Showing papers on "Slow-wave sleep published in 1987"

Sleep research in affective illness: state of the art circa 1987.

Abstract: Future sleep research in affective illness will probably continue the current evolution beyond cross-sectional to longitudinal studies, and beyond a largely descriptive emphasis to the testing of specific hypotheses and predictions derived from models of the pathophysiology of depression. These models are and will be variously neurochemical, chronobiological, genetic, and developmental in nature. Adequate testing of these models and predictions from them will require the use of pharmacologic and naturalistic probes and the use of sophisticated CNS imaging techniques. These probes will help further characterize the physiology of depression under conditions of disequilibrium or perturbation, such as following sleep deprivation, REM deprivation, phase advancement of the major sleep period, or the administration of antidepressant drugs with specific monoaminergic activity. Concurrently, if one is to understand further whether the sleep abnormalities of depression are part of a larger circadian rhythm disturbance, investigations will necessarily include 24-h measures of sleep-wake activity, psychomotor activity, and probably core body temperature rhythm under constant routine conditions. A complementary point of view would suggest that more intensive investigative efforts be focused on the first 100 min of sleep at night, since it is the first NREM-REM cycle that seems to show the greatest and most specific deviation in depressed patients from normal controls. Efforts to characterize further this part of the 24-h cycle, with respect to age- and gender-related variance as well as responses to physiologic, hormonal, pharmacologic, and naturalistic probes, are strongly warranted.

Temporal placement of a nap for alertness: contributions of circadian phase and prior wakefulness.

Abstract: Napping can enhance alertness during sustained wakefulness, but the importance of the temporal placement of the nap between days and within the circadian cycle remains controversial. To resolve these issues, a between-groups study was conducted with 41 healthy, young adults permitted a 2-h nap at one of five times during a 56-h period otherwise devoid of sleep. Naps were placed 12 h apart, near the circadian peak (P) or trough (T), and were preceded by 6, 18, 30, 42, or 54 h of wakefulness. Visual reaction time (RT) performance, Stanford Sleepiness Scale (SSS) ratings, and sublingual temperature were assessed every few hours throughout the 56 h, which took place in an environment free of time cues. All groups displayed a circadian-modulated decline in RT measures and increases in SSS functions as sleep loss progressed. A nap placed at any time in the protocol improved RT performance, particularly in the lapse domain, but not SSS ratings. Comparisons within groups of circadian temperature cycles for the first versus second day of the protocol indicated that early naps (P6, T18, P30) tended to prevent the mean drop in temperature across days. The earlier naps (P6, T18) yielded more robust and longer lasting RT performance benefits, which extended beyond 24 h after the naps, despite the fact that they were comprised of lighter sleep than later naps. Circadian placement of naps (P vs. T) did not affect the results on any parameter. In terms of temporal placement, therefore, napping prior to a night of sleep loss is more important for meeting subsequent performance demands than is the circadian placement of the nap. SSS ratings suggest that the napper is not aware of these performance benefits. Because the longest lasting RT gains followed early naps, which were composed of less deep sleep than later naps, napping during prolonged sleep loss may serve to prevent sleepiness more readily than it permits recovery from it.

Sleep and depression.

Abstract: Manifestations of sleep disturbances can potentially serve as external criteria for the diagnosis of specific subtypes of major depressive disorder (MDD). Depressed patients generally experience disturbances of sleep continuity and rapid eye movement (REM) sleep. Disturbances in nonrapid eye movement (NREM) sleep (stages III and IV) also occur. Characteristic of primary sleep disturbance in many depressed patients are shortened REM latency periods and instabilities in NREM sleep identified by increases in the number of stage shifts, decreases in the duration of stage III and IV sleep, and a shift towards lighter sleep stages (sleep efficiency disturbances). Treatment modalities for these sleep disturbances include sleep deprivation therapy and antidepressant therapy. Sleep deprivation alone has been only moderately successful, while antidepressant therapy usually results in symptomatic improvement. To restore normative sleep, REM sleep periods and stage III and IV sleep must be returned to normal. Trazodone therapy has been shown to reduce the frequency of arousals, the severity of drowsiness, and the duration of REM sleep, and increase restorative slow wave sleep and stage III and IV NREM sleep.

Electroencephalographic sleep of adolescents with major depression and normal controls.

Abstract: • Forty-nine, mostly outpatient (86%), nonbipolar adolescents, aged Tanner stage III to 18 years, with a current diagnosis of major depressive disorder and 40 adolescents without current presence or history of psychiatric disorder were studied polysomnographically for three consecutive nights. Sleep latency was significantly longer in the depressive groups. The nonendogenous depressive patients exhibited significantly more awake time and lower sleep efficiency during the sleep period. No significant group differences were found for first rapid eye movement (REM) period latency, REM density, or any other REM sleep measures. Age correlated significantly with REM latency and delta sleep time, especially among depressive patients. No significant correlations between sleep measures and severity of illness were found. It appears that the classic REM sleep findings associated with the adult depressive syndrome are not present among depressive adolescents, indicating a later ontogeny for these abnormalities.

Quantitative analysis of the effects of slow wave sleep deprivation during the first 3 h of sleep on subsequent EEG power density

Abstract: The relation between EEG power density during slow wave sleep (SWS) deprivation and power density during subsequent sleep was investigated. Nine young male adults slept in the laboratory for 3 consecutive nights. Sepctral analysis of the EEG on the 2nd (baseline) night revealed an exponential decline in mean EEG power density (0.25–15.0 Hz) over successive nonrapid eye movement — rapid eye movement sleep cycles. During the first 3 h of the 3rd night the subjects were deprived of SWS by means of acoustic stimuli, which did not induce wakefulness. During SWS deprivation an attenuation of EEG power densities was observed in the delta frequencies, as well as in the theta band. In the hours of sleep following SWS deprivation both the power densities in the frequency range from 1 to 7 Hz and the amount of SWS were enhanced, relative to the same period of the baseline night. Both the amount of EEG energy accumulating subsequent to SWS deprivation and its time course could be predicted accurately from the EEG energy deficit caused by SWS deprivation. The data show that the level of integral EEG power density during a certain period after sleep onset depends on the amount of EEG energy accumulated during the preceding sleep rather than on the time elapsed since sleep onset. In terms of the two-process model of sleep regulation (Borbely 1982; Daan et al. 1984) this finding indicates that EEG power density reflects the rate of decay of the regulating variable, S, rather than S itself, as was originally postulated.

Empirical Note: Self‐Report Versus Recorded Sleep in Healthy Seniors

Abstract: Although insomnia is a major public health problem in the elderly, little information concerning the relation between subjective reports of sleep and laboratory measures in the elderly has been published Also, while laboratory studies of the healthy elderly typically show that women steep better than men, epidemiologic studies suggest that women complain more often than men about disturbed sleep We report here a study of 20 healthy elderly subjects without sleep complaints (10M 10F), in which relations between subjective and objective measures of sleep were explored Both men and women showed significant correlations between objective measures of Sleep Latency (SL) and subjective estimates of fall asleep time; similarly, in both groups, subjective estimates of sleep duration were significantly and positively correlated with Time Spent Asleep (TSA) However, in the women, but not in the men, “restlessness” of sleep was significantly correlated with WASO (wake time after sleep onset), while “soundness” of sleep was positively related to amount of slow wave sleep In general, women showed a higher proportion of significant and more stable correlations between subjective and objective measures than did men These findings suggest that elderly women may report sleep loss more accurately than elderly men

Frequency analysis of the sleep EEG in depression.

Abstract: Eight patients with major depressive disorder (seven bipolar and one unipolar) and matched controls had sleep studies, on which frequency analysis of the electroencephalogram (EEG) was performed. Total sleep and sleep efficiency were decreased in the patients, but there was no significant difference in rapid eye movement (REM) latency between the two groups. Frequency analysis revealed no group differences in power in the delta band (0.23-2.5 Hz) or the whole EEG spectrum (0.23-25 Hz). These findings suggest that mean REM latencies are not always shorter in major depression. The results are discussed in light of a previous report of decreased delta energy in the sleep EEG of unipolar patients.

Slow wave sleep elevations after body heating: proximity to sleep and effects of aspirin.

Abstract: On three different occasions, six healthy young adult subjects ahd their body temperatures raised by an average of 2.0 degrees C for 30 min while sitting in baths of warm water. This was done once at 1700 h and on two occasions at 2100 h, once after the subjects had taken aspirin and once after a placebo. Nighttime sleep was recorded after each experimental condition and for baseline nights following nil heating. Records were scored both visually and by an automated sleep stager. Electroencephalographic (EEG) power was computed over the night. Results from the automated scoring were very similar to those of the visual method. While the early bath caused no changes in sleep, the late bath + placebo resulted in significant rises in stage 4 sleep and slow wave sleep (SWS) and significant falls in sleep onset and in REM sleep. Aspirin mostly counteracted these effects and, in particular, left stage 4 sleep and SWS at baseline levels. EEG power was significantly increased only after the late bath plus placebo, supporting the SWS outcome. These findings were assessed in light of other comparable results from our laboratory. It seems that as the time of the day of heating recedes from nighttime sleep, a larger "dose" of heating is required to produce the same effect.

Sleep-electroencephalography and the secretion of cortisol and growth hormone in normal controls.

Abstract: Sleep-electroencephalography, and the nocturnal secretion of cortisol and GH were investigated simultaneously in a sample of 25 male normal controls (27.1 +/- 1.3 years) in order further to examine interaction between sleep structure and concurrent endocrine activity. Slow wave sleep activity was increased during the first part of the night, whereas cortisol concentration was low and GH output reached maximal levels. The second half of the night was characterized by a relative preponderance of REM-sleep, low GH-concentration, and an increase in cortisol. However, no distinct reciprocal interaction between cortisol and GH concentration was noted. In all subjects, a pronounced GH surge between 22.00 and 02.00 h was recorded which occurred independently of the presence of slow wave sleep. Six out of the 25 subjects showed nocturnal GH increases even before sleep onset. These data indicate that somatotropic cell activity during night is less dependent upon the sleeping state or specific conventially defined sleep stages than originally reported.

The effects of chronic ritanserin treatment on sleep and the neuroendocrine response to L-tryptophan.

Abstract: A previous study has shown that acute administration of the 5-HT2 receptor antagonist ritanserin doubles Slow Wave Sleep (SWS) and increases the prolactin (PRL) response to l-tryptophan (LTP). The present study investigated the effect of repeated ritanserin treatment on sleep, neuroendocrine response to LTP and 5-HT2 platelet receptor binding. After 2 weeks, ritanserin administration SWS was persistently increased but the PRL response to LTP was unchanged. Platelet 5-HT receptor binding was undetectable at the end of ritanserin treatment but recovered 2 weeks after drug withdrawal. The results suggest that ritanserin causes a sustained effect on the 5-HT mechanisms mediating SWS and on platelet 5-HT2 receptors. However, adaptation occurs to its effect on 5-HT-mediated neuroendocrine responses.

Reversibility of deficient sleep entrained growth hormone secretion in a boy with achondroplasia and obstructive sleep apnea.

Abstract: Obstructive sleep apnea may lead to disordered sleep architecture and impair the physiologic slow wave sleep related growth hormone release. Obstructive sleep apnea occurs with craniofacial syndromes and in children with airway narrowing, pharyngeal hypoplasia, tonsillar adenoidal hypertrophy, micrognathia and achondroplasia. To examine the relationship between disordered sleep and growth hormone release we studied a 9 year old male with achondroplasia, growth failure (3 cm/year) and obstructive sleep apnea. Polysomnography data and a 20 min sampling for sleep entrained growth hormone showed before therapeutic tracheostomy numerous apneic episodes, absent slow wave sleep and abnormal low growth hormone secretion during sleep. Normalized slow wave sleep entrained growth hormone secretion after tracheostomy led to a sustained increase in growth rate. Normal growth rate (greater than 5 cm/year) continues 2 years after tracheostomy. We conclude that obstructive sleep apnea may impair sleep related growth hormone release. Obstructive sleep apnea may be a useful model for other diseases in which growth failure and sleep disturbances are linked.

Sleep deprivation as a probe in the elderly.

Abstract: • Decreased slow-wave sleep (SWS) and sleep continuity are major effects of healthy aging and of associated psychopathological states. Using sleep deprivation, we studied the extent to which age- and psychopathology-related sleep "decay" is reversible in aged normal, depressed, and demented subjects. Depression or probable Alzheimer's dementia compromised the augmentation of sleep continuity and SWS seen in healthy elderly following sleep deprivation. Rapid eye movement (REM) latency decreased during recovery sleep in the controls but increased in both patient groups. Compared with demented patients, depressed elderly had greater severity of sleep continuity disturbance both before and after sleep deprivation, a more protracted course of recovery sleep, and increased slow-wave density in the second non-REM (NREM) sleep period (during recovery). The REM sleep time was diminished in dementia compared with depression both at baseline and during recovery sleep. These differential effects of age, health, and neuropsychiatric disease on recovery from sleep loss are relevant to recovery or reversal theories of sleep and have implications for daytime well-being in the elderly.

Serotonin neurons and sleep. I. Long term recordings of dorsal raphe discharge frequency and PGO waves.

Abstract: Brain stem transection studies suggest that pontine neurons play a key role in regulating the mammalian sleep cycle. The serotonin (5-HT) hypothesis originally postulated that pontine 5-HT containing neurons directly initiated and maintained synchronized or NREM sleep and "primed" rapid eye movement (REM) sleep. Contrary to the predictions of this hypothesis, single unit recordings from the serotonergic dorsal raphe nucleus (DRN) have uniformly shown that DRN discharge rate is positively correlated with behavioral arousal but negatively correlated with both the NREM and REM phases of sleep. These findings required revision of the original 5-HT hypothesis and suggested instead that DRN discharge may influence the maintenance of behavioral arousal and, by ceasing to discharge, may contribute to the generation of NREM and REM sleep. The purpose of this paper was to quantitatively assess the strength of the correlation between DRN discharge, REM sleep, and PGO waves following the experimental perturbations of the sleep cycle. Since forced locomotor activity is known to powerfully alter the timing of sleep and wakefulness, the present experiments used forced activity in an attempt to dissociate DRN discharge from the sleep cycle. It was hypothesized that such dissociations would suggest DRN discharge is not involved in sleep cycle regulation. Contrastingly, preserved correlations would support the hypothesis of a possible causal relationship between DRN discharge, PGO waves activity, and the timing of sleep and wakefulness. Extracellular recordings were obtained from single cells in the DRN of intact, undrugged cats across greater than 300 sleep cycles with durations ranging from about 8 to 80 mins. Forced activity significantly reduced the amount of time spent in wakefulness and increased the number but not the duration of REM sleep epochs. The results revealed that DRN discharge rate was altered as a function of sleep cycle duration. In no case, however, was forced activity able to completely dissociate the characteristic DRN discharge rates from PGO waves or the ultradian sleep cycle. The inability of forced activity to disrupt the faithful relationships between DRN discharge, PGO waves, and sleep cycle phase thus provides a new form of correlative evidence consistent with the hypothesis that the DRN is involved in sleep cycle regulation.

Slow wave sleep deficiency insomnia: a problem in thermo-downregulation at sleep onset.

Abstract: The following review article attempts to develop the argument that a regulated, rapid drop in rectal, core-body temperature following sleep onset is a necessary prerequisite to the presence of sustained slow wave sleep (NREM Stage 4). Based upon this premise, a theory1 is presented to suggest that the slow wave sleep deficiency so commonly associated with chronic, primary insomnia (Gaillard, 1976, 1978) is the result of a failure in the thermoregulatory system to show a regulated, rapid decrease in body temperature with sleep onset which persists for the first 1–2 hrs into the sleep period.

Sleep EEG with or without sleep deprivation? Does sleep deprivation activate more epileptic activity in patients suffering from different types of epilepsy?

Abstract: A sleep EEG of 190 patients without sleep deprivation was recorded, followed by a sleep EEG after 24 h of sleep deprivation on the next day. The patients suffered from various types of epilepsy, in th

Response of polygraphic sleep to phenytoin treatment for epilepsy. A longitudinal study of immediate, short- and long-term effects.

Abstract: Report on a prospective longitudinal study of alterations in polygraphic sleep by phenytoin monotherapy for epilepsy. A first dose of 100mg already caused abbreviation of sleep latency and an increase of slow-wave sleep in the first NREM-REM cycle. In the course of adjustments to steady state, an increase of Stage 3 + 4 sleep in the later REM cycles developed, such that the percentage of slow-wave sleep for the whole night was also augmented, whereas the percentage of light sleep decreased. Sleep structure was affected particularly in the third NREM-REM cycle. With continuing therapy, however, these effects were reversed. The only permanent effect was an abbreviated sleep latency. There were only minimal differences in the response of generalized and of localization-related epilepsies. Serum drug levels had only a very limited influence, seizure control and length of follow-up had no influence on the results. As a collateral finding, a delayed further decrease of epileptic discharges during sleep was observed under long-term conditions in patients who were seizure-free and had been so since adjustment to the steady state.

Differential effects of hydrocortisone, fluocortolone, and aldosterone on nocturnal sleep in humans.

Abstract: Previous experiments have suggested that sleep processes are sensitive to influences of corticosteroids. The present experiment was designed to compare effects of three different corticosteroids on human sleep: fluocortolone (a synthetic pure glucocorticoid), cortisol which possesses glucocorticoid and mineralocorticoid activity, and aldosterone (the major mineralocorticoid). Ten male adult subjects were tested in four experimental nights according to a double-blind latin-square design under conditions of either 1.0 mg of aldosterone, 20 mg of fluocortolone, 80 mg of hydrocortisone, or placebo. Substances were administered orally (fluocortolone, 23.00 h) or infused iv throughout the night (hydrocortisone, aldosterone) starting at 23.00 h. Hydrocortisone and fluocortolone induced a substantial reduction of rapid eye movement sleep. Hydrocortisone increased slow wave sleep activity. No such effect was observed after fluocortolone. Effects on sleep processes of aldosterone, in general, seemed to be neglegible. The results demonstrate differential effects of synthetic glucocorticoid, cortisol, and aldosterone on sleep in humans, which may be attributed to the heterogeneity of corticosteroid receptors in the brain.

Effects of nighttime nap and age on sleep patterns of shift workers.

Abstract: The effects of nighttime nap and age on sleep patterns of shift workers were examined for two groups of young and older guards working a 24-h shift with a nighttime nap of approximately 3.2 h. For both groups, day sleep was reduced by approximately 4.1 h, mainly affecting stage 2 sleep, slow wave sleep (SWS), and REM sleep. The totals of the different sleep stages of the nighttime nap plus day sleep were shorter than those of the control night only in stage 2 sleep. The nighttime nap appears to compensate for the sleep loss caused by night duty. During day sleep, the older subjects had relatively more awakenings and stage shifts. In the older group, the acrophase of oral temperature exhibited a significant phase advance of circadian rhythm, with reductions of means in the mesor and amplitude. Morningness-eveningness questionnaires tended to show higher scores (morningness) for the older group. From these results, it was determined that for older workers, an aberration in the phase of the circadian rhythm would slightly increase the difficulty of day sleep following night duty.