Mental activity after early afternoon nap awakenings in healthy subjects

Despite the common misconception that rapid eye movement (REM) sleep is a unique correlate of dreaming, reports of mental activity can be elicited after awakenings from any stage of nocturnal sleep. We extended the investigation to naps and tried to explore the relationship between recall length and level of sleep stage and depth preceding the awakening. We hypothesized that dream report length would be related to arousal level. In 10 healthy young adults, sleep EEG and EOG were recorded for four non-consecutive early afternoon naps. Dream recalls were recorded following 10 s, 1 min, and 6 min of NREM Stage 2 and after 5 min of first REM period. We measured mental recall with total word count (TWC) method, sleep stages by using EEG visual scoring and Delta and Beta activity by period amplitude (PAA) and power spectral (PSA) analyses. All awakening conditions were followed by a dream report. TWC was significantly greater after REM than after 10 s and 1 min of NREM, and TWC did not differ among the NREM awakenings. Delta activity after REM was significantly lower compared to the NREM 6 and 1 min while Beta activity did not differ across the conditions. Assuming that arousal level decreased with increased NREM duration and increasing Delta EEG activity, the constant TWC across the three NREM awakenings indicates that arousal level cannot be the only factor affecting dream report length. Some other factor such as memory processing may explain the longer dream reports following REM sleep, or it may be that the EEG is an imperfect indicator of arousal level.     

Combined influence of cyclic arousability and EEG synchrony on generalized interictal discharges within the sleep cycle

PURPOSE: to analyze the activating role of cyclic alternating pattern (CAP) and EEG synchrony on generalized interictal paroxysms in the first part of the night, when all sleep patterns are represented. METHODS: nocturnal polysomnographic investigation was accomplished on a randomized series of 18 subjects with an active form of primary generalized epilepsy (PGE), but only six patients showed a complete and regular profile of the first two sleep cycles (SCs). Completeness and regularity of the selected SCs consisted in the absence of intervening wakefulness, in the presence of all sleep stages, and in the identification of three main units, (a) a descending branch, dominated by the build-up of EEG synchrony in the transition from light to deep non-rapid eye movement (NREM) sleep; (b) a trough, where the magnitude of EEG synchrony is greatest and gives rise to stages 3 and 4; (c) an ascending branch characterized by a decrease of EEG synchrony preceding the onset of rapid eye movement (REM) sleep. Generalized paroxysms were evaluated in terms of discharge rates (number of interictal bursts per minute of sleep) and distribution within the investigated sleep parameters. RESULTS: the discharge rates decreased from SC1 to SC2, with higher values quantified during NREM sleep (mean, 2.8) compared with REM sleep (mean, 0.8). Both SCs showed a progressive decrease of activation across the three units, from the highest discharge rates reached during the descending branches (mean, 3.6) to the more attenuated discharge rates during the troughs (mean, 2.4) down to the lowest rates during the ascending limbs (mean, 1.1). The magnitude of activation during the descending branches was closely related to the CAP condition (mean, 5.2) and to the powerful effect of phase A (mean, 13.9). The great majority (82%) of EEG discharges occurring in phase A were distributed within the A1 subtypes (identified by sequences of k-complexes or delta bursts). CONCLUSIONS: within the first two SCs, the features of NREM sleep endowed with the major activating power on generalized bursts are represented by the rise of EEG synchrony (descending branch) and by the A phases of CAP involved in the regulation of its build-up.     

Sleep Microstructure and EEG Epileptiform Activity in Patients with Juvenile Myoclonic Epilepsy

Clinical and EEG manifestations of juvenile myoclonic epilepsy (JME) occur in a strict relationship to the sleep-wake cycle, particularly to transition phases (awakening, falling asleep, afternoon relaxation after work). JME manifestations are deactivated during sleep. Because arousal fluctuations during NREM sleep may be controlled by the same neurophysiologic mechanisms regulating awakening, we studied the relationship between the cyclic alternating pattern (CAP) and JME manifestations. All-night polysomnographic recordings of 10 JME patients were analyzed for variations of epileptiform EEG abnormalities in relation to sleep stages and to different microstructural variables (NCAP, CAP, phases A and B). CAP rates (ratio between total CAP duration and total NREM sleep duration) were also calculated. Average CAP rate was 46.70%, significantly higher than that (23%) of an age-matched control group. Macrostructural analysis showed only a trend toward a slight predominance of EEG epileptiform activity during slow wave sleep but no significant correlation between spiking rates and sleep stages. Microstructural analysis confirmed the CAP modulation of EEG epileptiform activity, with maximum appearance of epileptiform abnormalities during phase A CAP (normalized spiking rate = 4.00 +/- 0.98) and strong inhibition during phase B (0.06 +/- 00.6). Intermediate values were noted during NCAP (0.54 +/- 0.27). No correlation was noted between spiking rates during NREM sleep and CAP rates, possibly indicating that in JME patients the increased CAP rate may be partially independent of epileptiform EEG activity. Our data suggest that in JME patients CAP may be a neurophysiologic oscillator organizing expression of the epileptiform discharges independent of the tendency of the individual patient to produce epileptiform EEG discharges.     

Influence of sleep stage and wakefulness on spectral EEG activity and heart rate variations around periodic leg movements.

OBJECTIVE: Typical changes in spectral electroencephalographic (EEG) activity and heart rate (HR) have been described in periodic leg movements (PLM) associated with or without microarousals (MA). We aimed to determine the effects of sleep stage and wakefulness on these responses to ascertain whether a common pattern of EEG and HR activation takes place. METHODS: The time course of EEG spectral activity and HR variability associated with PLM was analysed in 13 patients during light NREM sleep, rapid-eye-movement (REM) sleep and wakefulness. The same analysis was also conducted for PLM without MA occurring in stage 2. RESULTS: A significant EEG and electrocardiogram (ECG) activation was found associated with PLM during sleep, but not during wakefulness. While in light NREM sleep, an increase in delta and theta bands was detected before the PLM onset, in REM sleep the EEG activation occurred simultaneously with the PLM onset. Moreover, during stage 1 and REM sleep, alpha and fast frequencies tended to remain sustained after the PLM onset. In contrast, during wakefulness, a small and not significant increase in cerebral activity was present, starting at the PLM onset and persisting in the post-movement period. A typical pattern of cardiac response was present during NREM and REM sleep, the autonomic activation being lesser and prolonged during wakefulness. CONCLUSIONS: We conclude that the EEG and HR responses to PLM differ between sleep stages and wakefulness with lesser changes found during wakefulness. SIGNIFICANCE: These findings suggest that specific sleep state-dependent mechanisms may underlie the occurrence of PLM.     

Ischemic stroke selectively inhibits REM sleep of rats

Sleep disorders are important risk factors for stroke; conversely, stroke patients suffer from sleep disturbances including disruptions of non-rapid eye movement (NREM) and rapid eye movement (REM) sleep and a decrease in total sleep. This study was performed to characterize the effect of stroke on sleep architecture of rats using continuous electroencephalography (EEG) and activity monitoring. Rats were implanted with transmitters which enabled continuous real time recording of EEG, electromyography (EMG), and locomotor activity. Baseline recordings were performed prior to induction of either transient middle cerebral artery (MCA) occlusion or sham surgery. Sleep recordings were obtained for 60 h after surgery to identify periods of wakefulness, NREM, and REM sleep before and after stroke. Spectral analysis was performed to assess the effects of stroke on state-dependent EEG. Finally, we quantified the time in wake, NREM, and REM sleep before and after stroke. Delta power, a measure of NREM sleep depth, was increased the day following stroke. At the same time, there was a significant shift in theta rhythms to a lower frequency during REM and wake periods. The awake EEG slowed after stroke over both hemispheres. The EEG of the ischemic hemisphere demonstrated diminished theta power specific to REM in excess of the slowing seen over the contralateral hemisphere. In contrast to rats exposed to sham surgery which had slightly increased total sleep, rats undergoing stroke experienced decreased total sleep. The decrease in total sleep after stroke was the result of dramatic reduction in the amount of REM sleep after ischemia. The suppression of REM after stroke was due to a decrease in the number of REM bouts; the length of the average REM bout did not change. We conclude that after stroke in this experimental model, REM sleep of rats is specifically and profoundly suppressed. Further experiments using this experimental model should be performed to investigate the mechanisms and consequences of REM suppression after stroke.     

Painful nocturnal erection

Sleep related painful erection is a parasomnia occurring during rapid eye movement (REM) sleep. It is rarely dealt with in the literature, and is very often poorly understood. Because of repeated awakenings, it is interpreted as insomnia, and is attributed to anxiety. EEG recordings associated with nocturnal penile tumescence monitoring indicate the existence of disturbed sleep organization, with awakenings during REM sleep and frequent nocturnal erections, often unrelated to REM sleep. Though the pathophysiological mechanisms involved are not yet understood, an interpretation of sleep-related painful erections is proposed, based on the current understanding and physiology of diurnal and nocturnal erections.     

Coherent neocortical 40‐Hz oscillations are not present during REM sleep

During cognitive processes there are extensive interactions between various regions of the cerebral cortex. Oscillations in the gamma frequency band (≈40 Hz) of the electroencephalogram (EEG) are involved in the binding of spatially separated but temporally correlated neural events, which results in a unified perceptual experience. The extent of these interactions can be examined by means of a mathematical algorithm called ‘coherence’, which reflects the ‘strength’ of functional interactions between cortical areas. The present study was conducted to analyse EEG coherence in the gamma frequency band of the cat during alert wakefulness (AW), quiet wakefulness (QW), non‐rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep. Cats were implanted with electrodes in the frontal, parietal and occipital cortices to monitor EEG activity. Coherence values within the gamma frequency (30–100 Hz) from pairs of EEG recordings were analysed. A large increase in coherence occurred between all cortical regions in the 30–45 Hz frequency band during AW compared with the other behavioral states. As the animal transitioned from AW to QW and from QW to NREM sleep, coherence decreased to a moderate level. Remarkably, there was practically no EEG coherence in the entire gamma band spectrum (30–100 Hz) during REM sleep. We conclude that functional interactions between cortical areas are radically different during sleep compared with wakefulness. The virtual absence of gamma frequency coherence during REM sleep may underlie the unique cognitive processing that occurs during dreams, which is principally a REM sleep‐related phenomenon.     

Nocturnal sleep in infants with congenital cerebral malformation

Sleep EEG patterns in 17 infants with cerebral malformations (4 months to 4 years of age) were studied throughout nocturnal sleep and the following results were obtained. Seven cases evidenced normal sleep/wakefulness EEG patterns that could be classified into 6 stages. Ten cases showed abnormal sleep EEG patterns as follows: absence of sleep spindles (n = 7) which included cases of absence of EEG patterns characteristic of wakefulness, NREM sleep and REM sleep (n = 5), no characteristic EEG patterns of stages 1-4 (n = 1) and stages W, 1, 2 and REM (n = 1) and the remaining cases with absence of spindles (n = 1), and spindles with an extremely low incidence (n = 2). Short sleep and long awaking times, and no delta rhythmicity during the night, were noted in 5 out of 17 subjects. A significant decrease of DQ was found in subjects with indistinguishable stages including stages W, 1, 2 and REM, as compared with those patients whose stages were all distinguishable.     

The first phase of nocturnal sleep in mentally retarded children

The first phase of sleep observed in 104 mentally retarded children (from 3 months to 8 years of age) was studied throughout nocturnal sleep, and the following results were obtained. In 4 out of 104 subjects, REM sleep onset was observed, and in the remaining 100 subjects NREM sleep onset was found at the first wakefulness-sleep transition of the night. Following awakenings (lasting 4 min or more) during the night, 170 (51.7%) out of a total of 329 samples were REM sleep onset, and 159 (48.3%) showed NREM sleep onset. The phases of sleep onset and those following awakenings evidenced no correlation between the frequency of NREM sleep onset and DQ or clinical EEG, whereas a positive correlation was found between the frequency of NREM sleep onset and age.     

Sleep Alterations After Acute Administration of Carbamazepine in Cats

Little is known about the effects of carbamazepine (CBZ) on sleep despite the relationship between sleep and epilepsy and the common clinical use of CBZ. As part of a larger study on sleep and interictal activity in kindled cats, we performed sleep recordings in 11 normal cats before and after acute administration of CBZ. Epidural screws (frontooccipital) and depth electrodes (amygdala and hippocampus) were implanted bilaterally for EEG recording. Supraorbital screws and neck intramuscular electrodes were inserted for EOG and EMG. Ten days after electrode implantation, recordings were made of animals for 2 consecutive nights to assess baseline sleep patterns. Before the third night, cats received a single oral dose of 100 mg CBZ. After washout, a second similar drug administration was given before the fourth night. Recordings were scored for wakefulness, stage I and II of NREM sleep, REM sleep, number of stage shifts, awakenings, and REM onsets. The administration of CBZ produced a significant decrease in duration and percentage of REM sleep (p less than 0.001) and an increase in stage I NREM (p less than 0.05). Total sleep time was increased (p less than 0.05); awakenings were shorter (p less than 0.01), and stage I episodes were longer (p less than 0.01).     

Sleep modulation of interictal spike configuration in untreated children with partial seizures

Spontaneous changes in interictal spike morphology were evaluated before initiation of antiepileptic drug (AED) therapy in 38 children with uncontrolled partial seizures. Nonrapid eye movement (NREM) sleep during the first third of the night was associated with spikes of higher amplitude, longer duration, and lower degree of sharpness than those observed in wakefulness or REM sleep. Spike amplitude decreased in subsequent NREM epochs, but duration and sharpness remained relatively consistent. A NREM/REM modulatory pattern was identified, with REM periods exhibiting spikes of decreased amplitude, shorter duration, and increased sharpness as compared with NREM periods in each third of the night. The spike changes associated with REM sleep are similar to the alterations previously described as occurring coincidentally with attainment of seizure control and thus may reflect inherent modulation of epileptogenicity in synchrony with sleep cycles.     

Alpha activity and cardiac correlates: three types of relationships during nocturnal sleep.

OBJECTIVE: We examined simultaneously alpha activity and cardiac changes during nocturnal sleep, in order to differentiate non-rapid eye movement (NREM) sleep, REM sleep, and intra-sleep awakening. METHODS: Ten male subjects displaying occasionally spontaneous intra-sleep awakenings underwent EEG and cardiac recordings during one experimental night. The heart rate and heart rate variability were calculated over 5 min periods. Heart rate variability was estimated: (1) by the ratio of low frequency (LF) to high frequency (HF) power calculated from spectral analysis of R-R intervals; and (2) by the interbeat autocorrelation coefficient of R-R intervals (rRR). EEG spectral analysis was performed using a fast Fourier transform algorithm. RESULTS: Three types of relationships between alpha waves (8-13 Hz) and cardiac correlates could be distinguished. During NREM sleep, alpha activity and cardiac correlates showed opposite variations, with high levels of alpha power associated with decreased heart rate, rRR and LF/HF ratio, indicating low sympathetic activity. Conversely, during REM sleep, alpha activity was low whereas heart rate, rRR, and the LF/HF ratio peaked, indicating high sympathetic activity. During intra-sleep awakenings, alpha activity and cardiac correlates both increased. No difference in time-course between alpha 1 (8-10 Hz) and alpha 2 (10-13 Hz) activity could be shown. Alpha waves occurred in fronto-central areas during slow wave sleep (SWS), migrated to posterior areas during REM sleep, and were localized in occipital areas during intra-sleep awakenings. CONCLUSIONS: These results suggest that alpha waves are not simply a sign of arousal, as is commonly thought. Fronto-central alpha waves, associated with decreased heart rate, possibly reflect sleep-maintaining processes.     

Electrical activity of the human amygdala during all-night sleep and wakefulness

Objective

The aim of the present work was to characterize the dynamics of the human amygdala across the different sleep stages and during wakefulness.

Sleep alterations in juvenile neuronal ceroid-lipofuscinosis

In juvenile neuronal ceroid-lipofuscinosis (JNCL), sleep disorders are common. The purpose of this study was to investigate the sleep structure of 28 patients with JNCL compared with healthy controls subjects and to clarify the pathophysiology underlying the sleep disturbances in these patients. Each of 28 patients with JNCL (age range = 6-27 years), with or without sleep complaints, underwent one night of polysomnography. Electroencephalographic, electro-oculographic, electromyographic, and electrocardiographic findings were recorded. Sleep was scored and analyzed visually. The sleep parameters of the patients were compared with those of healthy control subjects. In most of the patients, the total sleep time, sleep efficiency, and percentages of rapid eye movement (REM) and non-REM (NREM) stage 2 sleep were significantly decreased, and the percentages of NREM stage 1 and slow-wave sleep and the number of nocturnal awakenings significantly increased. The percentage of NREM stage 1 and the number of awakenings increased with age and clinical stage. Paroxysmal epileptiform activity during light sleep (NREM stages 1-2) and high-amplitude delta-wave activity with intermingled sharp waves during slow-wave sleep were characteristic of the recordings. The present study revealed that in patients with JNCL, sleep is consistently altered.     

Nocturnal complex partial seizures precipitated by REM sleep. A case report

A 16-year-old patient presenting with complex partial seizures occurring in the transition from a REM period to wakefulness is described. His baseline EEG showed generalized and symmetrical slow spike and wave complexes, on a normal background activity, activated by NREM sleep. Polygraphic and videotape recordings, carried out for several nights, showed that after nearly each REM period, he would wake up briefly, presenting eye blinking followed by a burst of generalized hypersynchronous theta to start his seizures. These were characterized by moaning and autoaggressive behaviour, the ictal EEG showing generalized slow spike and wave complexes in the midst of several movement artifacts. At the end of each fit he fell back to REM sleep. Carbamazepine treatment completely resolved his symptoms, with full normalization of EEG activity.     

Electroencephalographic correlates of cataplectic attacks in narcoleptic canines

Cataplectic attacks were monitored behaviorally and polygraphically in 4 narcoleptic dogs, of which three inherited the disorder. The recorded EEG signals were evaluated by power spectral analysis. We found 3 distinct stages of cataplexy: an initial stage which resembled wakefulness with tonic suppression of EMG activity, a later stage which was highly similar to REM sleep, and a final transitional stage to wakefulness or NREM sleep. The first stage of cataplexy was characterized by full postural collapse, a waking-like EEG spectrum, visual tracking, and a hypotonic EMG. The second stage of cataplexy differed electrographically from the previous stage by the onset of hypersynchronous hippocampal theta activity, a REM-like EEG spectrum, larger amplitude EEG signals, and a higher peak theta frequency. Glazed eyes, sporadic rapid eye movements and muscle twitches were also present. The final stage of cataplexy was characterized by mixed amplitude, mixed frequency EEG activity, and by the absence of rapid eye movements, visual tracking, directed movements, and muscle twitches. The EEG spectra of two other narcoleptic phenomena, sleep-onset REM periods and NREM sleep onsets from cataplexy, were nearly identical to the spectra of the normally occurring REM and NREM sleep periods.     

Benign EEG variants in the sleep–wake cycle: A prospective observational study using the 10–20 system and additional electrodes

ObjectivesTo study the prevalence of benign EEG variants (BEVs) in the sleep–wake cycle among 1163 consecutive patients.MethodsProspective, observational EEG study using the 10–20 system with systematically two additional anterior-temporal electrodes. Depending on clinical indications, other electrodes were added. REM sleep identification was based on its characteristic EEG grapho-elements and rapid eye movements, clearly detectable with the additional anterior-temporal and fronto-polar electrodes due to eye proximity. The video-EEG monitoring duration was between 24 hours and eight days.ResultsWe identified 710 patients (61%) with BEVs. Positive occipital sharp transients of sleep (POSTs) were observed in 36.4% of participants, mu rhythm in 22.4%, lambda waves in 16.7%, wicket spikes (WS) in 15%, 14- and 6-Hz positive bursts in 8.3%, benign sporadic sleep spikes (BSSS) in 3.3%, rhythmic mid-temporal theta burst of drowsiness (RMTD) in 2.15%, midline theta rhythm in 2.1% and six-Hz spike and wave (SW) bursts in 0.1%. WS and RMTD were present during wakefulness, NREM (14.1%, 1.3%, respectively) and REM sleep (3.3%, 1.1%, respectively). Mu rhythm was also observed during NREM (1.5%) and REM sleep (7.7%). Fourteen- and 6-Hz positive bursts were present during NREM (4.5%) and REM sleep (6.5%). BSSS and six-Hz SW bursts were only observed during NREM sleep.ConclusionsThe prevalence of BEVs is much higher than current estimates. POSTs and WS can no longer be considered as unusual patterns but physiological patterns of NREM sleep. RMTD and mu rhythm may be observed during NREM and REM sleep.     

Sleep-induced changes in associative memory

The notion that dreaming might alter the strength of associative links in memory was first proposed almost 200 years ago. But no strong evidence of such altered associative links has been obtained. Semantic priming can be used to quantify the strength of associative links between pairs of words; it is thought to measure the automatic spread of activation from a "node" representing one word to nodes representing semantically related words. Semantic priming could thus be used to test for global alterations in the strengths of associative links across the wake-sleep cycle. Awakenings from REM and nonREM (NREM) sleep produce a period of state carry-over during which performance is altered as a result of the brain's slow transition to full wakefulness, and cognitive testing in this period can provide information about the functioning of the brain during the prior sleep period. When subjects were tested across the night--before and after a night's sleep as well as immediately following forced awakenings from REM and NREM sleep--weak priming (e. g., thief-wrong) was found to be state dependent (p = 0.016), whereas strong priming (e.g., hot-cold) was not (p = 0.89). Weak primes were most effective in the presleep and REM sleep conditions and least effective in NREM and postsleep conditions. Most striking are analyses comparing weak and strong priming within each wake-sleep state. Contrary to the normal pattern of priming, subjects awakened from REM sleep showed greater priming by weak primes than by strong primes (p = 0.01). This result was seen in each of three protocols. In contrast, strong priming exceeded weak priming in NREM sleep. The shift in weak priming seen after REM sleep awakenings suggests that cognition during REM sleep is qualitatively different from that of waking and NREM sleep and may reflect a shift in associative memory systems, a shift that we hypothesize underlies the bizarre and hyperassociative character of REM-sleep dreaming. Known changes in brainstem activity that control the transition into and maintenance of REM sleep provide a possible explanation of this shift.     

Sympathetic and cardiovascular changes during sleep in narcolepsy with cataplexy patients

ObjectiveNeural mechanisms underlying sleep-onset rapid eye movement (REM) periods (SOREMPs) in narcolepsy and the role of hypocretin in driving sympathetic changes during sleep are misunderstood. We aimed to characterize autonomic changes during sleep in narcolepsy with cataplexy (NC) patients to clarify the nature of SOREMP events and the effect of hypocretin deficiency on sympathetic activity during sleep.MethodsWe observed 13 hypocretin-deficient NC patients and five healthy controls who underwent nocturnal video-polysomnography (v-PSG) with blood pressure (BP) recording, heart rate (HR), skin sympathetic activity (SSA), and muscle sympathetic nerve activity (MSNA) from the peroneal nerve by microneurography.ResultsCompared to wake, control participants displayed a progressive significant decrease of BP and sympathetic activities during nonrapid eye movement (NREM) sleep and an increase of autonomic activity during REM sleep, as expected. NC patients showed: (1) a decrease of sympathetic activities during SOREMP comparable to NREM sleep stage 1 (N1) but in contrast to the increased activity typical of REM sleep; and (2) physiologic sympathetic change during the following sleep stages with a progressive decrease during NREM sleep stage 2 (N2) and NREM sleep stage 3 (N3) and a clear increase in REM sleep, though BP did not show the physiologic decrease during sleep (nondipper pattern).ConclusionsSOREMPs in NC patients lack the sympathetic activation occurring during physiologic REM sleep, thus suggesting a dissociated REM sleep condition. In addition, our data indicated that hypocretin plays a limited role in the regulation of sympathetic changes during sleep.     

24 hour polysomnographic evaluation in a patient with sleeping sickness

A 24 h polysomnographic recording was performed in a patient with sleeping sickness presenting an atypical neurological syndrome. Trypanosoma gambiense was found in a lymph gland puncture and the CSF, and a serologic immunofluorescence test was positive. The scoring technique of the polygraphic traces had to be adapted because of the presence of a permanent EEG delta wave activity during the NREM sleep stages, and the method used by Schwartz and Escande (1970) was applied. REM sleep and wakefulness presented normal polygraphic characteristics. The patient had 8 sleep episodes throughout the recording period, occurring during the daytime and at night, forming the classical diurnal sleepiness and nocturnal restlessness of sleeping sickness. All but one episode represented 1-3 complete REM-NREM sleep cycles. On all occasions, REM latency was short and 2 SOREM episodes were observed. The nychthemeral organization of the stages of vigilance differed from one state to another. Wakefulness and REM sleep had a circadian rhythmicity, while NREM sleep, total sleep time and deep sleep (corresponding to stages 3 and 4) had an ultradian periodicity. The concordance between the higher pressure for wakefulness and lower pressure for sleep around 20.00 h defined the time of occurrence of a 'forbidden zone' for sleep.