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At least 775 records · Page 43Linked to original sources
PubMed2002

Is the nonREM-REM sleep cycle reset by forced awakenings from REM sleep?

In selective REM sleep deprivation (SRSD), the occurrence of stage REM is repeatedly interrupted by short awakenings. Typically, the interventions aggregate in clusters resembling the REM episodes in undisturbed sleep. This salient phenomenon can easily be explained if the nonREM-REM sleep process is continued during the periods of forced wakefulness. However, earlier studies have alternatively suggested that awakenings from sleep might rather discontinue and reset the ultradian process. Theoretically, the two explanations predict a different distribution of REM episode duration. We evaluated 117 SRSD treatment nights recorded from 14 depressive inpatients receiving low dosages of Trimipramine. The alarms were triggered by an automatic mechanism for the detection of REM sleep and had to be canceled by the subjects themselves. The REM episodes were determined as in undisturbed sleep-they had to include the remaining REM activity and were separated by 30 min without REM epochs. The frequency histogram of REM episodes declined exponentially with episode duration for each of the first four sleep cycles. The duration of nonREM intervals revealed bimodal distributions. These results were found consistent with the model assuming a reset of the ultradian cycle upon awakening. Whether REM or nonREM activity is resumed on return to sleep can be modeled by a random decision whereby the probability for REM sleep might depend on the momentary REM pressure.

Activity Cycles↗
PubMed1997

Nasal obstruction as a risk factor for sleep-disordered breathing. The University of Wisconsin Sleep and Respiratory Research Group.

Nasal obstruction frequently has been associated with sleep-disordered breathing as a potential etiologic factor. Nasal obstruction results in pathologic changes in airflow velocity and resistance. Experimentally produced nasal obstruction increases resistance and leads to sleep-disordered breathing events, including apnea, hypopnea, and snoring. Clinical research examining the correlation between nasal obstruction and sleep-disordered breathing is limited, especially in regard to patients with conditions that increase nasal resistance, such as rhinitis and sinusitis. To further identify risk factors for sleep-disordered breathing, the role of chronic and acute nasal congestion was investigated in a population-based sample. Data on nasal congestion history and sleep problems were obtained by questionnaire (n = 4927) and by objective inlaboratory measurement (n = 911). Participants who often or almost always experienced nighttime symptoms of rhinitis (5 or more nights a month) were significantly (p < 0.0001) more likely to report habitual snoring (3 to 7 nights a week), chronic excessive daytime sleepiness, or chronic nonrestorative sleep than were those who rarely or never had symptoms. Habitual snorers had significantly (p < 0.02) lower air flow than nonsnorers, although a linear relation between decreased airflow and sleep-disordered breathing severity did not exist. Participants who reported nasal congestion due to allergy were 1.8 times more likely to have moderate to severe sleep-disordered breathing than were those without nasal congestion due to allergy. Men and women with nasal obstruction, especially chronic nighttime symptoms of rhinitis, are significantly more likely to be habitual snorers, and a proportion also may have frequent episodes of apnea and hypopnea, indicative of severe sleep-disordered breathing. Because allergic rhinitis is a common cause of nasal obstruction and it is a modifiable risk factor, further study of this association is warranted.

Adult↗
PubMed2000

Diurnal preference, sleep habits, circadian sleep propensity and melatonin rhythm in healthy human subjects.

After 24-h sleep deprivation, 33 healthy young subjects entered the 10/20 min ultra-short sleep-wake schedule for 26 h. Melatonin rhythm was hourly assessed simultaneously. Results indicated that morning preference was significantly correlated with habitual sleep onset (r=-0.41, P=0.04), habitual sleep offset (r=-0.52, P=0.002), melatonin peak time (r=-0.36, P=0.04), and sleep propensity onset time (r=-0.36, P=0.04). The intervals between habitual sleep mid-point and melatonin peak time and between habitual sleep mid-point and sleep propensity onset time were significantly longer in morning-preference subjects than in evening-preference subjects (P<0.05). These findings suggest that the variance of diurnal preference may be related to differences in phase relations between habitual sleep timing and the circadian pacemaker.

Adult↗
PubMed2005

Sleep, breathing, and menopause: the effect of fluctuating estrogen and progesterone on sleep and breathing in women.

BACKGROUND: Sleep-disordered breathing (SDB), such as obstructive sleep apnea (OSA), is more common in men than in women. However, menopause increases the risk for development of OSA. Administration of estrogen and progesterone to postmenopausal women with OSA decreases apnea and hypopnea during sleep. OBJECTIVE: Because beneficial changes can be observed soon after administration of a short course of hormones, we hypothesized that suppression of these hormones would rapidly result in the development of SDB. METHODS: Production of sex hormones was suppressed with daily administration of leuprolide acetate (LA), a gonadotropin-releasing hormone analogue, for 5 weeks in women who were participating in a study on pharmacologically induced menopause and physiology. The subjects underwent polysomnographic evaluation at baseline and after 5 weeks of LA administration. RESULTS: In the 12 healthy women aged 18 to 34 years who participated in the study, sleep architecture and respiration were normal at baseline. After LA administration, the subjects stopped their menses, and their plasma concentrations of l7beta-estradiol (preadministration, mean [SD] 33.9 [9.0] pg/mL; post administration, 10.2 [3.4] pg/mL) and progesterone (preadministration, 0.48 [0.05] ng/mL; post administration, 0.40 [0.06] ng/mL) reached menopausal levels. Sex hormone deficiency was associated with climacteric vasomotor symptoms such as hot flashes and sweating. Sleep latencies and architecture did not change significantly with LA administration. The participants subjectively noticed some increased snoring that was not confirmed by polysomnogram. Specifically, there was no change in arousal index and no evidence for sleep fragmentation to suggest the presence of increased upper-airway resistance during sleep. The apnea-hypopnea index, 0.07 (0.02) to 0.22 (0.11) events per hour of sleep, did not change with sex hormone deficiency. CONCLUSIONS: In this study, sex hormone deficiency in young women resulted in climacteric symptoms and cessation of menses, and was not associated with sleep fragmentation or clinically significant SDB.

Adolescent↗
PubMed2001

The relationship of sleep quality and posttraumatic stress to potential sleep disorders in sexual assault survivors with nightmares, insomnia, and PTSD.

Sleep quality and posttraumatic stress disorder (PTSD) were examined in 151 sexual assault survivors, 77% of whom had previously reported symptoms of sleep-disordered breathing (SDB) or sleep movement disorders (SMD) or both. Participants completed the Pittsburgh Sleep Quality Index (PSQI) and the Posttraumatic Stress Scale (PSS). High PSQI scores reflected extremely poor sleep quality and correlated with PSS scores. PSQI scores were greater in participants with potential SDB or SMD or both. PSQI or PSS scores coupled with body-mass index and use of antidepressants or anxiolytics predicted potential sleep disorders. The relationship between sleep and posttraumatic stress appears to be more complex than can be explained by the current PTSD paradigm; and, sleep breathing and sleep movement disorders may be associated with this complexity.

Adult↗
PubMed2004

Nightmares, insomnia, and sleep-disordered breathing in fire evacuees seeking treatment for posttraumatic sleep disturbance.

Eight months after the Cerro Grande Fire, 78 evacuees seeking treatment for posttraumatic sleep disturbances were assessed for chronic nightmares, psychophysiological insomnia, and sleep-disordered breathing symptoms. Within this sample, 50% of participants were tested objectively for sleep-disordered breathing; 95% of those tested screened positive for sleep-disordered breathing. Multiple regression analyses demonstrated that these three sleep disorders accounted for 37% of the variance in posttraumatic stress symptoms, and each sleep disorder was significantly and independently associated with posttraumatic stress symptoms severity. The only systematic variable associated with posttraumatic stress symptoms of avoidance was sleep-disordered breathing. The findings suggest that three common sleep disorders relate to posttraumatic stress symptoms in a more complex manner than explained by the prevailing psychiatric paradigm, which conceptualizes sleep disturbances in PTSD merely as secondary symptoms of psychiatric distress.

Adult↗
PubMed1998

Autonomic markers of arousal during sleep in patients undergoing investigation for obstructive sleep apnoea, their relationship to EEG arousals, respiratory events and subjective sleepiness.

Estimating the degree of sleep fragmentation is an important part of a respiratory sleep study and is conventionally measured using EEG micro arousals or is inferred indirectly from respiratory abnormalities such as apnoeas and desaturations. There is a need for less labour-intensive measures of sleep fragmentation, and transient rises in blood pressure and heart rate may fulfil this role. Forty unselected sleep clinic referrals undergoing investigation for possible obstructive sleep apnoea (OSA) were studied with one night of polysomnography. Three conventional indices of sleep fragmentation (EEG micro arousals, apnoea/hypopnoea index (AHI) and oxygen saturation dip rate (SaO2 dips)) and two autonomic indices (heart rate and blood pressure rises) have been compared. Correlations between these five indices ranged from r=0.38 to r=0.73. Of the two autonomic indices, the correlations for blood pressure rises with SaO2 dips and EEG micro arousals were stronger (r=0.71 and r=0.65, respectively) than those for heart rate rises (0.55 and 0.51). All indices of sleep fragmentation, apart from heart rate rises, were similar in their correlation with subjective sleepiness (r-values 0.21-0.36). Arousals implied from blood pressure rises (using pulse transit time) can be measured easily, are objective, and appear no worse at predicting subjective sleepiness than either EEG micro arousals or AHI. They may therefore provide a useful alternative to manual scoring of micro arousals from the EEG as an index of sleep fragmentation in sleep clinic patients undergoing investigation for possible OSA.

Adult↗
PubMed1998

Evolution of sleep-disordered breathing and sleep in infants.

OBJECTIVE: The evolution of sleep-disordered breathing and sleeping patterns in a group of high-risk infants was studied throughout the first year of life. METHODOLOGY: Eleven infants with documented sleep apnoea underwent overnight polysomnographic studies at monthly intervals to 6 months, then at 9 and 12 months of age. RESULTS: All infants had central apnoea and obstructive events recorded on their initial sleep studies. The sleep-disordered breathing in these infants was associated with disturbed sleeping patterns. The amount of rapid eye movement (REM) sleep recorded in each study was inversely proportional to the amount of apnoea. The amount of apnoea and sleep disturbances were highest at 2 months of age and then progressively improved and obstructive events resolved by 1 year of age. CONCLUSIONS: The respiratory abnormalities and sleep disturbances peaked in severity at the age reported to have the highest incidence of sudden infant death syndrome (SIDS) and may have implications for its aetiology.

Humans↗
PubMed1995

[Treatment of depression with sleep deprivation and sleep phase advancement].

Total sleep deprivation (TSD) exerts beneficial but only transient effects on mood in approximately 60% of the patients with a major depressive disorder (MDD). The positive effect of TSD is generally reversed after the next night of sleep. A pilot study of our group indicated that a consecutive one week phase advance of the sleep phase stabilized mood in more than half of the patients who responded to TSD. However, the majority of patients in our pilot study had been treated concomitantly with antidepressive medication. To exclude a possible synergistic effect of simultaneous antidepressive medication and the sleep-wake manipulation in the present study eleven medicated and sixteen drug-free depressed patients were investigated. In two thirds of the patients relapse into depression after successful TSD could be prevented. This effect seemed to be independent of adjunct antidepressant pharmacotherapy. Ten of these patients were studied polysomnographically prior to and during the treatment. Data analysis revealed that during the advance of the sleep phase no prolonged partial sleep deprivation took place. At the end of the study REM % had even increased and REM latency was still short in spite of clinical improvement, thus contradicting the assumption that REM sleep suppression is a necessary prerequisite for antidepressive therapy. The results support the hypothesis of a "critical phase" in the morning hours during which sleep can reinduce depressive mood and, vice versa, prevention of sleep during this time may act antidepressively.

Adult↗
PubMed1992

Sleep and wakefulness after treatment for craniopharyngioma in childhood; influence on the quality and maturation of sleep.

Craniopharyngiomas are situated in immediate vicinity of sleep regulating structures in the basal forebrain area, and the tumor and its treatment might influence the regulation of sleep and wakefulness. In 10 patients treated for craniopharyngioma nighttime sleep quality and daytime vigilance were examined with polygraphic sleep records and multiple sleep latency tests (MSLT). Two girls and 8 boys, 7.1-22.9 years of age, were studied after a follow-up time of 1.5-16.1 years postoperatively. The results were compared to those of 18 normal children. The regulation of the ultradian sleep rhythm was normal but the ability to maintain nighttime sleep was severely disturbed. The patients had an increased number of awakenings and spent long time awake during two recorded nights. Two patients had excessive daytime somnolence during this examination, one after severe sleep disturbance, the other without any known cause. The pattern of sleep and vigilance did not change in puberty in the expected fashion. The disturbances may well have an impact on the psychosocial situation of the patients.

Adolescent↗
PubMed2001

Sleep habits and sleep problems among a community sample of schoolchildren.

UNLABELLED: Sleep habits, sleep problems and subjective depth of sleep among 1413 schoolchildren aged 6.2-10.9 y were examined via a questionnaire, answered by the child and parent together. Total sleep time was approximately 10.5 h, with no difference between the sexes. Of 887 children who reported that they were awoken at night, parents considered that 75% were superficial sleepers and 25% were deep sleepers. The prevalence of frequent insomnia, sleepwalking and daytime sleepiness was 13, 7 and 4%, respectively. Logistic regression analyses indicated that onset insomnia was associated with fear of sleeping alone, bone pains, hypnagogic myoclonias, rhythmic movement disorder, enuresis, nocturia, confusion when awoken at night, nightmares, bodily movements during sleep, interrupted sleep, daytime sleepiness and daytime headache or stomach ache. Somnambulism was associated with rhythmic movement disorder, somniloquy, spontaneous confused arousals, nocturia and confusion when awoken at night. Increased risk of daytime sleepiness was found among children with fear of sleeping alone, onset insomnia, rhythmic movement disorder, spontaneous confused arousals, snoring, confusion when awoken, nightmares, bodily movements during sleep and headache or stomach ache. CONCLUSION: The results support the notion that onset insomnia is a problem with a predominantly psychological and behavioural background, while sleepwalking is a disorder of arousal without major psychological implications. The mechanisms behind daytime sleepiness seem to be multifactorial.

Age Factors↗
PubMed1998

Periodic leg movements during sleep and sleep disturbances in elders.

BACKGROUND: Periodic limb movements in sleep (PLMS) are an increasingly pervasive disturbance for aging adults. The aims of this experiment were: (a) to describe the index of periodic limb movements in sleep (myoclonus index [MI] in elderly subjects with complaints of poor sleep or depression (N = 22; 68 +/- 5.5 SD years); and (b) to correlate MI with sleep history, depression scores, and objective and subjective indices of sleep. METHOD: Sleep and leg movements were assessed for 5 consecutive nights. Between-subjects, nonparametric correlations were examined between mean MI and sleep history, depression scores, and objective and subjective sleep characteristics. Associations among within-subject night-to-night variabilities of MI, objective, and subjective variables were examined with repeated measures ANCOVA, entering MI as a covariate. RESULTS: A remarkably high level of MI was found (median 25.8 events per hour; 86% of subjects > 5). Nevertheless, no associations were found between MI and sleep disturbance measures. CONCLUSION: These results extend previous reports that PLMS are remarkably persuasive in elderly volunteers and support other reports questioning whether there is a distinct PLMS syndrome.

Aged↗
PubMed1989

Effects of continuous positive airway pressure on phasic events of REM sleep in patients with obstructive sleep apnea.

In patients with obstructive sleep apnea and associated rapid-eye-movement (REM) sleep deprivation and disruption, the first night of nasal continuous positive airway pressure (CPAP) is often associated with increases in REM sleep time and REM density (REM rebound). The amount of REM rebound, however, varies considerably. We sought to characterize the magnitude of REM rebound and to determine what factors determine individual differences in REM rebound with initial CPAP treatment. Twenty-six patients with sleep apnea had a baseline nocturnal polysomnogram and a second night with a trial of CPAP. REM sleep time increased by 69% with CPAP, REM density increased by 73%, and REM activity by 169%. REM density was highest in the second REM period. Improvement in respiratory disturbance index with CPAP correlated significantly with increased minutes of REM sleep with CPAP. Of polysomnographic measures on the baseline night, change in minutes of REM sleep with CPAP correlated best with minimum oxygen saturation and to a lesser degree with respiratory disturbance index, and minutes of Stage 1 sleep. One possible explanation for the effect of hypoxemia on subsequent REM rebound is that some physiological functions of REM sleep may fail when oxygen saturation falls below a certain level.

Adult↗
PubMed1992

Changes in the waking EEG as a consequence of sleep and sleep deprivation.

Electroencephalographic (EEG) activity was monopolarly recorded during resting wakefulness in 10 volunteers under the following conditions: at night before going to sleep, at night before total sleep deprivation, in the morning after waking, in the morning after sleep deprivation and at night after having slept during the day. Absolute and relative power and inter- and intrahemispheric correlation were established. After diurnal and nocturnal sleep as compared to sleep deprivation, we obtained the following significant results: interhemispheric correlations were higher; intrahemispheric correlations were lower; absolute power of alpha 2, beta 1 and beta 2 was lower; and relative power of alpha 2 and beta 2 was lower. EEG changes as a consequence of sleep or lack of sleep are dependent on prior sleep and/or wakefulness and not on circadian phase. EEG activity during wakefulness is a sensitive parameter and a useful tool to assess the consequences of sleep on brain functional organization.

Adult↗
PubMed1995

Sleep deprivation in the rat: XX. Differences in wake and sleep temperatures during recovery.

We examined the relationship between wake and sleep peritoneal temperature (T(ip)) during recovery from short-term (five rats, 5 days of deprivation) and long-term (nine rats, 14-21 days) total sleep deprivation (TSD). Mammalian body temperature normally declines in the passage from wakefulness to sleep. Recovery from TSD featured reductions of the typical wake-sleep T(ip) differences. Previous studies from our laboratory have shown that chronic TSD in the rat produces a progressive rise in energy production and an initial rise in wake T(ip), followed by a later fall in T(ip) to below baseline that becomes more acute as death becomes imminent. During recovery from both short-term TSD (wherein pre-recovery wake T(ip) was still above baseline) and long-term TSD (wherein pre-recovery wake T(ip) had fallen to below baseline), wake T(ip) and energy production quickly returned towards baseline. On the first recovery day, both short- and long-term TSD rats showed mean non-rapid eye movement (NREM) and paradoxical sleep (PS) T(ip) values that were slightly, although not significantly, above mean wake T(ip). In short-term TSD rats, wake-NREM and wake-PS T(ip) differences were reduced from baseline significantly (p < 0.0025) on the first recovery day and nonsignificantly on the remaining three recovery days. In long-term TSD rats, wake-NREM and wake-PS T(ip) differences were significantly (p < 0.001) reduced from baseline on the first four recovery day block. On the last four recovery day block, wake-sleep T(ip) differences tended to return toward baseline. Hypothalamic wake-sleep temperature differences in long-term TSD rats showed similar reductions during recovery. The reduction of wake-sleep temperature differences in recovery does not support either energy reduction or cooling functions for sleep.

Animals↗
PubMed1997

Effects of alcohol on sleep parameters of sleep-deprived healthy volunteers.

Both partial and total sleep deprivation frequently result in a rebound of paradoxical sleep (PS), as well as of slow-wave or delta sleep. Acute administration of ethanol inhibits PS in normal volunteers. This effect is dose-dependent and consists of increased latency to and reduced duration of paradoxical sleep. It has also been shown that PS rebound may occur on the same night, as blood alcohol concentration (BAC) declines. The present study examined the effects of sleep deprivation prior to ethanol administration on nocturnal-sleep parameters in healthy male volunteers. Polysomnograms were performed with a randomized, crossover design on baseline, placebo, post-placebo, ethanol (0.9 g/kg), and post-ethanol recovery nights. Subjects were submitted to partial (PSD) (n = 6) or total (TSD) (n = 6) sleep deprivation for 40 hours before placebo or ethanol conditions. Results evidenced a PS inhibition after ethanol treatment in both deprivation groups, despite their sleep debt (PSD, placebo = 103.7 minutes and ethanol = 72.7 minutes; TSD, placebo = 111.8 minutes and ethanol = 76.6 minutes). This inhibition was BAC-dependent and specific to PS, since delta sleep remained unaltered. These effects could be due to the reduction of cholinergic release and/or glutamatergic inhibition, both of which modulate acetylcholine release.

Adult↗
PubMed2004

Hypersynchronous delta sleep EEG activity and sudden arousals from slow-wave sleep in adults without a history of parasomnias: clinical and forensic implications.

STUDY OBJECTIVES: To determine the frequency of classical markers of non-rapid eye movement (NREM) parasomnias--hypersynchronous delta sleep (HSD) electroencephalogram waves and sudden arousals from slow-wave sleep (SWS)--in patients without histories of somnambulism or other NREM parasomnias. DESIGN: Retrospective review. SETTING: Sleep disorders center laboratory. PATIENTS: 82 consecutive patients without a history of parasomnias who underwent diagnostic polysomnograms; 57 men and 25 women, mean age 48+/-13.3 years, were included without regard to diagnosis or findings. All patients had at least 30 seconds of stage 3 or 4 sleep during the polysomnogram. MEASUREMENTS AND RESULTS: The primary diagnosis of all but 4 patients was obstructive sleep apnea (mean respiratory disturbance index, 30 +/- 23.6 [range, 2.7-117] per hour of sleep). Polysomnograms were then reviewed for the presence of HSD and SWS arousals. A total of 235 arousals (mean, 2.9 +/- 2.7; range, 0-14) from stage 3 or 4 sleep were noted. Eight-five percent of all patients had at least 1 SWS arousal and 45% had 3 or more SWS arousals; 85.1% of all arousals from SWS were secondary to sleep-disordered breathing, and 5.9% were secondary to leg movements. At least 1 episode of HSD (mean, 1.4 +/- 1.6; range, 0-9) was noted in 65.8% of patients. CONCLUSIONS: HSD and SWS arousals were a common finding in patients without clinical histories of sleepwalking or other parasomnias but who were found to have frequent respiratory-related arousals during sleep. HSD and SWS arousals thus have a low specificity for NREM parasomnias and, without further research, are not useful for the objective confirmation of parasomnias in clinical evaluations and in the forensic evaluation of sleepwalking as a legal defense.

Arousal↗
PubMed2006

Extracellular adenosine in the human brain during sleep and sleep deprivation: an in vivo microdialysis study.

STUDY OBJECTIVES: To examine the pattern of extracellular adenosine in the human brain during sleep deprivation, sleep, and normal wake. DESIGN: Following recovery from implantation of clinical depth electrodes, epilepsy patients remained awake for 40 continuous hours, followed by a recovery sleep episode. SETTING: Neurology ward at UCLA Medical Center. PATIENTS OR PARTICIPANTS: Seven male epilepsy patients undergoing depth electrode localization of pharmacologically refractory seizures. INTERVENTIONS: All subjects were implanted with depth electrodes, a subset of which were customized to contain microdialysis probes. Microdialysis samples were collected during normal sleep, sleep deprivation, and recovery sleep from human amygdalae (n = 8), hippocampus (n = 1), and cortex (n = 1). MEASUREMENTS AND RESULTS: In none of the probes did we observe an increase in extracellular adenosine during the sleep deprivation. There was a significant, though very small, diurnal oscillation (2.5%) in 5 of the 8 amygdalae. There was no effect of epileptogenicity on the pattern of extracellular adenosine. CONCLUSIONS: Our observations, along with those in animal studies, indicate that the role of extracellular adenosine in regulating sleep pressure is not a global brain phenomenon but is likely limited to specific basal forebrain areas. Thus, if energy homeostasis is a function of sleep, an increased rate of adenosine release into the extracellular milieu of the amygdala, cortex, or hippocampus is unlikely to be a marker of such a process.

Adenosine↗