EEG arousals in normal sleep: variations induced by total and selective slow-wave sleep deprivation

STUDY OBJECTIVES: Aim of the present study was to assess changes in arousal rates after selective slow-wave (SWS) and total sleep deprivations. DESIGN: Two-way mixed design comparing the arousal index (Al), as expressed by the number of EEG arousals divided by sleep duration, in totally or selectively sleep deprived subjects. SETTING: Sleep laboratory. PATIENTS OR PARTICIPANTS: Nineteen normal male subjects [mean age=23.3 years (S.E.M.=0.55)]. INTERVENTIONS: Al was measured in baseline nights and after selective SWS (N=10) and total sleep deprivation (N=9). MEASUREMENTS AND RESULTS: During the baseline nights AI values changed across sleep stages as follows: stage 1 > stage 2 and REM > SWS, but did not present any significant variations as a function of time elapsed from sleep onset. The recovery after deprivation showed a reduction in EEG arousals, more pronounced after total sleep deprivation; this decrease affected NREM but not REM sleep. During the baseline nights Al showed a close-to-significance negative correlation with REM duration, while during the recovery nights a significant positive relation with stage 1 duration was found. CONCLUSIONS: The present results suggest that recuperative processes after sleep deprivation are also associated with a higher sleep continuity as defined by the reduction of EEG arousals.     

Ambient temperature is associated with changes in infants' arousability from sleep

STUDY OBJECTIVE: To evaluate the influence of ambient temperature on infants' arousability from sleep. DESIGN: Two groups of healthy infants with a median age of 11 weeks were recorded polygraphically during one night: 31 infants were studied at 24 degreesC and 31 infants at 28 degreesC. To determine their arousal thresholds, the infants were exposed to white noises of increasing intensities during REM and NREM sleep. Arousal thresholds were defined by the auditory stimuli needed to induce arousals. SETTING: N/A. PATIENTS or PARTICIPANTS: N/A. INTERVENTIONS: N/A. MEASUREMENTS and RESULTS: The arousal thresholds decreased across the night in the infants sleeping at 24 degreesC (p=.017). The finding was not found for the infants sleeping at 28 degreesC. When analyzing the arousal responses according to time of the night, it was found that the auditory thresholds were significantly higher at 28 degreesC than at 24 degreesC between 03:00 hr and 06:00 hr (p=.003). These findings were only seen in REM sleep. CONCLUSION: High ambient temperature could add to the difficulty to arouse from REM sleep in the late hours of the night.     

Hypoxia impairs the arousal response to external resistive loading and airway occlusion during sleep

STUDY OBJECTIVES: Sustained hypoxia is a neurocognitive depressant, which has been shown to impair respiratory load sensation. Hypoxia has also been shown to impair arousal in animal models, but the effects of sustained hypoxia on arousal in humans have not been studied. The aim of this study was to assess the effects of sustained hypoxia on arousal from sleep in normal subjects. DESIGN: Twelve normal male subjects (age, 24.3 +/- 1.2 years; body mass index, 24.8 +/- 1.4 kg/m2) were studied during stable stage 2 non-rapid eye movement sleep on 2 separate nights 1 week apart. SETTING: Sleep physiology laboratory. PARTICIPANTS: Normal healthy volunteers. Interventions: Arousal responses to external resistive loads (18 cm H2O x L(-1) x sec(-1)) and occlusions were compared during room-air breathing following sustained normoxia and isocapnic hypoxia (SaO2 approximately 85%). Measurements and Results: Time to arousal and minimum esophageal pressure preceding arousal were measured. Time to arousal was significantly increased following hypoxia compared with normoxia for resistive loads (24.6 + 4.4 seconds vs. 12.6 +/- 1.9 seconds, p = .007) but not occlusions. Minimum esophageal pressure prior to arousal was more negative following hypoxia for both external loads (-16.8 +/- 1.2 vs. -13.5 +/- 1.3 cm H2O, p = .035) and occlusions (-19.6 +/- 2.2 vs. -15.1 +/- 1.5 cm H2O, p = .029). CONCLUSIONS: We conclude that sustained isocapnic hypoxia delays arousal to inspiratory loading during sleep and increases the respiratory arousal threshold. This has implications for disorders characterized by sustained nocturnal hypoxia, such as neuromuscular weakness, chronic obstructive pulmonary disease, obesity-hypoventilation syndrome, and severe obstructive sleep apnea.     

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.     

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.     

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.     

Motor responsiveness to stimuli presented during sleep: the influence of time-of-testing on sleep stage analyses.

The relationship between time-of-night of testing (circadian factors) and motor responsiveness to stimuli presented during different stages of sleep was examined. Nine males slept for two nonconsecutive nights in the laboratory. On Night 1, tympanic temperature was assessed at 30 min intervals. On Night 2, responsiveness was assessed with an incremental series of tones presented in sleep stages 2, 3/4, and REM throughout the night. Subjects were instructed to make a microswitch closure to the tones. Results showed that for all stages, responsiveness decreased across thirds of the night. Because the distribution of each sleep stage differed across the night, the effects on responsiveness due to time-of-testing and to sleep stage were confounded. When time-of-testing was held constant, responsiveness was greater in stages 2 and REM than in stage 3/4. When time-of-testing was not held constant, effects nearly opposite of the latter could be demonstrated.     

Performance during frequent sleep disruption

Performance on a simple addition task was measured during three schedules of frequent sleep disruption for 2 nights. Five young adults had their sleep briefly disturbed for 2 nights in 3 separate weeks either every 1 min, every 10 min, or at sleep onset after an undisrupted 2.5-h sleep period. Subjects were required to perform a two-number, two-digit addition problem as rapidly as possible on awakening. Main effects were found for sleep disruption condition and time of night, and a significant interaction between the two was also observed. Latency to response was longest for the 10-min condition on night 1, on night 2, however, response latencies were longest in the 1-min condition. Response latencies were fastest in the 2.5-h condition for both nights of disruption. Arousal thresholds were also gathered across both nights. Arousal thresholds were consistently the highest in the 1- and 10-min conditions for both nights of disruption, reaching maximum threshold levels at the end of night 1. Arousal threshold was significantly positively correlated with response latency. Sleep stages (slow-wave sleep (SWS), SWS + REM (SWSR), and total sleep time minus stage 1 sleep) were poor predictors of performance changes across the 2 disruption nights. The data were best explained by sleep continuity theory, which posits that a period of at least 10 min of uninterrupted sleep is required for restoration to take place.     

The effect of clustered versus regular sleep fragmentation on daytime function

Previously, we found that regular sleep fragmentation, similar to that found in patients with sleep apnoea/hypopnoea syndrome (SAHS), impairs daytime function. Apnoeas and hypopnoeas occur in groups in patients with REM or posture related SAHS. Thus, we hypothesised that clustered sleep fragmentation would have a similar impact on daytime function as regular sleep fragmentation. We studied 16 subjects over two pairs of 2 nights and 2 days. The first night of each pair was for acclimatisation. On the second night, subjects either had their sleep fragmented regularly every 90 s, or fragmented every 30 s for 30 min every 90 min, the remaining 60 min being undisturbed. We fragmented sleep with tones to produce a minimum 3 s increase in EEG frequency. During the days following each pair of nights we tested subjects daytime function. Total sleep time (TST) and microarousal frequency were similar no both study nights. We found significantly less stage 2 (55 SD 4, 62 +/- 7%; P = 0.001) and more slow wave sleep (21 SD 3, 12 +/- 6%; P < 0.001) on the clustered night. Mean sleep onset latency was similar on MSLT (clustered 10 SD 5, regular 9 +/- 4 min; P = 0.7) and MWT (clustered 32 SD 7, regular 30 +/- 7 min; P = 0.2). There was no difference in subjects mood or cognitive function after either study night. These results suggest that although there is more slow wave sleep (SWS) on the clustered night, similar numbers of sleep fragmenting events produced similar daytime function whether the events were evenly spaced or clustered.     

Increased production of evoked and spontaneous K-complexes following a night of fragmented sleep

STUDY OBJECTIVES: To determine whether K-complex production is better interpreted as being an arousal response or reflective of a sleep protective micro-state. DESIGN: A 3-night study--night 1 as a baseline night, night 2 as a sleep fragmentation night, followed immediately by night 3 as a recovery night. On nights 1 and 3, approximately 400 auditory stimuli were presented during nonREM sleep in the first two sleep cycles, using stimulus parameters previously found to be optimal for K-complex production. SETTING: The sleep research laboratory at the University of Melbourne. PARTICIPANTS: Six young healthy subjects (3 female). INTERVENTIONS: One night of sleep fragmentation. Ten-second auditory tones of up to 110 dB were presented throughout the entire night at approximately 1-minute intervals. MEASUREMENTS AND RESULTS: Sleep drive was increased on the recovery night, as indicated by increased amounts of slow wave sleep, increased sleep efficiency, and a reduction in stimulus-related alpha activity. The incidence of both evoked and spontaneous K-complexes increased significantly on the recovery night. When K-complex trials were averaged, neither N550 (Fz) amplitude nor latency differed between the 2 nights. When vertex sharp waves were averaged, N350 (Cz) amplitude was increased significantly on the recovery night. CONCLUSIONS: The increase in K-complex frequency together with the decrease seen in stimulus-related alpha activity supports the view that they reflect a sleep maintenance, rather than an arousal, response.     

Increased homeostatic response to behavioral sleep fragmentation in morning types compared to evening types

STUDY OBJECTIVES: To evaluate the influence of chronotype on sleep stages and quantitative sleep EEG when sleep pressure is increased and sleep schedule remains constant. DESIGN: A 5-day session comprising an adaptation night, a baseline night, two nights of sleep fragmentation, and a recovery night. SETTING: Chronobiology laboratory. PARTICIPANTS: Twenty-four healthy subjects aged 19-34 years: 12 morning types and 12 evening types selected by questionnaire. Each group included 6 men and 6 women with a habitual sleep duration of 7 to 9 hours. Interventions: Two nights of behavioral sleep fragmentation induced by forced 5-min awakenings every half-hour. MEASUREMENTS AND RESULTS: Each night of polysomnography recording lasted 8 hours and was based on each subject's preferred sleep schedule. On both nights of sleep fragmentation, stage 1 sleep increased, while both total sleep time and minutes of slow wave sleep decreased. No difference was observed in sleep architecture between morning types and evening types during sleep fragmentation nights or during recovery night. Spectral analysis of all-night NREM sleep EEG showed that during the recovery night, morning types had a larger fronto-central increase in low frequency activities and a larger centro-parietal decrease in 14-15 Hz activity than evening types. The largest group difference was for slow wave activity in the fronto-central area during the first part of the sleep episode. CONCLUSIONS: These results add further support to a postulated difference in homeostatic sleep regulation between morning types and evening types, with morning types showing indications of a higher homeostatic response to sleep disruption.     

Ontogenetic variations in auditory arousal threshold during sleep

Developmental variations in auditory arousal thresholds during sleep were investigated in four groups of normal male subjects - children, preadolescents, adolescents, and young adults. Arousal thresholds were determined during NREM and REM sleep for tones presented via earphone insert on a single night following two adaptation nights of undisturbed sleep. Age-related relationships were observed for both awakening frequency and stimulus intensity required to effect awakening, with awakenings occurring more frequently in response to lower stimulus intensities with increasing age. Although stimulus intensities required for awakening were high and statistically equivalent across sleep stages in nonadults, higher intensity stimuli were required in Stage 4 relative to Stage 2 and REM sleep in adults. These results confirm previous observations of marked resistance to awakening during sleep in preadolescent children and suggest that processes underlying awakening from sleep undergo systematic modification during ontogenetic development.     

Effect of 64 hours of sleep deprivation upon sleep in geriatric normals and insomniacs

Fifty-eight geriatric normal and chronic insomniac sleepers were screened with sleep recordings to define groups of 12 Normal (Sleep Efficiency greater than 85%) and Insomniac (Sleep Efficiency less than 80%) sleepers. All subjects then had 4 baseline sleep nights, 64 hours of total sleep loss, and 4 recovery nights. Insomniacs, had lower sleep efficiencies and less REM than Normals during baseline. Sleep efficiency was high (97%) in both groups on the first recovery night but decreased toward baseline values in both groups between the second (Normal) and fourth (Insomniac) recovery night. The groups had relatively little slow wave sleep, but had a significant increase on the first recovery night. Five Normals and one Insomniac had REM latency of less than 15 min on their first recovery night. This REM latency was found to be significantly correlated with the amount of slow wave sleep on baseline. Decreased REM latency in initial recovery sleep was interpreted as evidence of decreased pressure for slow wave sleep in aging.     

Arousals and sleep stages in patients with obstructive sleep apnoea syndrome: changes under nCPAP treatment

Nocturnal arousals are the essential cause of disturbed sleep structure in patients with obstructive sleep apnoea syndrome (OSAS). The aim of this study was to analyse the relationship between sleep stages, respiratory (type-R) and movement (type-M) related EEG arousals. Furthermore, the value of these arousals as a criterion for the efficiency of nCPAP treatment was estimated. We examined 38 male patients aged between 30 and 71 (49.1±20.9 SD) y. All patients suffered from OSAS. The mean respiratory disturbance index (RDI) was 47.3±27.8 per h. Polysomnographic monitoring was carried out on 4 subsequent nights: baseline night, 2 nights of nCPAP titration and nCPAP control night. Sleep was visually scored and EEG arousals were classified into type R and M, depending on whether changes of respiration or movement caused the arousal. The RDI, the R index (type-R/h), the M index (type-M/h) and the R and M indices in different sleep stages were calculated. During the baseline night a deficit of slow wave sleep (SWS) and REM sleep was found. Furthermore there were more type-R than type-M arousals registered (17.4 h^?1[3.6–43.6] vs. 5.9 h^?1[1.6–11.8]) ( P <0.01). They occurred during stages NREM 1, NREM 2 and REM ( P <0.01). An SWS sleep rebound and a reduction of the SWS and REM latencies were already found during the first CPAP night. The R index was reduced during the first CPAP night in all sleep stages ( P <0.01) and remained approximately the same in the following 2 nights (3. CPAP night: 1.1 h^?1[0.3–5.0]). Type M arousals occurred more in stages 1 and 2 ( P <0.01), and remained unchanged under nCPAP. We concluded that differentiation of nocturnal arousals may provide more detailed information regarding the influence of breathing disturbances on sleep. Respiratory related, not movement related, arousals may be a useful additional tool in judging the efficiency of OSAS.     

The effects of sleep inertia on decision-making performance

Sleep inertia, the performance impairment that occurs immediately after awakening, has not been studied previously in relation to decision-making performance. Twelve subjects were monitored in the sleep laboratory for one night and twice awoken by a fire alarm (slow wave sleep, SWS and REM sleep). Decision making was measured over 10 3-min trials using the ‘Fire Chief’ computer task under conditions of baseline, SWS and REM arousal. The most important finding was that sleep inertia reduces decision-making performance for at least 30 min with the greatest impairments (in terms of both performance and subjective ratings) being found within 3 min after abrupt nocturnal awakening. Decision-making performance was as little as 51% of optimum (i.e. baseline) during these first few minutes. However, after 30 min, performance may still be as much as 20% below optimum. The initial effects of sleep inertia during the first 9 min are significantly greater after SWS arousal than after REM arousal, but this difference is not sustained. Decision-making performance after REM arousal showed more variability than after SWS arousal. Subjects reported being significantly sleepier and less clear-headed following both SWS and REM awakenings compared with baseline and this was sustained across the full 30 min. In order to generalize this finding to real-life situations, further research is required on the effects of continuous noise, emotional arousal and physical activity on the severity and duration of sleep inertia.     

Chemosensory induced arousals during sleep in premenopausal women

Only a limited number of studies is available addressing chemosensory stimulation during sleep. Recent work indicates that stimulation with a nasal irritant produces an increase in arousal frequency in non-REM sleep, whereas a selective olfactory stimulant does not. The present study focused on arousal reactions in REM sleep. Five young healthy volunteers were investigated during 27 nights. Using air-dilution olfactometry CO(2) was used for nasal irritation and H(2)S was used as a specific olfactory stimulant. Both stimuli were presented at four concentrations, odorless stimuli served as control. Other than in previous studies arousal latency was used as a dependent measure. Even the strongest olfactory stimulus did not produce an increase in arousal frequency in REM sleep whereas for irritation such an increase was clearly present. Latencies of arousal responses to CO(2) shortened with increasing stimulus concentrations. Olfactory stimulation does not lead to arousal reactions. In contrast, trigeminal stimulation produces a concentration-dependent increase in arousal frequency and decrease in arousal latency across all sleep stages. The present data shows for the first time that arousals are not present during REM sleep in response to selective olfactory stimuli. However, such changes are easily evoked by irritants activating the trigeminal nerve.     

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.     

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.     

Recovery sleep following different visual conditions during total sleep deprivation in man.

The findings of visual impairment during total sleep deprivation were used as a basis for a possible link between vision and sleep. It was proposed that the level of visual load imposed during sleep deprivation was an important variable, and would have a substantial effect upon recovery sleep. Six young male subjects underwent two conditions of 64 h of sleep deprivation on separate occasions. One condition incorporated a high visual load, and the other a low load. Exercise and sound were balanced. All night sleep EEGs were taken for two baseline nights, and also for two recovery nights following each condition. There was a significant increase of stage 4 on all recovery nights and a REM rebound on the second recovery night. SWS, particularly stage 4, TST and REM density, were significantly greater following the high load. Implications of these findings for sleep theories and for sleep deprivation research are discussed.     

Relationship of epileptic seizures to sleep stage and sleep depth

STUDY OBJECTIVES: Interictal epileptiform discharges (IEDs) are facilitated by NREM stages 3 and 4 sleep and as sleep is deepening. To determine whether sleep influences seizures in a similar way to IEDs, we examined seizure rates in various stages of sleep in epilepsy patients undergoing overnight video-EEG-polysomnography (VPSG). DESIGN: Cross-sectional study. SETTING: Neurology Department. PATIENTS, MEASUREMENTS, AND INTERVENTIONS: We reviewed VPSGs from our Sleep and Epilepsy Laboratories to identify patients with recorded seizures during sleep. A total of 55 patients having 117 seizures were identified. RESULTS: Ninety-five percent of seizures occurred in NREM sleep (61% in stage 2, 20% in stage 1, 14% in stages 3 and 4 combined), and 5% in REM sleep. Adjusting for time spent in each stage of sleep, patients had 0.34 seizures per hour in stage 1, 0.38 seizures per hour in stage 2, 0.29 seizures/hr in stage 3 and 4 combined, and 0.09 seizures per hour in REM sleep. Seizures/hour was higher in NREM sleep (0.35 for NREM and 0.09 for REM; p=0.0001). For single seizures occurring in 1 night, seizure rate was significantly higher in NREM stages 1 and 2 as compared to NREM stages 3 and 4 sleep. A significant increase in log delta power, an automated measure of sleep depth, was observed in the 10 minutes prior to seizures. CONCLUSIONS: Both seizures and IEDs are facilitated by NREM sleep. While deeper stages of NREM sleep activate IEDs, lighter stages of NREM sleep promote seizures, at least for single seizures occurring in 1 night.