All-night Sleep Research Articles

Lack of an acute modulatory effect of melatonin on human nocturnal thyrotropin and cortisol secretion.

Using a recently developed model for investigating the neuroendocrine role of melatonin in man, we studied melatonin's effect on the nocturnal secretion of thyrotropin and cortisol in 17 normal male volunteers. The model consists of sleep in the dark and all-night sleep deprivation in conditions of: bright light with and without a melatonin infusion, and dim light. We have improved our infusion paradigm so that levels of melatonin during infusion are now indistinguishable from those occurring during sleep in the dark or dim light sleep deprivation. Sleep deprivation per se raised TSH levels compared to normal sleep. However, the three conditions of sleep deprivation could not be distinguished from each other, which suggests that the suppression of TSH by sleep (or the stimulation of TSH by sleep deprivation) is not mediated by melatonin. Cortisol secretion was unaffected by sleep deprivation regardless of melatonin's presence or absence. However, a difference in the pattern of secretion of cortisol in the sleep condition in the early morning (compared to the sleep deprivation conditions) was noted. These data do not implicate melatonin in the acute regulation of TSH or cortisol in normal man. These data also provide a method of melatonin infusion that replicates the pattern and levels seen in sleep.

Changes in the auditory middle latency responses during all-night sleep recording.

The middle latency response (MLR) using wide band-pass filters shows marked changes in amplitude, latency and configuration in sleep. The components with latencies greater than 20 ms show the greatest variability. There is a significant increase in Pa latency in stages 2 and stages 3/4, and in some cases a disappearance of the Nb component with the development of a broad positivity of latency intermediate to Pa and Pb which dominates the response. The responses in REM are of similar latency and configuration as in wakefulness but of reduced amplitude. The 40 Hz response is markedly reduced in amplitude in all sleep stages reflecting a decrease in the contribution of the middle latency components to this composite response. This appears to arise through a loss of 40 Hz periodicity in slow wave sleep and an increase in the slow 10 Hz component. In REM sleep, there is an overall reduction in amplitude. Much of the reported variability of the MLR in the literature arises from the widely differing band-pass filters used and the inadequate control for level of arousal. Both these factors have been shown to produce significant changes in the response.

Rhythmic Slow Wave Observed on Nocturnal Sleep Encephalogram in Children with Idiopathic Nocturnal Enuresis

All-night sleep polygraphs, except the first night, were recorded for 15 patients with idiopathic nocturnal enuresis and 10 normal controls. Relations between sleep and the mechanism by which nocturnal enuresis is caused, with special emphasis on the occurrence of rhythmic slow waves (RSW), was studied. The following results were obtained. (a) There was no significant difference between the two groups in the proportions of the electroencephalographic (EEG) sleep stages, under the same conditions. (b) Nocturnal enuresis occurred with almost the same frequency in all sleep stages except stage 1 sleep and was higher in the second and third cycles. (c) Immediately before a nocturnal enuretic event, 6-7 Hz RSW continued for as long as 15-40 s in NREM sleep, or 3-5 Hz RSW was observed in REM sleep. (d) RSW was observed in enuretics and controls, and decreased with increase in age. However, RSW occurred more often, and age-related decrease was delayed in enuretic children. (e) RSW was induced by stimuli such as changes in sleep stages or body movement. During RSW, the variance of heart rate and respiration tended to be low. These results and the similarity between RSW and diffuse rhythmic theta suggest that RSW may be an expression of the process of maintaining a given sleep stage in children. These results may also be caused by the immaturity of the sleep mechanism in enuretic children. The long-lasting RSW on the sleep EEG was considered to be a sign of the onset of nocturnal enuresis.

Classification of Sleep Patterns by Means of Markov Modeling and Correspondence Analysis

Shown is how correspondence analysis can be used to track changes in an individuals' sleep pattern. Correspondence analysis was applied to sleep stage transition matrices computed from all-night sleep of normal, obese, and apnoetic subjects. Differences between the groups, and intraindividual changes in sleep patterns could be visualized better than with a x2-based clustering approach.

Sleep EEG in bulimia

To evaluate the sleep electroencephalogram (EEG) characteristics of bulimia, all-night sleep EEGs were performed on 11 women meeting DSM-III criteria for bulimia. Comparison groups consisted of young women outpatients with major depression ( n = 44) and young normal women ( n = 20). The sleep EEGs of the bulimic patients were largely indistinguishable from those of the normal controls, except for a trend toward increased rapid eye movement (REM) density in the first REM period among the bulimic subjects. No differences in any sleep EEG measure were observed between bulimic patients with major depression and those without affective disorder. By contrast, the outpatients with major depression displayed marked sleep continuity disturbances, as well as significantly increased REM intensity and REM density, as compared to normal controls. Implications of these results with respect to the hypothesis that bulimia is related to major affective disorder are discussed.

Sleep deprivation effects in older endogenous depressed patients

In a drug-free group of 15 older endogenous depressed inpatients, all-night sleep deprivation (SD) was associated with a significant decrease in Hamilton depression scores and in Profile of Mood States self-ratings of depression. Six of 15 patients (40%) were responders to SD, as evidenced by ⩾ 30% improvement in Hamilton ratings. While symptomatic improvement was short-lived (8 of 15 patients worsened after 1 night of recovery sleep), five patients showed further improvement after 1 night of recovery sleep. The final two patients had an increase in Hamilton ratings after sleep deprivation, with a return to baseline values after 1 night of recovery sleep. Responders (but not nonresponders) showed significant improvement in sleep latency, sleep efficiency, and slow wave sleep during recovery sleep (as did controls). The SD Hamilton depression rating (at 9 a.m. after all-night sleep deprivation) showed a significant inverse correlation with the increase in slow wave sleep (SWS) minutes and in SWS % from baseline to first recovery night. Responders also had significantly larger increases in SWS minutes than did nonresponders (53.8 vs. 7 minutes). Similarly, the % change in Hamilton depression ratings was predicted by baseline Stage 4 sleep. These findings suggest that there is a mutual interaction between the process of sleep regulation and the symptoms of depression. They also confirm a prediction from the two-process model of sleep regulation—namely, that improved sleep initiation and maintenance and increased SWS, attained by SD, are associated with clinical improvement.

Effect of aging on sleep-related changes in respiratory variables.

Several respiratory variables were examined in 11 healthy elderly (greater than 60 years) and 12 younger (30-39 years) control subjects during all-night sleep runs, with a view to determining the effect of the aging process on breathing during sleep. O2 saturation, end-tidal PCO2, and transcutaneous PCO2 were monitored, together with standard sleep staging measures. Estimates of tidal volume (Vt) and ventilation (Ve) were obtained using a Respitrace inductive plethysmography system, from which respiratory rate (fb) was also measured. Older subjects had more sleep apnea/hypopnea than younger subjects, an incidence of 55 versus 8%, respectively. More of their arousals were associated with respiratory disturbance than those of the younger subjects, and they had more brief, but not longer, arousals. Mean O2 saturation was lower in older subjects during wakefulness but did not decrease more in older subjects than in control subjects during sleep. Mean end-tidal/transcutaneous PCO2 did not differ between groups during wakefulness or sleep. Vt and Ve estimates did not decrease during slow wave sleep in older subjects as they did in the younger subjects. It was concluded that aging by itself does not significantly alter average sleep-related changes in O2 saturation or PCO2, although the increased incidence of respiratory disturbance does produce transient swings in these variables. The lack of a decrease in ventilation estimates during sleep in spite of the usual changes in O2 saturation and PCO2 in the older group indicates a possible decrease in effective gas exchange.

Sleep Studies in Benign Epilepsy of Childhood with Rolandic Spikes. II. Analysis of Discharge Frequency and Its Relation to Sleep Dynamics

Polygraphic all-night sleep recordings of 11 children with benign epilepsy of childhood with rolandic spikes (BERS) were investigated from the viewpoint of spike distribution. Spike/min ratios were calculated with regard to different sleep stages and waking, identical stages of the consecutive cycles, and stages 1-2 taking place on the descending versus the ascending slopes of sleep cycles. Maximum spike/min ratios were related to slow sleep stages, especially delta sleep, and in general to the first cycle. Stages 1-2 on the descending (DESC) slopes of consecutive cycles showed a decrease in spike density during the night, as opposed to the increasing rate of activation of the same stages on the ascending (ASC) slopes. Based on our results, we suggest that the actual drive of spiking as well as seizures in BERS is the functional overweight of sleep-inducing mechanisms.

Sleep studies in benign epilepsy of childhood with rolandic spikes. I. Sleep pathology.

Polygraphic all-night sleep records of 11 children with typical benign epilepsy of childhood with rolandic spikes (BERS) and those of eight nonepileptic controls were investigated with regard to sleep pathology. Basic properties of sleep organization and electromorphology were preserved in both groups. Seventeen quantitative sleep parameters were measured. Except for more waking in the BERS group, no sleep parameter showed significant differences between the BERS and the control group, but differences existed in comparison to normative values. We interpret our results as showing that in BERS epileptic neuronal malfunctioning does not affect sleep organization in a characteristic manner. The lack of detrimental interactions between epileptic neuronal behavior and pathological sleep alterations may be an additional cause of the benign course of BERS.

Midlatency auditory evoked responses: Differential effects of sleep in the human

Middle latency responses (MLRs) in the 10–100 msec latency range, evoked by click stimuli, were studied in 14 adult volunteer subjects during sleep-wakefulness to determine whether such changes in state were reflected by any MLR component. Evoked potentials were collected in 500 trial averages during continuos presentation of 1/sec clicks during initial awake recordings and thereafter during a 2 h afternoon nap or all-night sleep session. Continuously recorded EEG, EOG and EMG were scored for wakefulness, stages 2–4 of slow wave sleep (SWS), and rapid eye movement (REM) sleep during each evoked potential epoch. The major components included in this study and their latency ranges, as determined by peak latency measurements from the awake records, were: ABR V, 5–8 msec, Pa, 30–40 msec, Nb, 45–55 msec, and P1, 55–80 msec. In agreement with previous reports, ABR V and Pa showed no amplitude changes from wakefulness to either SWS or REM. Not previously reported, however, was the dramatic decrease and disappearance of P1 during SWS and its reappearance during REM to an amplitude similar to that during wakefulness. This unique linkage between a particular evoked potential component and sleep-wakefulness indicates that its generator system must be functionally related to states of arousal. Relevant data from the cat model suggest that the generator substrate for P1 may be within the ascending reticular activating system.

Midlatency auditory evoked responses: Differential effects of sleep in the cat

Middle latency responses (MLRs) in the 10–100 msec latency range, evoked by click stimuli, were studied in 8 adult cats during sleep-wakefulness to determine whether such changes in state were reflected by any MLR component. In particular, we wanted to determine whether the 20–22 msec positivity recorded at the vertex, ‘wave A,’ shown in previous studies to reflect a generator substrate within the ascending reticular formation, was tightly linked to changes in sleep-wakefulness, as reported for single neurons in the ascending reticular activating system. Evoked potentials were collected in 100 trial averages during continuous presentation of 1/sec clicks during initial awake recordings and thereafter during all-night sleep sessions. Continuously recorded EEG, EOG and EMG were scored for wakefulness, slow wave sleep (SWS), and rapid eye movement (REM) sleep during each evoked potential epoch. Recordings were obtained from electrodes implanted at the vertex and overlying the primary auditory cortex referenced to frontal sinus or to neck. In agreement with others, components of the auditory brain-stem response and the 12 msec primary cortical response showed no change in amplitude from wakefulness to either SWS or REM. Only wave A, among the components evaluated in the 1–100 msec range, decreased and disappeared during SWS and dramatically reappeared during REM to an amplitude equal to that during wakefulness. These data lend particular support to a functional relation between wave A and the ascending reticular activating system and suggest that this potential may provide a unique and dynamic probe of tonic brain activity. Moreover, this animal model provides a hypothetical basis for expecting a similar surface recorded potential in the human, a potential which has consequently been discovered.

Hemifacial spasm in sleep.

We conducted polygraphic studies during wakefulness and all-night sleep in 13 patients with cryptogenic and 3 with postparalytic hemifacial spasm. The movements decreased progressively with deepening sleep stages, reaching lowest values in REM sleep. The reduction was inversely related to the severity of movements during wakefulness. There was no relation between hemifacial spasm and mimic activity on the unaffected side. Central inhibitory processes may account for the partial decline in intensity of the movements in sleep.

Interaction sleep and epilepsy.

In order to improve the diagnosis of epilepsy, a routine EEG recording can be supplemented with a long-lasting sleep recording or with an ambulatory EEG recording. In this paper we compare the all-night polygraphic sleep recording with the 3- to 5-hour recording after 1 night total sleep deprivation, and we discuss the outcome with each. In the first part we have analyzed the relationship between the clinical form of epilepsy and the kind and depth of sleep and we have tried to determine the optimal registration time (in hours) to obtain a maximum diagnostic gain. In the second part we have evaluated the changes in the sleep composition induced by the occurrence of epileptic EEG phenomena and by the intake of antiepileptic drugs. In the third part we have analyzed the changes in the morphological aspects of the epileptic EEG phenomena which can occur under influence of light (NREM 1-2) and deep (NREM 3-4) slow-wave sleep and REM sleep. A sufficient knowledge of these changes is very important to avoid misinterpretations.

Respiratory muscle activity and thoracoabdominal motion during acute episodes of asthma during sleep.

To understand the mechanisms of respiratory system compensation to internal loading during sleep, all-night sleep studies were performed in 10 patients with chronic stable asthma. We used noninvasive measurements to identify the onset of increased airway resistance in sleep. In each sleep study, we recorded arterial oxygen saturation (SaO2) and an array of electromyograms (diaphragm, external intercostal and sternomastoid) as well as thoracoabdominal motion. Only 4 patients developed acute asthma during sleep. A total of 6 such attacks were recorded. The attacks were detected by audible wheeze, augmentation of diaphragm, external intercostal and sternomastoid activity, associated with distinctive changes in thoracoabdominal motion. The duration of these acute asthmatic attacks ranged between 20 and 140 min. One attack started in stage I/II non-rapid-eye-movement (NREM) sleep, 3 in stage III/IV NREM sleep, and 2 in rapid-eye-movement (REM) sleep. Acute asthma in NREM sleep resulted in a paradoxical inward displacement of the abdomen during early inspiration. Attacks occurring during REM sleep resulted in rib cage inward displacement during inspiration. Attacks occurring during REM sleep resulted in rib cage inward displacement during inspiration. Attacks occurring in both NREM and REM sleep did not result in a significant fall in SaO2. We conclude that acute internal respiratory loading during sleep can provoke different compensatory mechanisms in order to provide adequate ventilation in adult asthmatics.

Sleeping position and sleep apnea syndrome

Four patients who were evaluated for hypersomnia-sleep apnea syndrome were found in all-night sleep studies to have obstructive or mixed apneas related to their sleeping positions. All four were available for comprehensive follow-up and were subsequently restudied while avoiding the supine position. Supine, prone, and lateral decubitus apnea indices were calculated for each patient for each night. The supine sleeping position was associated with significantly more apneas than the non-supine positions. Keeping these patients off their backs when they slept was effective treatment. Additionally, when results of surgical or pharmacologic treatments of apnea are evaluated, positional apnea indices should be considered.

Human auditory steady state evoked potentials during sleep.

The human auditory steady state evoked potentials were recorded during all-night sleep in 10 subjects. The effects of stimulus rate and intensity on these potentials were measured using on-line Fourier analysis. The amplitude of the response was greatest at stimulus rates of 30 to 50/sec. Although the response amplitude was lower during sleep, the rate at which the amplitude was greatest did not change between sleep and wakefulness. As the intensity was increased above threshold, the amplitude of the response increased linearly. The responses recorded during wakefulness showed a larger amplitude change with increasing intensity than during sleep. The estimated thresholds for the responses, however, did not differ significantly between wakefulness and sleep.

Measurement error in visually scored electrophysiological data: respiration during sleep

Electrophysiological sleep studies employ the simultaneous recording of multiple physiological parameters. These data are often scored and analyzed visually, i.e. by trained human scorers. In this study, we investigated the measurement error inherent in visual evaluation of respiratory disturbances during human sleep. Three trained scorers independently evaluated twenty-eight all-night sleep recordings. Results indicated that the scorers achieved high agreement on only selected variables. Scorers' experience did not affect the reliability and independent judgements of recording quality did not account for the discrepancies. These findings, although most relevant for the specific parameters studied here, as well as for these scoring criteria, subjects, and techniques, document the unreliability of certain visually scored sleep data. The present paradigm may be useful in evaluating other types of measurement error.

Patterning of NREM sleep periods in normals: an observation revisited

Both the visual examination of all-night sleep recordings in both normals and patients, generated by a delta wave analyzer, and spectral analysis have suggested that delta wave sleep often appear to rise gradually during a NREM period and then to cease abruptly. Such observations by minute-by-minute computer plots of delta wave activity have strengthened the notion of a REM generator and/or a delta sleep generator in the central nervous system. We now report observations on a sample of 23 normal subjects under the age of 45 in which we investigated the ‘rise and fall’ of delta sleep activity during successive NREM periods. For these 23 normal subjects, significantly greater maximal decreases throughout the night were noted in each of these 4 NREM periods as compared to the maximal increases. Furthermore, these findings have implications for the understanding of the physiology of sleep and particularly the on- and off-generator of REM and NREM sleep.

Behavioral control of respiration in sleep.

Three experiments are presented involving behavioral control of sleeping respiration during all-night sleep recording. Probability and latency of the breathing response to an auditory signal revealed that control over sleeping respiration was obtained in all sleep stages and was maintained over several nights. This control was especially marked when failure to respond was punished (contingency procedure) by increasing the intensity of the signal (Experiments 2 and 3). Few awakenings occurred to the signal but signs of brief arousal (bursts of alpha activity, increases in EMG activity, EEG “speeding”) often accompanied the behavioral response. Overall sleep patterns were only minimally disrupted by the procedure. Demonstrating behavioral control over sleeping respiration may be a promising step toward the development of behavioral therapies for certain sleep apnea disorders and hypoventilation syndromes.

EEG-based multivariate statistical analysis of sleep stages.

All-night sleep of 5 healthy male subjects was scored on the basis of EEG (paper records), EMG and EOG into the stages of wakefulness, REM sleep and slow sleep stages 1-4 according to Rechtschaffen and Kales. Spectral analysis for 8 EEG channels was then performed and spectral parameters (total power and coherence for certain frequency bands) extracted. Stepwise linear discriminant analysis was applied to these spectral parameters to see how well the polygraphically defined sleep stages were recognized. While the results of each intrasubject analysis were satisfactory (error rates between 10 and 15%), a more detailed analysis revealed that most errors occur between nearby slow sleep stages or between S1 and REM or wakefulness. This is related to the fact that Rechtschaffen and Kales classify into discrete stages an essentially continuous process and this is, to some extent, arbitrary. This interpretation is supported by examples. Cross-classification of each subject on the basis of the remaining 4 increases the error rates drastically. A simple way of avoiding this effect, by standardizing the individual data, is shown to work nicely in this case.