Respiratory arousals in mild obstructive sleep apnea syndrome.

The objective of the study is to identify patients with mild sleep apnea by counting not only apneas and hypopneas, but also mild respiratory events, which do not fulfill apnea or hypopnea criteria, but result in an arousal (Type-R arousal). Arousals related to body movements (Type-M arousal) were separately counted. The influence of nasal continuous positive airway pressure (nCPAP) on respiratory and movement arousals was analyzed. Daytime sleepiness before and after nCPAP and its relationship to arousal types was investigated using the Multiple Sleep Latency Test (MSLT) and a standardised questionnaire. Twenty-two patients with a mean age of 43.6 +/- 9.2 years underwent polysomnographic evaluation on a baseline night, and during three nights with nCPAP. On the baseline night, subjects presented with a mean RDI of 10.5 +/- 7.2/h, an apnea index (AI) of 1.2 +/- 1.5/h, a hypopnea index (HI) of 9.3 +/- 6.6/h, a R index of 5.2 +/- 5.9/h, and a M index of 9.7 +/- 5.6/h. Use of nCPAP lowered the RDI (p < 0.001) and the R index (p < 0.01). Mean sleep latency in the MSLT increased with nCPAP (p < 0.05) and the patient's subjective well being improved (p < 0.01). Correlation analysis revealed a relationship between Type-R arousals and RDI and HI (r = 0.5, p < 0.01) as well as between questionnaire scores and mean sleep latency. The decrease of Type-R indicates the positive effect of nCPAP. Arousal analysis and detection of mild respiratory events associated with arousals are helpful in investigating the sleep structure and in objectifying clinical symptoms and treatment success in patients with mild OSAS.     

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.     

Changes in dreaming induced by CPAP in severe obstructive sleep apnea syndrome patients

To study dream content in patients with severe obstructive sleep apnea syndrome (OSAS) and its modification with Continuous Positive Airway Pressure (CPAP) therapy. We assessed twenty consecutive patients with severe OSAS and 17 healthy controls. Polysomnograms were recorded at baseline in patients and controls and during the CPAP titration night, 3 months after effective treatment and 2 years later in patients. Subjects were awakened 5-10 min after the beginning of the first and last rapid eye movement (REM) sleep periods and we measured percentage of dream recall, emotional content of the dream, word count, thematic units, sleep architecture and REM density. Dream recall in REM sleep was similar in patients at baseline and controls (51.5% versus 44.4% respectively; P = .421), decreased to 20% and 24.3% the first and third month CPAP nights, and increased to 39% 2 years later (P = 0.004). Violent/highly anxious dreams were only seen in patients at baseline. Word count was higher in patients than in controls. REM density was highest the first CPAP night. Severe OSAS patients recall dreams in REM sleep as often as controls, but their dreams have an increased emotional tone and are longer. Despite an increase in REM density, dream recall decreased the first months of CPAP and recovered 2 years later. Violent/highly anxious dreams disappeared with treatment. A dream recall decrease with CPAP is associated with normalization of sleep in OSAS patients.     

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.     

Thinking and hallucinating: reciprocal changes in sleep

Internal deliberations (focused thoughts) and endogenous percepts (hallucinations) vary in a reciprocal manner across the states of waking and sleep, paralleling changes in regional brain activation. As subjects go from waking through sleep onset to NREM sleep and then to REM sleep, they report progressively more hallucinoid imagery and progressively less thinking. We have investigated whether this reciprocity in cognition between NREM and REM is maintained throughout the night. To do so, we analyzed 229 REM and 165 NREM reports collected with the Nightcap sleep monitoring system from 16 participants in their homes over 14 nights. The reports were scored for the presence of hallucinations and directed thinking by external judges. As predicted, hallucinations were more frequent in REM than in NREM for each segment of the night, and directed thinking was more frequent in NREM in the first 5 h of the night. Late in the night, directed thinking was equally infrequent in NREM and REM. At the same time, hallucinations increased within both NREM and REM as the night progressed, whereas directed thinking decreased in NREM and remained at a stable, low level in REM. These findings suggest that a reciprocal shift in focused thinking and hallucinating is a general property of cognitive activity across the wake-sleep cycle. Biological evidence supports the hypothesis that these cognitive changes are governed by specific state regulatory and neurocognitive processes at several levels of the brain.     

Slow wave activity and slow oscillations in sleepwalkers and controls: effects of 38 h of sleep deprivation

Sleepwalkers have been shown to have an unusually high number of arousals from slow wave sleep and lower slow wave activity (SWA) power during the night than controls. Because sleep deprivation increases the frequency of slow wave sleep (SWS) arousals in sleepwalkers, it may also affect the expression of the homeostatic process to a greater extent than shown previously. We thus investigated SWA power as well as slow wave oscillation (SWO) density in 10 sleepwalkers and nine controls at baseline and following 38 h of sleep deprivation. There was a significant increase in SWA during participants' recovery sleep, especially during their second non‐rapid eye movement (NREM) period. SWO density was similarly increased during recovery sleep's first two NREM periods. A fronto‐central gradient in SWA and SWO was also present on both nights. However, no group differences were noted on any of the 2 nights on SWA or SWO. This unexpected result may be related to the heterogeneity of sleepwalkers as a population, as well as our small sample size. SWA pressure after extended sleep deprivation may also result in a ceiling effect in both sleepwalkers and controls.     

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.     

Periodic leg movements in patients with obstructive sleep apnea syndrome during nCPAP therapy

Summary Excessive daytime sleepiness and concentration deficits are complained by patients with obstructive sleep apnea syndrome (OSAS) as well as by patients with periodic leg movements (PLM). PLM observed during nCPAP (nasal continuous airways pressure) therapy may therefore cause persistent complaints of diurnal symptoms despite sufficient treatment. 65 OSAS-patients (58 men, 7 women, aged 55.6 ± 8.0 years) were investigated before starting and after the first two nights of nCPAP therapy. Apnea/Hypopnea index decreased in all patients (28.8 ± 18.4/h to 11.5 ± 13.0/h, p ≤ 0.01). 26 patients had an initial PLM index > 5/­h which decreased during treatment (14.6 ± 6.4/h to 10.7 ± 7.8/h) with significant increase of sleep stages 3 and 4. In 22 patients with PLM index < 5/h index increased during therapy (2.7 ± 1.2 to 5.6 ± 7.7/h, p ≤ 0.01). 17 patients developed PLM for the first time during nCPAP-therapy (10.9 ± 3.2 PLM/h). Optimizing of nCPAP therapy did not change PLM frequency. Though the pathogenesis and daytime consequences of PLM in OSAS are not fully proved yet our study may entail different therapeutic approaches. In patients with a decrease of PLM during CPAP-therapy movements seemed at least partially induced by OSAS and CPAP may be the sufficient treatment. In the majority of our cases PLM was demasked during nCPAP therapy thus indicating an independent coexistence of periodic limb movement disorder and OSAS. These patients may profit from a treatment similar to the one in restless legs syndrome when daytime symptoms persist during CPAP therapy.     

Sleep disturbance at simulated altitude indicated by stratified respiratory disturbance index but not hypoxic ventilatory response

At high altitudes, the clinically defined respiratory disturbance index (RDI) and high hypoxic ventilatory response (HVR) have been associated with diminished sleep quality. Increased RDI has also been observed in some athletes sleeping at simulated moderate altitude. In this study, we investigated relationships between the HVR of 14 trained male endurance cyclists with variable RDI and sleep quality responses to simulated moderate altitude. Blood oxygen saturation (SpO₂%), heart rate, RDI, arousal rate, awakenings, sleep efficiency, rapid eye movement (REM) sleep, non-REM sleep stages 1, 2 and slow wave sleep as percentages of total sleep time (%TST) were measured for two nights at normoxia of 600 m and one night at a simulated altitude of 2,650 m. HVR and RDI were not significantly correlated with sleep stage, arousal rate or awakening response to nocturnal simulated altitude. SpO₂ was inversely correlated with total RDI (r=–0.69, P=0.004) at simulated altitude and with the change in arousal rate from normoxia (r=–0.65, P=0.02). REM sleep response to simulated altitude correlated with the change, relative to normoxia, in arousal (r=–0.63, P=0.04) and heart rate (r=–0.61, P=0.04). When stratified, those athletes at altitude with RDI >20 h^–1 (n=4) and those with <10 h^–1 (n=10) exhibited no difference in HVR but the former had larger falls in SpO₂ (P=0.05) and more arousals (P=0.03). Neither RDI (without stratification) nor HVR were sufficiently sensitive to explain any deterioration in REM sleep or arousal increase. However, the stratified RDI provides a basis for determining potential sleep disturbance in athletes at simulated moderate altitude.     

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.     

Automatic CPAP based on impedance-comparison of constant CPAP with an individual pressure range

Summary Introduction   Self-adjusting positive airways pressure treatment based on the impedance of the airways (APAP_FOT) has proven effective in obstructive sleep apnoea syndrome. To avoid patient discomfort during periods of high treatment pressure we lowered the upper pressure limit with APAP_FOT and investigated whether this provided equally as effective treatment as constant CPAP. Methods   37 patients (33 males, 57.9 ± 9.9 years, BMI 32.5 ± 3.8 kg/m²) underwent after diagnostic polysomnography and manual nCPAP titration two treatment nights in randomized order, one with constant nCPAP (mode 1), one with APAP_FOT (mode 2). Under APAP_FOT treatment pressure varied between 4 hPa (set lower limit for all patients) and 13.3 ± 1.4 hPa (individually variable upper pressure limit). Results   AHI was reduced from 32.8 ± 18.1/h to 4.6 ± 4.9/h (mode 1, p < 0.01) and to 5.0 ± 4.1/h (mode 2, p < 0.01). Rapid eye movement sleep (REM) and respiratory arousals improved significantly with both modes. With APAP_FOT, the mean pressure was 5.7 ± 1.7 hPa as compared to 8.3 ± 1.4 hPa with constant nCPAP (p < 0.01). Conclusions   APAP_FOT with a reduced upper pressure is as effective as constant nCPAP for OSAS. With APAP_FOT the mean pressure is substantially reduced.     

Effects of sleep on endotoxin-induced host responses in healthy men

OBJECTIVE: To examine whether increased sleep during viral or bacterial infections supports host defense mechanisms. METHODS: To test this assumption in humans, healthy male subjects were assigned either to sleep from 2300 to 0700 hours (n = 10) or to stay awake through the night (n = 10). In the sleeping subjects Salmonella abortus equi endotoxin (0.4 ng/kg) or placebo were intravenously injected in balanced order during the first SWS episode. The age-matched, sleep-deprived subjects were injected at the same time point. RESULTS: As expected, endotoxin significantly increased rectal temperature, the plasma levels of cortisol, tumor necrosis factor-alpha (TNF-alpha), the soluble TNF receptors p55 and p75, Interleukin (IL)-6, the IL-1 receptor antagonist (RA), leukocyte, and granulocyte counts in both sleeping and sleep-deprived subjects, whereas lymphocyte and monocyte counts were transiently reduced. Time courses of endotoxin-induced host responses did not differ between the sleep and sleep deprivation groups. Endotoxin did not affect the amount of nocturnal wakefulness, nonrapid-eye-movement (NREM) sleep, or rapid-eye-movement (REM) sleep across the total night compared with placebo, but significantly increased electroencephalogram-arousals (EEG-arousals) in stage 2 and decreased arousals in SWS. In addition, the amount of SWS, spectral EEG-delta and -theta power was increased at the beginning and at the end of the sleep period, respectively, when the degree of immune activation was relatively low. CONCLUSION: The present results support the notion that short-term sleep deprivation is unlikely to harm the immune system as far as unspecific acute responses are concerned. The effects of endotoxin on sleep in this case support prior observations that in humans, enhanced SWS and intensified NREM sleep occur when host defense activation is subtle.     

Effects of sleep fragmentation on the arousability to resistive loading in NREM and REM sleep in normal men

STUDY OBJECTIVE: In healthy subjects, arousability to inspiratory resistive loading is greater during rapid eye movement (REM) sleep compared with non-REM (NREM) sleep but is poorest in REM sleep in patients with sleep apnea. We therefore examined the hypothesis that sleep fragmentation impairs arousability, especially from REM sleep. DESIGN: Two blocks of 3 polysomnographies (separated by at least 1 week) were performed randomly. An inspiratory-loaded night followed either 2 undisturbed control nights (LN(C)) or 2 acoustically fragmented nights (LN(F)) SETTING: Sleep laboratory. PARTICIPANTS: Sixteen healthy men aged 20 to 29 years. INTERVENTIONS: In both loaded nights, an inspiratory resistive load was added via a valved facemask every 2 minutes during sleep and turned off either when arousal occurred or after 2 minutes. MEASUREMENTS AND RESULTS: During LN(F), arousability remained significantly greater in REM sleep (71% aroused within 2 minutes) compared with stage 2 (29%) or stage 3/4 (16%) sleep. After sleep fragmentation, arousability was decreased in stage 2 sleep (LN(F): 29%; LN(C): 38%; p < .05) and low in early REM sleep, increasing across the night (p < .01). In stage 3/4 sleep, neither an attenuation nor a change across the night was seen after sleep fragmentation. CONCLUSIONS: Mild sleep fragmentation is already sufficient to attenuate arousability in stage 2 sleep and to decrease arousability in early, compared with late, REM sleep. This means that sleep fragmentation affects the arousal response to increasing resistance and that the effects are different in stage 2 and REM sleep. The biologic reason for this increase in the arousal response in REM sleep across the night is not clear.     

Proton magnetic resonance spectroscopy study of brain metabolism in obstructive sleep apnoea syndrome before and after continuous positive airway pressure treatment

STUDY OBJECTIVES: Obstructive sleep apnoea syndrome (OSAS) causes sleep related oxygen desaturation, excessive daytime sleepiness (EDS), and cognitive impairment. The role of hypoxic brain damage, sleep fragmentation, and the associated comorbidities (hypertension, vascular disorders) in the pathogenesis of cognitive deficits remains controversial. The aim of this study was to evaluate the cerebral metabolism of OSAS patients in vivo before and after CPAP treatment. DESIGN AND PATIENTS: Fourteen OSAS patients without cardiovascular or cerebrovascular impairment underwent the same protocol before and after 6 months of CPAP including: overnight videopolysomnography (VPSG), Multiple Sleep Latency Test (MSLT), and within the next 2 days neuropsychological and 1H-MRS evaluations. Single voxel 1H-MRS was performed in the parietal-occipital cortex, and absolute concentrations of N-acetyl-aspartate (NAA), creatine, and choline were measured, acquiring spectra at multiple echo-times and using water as internal standard. Ten matched controls were also studied. RESULTS: OSAS patients had a mean RDI of 58/hr, a mean arousal index of 57/hr, and a mean nadir SpO2 of 71%. Before CPAP, all patients showed a normal global cognitive functioning, with only a small number of pathological tasks in working memory and attention tests in a minority of patients. CPAP therapy was effective in resolving sleep apnoea and normalizing sleep structure, and improving EDS and neuropsychological alterations. Before CPAP treatment cortical [NAA] in OSAS (11.86 mM +/- 0.80, mean +/- SD) was significantly lower than in controls (12.85 +/- 0.93; P = 0.01) and positively correlated with minimum SpO2 during sleep (r = 0.69; P = 0.006) and MSLT scores (r = 0.62; P = 0.01). Cortical [NAA] reduction persisted after therapy (11.94 +/- 1.33; P = 0.87 versus pre-CPAP). CONCLUSIONS: OSAS patients have cortical metabolic changes consistent with neuronal loss even in the absence of vascular comorbidities. Metabolic changes persisted after CPAP in the absence of EDS, nocturnal arousals, and major cognitive deficits, likely related to hypoxic damage prior to CPAP treatment.     

Benefit of nasal CPAP in obstructive sleep apnea is due to positive pharyngeal pressure

The purpose of this study was to determine if the mechanism of nasal continuous positive airway pressure's (CPAP's) effectiveness is to act as a pneumatic splint or to increase functional residual capacity (FRC) and consequently, upper airway caliber. Four subjects with obstructive sleep apnea underwent 3 nights of polysomnography: night 1, control; night 2, nasal CPAP; night 3, external subatmospheric pressure (ESAP). ESAP, a negative pressure body suit, increases FRC. We measured the changes in FRC with nasal CPAP and ESAP using the weighted spirometer technique. The dose used for the ESAP night was the dose that produced the same FRC as the subject's prescribed nasal CPAP dose. The mean number of arousals and the respiratory events index were higher on ESAP and control nights. Less severe oxygen desaturation occurred during non-rapid-eye-movement sleep on the nasal CPAP and ESAP nights. These preliminary results show that increasing FRC alone does not account for the effectiveness of nasal CPAP, and splinting of the collapsible upper airway is necessary.     

The effects of total sleep deprivation, selective sleep interruption and sleep recovery on pain tolerance thresholds in healthy subjects

The aim of this study was to compare the effects of total sleep deprivation (TSD), rapid eye movement (REM) sleep and slow wave sleep (SWS) interruption and sleep recovery on mechanical and thermal pain sensitivity in healthy adults. Nine healthy male volunteers (age 26--43 years) were randomly assigned in this double blind and crossover study to undergo either REM sleep or SWS interruption. Periods of 6 consecutive laboratory nights separated by at least 2 weeks were designed as follows: N1 Adaptation night; N2 Baseline night; N3 Total sleep deprivation (40 h); N4 and N5 SWS or REM sleep interruption; N6 Recovery. Sleep was recorded and scored using standard methods. Tolerance thresholds to mechanical and thermal pain were assessed using an electronic pressure dolorimeter and a thermode operating on a Peltier principle. Relative to baseline levels, TSD decreased significantly mechanical pain thresholds (-8%). Both REM sleep and SWS interruption tended to decrease mechanical pain thresholds. Recovery sleep, after SWS interruption produced a significant increase in mechanical pain thresholds (+ 15%). Recovery sleep after REM sleep interruption did not significantly increase mechanical pain thresholds. No significant differences in thermal pain thresholds were detected between and within periods. In conclusion this experimental study in healthy adult volunteers has demonstrated an hyperalgesic effect related to 40 h TSD and an analgesic effect related to SWS recovery. The analgesic effect of SWS recovery is apparently greater than the analgesia induced by level I (World Health Organization) analgesic compounds in mechanical pain experiments in healthy volunteers.     

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.     

Modafinil, d-amphetamine and placebo during 64 hours of sustained mental work. II. Effects on two nights of recovery sleep

Polysomnograms were obtained from 37 volunteers, before (baseline) and after (two consecutive recovery nights) a 64-h sleep deprivation, with (d-amphetamine or modafinil) or without (placebo) alerting substances. The drugs were administered at 23.00 hours during the first sleep deprivation night (after 17.5 h of wakefulness), to determine whether decrements in cognitive performance would be prevented; at 05.30 hours during the second night of sleep deprivation (after 47.5 h of wakefulness), to see whether performance would be restored; and at 15.30 hours during the third day of continuous work, to study effects on recovery sleep. The second recovery night served to verify whether drug-induced sleep disturbances on the first recovery night would carry over to a second night of sleep. Recovery sleep for the placebo group was as expected: the debt in slow-wave sleep (SWS) and REM sleep was paid back during the first recovery night, the rebound in SWS occurring mainly during the first half of the night, and that of REM sleep being distributed evenly across REM sleep episodes. Recovery sleep for the amphetamine group was also consistent with previously published work: increased sleep latency and intrasleep wakefulness, decreased total sleep time and sleep efficiency, alterations in stage shifts, Stage 1, Stage 2 and SWS, and decreased REM sleep with a longer REM sleep latency. For this group, REM sleep rebound was observed only during the second recovery night. Results for the modafinil group exhibited decreased time in bed and sleep period time, suggesting a reduced requirement for recovery sleep than for the other two groups. This group showed fewer disturbances during the first recovery night than the amphetamine group. In particular, there was no REM sleep deficit, with longer REM sleep episodes and a shorter REM latency, and the REM sleep rebound was limited to the first REM sleep episode. The difference with the amphetamine group was also marked by less NREM sleep and Stage 2 and more SWS episodes. No REM sleep rebound occurred during the second recovery night, which barely differed from placebo. Hence, modafinil allowed for sleep to occur, displayed sleep patterns close to that of the placebo group, and decreased the need for a long recovery sleep usually taken to compensate for the lost sleep due to total sleep deprivation.     

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.