the 10 min preceding and following each REM period. PIPs and MEMAs displayed high levels of internight reliability. PIPs were more abundant than MEMAs; in REM the average PIP rate was almost 8 times the average MEMA rate. Within REM, the proportion of MEMAs and PIPs with concurrent eye movement activity was very similar, 66 and 70%, respectively. Both PIPs and MEMAs had higher rates within REM than within NREM. NREM PIP activity was similar both before and after the REM period, whereas NREM MEMA activity was higher before the REM period than after the REM period. Within REM, the distribution of PIPs and MEMAs was similar for REM periods exceeding 30 min. Within-night trends could nor be established for MEMAs due to limitations of the recording technique; PIPs, however, were generally highest in the middle of the night but still higher at the end of the night than at the beginning. Correlations with psychometric test data showed PIP rate in REM to be related to the psychoticism scale of the Minnesota Multiphasic Personality Inventory and MEMA rate in REM to be inversely related to the Barron Ego Strength scale. No associations were found between the psychometric data and measures of PIP and MEMA leakage from REM into NREM. The potential for pathological intrusion of REM phasic events into the waking stage might be conceptualized in terms of a general ungating of activity with PIP and MEMA rates increasing in both NREM and REM alike.     

REM sleep characteristics in narcolepsy and REM sleep behavior disorder

STUDY OBJECTIVES: To assess the presence of polysomnographic characteristics of REM sleep behavior disorder (RBD) in narcolepsy; and to quantify REM sleep parameters in patients with narcolepsy, in patients with "idiopathic" RBD, and in normal controls. DESIGN: Sleep laboratory study PARTICIPANTS: Sixteen patients with narcolepsy and cataplexy matched for age and sex with 16 patients with "idiopathic" RBD and with 16 normal controls were studied. MEASUREMENTS AND RESULTS: Higher percentages of REM sleep without atonia, phasic electromyographic (EMG) activity, and REM density were found in patients with narcolepsy than normal controls. In contrast, RBD patients had a higher percentage of REM sleep without atonia but a lower REM density than patients with narcolepsy and normal controls. Based on a threshold of 80% for percentage of REM sleep with atonia, 50% of narcoleptics and 87.5% of RBD patients had abnormal REM sleep muscle activity. No significant behavioral manifestation in REM sleep was noted in either narcoleptics or controls. We also found a higher frequency of periodic leg movements during wake (PLMW) and during sleep (PLMS) in narcoleptic patients compared to controls. CONCLUSIONS: The present study demonstrates abnormalities in REM sleep motor regulation with an increased frequency of REM sleep without atonia, phasic EMG events and PLMS in narcoleptic patients when compared to controls. These abnormalities were seen more prominently in patients with RBD than in narcoleptics, with the exception of the PLMS index. We proposed that dysfunctions in hypocretin/dopaminergic system may lead to motor dyscontrol in REM sleep that results in dissociated sleep/wake states.     

A sensitive air pressure-measuring transducer for indirect middle ear muscle recording in humans.

In the past, the recording of middle ear muscle activity (MEMA) during sleep was accomplished with the use of the acoustic impedance bridge (AIB). However, two major concerns with this technique are: 1. augmentation of MEMA (and possible impairment of the auditory apparatus), as a consequence of the 85-95 dB probe tone, which is necessary for acoustic tympanometry; 2. the AIB recording method is susceptible to snoring artifact so that determination of true MEMA events is difficult. By utilizing a highly sensitive air-pressure measuring transducer (AMPT), we were able to record MEMA accurately without artifactual stimulation of this endogenously occurring REM sleep phasic activity. Possible damage to inner ear structures is precluded because no sound input is required with the AMPT.     

Brain-mind states: I. Longitudinal field study of sleep/wake factors influencing mentation report length

STUDY OBJECTIVES: To collect and analyze reports of mental activity across sleep/wake states. DESIGN: Mentation reports were collected in a longitudinal design by combining our Nightcap sleep monitor with daytime experience sampling techniques. Reports were collected over 14 days and nights from active and quiet wake, after instrumental awakenings at sleep onset, and after both spontaneous and instrumental awakenings from REM and NREM sleep. SETTING: All reports were collected in the normal home, work and school environments of the subjects. PARTICIPANTS: Subjects included 8 male and 8 female undergraduate students (19-26 years of age). INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: A total of 1,748 reports, averaging 109 per subject, were collected from active wake across the day (n=894), from quiet wake in the pre-sleep onset period (n=58), from sleep onset (n=280), and from later REM (n=269) and nonREM (n=247) awakenings. Median report lengths varied more than 2-fold, in the order REM > active wake > quiet wake > NREM = sleep onset. The extended protocol allowed many novel comparisons between conditions. In addition, while spontaneous REM reports were longer than those from forced awakenings, the difference was explained by the time within the REM period at which the awakenings occurred. Finally, intersubject differences in REM report lengths were correlated with similar differences in waking report lengths. CONCLUSIONS: The use of the Nightcap sleep monitoring system along with waking experience sampling permits a more complete sampling and analysis of mental activity across the sleep/wake cycle than has been previously possible.