Severity of obstructive sleep apnoea/hypopnoea syndrome and subsequent waking EEG spectral power.

It is well known that most patients with obstructive sleep apnoea/hypopnoea syndrome (OSAHS) suffer sleepiness, although the underlying mechanisms of this relationship remain unclear. The present study examined the relationship between nocturnal variables and the subsequent waking electroencephalogram (EEG), in order to determine if sleepiness was related to OSAHS severity and due to sleep fragmentation or to nocturnal hypoxaemia. In total, 12 moderate-to-severe OSAHS patients underwent a total sleep night followed by a 24-h period of sustained wakefulness where the waking EEG was measured every hour. The results showed that alpha (7.9-12.6 Hz) and beta (12.7-29.2 Hz) activities were strongly related to OSAHS severity, mainly reflected by the apnoea index. Moreover, spectral power in most of the waking EEG components was significantly correlated with nocturnal hypoxaemia indices, namely alpha and beta activity when hypoxaemia becomes severe. However, no correlation was found between the waking EEG and sleep fragmentation parameters. In conclusion, the present results suggest that the difficulty in maintaining an optimal level of alertness, reflected by a higher activity in awake alpha and beta bands (7.9-29.2 Hz) in obstructive sleep apnoea/hypopnoea syndrome, was better explained by: 1) the apnoea as opposed to the hypopnoea index; and 2) nocturnal hypoxaemia as opposed to sleep fragmentation.

EEG spectral power and sleepiness during 24 h of sustained wakefulness in patients with obstructive sleep apnea syndrome.

OBJECTIVE: This study investigated if obstructive sleep apnea syndrome (OSAS) may be associated with higher activity in different frequency bands of the EEG during a sustained wakefulness paradigm. METHODS: Twelve OSA patients and 8 healthy controls were studied with the Karolinska Drowsiness Test (KDT) and subjective ratings of sleepiness (VAS and KSS) conducted every hour during 24 h of sustained wakefulness. RESULTS: The waking EEG activity, mainly in the low (0.5-7.8 Hz) and fast (12.7-29.2 Hz) frequency band, increased as time awake progressed in both groups but more obviously in OSA patients. A similar pattern was observed for rated sleepiness in both groups. Moreover, VAS ratings of alertness were closely related to the awake theta, fast alpha and beta bands in controls but not in OSA patients. CONCLUSIONS: OSAS was associated with a wake-dependent increase in low (0.5-7.8 Hz) and fast (12.7-29.2 Hz) frequency range activity. Variations in behavioural sleepiness measured by VAS ratings closely reflect most of the waking EEG parameters in controls but not in OSA patients. SIGNIFICANCE: In a sustained wakefulness paradigm, higher activity in delta, theta and beta bands associated with OSAS indicates that OSA patients show marked signs of higher sleepiness and stronger efforts than controls to stay awake, even though they tend to underestimate their sleepiness.

Are OSAS patients impaired in their driving ability on a circuit with medium traffic density?

OBJECTIVES: Many studies have demonstrated that patients with Obstructive Sleep Apnea Syndrome (OSAS), a very common sleep-related breathing disorder, are usually impaired in their driving ability because of decreased sleep quality. However, most of the simulation procedures in laboratories are designed to create monotonic conditions with low traffic density, if any, thereby leading to a dramatic decrease in performance in OSAS patients because of the lack of stimulation. The aim of this study was therefore to evaluate driving abilities in OSAS patients involved in a driving simulation task with medium traffic density, in order to replicate as far as possible real world conditions. The behavioral and physiological attributes likely to predict driving performance in these patients were also investigated. METHODS: After a normal night of sleep, 12 OSAS patients and 8 healthy controls performed 6 driving sessions during a 24-h period of sustained wakefulness. Driving performances (speed, lateral position, distances...) were measured and correlated to sleep parameters and to a waking EEG recorded during the task. RESULTS: Compared to controls, patients showed difficulties in speed adjustment. However, they maintained longer inter-vehicle distances, including during overtaking. Their waking EEG, while driving, showed increased spectral power in theta (3.9-7.8Hz) but also in beta (12.7-29.2Hz) activity, alpha power (7.9-12.6Hz) being increased in both groups due to sustained wakefulness. Poor sleep indices were correlated to increased theta and beta activities, as well as to more cautious behavior. DISCUSSION: In medium traffic density conditions, driving performance in OSAS patients remained at near normal levels, but with more cautious behavior than controls. This could be the result of a bigger effort to stay awake, as suggested by an increased beta activity in these patients.

Oculomotor changes due to road events during prolonged monotonous simulated driving.

The possible influence of occuring external events on driver attention and vigilance level was assessed during a prolonged simulated driving task. Special attention was given to the duration of the task, as well as to the influence of time of day and of individual factors. Thirty six subjects drove for two hours. Blinking activity and eye movements associated with glances to the speedometer were recorded during the entire driving task and particularly during specific road events. During significant events, blinking and ocular activity decreased, attesting a higher attention of the driver. With increased duration of driving, the reduction in blinking and ocular activity was progressively smaller for the less significant events, indicating a reduction in attention. During driving, women blinked more frequently than men. With increased duration of driving, drivers adopted different behavioural strategies depending on their age and sex to reach a safe and adapted method of driving.

Defining the states of consciousness.

Consciousness remains an elusive concept due to the difficulty to define what has been regarded for many years as a subjective experience, therefore irrelevant for scientific study. Recent development in this field of research has allowed to provide some new insight to a possible way to define consciousness. Going through the extensive literature in this domain, several perspectives are proposed to define this concept. (1) Consciousness and Attention may not reflect the same process. (2) Consciousness during wake and sleep may not involve the same mechanisms. (3) Besides physiological states of consciousness, human beings can experience modified states of consciousness either by self-training (transcendental meditation, hypnosis, etc.) or by drug intake (hallucinogens, anaesthetics, etc.). Altogether, we address the question of a more precise terminology, given the theoretical weight words can convey. To this respect, we propose different definitions for concepts like consciousness, vigilance, arousal and alertness as candidates to separate functional entities.

Interactions between spontaneous and provoked cortisol secretory episodes in man.

This study describes the interactions between cortisol peaks due to spontaneous episodic release and peaks provoked by external stimuli. Successive and equidistant transitory rises of similar amplitude and duration were produced either by muscular exercise (30 min, 75% VO2max) or by injecting ACTH1-24 (Synacthen: 250 ng) before and after the midday meal-related peak. ACTH1-24 was also injected during sleep before the nocturnal sequence of the major secretory episodes. In all instances, cortisol levels had reverted to basal levels when the second stimulus was applied. ACTH-induced cortisol peaks depressed the subsequent meal-related peaks, the exercise-induced peaks, and the spontaneous secretory episodes at the end of the night, and thus had a strong depressor capacity. When exercise was the prior stimulus, the subsequent meal-related peaks were depressed, but the response to later exercise was not affected. Meal-related peaks and the spontaneous diurnal or nocturnal peaks did not depress the subsequent secretory episodes. These quantitatively comparable cortisol episodes were preceded by ACTH rises whose amplitude and duration were not identical: spontaneous and meal-related ACTH peaks were smaller than the provoked one; exercise-induced ACTH peaks were of longer duration than those after ACTH1-24 injection. The different depressor capacities of similar sized cortisol episodes and the lack of proportionality between spontaneous and provoked ACTH and cortisol peaks suggest that there are separate adrenocortical activation channels, which depend on the origin of the stimulation.

Ultradian oscillations in plasma renin activity: their relationships to meals and sleep stages.

The 24-h pattern of PRA was studied in 6 supine normal subjects, and the relationship between sleep stages and PRA oscillations was analyzed using 18 nighttime profiles and the concomitant polygraphic recordings of sleep. Blood was collected at 10-min intervals. The slow trends obtained by adjusting a third degree polynomial to the 24-h data were not reproducible among individuals, and no circadian pattern was detected. Sustained oscillations in PRA occurred throughout the day. Spectral analysis revealed that PRA oscillated at a regular periodicity of about 100 min during the night. This periodicity was modified during the daytime by meal intake, which induced PRA peaks with large interindividual variations in size. A close relationship was found between the nocturnal PRA oscillations and the alternance of rapid eye movement (REM) sleep and non-REM sleep. Non-REM sleep invariably coincided with increasing or peaking PRA levels. REM sleep occurred as PRA was declining or at nadirs. More precisely, increases in PRA marked the transition from REM sleep to stage II, whereas stages III and IV usually occurred when PRA was highest. This relationship between the periodic nocturnal oscillations in PRA and the alternance of the REM-non-REM cycles may translate a similar oscillatory process in the central nervous system or may be linked to hemodynamic changes during sleep that might be partly controlled by the renin-angiotensin system.

Cortisol secretion is related to electroencephalographic alertness in human subjects during daytime wakefulness.

To determine whether human hypothalamo-pituitary-adrenal axis activity is related to the alertness level during wakefulness, 10 healthy young men were studied under resting conditions in the daytime (0900-1800 h) after an 8-h nighttime sleep (2300-0700 h). A serial 70-sec gaze fixation task was required every 10 min throughout the daytime experimental session. The corresponding waking electroencephalographic (EEG) segments were submitted to quantitative spectral analysis, from which EEG beta activity (absolute power density in the 13-35 Hz frequency band), an index of central alertness, was computed. Blood was collected continuously through an indwelling venous catheter and sampled at 10-min intervals. Plasma cortisol concentrations were measured by RIA, and the corresponding secretory rates were determined by a deconvolution procedure. Analysis of individual profiles demonstrated a declining tendency for EEG beta activity and cortisol secretory rate, with an overall temporal relationship indicated by positive and significant cross-correlation coefficients between the two variables in all subjects (average r=0.565, P < 0.001). Changes in cortisol secretion lagged behind fluctuations in EEG beta activity, with an average delay of 10 min for all the subjects. On the average, 4.6+/-0.4 cortisol secretory pulses and 4.9+/-0.5 peaks in EEG beta activity were identified by a detection algorithm. A significant, although not systematic, association between the episodes in the two variables was found: 44% of the peaks in EEG beta activity (relative amplitude, near 125%; P < 0.001) occurred during an ascending phase of cortisol secretion, cortisol secretory rates increasing by 40% (P < 0.01) 10-min after peaks in EEG beta activity. However, no significant change in EEG beta activity was observed during the period from 50 min before to 50 min after pulses in cortisol secretion. In conclusion, the present study describes a temporal coupling between cortisol release and central alertness, as reflected in the waking EEG beta activity. These findings suggest the existence of connections between the mechanisms involved in the control of hypothalamo-pituitary-adrenal activity and the activation processes of the brain, which undergoes varying degrees of alertness throughout daytime wakefulness.

Changes in EEG power density during sleep laboratory adaptation in depressed inpatients.

BACKGROUND: The aim of the present study was to evaluate the first-night effect in depressed inpatients, using standard sleep measures as well as all-night spectral analysis of the sleep electroencephalogram (EEG). METHODS: Eighteen drug-free, depressed inpatients were studied for 3 consecutive nights in the hospital sleep laboratory. RESULTS: Visual sleep scoring results showed a slight but measurable first-night effect, characterized by a reduction of rapid eye movement (REM) sleep amount and increased wakefulness. Sleep EEG spectral analysis showed significantly reduced delta (p <.01) and theta (p <.05) power density in non-REM (NREM) sleep of the first night compared with that of the second and third nights. These differences were limited to the early part of the sleep period, a time during the night that is particularly vulnerable to the effects of depressive disorder. In contrast to the NREM sleep findings, spectral REM variables studied did not significantly vary across the three nights. CONCLUSIONS: The results obtained suggest that first-night data should not be simply discarded but could be used in subsequent analyses and could be considered useful in the evaluation of the sleep of depressed patients.

Effects of a nocturnal environment perceived as warm on subsequent daytime sleep in humans.

We studied the influence of a nocturnal environment perceived as warm on the subsequent daytime sleep of healthy human subjects (20-25 years old). From 00:00 to 8:00, they were kept awake and exposed to either a thermoneutral and comfortable (CN) or a warm and uncomfortable (EW) environment, as assessed by the predicted mean vote/percentage of persons dissatisfied questionnaire (PMV/PPD). The subjects then slept from 8:00 to 14:00 in a thermoneutral environment. Sleep was scored according to the Rechtschaffen and Kales criteria. Rectal temperature was recorded from 22:00 to the end of the sleep period. Compared to CN, a significant but moderate hyperthermia (0.3-0.4 degrees C) occurred rapidly in EW, and was maintained throughout the night. This modest difference disappeared during subsequent sleep spent at thermal comfort. Exposure to a warm uncomfortable environment before bedtime significantly increased the duration (+37%) and percentage of rapid eye movement sleep (REMS). This hypnic response could be due to interactions occurring between thermoregulatory, circadian, and sleep mechanisms. It could also be ascribed to synergic actions of the neurophysiological (among others, involving the hypothalamo-pituitary-adrenal axis) and psychological (involving memory processing) processes developed when the organism faces a moderate stress.

Benzodiazepine hypnotics increase heart rate during sleep.

The cardiovascular effects of benzodiazepines administered intravenously as preoperative sedatives have received considerable study, but sleep laboratory research on benzodiazepines administered orally as hypnotics has not focused on assessment of cardiovascular changes. Analysis of heart rate (HR) data collected in sleep laboratory studies on the effects of 0.5 mg of triazolam (Halcion) and 30 mg of flurazepam (Dalmane) demonstrated that both benzodiazepine hypnotics produced a significant HR elevation that was present for up to 4 h during sleep. By the 3rd night of bedtime administration of triazolam, the HR increase was no longer statistically significant, but on the 5th night of flurazepam administration, HR was still significantly elevated over baseline levels. The HR elevation does not appear to be of clinical significance for most patients. However, this finding indicates that benzodiazepines administered at hypnotic-dose levels have peripheral as well as central effects.

Dynamic relation of sleep spindles and K-complexes to spontaneous phasic arousal in sleeping human subjects.

K-complexes unaccompanied by sleep spindles (K0-complexes) and isolated sleep spindles during stage 2, non-rapid eye movement (NREM) sleep were examined before and after transient activation phase (AP) and also pseudo-AP during human sleep to determine the relationship of K0-complexes and sleep spindles to APs. Sixteen sleep records obtained from 16 young adult males were scanned for isolated APs during stage 2 NREM sleep. One hundred APs and 62 pseudo-APs were identified and analyzed. The number of sleep spindles decreased and reached its minimum at the onset of APs, when an increase was observed in the number of K0-complexes. APs occurred when a decrease in sleep spindles was coupled with an increased incidence of K0-complexes, thus forming an antagonistic relation. A similar antagonism was observed between sleep spindles and slow waves. A working hypothesis was formulated to interpret a triad of sleep events: sleep spindles. K0-complexes, and slow wave sleep. Three kinds of sleep--REM, spindles-dominant, and slow-wave-dominant--are suggested as more useful classifications than the Rechtschaffen and Kales categories.

Comparison of cardiovascular responses to noise during waking and sleeping in humans.

Eighty subjects, 40 men and 40 women, were allocated to one of two groups according to their self-estimated high or low sensitivity to noise. In the first part of the experiment, they were exposed to sequences of common noises during the morning or the afternoon. The heart-rate and finger-pulse responses were measured and recorded in relation to sensitivity, sex of subjects, and time of day. The different types of noise were compared for both responses. The heart-rate response showed differences between sensitivity groups but not between noises. In contrast, no significant differences were obtained between sensitivity groups when using the finger-pulse response, but clear differences were observed between noises. In a second part of the experiment, 10 men and 10 women subjects were selected from the previous two sensitivity groups. These 20 subjects were exposed during sleep to the same noises as during the daytime. Heart-rate and finger-pulse responses during sleep were significantly greater than during waking, and they did not differ significantly with respect to sensitivity to noise or gender. These two autonomic responses showed differences between noises that appeared to be related to their noise-equivalent-level value. Compared with the silent baseline night, the sleep pattern showed no significant modification in the night of noise disturbance, except for the frequency of transient activation phases, which was significantly increased in the latter.

K-complexes and sleep spindles before transient activation during sleep.

Six subjects spent three consecutive nights in the sleep laboratory. Activation phases (PATs), spontaneous K-complexes, and sleep spindles were visually detected in sleep stages 2 and 3 for nights 2 and 3. The K-complex rate was significantly greater in the 10 sec prior to the PATs than at any other time spent in stage 2 or 3. K-complexes associated with sheep spindles occurred significantly less frequently during the epochs just preceding the PATs. In all subjects, there was a sharp increase of sleep spindles associated with K-complexes when PATs did not follow within 10 sec. These results suggest that spontaneous K-complexes and sleep spindles act antagonistically with respect to the occurrence of PATs. These two phasic events are significantly related to regulating the probability of occurrence of PATs in sleep stages 2 and 3; K-complexes may reflect an organismic state leading towards PAT, whereas sleep spindles may inhibit the occurrence of PAT.

Effect of continuous heat exposure on sleep stages in humans.

Six young men were exposed to a thermoneutral environment of air temperature (Ta) 20 degrees C for 5 days and nights followed by an acclimation period of 5 days and nights at Ta 35 degrees C and 2 recovery days and nights at Ta 20 degrees C. Electrophysiological measures of sleep, esophageal temperature, and mean skin temperature were continuously monitored. The total nocturnal body weight loss was measured by a sensitive platform scale. Compared with the 5 nights of the baseline period at 20 degrees C, sleep patterns showed disturbances at 35 degrees C. Total sleep time was significantly reduced, while the amount of wakefulness increased. The subjects exhibited fragmented sleep patterns. The mean duration of REM episodes was shorter at 35 degrees C than at 20 degrees C of Ta, while the REM cycle length shortened. In the acclimation period, there was no change in sleep pattern from night to night, despite adaptative adjustments of the thermoregulatory response. The protective mechanisms of deep body temperature occurring with heat adaptation did not interact with sleep processes. Upon return to baseline condition, a recovery effect was observed on a number of sleep parameters which were not significantly affected by the preceding exposure to prolonged heat. This would suggest that during exposure to dry heat, the demand for sleep could overcome that of other regulatory functions that are temperature-dependent. Therefore, a complete analysis of the effect of heat on sleep parameters can be assessed only if heat exposure is compared with both baseline and recovery periods.

Effect of continuous heat exposure on sleep during partial sleep deprivation.

This study examined the effects of continuous heat exposure on sleep structure during a partial sleep-deprivation regime. The experimental protocol was divided into three periods. After a baseline period (5 days and nights at 20 degrees C), the sleep of the subjects was restricted to the second half of the night (3 a.m.-7 a.m.) for four consecutive nights. The restricted-sleep period was followed by two recovery days and nights. During the deprivation and recovery periods, the ambient temperature was 20 degrees C for six of the 12 subjects and 35 degrees C for the others. Sleep, esophageal and mean skin temperatures were continuously recorded. At 20 degrees C, the expected effect of sleep debt was apparent. There were significant reductions in time spent awake and in latencies for sleep and stage 4 sleep. The duration of stage 4 sleep significantly increased during the four successive restricted-sleep nights, whereas esophageal temperature significantly decreased over the successive days. When heat was added, esophageal temperature decrease was weakened, and the significant increase in stage 4 duration seen at 20 degrees C was not found. The findings suggest that the heat load imposed in our experimental condition has a suppressive effect on sleep stage 4 increase, which is induced by sleep restriction. The hypothesis that an increase in this sleep stage serves as a mechanism for energy conservation should be also considered.

A quantitative evaluation of the relationships between growth hormone secretion and delta wave electroencephalographic activity during normal sleep and after enrichment in delta waves.

The existence of a relationship between growth hormone (GH) release and slow-wave sleep (SWS), often studied in the past using conventional scoring of sleep stages, remains controversial. In the present study, this relationship was reevaluated by spectral analysis of the sleep electroencephalogram (EEG) and deconvolution analysis of the plasma GH concentrations during normal nocturnal sleep and after enrichment in SWS by means of ritanserin, a selective 5-HT2 receptor antagonist. Eight healthy male subjects each participated in two randomized night studies after having received either a placebo or a 5-mg dose of ritanserin. They were subjected to 8 hours of polysomnography, including spectral analysis of the sleep EEG. Plasma GH levels were measured at 10-minute intervals. The mean delta absolute power and the mean GH secretory rates were significantly higher under ritanserin than under placebo for the first 3 hours after sleep onset (+24% and +29%, respectively). Their nocturnal profiles were significantly and positively correlated in all subjects (average r = 0.710 under placebo, 0.567 under ritanserin; p < 0.0001 in both cases). GH secretory pulses were found to be coincident with delta activity peaks in both directions. The amount of GH secreted during significant GH pulses was correlated with the amount of concomitant delta wave activity (r = 0.803 under placebo, r = 0.764 under ritanserin, p < 0.0001). Similarly, the amount of delta wave activity found during delta wave peaks was correlated with the amount of GH secreted concomitantly (r = 0.715 under placebo, r = 0.723 under ritanserin: p < 0.0001). These results demonstrate a close temporal and quantitative relationship between GH secretion and delta wave activity, which may be evidence of common stimulatory mechanisms.

Temporal relationship between prolactin secretion and slow-wave electroencephalic activity during sleep.

It is well established that plasma prolactin (PRL) concentrations exhibit a sleep-dependent pattern, with the highest levels occurring during sleep and the lowest during waking. Still, controversy exists concerning an association between rapid eye movement (REM) and non-REM sleep cycles and plasma PRL pulses. These studies were all based on conventional scoring of sleep stages. In the present study, plasma PRL concentrations were analyzed at 10-minute intervals in 10 subjects during the night when sleeping. PRL secretory rates were calculated by a deconvolution procedure. Spectral parameters of sleep electroencephalographic (EEG) recordings were analyzed together with PRL secretion using cross-correlation. Slow-wave activity of the EEG and PRL secretion ran parallel in all individuals. Conversely, alpha and beta bands and the EEG mean frequency were inversely proportional to PRL secretion. In 9 of the 10 subjects studied, PRL secretion was concomitant with delta waves or lagged behind by 10-20 minutes, depending on subjects, with maximum cross-correlation coefficients ranging between 0.40 and 0.67. This temporal relationship between PRL secretion and delta waves was further assessed by a pulse-by-pulse analysis based on the calculation of probability levels after computer simulations. Nine of the 10 subjects displayed significant concomitance between delta wave activity and PRL secretory oscillations. These results demonstrate that PRL secretion during sleep is coupled to delta waves in young healthy men.

Sleep stage scoring using the neural network model: comparison between visual and automatic analysis in normal subjects and patients.

In this paper, we compare and analyze the results from automatic analysis and visual scoring of nocturnal sleep recordings. The validation is based on a sleep recording set of 60 subjects (33 males and 27 females), consisting of three groups: 20 normal controls subjects, 20 depressed patients and 20 insomniac patients treated with a benzodiazepine. The inter-expert variability estimated from these 60 recordings (61,949 epochs) indicated an average agreement rate of 87.5% between two experts on the basis of 30-second epochs. The automatic scoring system, compared in the same way with one expert, achieved an average agreement rate of 82.3%, without expert supervision. By adding expert supervision for ambiguous and unknown epochs, detected by computation of an uncertainty index and unknown rejection, the automatic/expert agreement grew from 82.3% to 90%, with supervision over only 20% of the night. Bearing in mind the composition and the size of the test sample, the automated sleep staging system achieved a satisfactory performance level and may be considered a useful alternative to visual sleep stage scoring for large-scale investigations of human sleep.

First-night effect in normal subjects and psychiatric inpatients.

The goal of the present study was to evaluate the first-night effect in psychiatric inpatients using large subject samples (n > 30) in order to obtain a good statistical evaluation. Thirty-two normal subjects and 94 psychiatric inpatients (38 depressives and 56 insomniacs) were studied for three consecutive nights in the hospital sleep laboratory. Our results showed clearly that there was a first-night effect in normal subjects, similar to that reported in previously published data, characterized by a longer rapid eye movement (REM) sleep latency (p < 0.05), increased wakefulness (p < 0.01) and total sleep time (p < 0.02) and a decreased sleep efficiency (p < 0.01). REM sleep latency and stage REM in the first third of the night were still altered in the second night. Both clinical groups had a less marked first-night effect than normal subjects, showing alterations only observed in REM sleep (p < 0.01) (decreased REM sleep, longer REM sleep latency, increased REM sleep gravity center). However, the first-night effect was more pronounced in insomniacs than in depressed patients. No statistical differences between the second and third nights' recordings were found in sleep parameters. It is suggested that first-night data should not be simply discarded but could be used in subsequent analyses.