Showing papers on "Slow-wave sleep published in 1994"

Effect of unilateral somatosensory stimulation prior to sleep on the sleep EEG in humans.

Abstract: SUMMARY The hypothesis that local activation of brain regions during wakefulness affects the EEG recorded from these regions during sleep was tested by applying vibratory stimuli to one hand prior to sleep. Eight subjects slept in the laboratory for five consecutive nights. During a 6-h period prior to night 3, either the left or the right hand was vibrated intermittently (20 min on-8 min off), while prior to night 5 the same treatment was applied to the contralateral hand. The sleep EEG was recorded from frontal, central, parietal and occipital derivations and subjected to spectral analysis. The interhemispheric asymmetry index (IAI) was calculated for spectral power in nonREM sleep in the frequency range 0.25-25.0 Hz for 0.5-Hz or 1-Hz bins. In the first hour of sleep following right-hand stimulation, the IAI of the central derivation was increased relative to baseline, which corresponds to a shift of power towards the left hemisphere. This effect was most prominent in the delta range, was limited to the first hour of sleep and was restricted to the central derivation situated over the somatosensory cortex. No significant changes were observed following left-hand stimulation. Although the effect was small, it is consistent with the hypothesis that the activation of specific neuronal populations during wakefulness may have repercussions on their electrical activity pattern during subsequent sleep.

Microbial Products and Cytokines in Sleep and Fever Regulation

Abstract: Excessive sleepiness and fever are constitutional symptoms associated with systemic infection. Although fevers have been investigated for many years, sleep responses to infectious challenge have only recently been investigated. Inoculation of animals with bacterial, viral, protozoan and fungal organisms result in complex sleep responses dependent upon the microbial agent and route of administration. The general pattern is characterized by an initial robust increase in non-rapid eye movement sleep (NREMS) followed by a period of NREMS inhibition. REMS is inhibited after infectious challenge. The sleep responses are accompanied by fever but the two responses are, in part, independent from each other. Sleep responses, like fevers, may be beneficial to host defense although this area is relatively uninvestigated. Microbial products likely responsible for sleep and fever responses include bacterial muramyl peptides and endotoxin, and viral double stranded RNA. These microbial products induce sleep and fever responses in animal models. The exact mechanism of how these structurally diverse microbial products elicit sleep and fever remain unknown; however these substances share the ability to induce cytokine production. Cytokines such as interleukin-1 (IL-1), tumor necrosis factor, acidic fibroblast growth factor (FGF), and interferon-alpha (IFN-alpha) are somnogenic whether given directly into brain or intravenously. Other cytokines lack somnogenic activity, e.g., IL-2, IL-6, IFN beta and basic FGF. The somnogenic actions of cytokines probably involve growth hormone-releasing hormone (GHRH) and nitric oxide. Anti-GHRH or inhibition of NO production inhibits normal sleep and inhibits IL-1-induced sleep. In conclusion, cytokines are likely key mediators of fever and sleep responses to infection. The microbial-cytokine altered sleep likely results from an amplification of physiological sleep mechanisms which include cytokines, several neuropeptides and neurotransmitters such as nitric oxide.

Sleep cycles and alpha-delta sleep in fibromyalgia syndrome.

Abstract: Objective Fibromyalgia syndrome (FMS) is a musculoskeletal disorder characterized by generalized pain, localized tender points, chronic fatigue and nonrestorative sleep. Since sleep disturbances frequently occur in FMS and alpha intrusion in nonrapid eye movement (NREM) sleep probably associates with the nonrefreshing sleep, we prospectively studied the delta and alpha activity and alpha-delta ratio across sleep cycles, performing polysomnography in 10 patients with FMS and in 14 healthy control subjects. Methods Night long polysomnography recordings were performed in all subjects. Sleep scoring was done visually according to Rechtschaffen and Kales criteria. By means of spectral analysis the conventional electroencephalogram (EEG) frequency bands were automatically computed for the all night recordings. For alpha and delta power the integrated and normalized values were calculated for each sleep cycle, the evolution of these activities across successive sleep cycles was studied. Results Alpha-delta patterns occurred in almost all the patients who had also superficial and fragmented sleep with increased awakenings and reduced REM and slow wave sleep. Delta decay across sleep cycles was different in FMS and alpha activity was greater and declined, whereas the controls were persistently low throughout their sleep. Alpha-delta ratio increased progressively in successive sleep cycles; this was again different from controls. Conclusion Patients with FMS presented a high frequency of subjective sleep disturbances, an increased incidence of alpha EEG NREM sleep and clear abnormalities in sleep cycle organization.

Changes in Sleep and Sleep Electroencephalogram During Pregnancy

Abstract: The impairment of sleep quality is a common complaint during pregnancy. To investigate the changes in sleep in the course of pregnancy, the sleep electroencephalogram (EEG) was recorded and analyzed in nine healthy women on 2 consecutive nights during each trimester of pregnancy. Waking after sleep onset increased from the second (TR2) to the third (TR3) trimester, whereas rapid eye movement (REM) sleep decreased from the first trimester (TR1) to TR2. Spectral analysis of the EEG in nonrapid eye movement (NREM) sleep revealed a progressive reduction of power density in the course of pregnancy. In comparison to TR1, the values in TR2 were significantly lower in the 10.25-11.0-Hz and 14.25-17.0-Hz bands. In TR3, the significant reduction extended over the ranges of 1.25-12.0 Hz and 13.25-16.0 Hz. The largest decrease (30%) occurred in the 14.25-15.0-Hz band. In REM sleep, the spindle frequency range was not affected, and a minor reduction of power density in some frequency bins below 12 Hz was present only in TR3. The study documents major alterations of the sleep EEG that are not evident from the sleep scores and that may be associated with the characteristic hormonal changes occurring during pregnancy.

The Thermoregulatory Effects of Menopausal Hot Flashes on Sleep

Abstract: Menopausal hot flashes are thought to be a disorder of thermoregulation initiated centrally within the medial preoptic area of the hypothalamus. These heat-loss mechanisms appear to be activated in the presence of normal core body temperature. Previous studies have demonstrated that thermal stimuli have the potential to alter sleep stages. We performed 24-hour ambulatory recordings of hot flashes and all-night sleep parameters on 12 postmenopausal women with hot flashes and seven postmenopausal women without flashes to determine whether the presence of hot flashes prior to sleep or during sleep itself would result in alterations in sleep pattern. The results show that hot flashes are associated with increased Stage 4 sleep and a shortened first rapid eye movement period. Hot flashes occurring in the 2 hours prior to sleep onset were positively correlated with the amount of slow-wave sleep. The central thermoregulatory mechanism underlying hot flashes may affect hypnogenic pathways inducing sleep and heat loss in the absence of a thermal load.

Hypothalamo‐preoptic Histaminergic Projections in Sleep‐Wake Control in the Cat

Abstract: Cats were chronically implanted with electrodes for polygraphic recordings and cannulae for intracerebral microinjections in order to study the functional role of histaminergic innervation of the preoptic-anterior hypothalamus in sleep-wake control. alpha-Fluoromethylhistidine (alpha FMH, 50 micrograms in 1 microliter), a specific inhibitor of the histamine-synthesizing enzyme, when injected bilaterally into the preoptic area, where numerous histaminergic fibres and terminal-like structures are present, caused a significant increase in deep slow wave sleep (S2) and paradoxical sleep (PS) and a decrease in wakefulness. In contrast, microinjections of histamine (5 or 30 micrograms in 1 microliter) in the same area dose-relatedly increased wakefulness and decreased both slow wave sleep and paradoxical sleep. The effects of histamine were reduced by pretreatment with mepyramine (1 mg/kg i.p.), a well known histamine H1 receptor antagonist, and were mimicked by a local injection of impromidine (1 microgram in 1 microliter), a potent histamine H2 receptor agonist. Microinjections of mepyramine alone (120 micrograms in 1 microliter) caused an increase in slow wave sleep. These results suggest that preoptic histaminergic innervation is involved in sleep-wake control and that the action might be mediated via both H1 and H2 receptors.

Experimental sleep fragmentation

Abstract: Thirty-six healthy young men and women (age range 21-35 years) were studied in an experimental model of sleep fragmentation. On 2 nights sleep was disrupted by presenting tones to produce brief electroencephalogram (EEG) arousals (without shortening sleep time) and daytime function was assessed the following day with the Multiple Sleep Latency Test and a divided attention performance test. The fragmentation of sleep produced significant disruption of nocturnal sleep and reduced daytime alertness. Adaptation in EEG-defined arousals occurred from the 1st to the 2nd night of fragmentation. Threshold (measured indirectly) characteristics of EEG-defined arousals were somewhat different than those of previous studies requiring behavioral awakening. The percent of tone series producing arousal, number of tones necessary for arousal and duration of the arousal all reflected heightened thresholds in stage 3/4 and rapid eye movement (REM) sleep compared to stage 1 and stage 2 sleep. In the last 3 hours of sleep versus the first 3 hours, arousals occurred less frequently, required more tones to produce, resulted in shorter durations and in fewer sleep stage changes, except for REM sleep where the converse was the case.

Sleep fragmentation in normals: a model for sleepiness associated with upper airway resistance syndrome.

Abstract: Summary: Eight young adults underwent I night of auditory sleep fragmentation followed by four naps of the multiple sleep latency test and performance testing the next day. A latin-square design was used to compare results with baseline. Efforts were made to eliminate effects of learning on repeated performance tests. A mean of 303 arousals, lasting a mean of II seconds, disrupted nocturnal sleep. This sleep fragmentation was induced to mimic as closely as possible the nocturnal sleep disruption seen in subjects with upper airway resistance syndrome. There was a significant disruption of nocturnal sleep architecture with a significant overall decrease in slow-wave sleep (SWS) and a significant but more moderate decrease in rapid eye movement (REM) sleep during the fragmented night. The most interesting finding related to analysis by thirds of the night, which indicated an important increase over time in arousal threshold during SWS followed by REM sleep. This threshold increase was associated with a parallel increase in dB(A) levels needed to induce an arousal. Stages I and 2 nonrapid eye movement (NREM) sleep were less affected by the stimulation, but the amount of stage I NREM sleep decreased from the beginning to the end of the night, again indicating an increase in pressure to sleep. Following I night of sleep fragmentation, subjects had significantly shorter sleep latencies on the multiple sleep latency test for naps 2, 3 and 4. There was a significant relationship between percent nocturnal SWS and mean sleep latencies. The selected performance tests were not affected by I night of sleep fragmentation, despite the obvious sleepiness. Key Words: Sleep fragmentation­ Upper airway resistance syndrome-Sleepiness-Performance testing.

Ontogenetic variations in auditory arousal threshold during sleep

Abstract: Developmental variations in auditory arousal thresholds during sleep were investigated in four groups of normal male subjects--children, preadolescents, adolescents, and young adults. Arousal thresholds were determined during NREM and REM sleep for tones presented via earphone insert on a single night following two adaptation nights of undisturbed sleep. Age-related relationships were observed for both awakening frequency and stimulus intensity required to effect awakening, with awakenings occurring more frequently in response to lower stimulus intensities with increasing age. Although stimulus intensities required for awakening were high and statistically equivalent across sleep stages in nonadults, higher intensity stimuli were required in Stage 4 relative to Stage 2 and REM sleep in adults. These results confirm previous observations of marked resistance to awakening during sleep in preadolescent children and suggest that processes underlying awakening from sleep undergo systematic modification during ontogenetic development.

Epilepsy with Electrical status epilepticus during slow sleep and secondary bilateral synchrony

Abstract: In 3 children with "epilepsy with electrical status epilepticus during slow sleep" (ESES), we estimated interhemispheric small time differences (TDs) during spike-wave activity in EEG by coherence and phase analysis by the two-dimensional autoregressive model to differentiate their continuous diffuse spike-waves during slow-wave sleep (CSWS) between primary bilateral synchrony and secondary bilateral synchrony (SBS). Maximal TDs at onset of apparently bilateral synchronous spike-wave bursts (BSSWs) during slow-wave sleep were 12.0-26.5 ms (mean 20.3 ms) with consistent leading hemispheres in eight bursts of the 3 patients, indicating SBS as pathophysiology of their CSWS. This suggestion was supported by their clinico-EEG findings, including the effect of a single oral dose of clobazam (CLB) on EEG. Three ictal BSSWs of atypical absence seizures in 2 patients were also analyzed to obtain maximal TDs of 17.9-41.7 ms (mean 26.3 ms) at onset, with the same leading sides as in sleep, also indicating SBS. Examination of intraburst TD variations showed no consistent disappearance of TDs during the latter part of the bursts, in either sleep or the ictal EEGs of atypical absences, and a role of the corpus callosum was suggested in the generation of SBS in ESES.

Memory self-report in Alzheimer's disease and in age-associated memory impairment.

Abstract: The effects of treatment with high doses (300 mg three times daily) of hypericum extract LI 160 on sleep quality and well-being were investigated over a 4-week period. The double-blind, placebo-controlled study was conducted with 12 older, healthy volunteers in a cross-over design, which included a 2-week wash-out phase between both treatment phases. A hypostatic influence of the REM sleep phases, which is typical for tricyclic antidepressants and MAO inhibitors, could not be shown for this phytopharmacon. Instead, LI 160 induced an increase of deep sleep during the total sleeping period. This could be shown consistently in the visual analysis of the sleeping phases 3 and 4, as well as in the automatic analysis of slow-wave EEG activities. The continuity of sleep was not improved by LI 160; this was also the case for the onset of the sleep, the intermittent wake-up phases, and total sleep duration.

Effects of pulsatile cortisol infusion on sleep‐EEG and nocturnal growth hormone release in healthy men

Abstract: SUMMARY This study investigates the short-term effects of pulsatile cortisol administrations upon sleep electroencephalogram (EEG) and spontaneous release of growth hormone (GH) in humans. Ten young healthy male volunteers received intravenous injections of either placebo or cortisol every 60 min between 17.00 hours and 06.00 hours (1 mg kg-1 BW with a loading dose of 20% starting at 17.00 hours, followed by a dose of 6% every hour until 06.00 hours). The amount of rapid eye-movement (REM) sleep was significantly reduced (placebo: 19.9 ± 1.8; cortisol: 12.2 ± 1.5%; P < 0.05), whereas the time spent in slow-wave sleep (SWS) was significantly increased (placebo: 9.4 ± 1.6; cortisol: 13.9 ± 1.9%; P < 0.05). The SWS-promoting effect was most prominent during the first hours of sleep, but tended to persist also during the second half of the night. The pulsatile cortisol administration augmented the total amount of plasma GH concentrations (mean area under the time course curve, AUC, placebo: 3.2 ± 0.5; cortisol: 4.4 ± 0.6 [ng × 1000 × ml min-1]; P < 0.05) due to an increase of GH release before sleep onset, and during the second half of the night, while the GH surge at sleep onset remained unchanged. Our data are in accordance with the hypotheses that cortisol-induced changes of both sleep-EEG and GH secretion involve a common mechanism that includes activation of the hypothalamic-somatotrophic (growth hormone releasing hormone-growth hormone) system.

Sleep in depression: the influence of age, gender and diagnostic subtype on baseline sleep and the cholinergic REM induction test with RS 86

Abstract: One hundred and eight healthy controls and 178 patients with a major depressive disorder according to DSM-III were investigated in the sleep laboratory after a 7-day drug wash-out period. Subsamples of 36 healthy controls and 56 patients additionally took part in the cholinergic rapid eye movement (REM) sleep induction test with RS 86. Data analysis revealed that age exerted powerful influences on sleep in control subjects and depressed patients. Sleep efficiency and amount of slow wave sleep (SWS) decreased with age, whereas the number of awakenings, early morning awakening, and amounts of wake time and stage 1 increased with age. REM latency was negatively correlated with age only in the group of patients with a major depression. Statistical analysis revealed group differences for almost all parameters of sleep continuity with disturbed indices in the depressed group. Differences in SWS were not detected. REM latency and REM density were altered in depression compared to healthy subjects. Sex differences existed for the amounts of stage 1 and SWS. The cholinergic REM induction test resulted in a significantly more pronounced induction of REM sleep in depressed patients compared with healthy controls, provoking sleep onset REM periods as well in those depressed patients showing baseline REM latencies in the normal range. Depressed patients with or without melancholia (according to DSM-III) did not differ from each other, either concerning baseline sleep or with respect to the results of the cholinergic REM induction test. The results stress the importance of age when comparing sleep patterns of healthy controls with those of depressed patients. Furthermore they underline the usefulness of the cholinergic REM induction test for differentiating depressed patients from healthy controls and support the reciprocal interaction model of nonREM-REM regulation and the cholinergic-aminergic imbalance hypothesis of affective disorders.

Clinical and polysomnographic effects of trazodone CR in chronic insomnia associated with dysthymia.

Abstract: Six middle aged subjects complaining of chronic insomnia associated with dysthymia were investigated in a 2-month single blind study: a 7-day placebo treatment period, followed by a 6-week phase with increasing doses of trazodone controlled release (CR) formulation (50 mg through days 8-10; 75 mg through days 11-13; 150 mg through days 14-49) and then a final 7-day withdrawal period under placebo. Medication was always administered at bedtime. Five polysomnographic recordings were accomplished by each subject (sleep 1: under baseline placebo; sleep 2-3-4; under active treatment; sleep 5: after drug discontinuation). A "blind" EEG reader analysed the traditional polysomnographic variables (macrostructure of sleep) and the amount and percentage ratio (CAP rate) of cyclic alternating pattern (CAP), the microstructural parameter that measures the instability of arousal during sleep. Visual analogue scales (VAS) for the evaluation of subjective sleep quality and the Hamilton rating scale for depression (HAM-D) were regularly assessed across the study. Statistical analysis was based on an ANOVA test with repeated measures completed by means of Bonferroni adjusted probabilities. No significant differences emerged from the macrostructural parameters referred to sleep initiation and maintenance, while significant overall modifications emerged from stage 2 (P < 0.0005), slow wave sleep (P < 0.0001), total CAP time (P < 0.0001) and CAP rate (P < 0.0001). Compared to the placebo baseline night, a significant increase of slow wave sleep (+40 min) and significant reductions of stage 2 (-67 min), CAP time (-90 min) and CAP rate (-23%) were already found on day 4 of treatment (sleep 2).(ABSTRACT TRUNCATED AT 250 WORDS)

Sleep EEG of patients with obsessive-compulsive disorder

Abstract: Twenty-two patients suffering from an obsessive and compulsive disorder (OCD) according to DSM-III-R were investigated by polysomnographic sleep EEG recordings under drug-free conditions and compared to age- and sex-matched healthy controls. Sleep efficiency was significantly lower and wake % SPT was significantly increased in the patient group compared to healthy subjects. Sleep architecture did not differ among the two samples. Especially REM sleep measures, in particular, REM latency did not differ among the groups. No positive correlation was found between sleep variables and rating inventories for obsession and compulsions (Y-BOCS), depression (Hamilton) and anxiety (CAS). A secondary depression did not influence sleep EEG variables. The results of this study contradict the assumption that OCD patients show REM sleep and slow wave sleep abnormalities similar to those shown by patients with primary depression.

Changes in Sleep-Wakefulness after Kainic Acid Lesion of the Preoptic Area in Rats.

Abstract: The role of the preoptic area (POA) neurons in the regulation of sleep-wakefulness (S-W) has been investigated in this study. The cell-specific neurotoxin, kainic acid (KA), was injected (0.8 microgram in 0.2 microliter) intracerebrally for lesioning of the POA. S-W was assessed (on the basis of EEG, EMG, and EOG recordings) for a day before bilateral lesion of the POA, and for 3 weeks after the lesion. There was an increase in wakefulness, and a decrease in all the stages of sleep after KA lesion of the POA. The reduction in deep slow wave sleep (S2) and REM sleep (PS) were more marked than light slow wave sleep (S1), and these had not shown any recovery even after 3 weeks of lesion. Two days after the lesion, the reduction in sleep was much more marked during the daytime than at night. There was an increase in locomotor activity, especially during the daytime, though it was only statistically significant on the 6th and the 10th day after the lesion. This study shows that the POA neurons are involved in the induction and maintenance of sleep. The lesion did not have a long lasting effect on the circadian distribution of sleep but the changes in locomotor activity seem to persist for a longer period.

Influence of the cholinesterase inhibitor galanthamine hydrobromide on normal sleep

Abstract: Evidence from animal experiments has suggested that the triggering and maintenance of rapid eye movement (REM) sleep is mainly under the control of cholinergic neurons in the brain stem. Correspondingly, studies in humans have demonstrated that the application of cholinergic agonists or cholinesterase inhibitors provokes an earlier onset of REM sleep. The present study investigated the influence of galanthamine hydrobromide, a reversible cholinesterase inhibitor, on REM sleep regulation in 18 healthy volunteers. After an adaptation night, the subjects were given two doses of galanthamine (10 mg and 15 mg) or placebo at 10 p.m. in a randomized double-blind design. Both doses of galanthamine shortened REM latency (with statistical significance depending on the definition of REM latency used), increased REM density, and reduced slow wave sleep mainly in the first non-REM cycle. Higher doses of galanthamine (15 mg) seem to be accompanied by unwanted side effects that warrant the application of a peripheral antidote. These results are comparable to those for other cholinomimetics and stress the usefulness of galanthamine for pharmacological challenge studies in healthy subjects and depressed patients.