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Sleep electroencephalograms and sleep stages in hypoparathyroidism.

2 patients with hypoparathyroidism, one idiopathic and the other pseudoform, were studied by overnight polygraphic recording of the sleep EEG and related activities before and after start of treatment to investigate their sleep EEG patterns and states, with the results as follows. (1) Conspicuous abnormalities were noted in the sleep record, namely, disappearance of humps, spindles and hill waves, emergence of the mitten pattern and rather monotonous delta rhythm bursts. The EEGs, both awake and asleep, showed findings suggestive of a possible disorder of the desynchronizing mechanism of the brain stem. Normal sleep EEG patterns were restored after the serum calcium level had returned to the normal range. (2) In the course of overnight sleep, disturbance in the cyclic changes of sleep EEG pattern and absence of REM sleep were observed. Restoration to the normal course of sleep was achieved following the normalization of serum calcium level. Divalent calcium ion is considered to have intimate bearing upon the mechanism whereby synaptic chemical transmitters are activated. When viewed with reference to the monoamine hypothesis of Jouvet, the disturbance in the course of sleep observed in the present cases, especially the absence of or disturbed REM sleep, is inferred to be related to the hypocalcemia.

Child↗

Sleep fragmentation, awake blood pressure, and sleep-disordered breathing in a population-based study.

Arousal from sleep produces transient increases in systemic blood pressure, leading to the suggestion that repeated arousals are associated with a sustained increase in daytime blood pressure. Using data from the Wisconsin Sleep Cohort Study, a population-based study, we tested the hypothesis that sleep fragmentation is associated with elevated awake blood pressure. Sleep, breathing, and seated blood pressure measurements from 1,021 participants (age 42 +/- 8 yr; 590 males) were analyzed. Sleep fragmentation was defined as the total number of awakenings and shifts to Stage 1 sleep divided by the total sleep time (sleep fragmentation index: SFI). To reduce the confounding influence of sleep-disordered breathing, which is related to both increased daytime blood pressure and sleep fragmentation, all participants with an apnea-hypopnea index (AHI) > or = 1 were analyzed separately. Accounting for the influences of sex, age, body mass index, and antihypertensive medication use, the SFI was significantly associated with higher levels of awake systolic blood pressure in people with an AHI < 1; a 2 standard deviation increase in the SFI was associated with a 3.1 mm Hg rise in awake systolic blood pressure. In participants with an AHI > or = 1, there was no independent association between the SFI and awake blood pressure after controlling for the influence of the AHI.

Adult↗

Localization of upper airway collapse during sleep in patients with obstructive sleep apnea.

The present study was conducted to determine the effects of body position and sleep state, as well as the effect of uvulopalatopharyngoplasty (UPPP) on the regions over which the upper airway (UA) collapses during sleep. To accomplish this goal, 18 male patients with obstructive sleep apnea (OSA) underwent overnight polysomnography with simultaneous monitoring of pressures in the posterior nasopharynx, oropharynx, hypopharynx, and esophagus. From the profile of pressures recorded in the UA and esophagus, the regions over which the UA collapses during apneas could be determined. The patients were 54 +/- 14 y of age and were grossly obese with a body mass index of 37 +/- 2 kg/m2. They had moderately severe OSA with a mean apnea plus hypopnea index of 62 +/- 8 per hour. During NREM sleep, 10 of the 18 (56%) patients had collapse confined to the velopharyngeal or retropalatal segment of the upper airway. The remaining 44% of the patients demonstrated collapse of the retroglossal segment of the oropharynx located caudal to the inferior margin of the soft palate. Upper airway collapse at the level of the hyoid bone was not observed during NREM sleep. Observations made during REM sleep in nine patients demonstrated that collapse occurred in a more caudal segment of the UA in seven patients during REM than during NREM sleep. The effect of sleep position was evaluated in 10 patients and found to have little affect on the extent over which the UA collapsed during sleep independent of sleep state. The effects of UPPP on regional UA collapse were evaluated in a small group of six patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Neurobiology of the sleep-wake cycle: sleep architecture, circadian regulation, and regulatory feedback.

This mini-review article presents the remarkable progress that has been made in the past decade in our understanding of the neural circuitry underlying the regulation of sleep-wake states and circadian control of behaviors. Following a brief introduction to sleep architecture and physiology, the authors describe the neural circuitry and neurotransmitters that regulate sleep and cortical arousal (i.e., wakefulness). They next examine how sleep and wakefulness are regulated by mutual inhibition between sleep-and arousal-promoting circuitry and how this interaction functions analogously to an electronic "flip-flop" switch that ensures behavioral state stability. The authors then discuss the role of circadian and homeostatic processes in the consolidation of sleep, including the physiologic basis of homeostatic sleep drive (i.e., wake-dependent increase in sleep propensity) and the role of the SCN in the circadian regulation of sleep-wake cycles. Finally, they describe the hypothalamic circuitry for the integration of photic and nonphotic environmental time cues and how this integration allows organisms to sculpt patterns of rest-activity and sleep-wake cycles that are optimally adaptive.

Animals↗

On the interactions of the hypothalamic-pituitary-adrenal (HPA) axis and sleep: normal HPA axis activity and circadian rhythm, exemplary sleep disorders.

The hypothalamic-pituitary-adrenal (HPA) axis plays important roles in maintaining alertness and modulating sleep. Dysfunction of this axis at any level (CRH receptor, glucocorticoid receptor, or mineralocorticoid receptor) can disrupt sleep. Herein, we review normal sleep, normal HPA axis physiology and circadian rhythm, the effects of the HPA axis on sleep, as well as the effects of sleep on the HPA axis. We also discuss the potential role of CRH in circadian-dependent alerting, aside from its role in the stress response. Two clinically relevant sleep disorders with likely HPA axis dysfunction, insomnia and obstructive sleep apnea, are discussed. In insomnia, we discuss how HPA axis hyperactivity may be partially causal to the clinical syndrome. In obstructive sleep apnea, we discuss how HPA axis hyperactivity may be a consequence of the disorder and contribute to secondary pathology such as insulin resistance, hypertension, depression, and insomnia. Mechanisms by which cortisol can affect slow wave sleep are discussed, as is the role the HPA axis plays in secondary effects of primary sleep disorders.

Circadian Rhythm↗

Inhibition of serotonergic neurons in the nucleus paragigantocellularis lateralis fragments sleep and decreases rapid eye movement sleep in the piglet: implications for sudden infant death syndrome.

Serotonergic receptor binding is altered in the medullary serotonergic nuclei, including the paragigantocellularis lateralis (PGCL), in many infants who die of sudden infant death syndrome (SIDS). The PGCL receives inputs from many sites in the caudal brainstem and projects to the spinal cord and to more rostral areas important for arousal and vigilance. We have shown previously that local unilateral nonspecific neuronal inhibition in this region with GABA(A) agonists disrupts sleep architecture. We hypothesized that specifically inhibiting serotonergic activity in the PGCL would result in less sleep and heightened vigilance. We analyzed sleep before and after unilaterally dialyzing the 5-HT1A agonist (+/-)-8-hydroxy-2-(dipropylamino)-tetralin (8-OH-DPAT) into the juxtafacial PGCL in conscious newborn piglets. 8-OH-DPAT dialysis resulted in fragmented sleep with an increase in the number and a decrease in the duration of bouts of nonrapid eye movement (NREM) sleep and a marked decrease in amount of rapid eye movement (REM) sleep. After 8-OH-DPAT dialysis, there were decreases in body movements, including shivering, during NREM sleep; body temperature and heart rate also decreased. The effects of 8-OH-DPAT were blocked by local pretreatment with N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinylcyclohexane-carboxamide, a selective 5-HT1A antagonist. Destruction of serotonergic neurons with 5,7-DHT resulted in fragmented sleep and eliminated the effects of subsequent 8-OH-DPAT dialysis on REM but not the effects on body temperature or heart rate. We conclude that neurons expressing 5-HT1A autoreceptors in the juxtafacial PGCL are involved in regulating or modulating sleep. Abnormalities in the function of these neurons may alter sleep homeostasis and contribute to the etiology of SIDS.

Animals↗

[Relation between changes in arousal level with shift of sleeping time and subsequent sleep stage pattern].

The relationship between decrease in cerebral arousal level and sleep stage pattern was examined when a cycle of 22 h-wake and 8 h-sleep was repeated four times. The subjects of the experiment were six healthy male university students. The results of the experiment showed that the period between the time when the average score of Stanford Sleepiness Scale (SSS) reached point four (a little foggy) and the rising time was gradually decreased by repetition of the 22 h-wake and 8 h-sleep cycle. It was also found that the average score for the 6th experimental day after the third cycle was significantly increased, compared with that for the 1st 22 h waking period. These results show that the cerebral arousal level, which was indicated on the scores of SSS, was gradually decreased under the present experimental wake-sleep condition. The day-to-day variation of critical fusion frequency showed a tendency similar to that of SSS, demonstrating a gradual decrease in arousal level. On the other hand, stage 4 sleep (S4) was significantly increased during sleep after the 1st 22 h waking period, compared with baseline sleep after 16 h waking time. However, a significant increase in S4 was not seen during the sleeping periods in the second to the fourth cycles of 22 h-wake and 8 h-sleep, compared with that during the sleep after the 1st 22 h waking period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Changes in the arterial PCO2 during a single night's sleep in patients with obstructive sleep apnea.

To investigate the relationship between hypercapnia during sleep and its influence on the PaCO2 during the morning after sleep in patients with obstructive sleep apnea syndrome (OSAS), the transcutaneous PCO2 (PtcCO2) was measured throughout the night, and the arterial blood gases (ABG) were also measured while awake before and after polysomnography in 30 OSAS patients with (n=13, hypercapnic group: HC) and without (n=17, normocapnic group: NC) hypercapnia. Significant differences were observed in the body mass index (p=0.03), the difference between the highest PtcCO2 during sleep and the PtcCO2 during awake before sleep (D-PtcCO2), (HC: 11.l+/-1.7 mmHg; NC: 6.3+/-0.5 mmHg; p=0.0057) and the lowest SaO2 during sleep (p=0.0007). In the HC, the PaCO2 on the morning after sleep (50.0+/-0.14 mmHg) was significantly increased (p=0.0029) compared with the PaCO2 on the night before sleep (47.4+/-1.1 mmHg). In the NC, this phenomenon was not observed. Severe hypercapnia (high D-PtcCO2) during a single night's sleep has a significant effect on the waking PaCO2 immediately following sleep in the HC.

Body Mass Index↗

[Diurnal sleep study for sleep related breathing disorders--comparative study of diurnal polysomnography using diazepam with nocturnal polysomnography].

UNLABELLED: Nocturnal polysomnography (n-PSG) and diurnal polysomnography using diazepam (d-PSGD) were performed on 46 patients with sleep related breathing disorders including sleep spnea syndrome (SAS) patients and simple snorers. Sleep stage, apnea type, and various indices of breathing disorders were examined, and the results obtained by the two different sleep studies were compared. There were no significant differences in either the apnea type or the indices of breathing disorders between the two sleep studies. Concerning the sleep stage, significant differences in the duration of REM sleep between the two sleep studies were observed. In the duration of each stage of NREM sleep, however, there were no significant differences. Also, no significant differences were observed in the indices of breathing disorders between SAS patients and simple snorers. IN CONCLUSION: d-PSGD can be utilized as a substitute for n-PSG clinically, in patients with sleep related breathing disorders, as far as the study of NREM stages is concerned.

Adolescent↗

Effects of modafinil and amphetamine on sleep-wake cycle after sleep deprivation in cats.

AIM: The effects of modafinil and amphetamine on sleep-wake cycle and cortical power spectrum were assessed in the cats before and after sleep deprivation. METHODS: The sleep deprivation in the cats was used with the water tank technique. Cats were administrated with modafinil (5 mg.kg-1 p.o.) or amphetamine (1 mg.kg-1) before and after sleep deprivation. RESULTS: The waking effect of 8-10 h induced by modafinil before and after sleep deprivation was similar and was not followed by an increase in sleep rebound. On the contrary, the arousal effect about 8 h evoked by amphetamine after sleep deprivation was less lasting than that of 10-12 h observed in normal conditions and followed by an amplified rebound in both deep slow wave sleep and paradoxical sleep. CONCLUSION: These results suggest the efficiency of modafinil against somnolence and hypersomnia without increasing subsequent sleep.

Amphetamine↗

The effect of surgical weight reduction on sleep quality in obesity-related sleep apnea syndrome.

Obesity-related sleep apnea syndrome (SAS) was diagnosed in 13 patients evaluated for gastric bypass surgery. A diagnostic sleep study was performed whenever a specially designed questionnaire revealed characteristic signs of sleep disturbances. Pretreatment polyhypnographic recordings of patients with SAS demonstrated considerable reduction of deep and rapid eye movement (REM) sleep stages with a correspondent prolongation of wake within sleep or non-REM sleep stages I and II. After surgical weight reduction repeated polyhypnographic recordings revealed considerable improvement or even a complete recovery of breathing in sleep and a normalization of sleep structure. Non-REM deep sleep stages (III and IV) augmented from 5.51% +/- 2.53% (mean + SEM) to 22.69% +/- 3.56% (p less than 0.002), and the REM stage increased from 9.91% +/- 1.78% to 18.15% +/- 2.13% (p less than 0.005). Surgical weight reduction in obesity-related SAS is a valuable therapeutic measure for this respiratory derangement, as well as for sleep quality.

Female↗

Effects of sleep deprivation on naval seamen: II. Short recovery sleep on performance.

Twenty male naval volunteers, aged 18 to 20 years, with 12 to 14 years of education, underwent a total sleep deprivation experiment on board a Republic of Singapore Navy landing ship in the South China Sea for a period of 42-102 hours. The sleep group comprised eight volunteers who dropped out at the 44th-46th h of the experiment and were randomly assigned to a 2 or 4 h sleep regime. The rest served as sleep-deprived controls. Neurobehavioural performance tests, profile of mood state and the Stanford Sleepiness Scale were applied 6 hourly starting from 6.00 am on the first experimental day. No thresholds were observed in the performance of tests related to manual tasks and subjective feeling, including naval tasks, mood and sleepiness scale during the sleep deprivation experiment. However, thresholds were observed in the performance of tests requiring cognitive and perceptive skills, including the grooved peg board, trail making, sea-shore rhythm, addition, digit span, digit symbol, flicker fusion and dynamometer tests. Performances in these tests were observed to deteriorate only after approximately 30 h of sleep deprivation. The Z score for the non-threshold tests (Z-N) deteriorated from -0.01 at the start of the experiment to 1.25 at the 42nd h of the experiment just before the imposed sleep and improved to 0.81 at the 48th h of the experiment just after the imposed sleep; and the Z score for the threshold tests (Z-T) varied from -0.07 at the start to 0.49 just before sleep (at the 42nd h) and to continuously deteriorate to 0.83 just after sleep (at the 48th h).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

The echidna Tachyglossus aculeatus combines REM and non-REM aspects in a single sleep state: implications for the evolution of sleep.

Placental and marsupial mammals exist in three states of consciousness: waking, non-REM sleep, and REM sleep. We now report that the echidna Tachyglossus aculeatus, a representative of the earliest branch of mammalian evolution (the monotremes), does not have the pattern of neuronal activity of either of the sleep states seen in nonmonotreme mammals. Echidna sleep was characterized by increased brainstem unit discharge variability, as in REM sleep. However, the discharge rate decreased and the EEG was synchronized, as in non-REM sleep. Our results suggest that REM and non-REM sleep evolved as a differentiation of a single, phylogenetically older sleep state. We hypothesize that the physiological changes that occur during postnatal sleep development parallel certain aspects of the changes that have occurred during the evolution of sleep-waking states in mammals.

Animals↗

REM-sleep-hypertension in obstructive sleep apnea.

Previous investigations involving continuous blood pressure (BP) monitoring have shown an important alteration of the 24-hour BP profile in patients with obstructive sleep apnea syndrome (OSAS). We investigated the impact of REM sleep on the 24-hour BP cycle in 16 severe OSAS male patients (mean respiratory disturbance index = 66 +/- 16 events/hour of sleep), with hypertension (mean BP 162 +/- 21/105 +/- 11 mmHg World Health Organization (WHO) protocol). Two successive nights of polysomnography were performed, and arterial BP was monitored continuously during the second 24-hour period after brachial artery cannulation. During the daytime, subjects were kept awake and supine. At 3 p.m. BP was continuously monitored during quiet supine wakefulness for 20 minutes. Systolic, diastolic and mean BP and heart rate (HR) were analyzed and tabulated in mean values of 5 minute segments. Sleep/wake information were correlated with cardiovascular variables. Each uninterrupted REM sleep period was identified and comparison between the period of quiet supine wakefulness and REM sleep HR and BP values was performed. 8 OSAS patients presented a normal drop of the mean arterial BP during the nocturnal REM sleep periods compared to quiet supine wakefulness (mean value = -10.8 +/- 7.3 mmHg) ("dippers") while the other 8 subjects ("REM sleep non dippers"), revealed an elevated mean arterial BP during REM sleep (mean value = 18.9 +/- 10.9 mm Hg). The absence of the normal circadian BP dip seen during the nocturnal sleep period is considered as an indication of vascular risk. The REM sleep non dipping may play a role in this risk.

Adult↗

[Disorders of sleep structure and autonomic regulation in sleep of patients with stroke].

Peculiarities of both the structure of night sleep and autonomic regulation in the sleep were studied in 30 patients with ischemic stroke of different location. Clinical, polysomnographic (including autonomic indices) and psychologic methods were used. Considerable alterations in the structure of night sleep were observed, namely: lengthening of the period of falling asleep, increase of the time of awakening inside the sleep, impossibility to support necessary duration of both stages and phases of sleep. The indices of cardiovascular system's activity such as heart rate (HR) and arterial pressure (AP) were altered most of all. The most dramatic disorders of both the structure of sleep and autonomic regulation in the sleep were found in right hemispheric and medial location of ischemic stroke. High values of HR and AP in the sleep (especially in phase of the fast sleep), high HR and AP variability as well as the decrease of these indices from the first cycle of the sleep to the third one were prognostically unfavourable factors.

Adult↗

Effects of sleep and sleep loss on immunity and cytokines.

Sleep is hypothesized to be a restorative process that is important for the proper functioning of the immune system. Severity of disordered sleep in depressed- and alcoholic subjects correlates with declines in natural- and cellular immunity and is associated with alterations in the complex cytokine network. Sleep loss has a role in mediating these immune changes as experimentally induced partial night sleep deprivation replicates the kind of sleep loss found in clinical samples and induces a pattern of immune alterations similar to that found in depressed- and alcoholic patients. Despite evidence that sleep and sleep loss have effects on immune processes and nocturnal secretion of cytokines, the clinical significance of these immune changes is not known. Moreover, in view of basic evidence of a reciprocal interaction between sleep and cytokines, further research is needed to understand whether alterations in cytokines contribute to disordered sleep in patient populations.

Alcoholism↗

Lack of delta waves and sleep disturbances during non-rapid eye movement sleep in mice lacking alpha1G-subunit of T-type calcium channels.

T-type calcium channels have been implicated as a pacemaker for brain rhythms during sleep but their contribution to behavioral states of sleep has been relatively uncertain. Here, we found that mice lacking alpha1(G) T-type Ca(2+) channels showed a loss of the thalamic delta (1-4 Hz) waves and a reduction of sleep spindles (7-14 Hz), whereas slow (<1 Hz) rhythms were relatively intact, when compared with the wild-type during urethane anesthesia and non-rapid eye movement (NREM) sleep. Analysis of sleep disturbances, as defined by the occurrence of brief awakening (BA) episodes during NREM sleep, revealed that mutant mice exhibited a higher incidence of BAs of >16 sec compared with the wild-type, whereas no difference was seen in BAs of <16 sec between the two genotypes. These results are consistent with the previous idea of the distinct nature of delta oscillations and sleep spindles from cortically generated slow waves. These results also suggest that the alpha1(G)-subunit of T-type calcium channels plays a critical role in the genesis of thalamocortical oscillations and contributes to the modulation of sleep states and the transition between NREM sleep and wake states.

Animals↗

[Sleep disorders in elderly, the sleep apnea syndrome in particular: are they a cause of insomnia? A review of literature].

In this publication a review is presented based on the findings resulting from sleep-wake investigations searching for sleep disorders associated with insomnia in relatively healthy elderly. 44 Relevant journal articles published between 1980-1998 were found. The four most important sleep disorders which can be accompanied by sleeplessness in relatively healthy elderly people are periodic leg movements disorder (PLM), restless legs syndrome (RLS), REM sleep behaviour disorder (RBD) and sleep apnea syndrome (SAS). Of these disorders, sleep apnea and periodic leg movements occur most frequently, in a quarter of the elderly. The latter, however, seldom complain about sleeplessness. Within the category of older people disorders characterized by movements during sleep increase significantly with age, nightly respiration disorders do not. SAS, PLM and RBD appear most frequently in men and RLS in women. The disorders characterized by movements during sleep (especially RLS and RBD) are often accompanied by sleeplessness. SAS, however, is more closely associated with day-time sleepiness than with sleeplessness. No combination of demographic variables and symptoms allows a reliable prediction of these sleep disorders. Fortunately, these disorders are not a major threat to the health of older people.

Adult↗