Changes In Sleep Architecture Research Articles

A rodent model of sleep disturbances in posttraumatic stress disorder: The role of context after fear conditioning

A prominent sleep disturbance, likely including a disruption of rapid eye movement sleep (REMS) continuity, characterizes posttraumatic stress disorder (PTSD). We set out to develop a fear conditioning paradigm in rats that displays alterations in sleep architecture analogous to those in PTSD. Baseline polysomnographic recordings of rats were performed in a neutral context to which the rats had been habituated for several days. Rats were then shock- or mock-trained in a distinctly different context, and their sleep was studied the following day in that context. A separate group of rats was shock-trained and studied in the neutral context on the following 2 days. Rats that slept in the neutral context exhibited a REMS-selective increase in sleep 24 hours after training and increases in REMS and non-REMS 48 hours after training. In contrast, rats that slept in the presence of situational reminders of the training context exhibited a REMS-selective decrease in sleep 24 hours later. Animals that were mock-trained showed no changes in sleep. Shock training induced days-long changes in sleep architecture that were disrupted when the animal was exposed to situational reminders of the training context.

Vigilance states in a parkinsonian model, the MPTP mouse

Sleep disturbances and vigilance disorders are frequently observed in Parkinson's disease. Despite the fact that the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse is one of the best-known animal models of Parkinson's disease, sleep analysis has never previously been performed in this system. In the present study, we explored sleep-wakefulness cycles in MPTP-treated mice and compared the results to data from untreated mice. MPTP (25 mg/kg) was injected daily for 5 days. After recovery, polysomnography was recorded over 48 h. Dopaminergic lesions of the substantia nigra and striata were evaluated using immunohistochemical markers. Immunohistochemical analysis showed a loss of dopaminergic neurons in MPTP mice. Compared with controls, MPTP-treated mice presented changes in sleep architecture throughout the nycthemeral period, with longer wakefulness and paradoxical sleep episodes and an increase in the amount of paradoxical sleep. We observed changes in sleep architecture in MPTP-treated mice, compared with saline-treated mice. MPTP mice show more consolidated vigilance states with higher amount of paradoxical sleep than controls. Although the MPTP-treated mouse is not a good model of sleep disturbances in PD, our results suggest that it could be a good pharmacological model for studying the effects of dopaminergic treatments on animal sleep-wakefulness cycles.

Sleep Disorders During Pregnancy

This paper reviews the topic of sleep disorders in pregnant women. We describe changes in sleep architecture and sleep pattern during pregnancy, discuss the impact of the physical and biochemical changes of pregnancy on sleep in pregnant women and examine whether maternal-fetal outcomes may be adversely affected in women with disordered sleep. The literature on common sleep disorders affecting pregnant women, including insomnia, sleep-disordered breathing and restless legs syndrome, is reviewed and recommendations are made for the management of these disorders during pregnancy.

Sleep at high altitude.

New arrivals to altitude commonly experience poor-quality sleep. These complaints are associated with increased fragmentation of sleep by frequent brief arousals, which are in turn linked to periodic breathing. Changes in sleep architecture include a shift toward lighter sleep stages, with marked decrements in slow-wave sleep and with variable decreases in rapid eye movement (REM) sleep. Respiratory periodicity at altitude reflects alternating respiratory stimulation by hypoxia and subsequent inhibition by hyperventilation-induced hypocapnia. Increased hypoxic ventilatory responsiveness and loss of regularization of breathing during sleep contribute to the occurrence of periodicity. Interventions that improve sleep quality at high altitude include acetazolamide and benzodiazepines.

Psychiatric aspects of late-life insomnia.

Epidemiological trends towards a 'graying' population make the issue of insomnia in the elderly an increasingly important research and clinical topic. It is often challenging to determine how much of a psychiatric dimension there is to a clinical condition that is best viewed as both as a symptom and a true psychosomatic entity in its own right. To categorize insomnia as either psychiatric or medically based risks oversimplification of the complexities of sleep disruption in the elderly. Normal senescence-related changes in sleep architecture and circadian rhythms must be considered, as well as the frequent medical comorbidities that may affect sleep. Psychiatric diagnoses to consider include mood and anxiety disorders, which may be affected equally by physiological and psychological changes implicit in old age. Sleep disruption related to dementia is of particular interest to clinicians involved with patients in long-term care facilities. Insomnia may occasionally be iatrogenically induced or exacerbated, and particularly antidepressants must be carefully selected for this reason. Light therapy and behavior therapies are important in multimodal treatment of insomnia, and sleep hygiene includes both regular physical and social activities to preserve entrainment of circadian rhythms affecting sleep.

Kyphoscoliotic Ventilatory Insufficiency: Effects of Long-term Intermittent Positive-Pressure Ventilation

To determine the effects of long-term nocturnal intermittent positive-pressure ventilation (NIPPV) on symptoms, pulmonary function test results, sleep, and respiratory muscle performance in patients with ventilatory insufficiency due to severe kyphoscoliosis. A prospective study in which 16 severe kyphoscoliotic patients were treated with NIPPV delivered by volume-cycled and pressure-cycled ventilators, over a period of 36 months. At baseline, pulmonary function tests, blood gas measurements, polysomnography, and respiratory muscle strength (measured by noninvasive indexes) were obtained. Symptoms and the number of hospitalizations in the previous 6 months also were recorded. Patients then began using a ventilator for > 1 to 2 days, in order to select the type of ventilator and the appropriate interface. Patients returned for evaluation (in outpatient setting) every 6 months for a follow-up period of 3 years. At 6 months, polysomnography was repeated, and by the third year clinical and functional parameters had been reassessed. All symptoms improved significantly with NIPPV therapy, when compared with the baseline values. The mean (+/- SD) PaO(2) and FVC values increased at 36 months compared with baseline values (62.6 +/- 7.1 vs 67.8 +/- 8.8 mm Hg, respectively; and 37.9 +/- 7.2% vs 47.5 +/- 11.9%, respectively; p < 0.05 for both). There were significant improvements in mean maximal inspiratory pressure (55.8 +/- 17.4 to 78.5 +/- 17.5 cm H(2)O), maximal expiratory pressure (53.8 +/- 17.7 to 72.3 +/- 11.0 cm H(2)O), mouth pressure (0.28 +/- 0.08 to 0.22 +/- 0.02 cmH(2)O), and pressure-time index (0.18 +/- 0.05 to 0.11 +/- 0.02; p < 0.05 for all comparisons). There were no significant differences in breathing pattern and ventilatory drive. After 6 months, nocturnal oxyhemoglobin saturation improved, however, there was no significant change in sleep architecture. All patients subjectively perceived a better quality of life after beginning ventilation, which persisted over the course of the study. Long-term NIPPV therapy improves daytime blood gas levels, respiratory muscle performance, and hypoventilation-based symptoms in patients with severe kyphoscoliosis.

Sleep Dysfunction in Alzheimer's Disease and Other Dementias.

Changes in sleep architecture and circadian rhythms, including increased sleep latency and nighttime awakenings, decreased slow-wave sleep, rapid eye movement sleep, and total sleep time, and increased daytime napping are widespread in people with dementia. In addition, cyclic agitation episodes ("sundowning"), nightmares or hallucinations, sleep attacks, and nocturnal behavioral outbursts are associated with specific dementia syndromes. Sleep hygiene recommendations, particularly those aimed at reducing daytime sleep and improving the sleep environment and routine, can offset the circadian disturbances of some dementia patients. However, they can be burdensome for caregivers to implement, and must be targeted to the specific patterns of sleep disturbances patients are experiencing. Pharmacologic treatments may be useful for symptomatic treatment of insomnia and nighttime behavioral disturbances in dementia patients, but there have been few controlled trials demonstrating their efficacy or long-term safety. Clonazepam is highly effective for treating the nighttime behaviors associated with rapid eye movement behavior disorder. For most dementia patients, however, the side effect risks of prolonged use of sedating medications must be weighed against the potential benefits. Dementia patients should be evaluated for common primary sleep disorders that may contribute to nighttime behavioral disturbances and impact treatment decisions. Continuous positive airway pressure, the gold standard for treating obstructive sleep apnea, can be tolerated by mild to moderately demented individuals with support from supervising caregivers. Increased daily light exposure and physical activity may help normalize circadian rest-activity rhythms in some dementia patients, although the frequency and dose needed to maintain treatment effects is currently not known.

Effect of acute exposure to loud occupational noise during daytime on the nocturnal sleep architecture, heart rate, and cortisol secretion in healthy volunteers.

Noise is one of the commonest physical stressors to which industrial workers are exposed. Many workers complain of symptoms associated with a non-specific generalized stress response, including disturbed sleep. However, industrial workers may be exposed to more than one source of stress and it is not possible to completely attribute the disturbed nocturnal sleep and changes in heart rate to the effects of loud noise alone. This study was done to find out whether acute exposure of healthy individuals to loud occupational noise during the daytime would cause changes in their nocturnal sleep architecture, heart rate during sleep and serum cortisol levels. Baseline polysomnography was done on ten subjects who were exposed for eight hours either to continuous occupational background noise levels of >75dB(A), or a quiet environment. Sleep polysomnography was done on the night prior to and after exposure. Blood was collected for serum cortisol estimation at night prior to sleep and in the morning after waking up. Statistical analysis was done by repeated measures ANOVA with Tukey's post test. The sleep efficiency was less than 80% and the total time spent in Rapid Eye Movement (REM) sleep, Slow Wave Sleep (SWS) and the REM onset latency were significantly decreased on the night after exposure to noise. There was a significant increase in stage shifts. The percentage fall in heart rate during sleep was decreased compared to the baseline values. The serum cortisol levels in the morning after exposure to noise was significantly increased. Workers exposed to loud background occupational noise react to the stress and show changes in nocturnal sleep architecture and heart rate which may be contributed to the exposure to noise.

Sleep apnea and the nasal airway.

Sleep apnea and the nasal airway.

Long-term vs. short-term processes regulating REM sleep.

In cats, rats, and mice, the amount of rapid eye movement sleep (REMS) lost during a sleep deprivation (SD) predicts the subsequent REMS rebound during recovery sleep. This suggests that REMS is homeostatically regulated and that a need or pressure for REMS accumulates in its absence, i.e. during both wakefulness and non-rapid eye movement sleep (NREMS). Conversely, it has been proposed that REMS pressure accumulates exclusively during NREMS [Benington and Heller, Am. J. Physiol. 266 (1994) R1992; Prog. Neurobiol. 44 (1994b) 433]. This hypothesis is based on the analysis of the duration of successive NREMS and REMS episodes and of electroencephalogram (EEG) events preceding REMS. Pre-REMS events (PREs) do not always result in sustained REMS and can thus be regarded as REMS attempts that increase as NREMS progresses. It is assumed that two processes regulating REMS can resolve the apparent contradiction between these two concepts: a 'long-term' process that homeostatically regulates the daily REMS amount and a 'short-term' process that regulates the NREM--REMS cycle. These issues were addressed in two SD experiments in rats. The two SDs varied in length (12 and 24 h) and resulted in very similar compensatory changes in NREMS but evoked very different changes for all REMS parameters studied. The large REMS increase observed after 24-h SD was accompanied by a reduction in unsuccessful PREs and an increase in sustained REMS episodes, together resulting in a threefold increase in the success-rate to enter REMS. Changes in success-rate matched those of a theoretically derived long-term REMS pressure. The SD induced changes in sleep architecture could be reproduced by assuming that the increased long-term REMS pressure interacts with the short-term process by increasing the probability to enter and remain in REMS.

Fluoxetine and Sleep EEG: Effects of a Single Dose, Subchronic Treatment, and Discontinuation in Healthy Subjects

The goals of the current study were to evaluate whether a single dose of fluoxetine causes qualitatively different changes in sleep architecture and NREM sleep EEG than subchronic administration in healthy subjects and to determine degree and duration of such changes after the single dose and after discontinuation from subchronic administration. Our hypothesis was that subchronic intake should cause changes qualitatively different from the single dose and that such changes could be sufficiently long-lived to suggest the possibility of a dosing in intervals of several days. Ten healthy volunteers first took one single 60-mg dose of fluoxetine and a week later started to take a 40-mg dose every morning for three weeks. Sleep laboratory nights included two nights before and four nights after the single dose and every second night for two weeks after discontinuation from subchronic administration. The single dose caused only a slight increase in drug plasma concentrations but relatively clear changes in sleep structure. After discontinuation from subchronic administration, sleep quality indices normalized quickly (within 2–4 days), whereas REM latency and spectral power effects correlated with total SSRI plasma concentration and normalized more slowly, corresponding to the drug plasma half-life of about 10 days. The REM fraction of the sleep period showed a rebound, whereas the delta sleep ratio did not correlate with drug plasma levels and yet remained increased after the medication interval. Thus, the only qualitative difference seen between acute and subchronic medication was the initial sleep disturbance. REM latency and especially the delta sleep ratio remained increased for several days after discontinuation from subchronic administration, indicating the possibility of a less-than-daily maintenance medication after an initial daily interval. Finally, the pattern of change observed for the delta sleep ratio indicates that it may be due to secondary, adaptive effects possibly linked to the antidepressant effect of fluoxetine in depressed patients.

Effects of waking-auditory stimulation on human sleep architecture

Evidence suggests that sleep architecture is affected by endogenous homeostatic mechanisms as well as by behavioral and sensory demands during the prior wakefulness. Regarding the auditory system, sensory deprivation has shown to drastically modify the sleep structure, stressing the relevance of such sensory system for sleep organization. Changes in sleep architecture following prolonged auditory stimulation during prior wakefulness would provide additional support to this hypothesis. In the present study, auditory stimulation was administered over a 6 h period prior to sleep. Sleep parameters obtained from visual scoring were quantified across the total sleep period, for each sleep cycle, and for the two halves of the night, separately. Results showed that 6 h of waking-auditory stimulation were followed by an increase in the duration of slow wave sleep, a shortening of the latency between slow wave sleep periods, and a longer sleep onset latency as compared with the baseline night. In contrast, REM sleep parameters were unaffected by the pre-sleep auditory stimulation. These results indicate that sleep architecture depends on auditory demands during the prior wakefulness, suggesting that the local neural activation underlying auditory stimulation may trigger brain control mechanisms selectively involved in both the slow wave sleep maintenance and organization.

Insomnia and ageing: Implications for healthcare practice and policy

Although ageing itself does not lead to insomnia, changes in sleep architecture (the ‘typical’ physiological progression from wakefulness to deep sleep) and health status create a vulnerability to the development of insomnia, which can be precipitated by a trigger event. This review highlights some of the problems associated with insomnia in older people and offers insights into the possible approaches to stop insomnia from becoming a ‘rite of passage’. The main conclusion from this review however, is that sleep research focusing specifically on the ageing population is badly needed, alongside a unified diagnostic system and research structure (Leger, 2000). These findings are also discussed in relation to both healthcare policy and practice.

Cognitive and behavioural performance in children with sleep-related obstructive breathing disorders.

Sleep-related obstructive breathing disorders (SROBD) are common in children. While the sequelae of cor pulmonae, and growth and developmental impairment have been well documented, neurocognitive deficits have been less well studied. There is emerging evidence that children with SROBD show reduced neurocognitive functioning especially in the inter-related areas of attentional capacity, memory and cognitive function. In addition, these children show increased problematic behaviour and reduced school performance. Early reports suggest that some of these deficits may be reversible with treatment. The genesis of the defects is unclear but may include hypoxaemia and subtle changes in sleep architecture. The natural history of SROBD and long-term effects on neurocognitive functioning and behaviour remain to be fully examined.

Heart rate variability during sleep: effects of aging and cardiac denervation

Cardiac vagal predominance increases RR interval (RR) and RR high frequency (HF) variability during non rapid-eye- movement sleep (non-REM, stage I-IV) in young subjects. Aging suppresses deep sleep but effects of age-related changes in sleep architecture on RR are unknown. Whether mechanical effects of changes in the breathing pattern on the sinus node during sleep affect RR variability is unclear. Methods: Polygraphic sleep recordings, RR and RR spectral profiles were determined in 8 young (22.5±3.3 yr.) and 8 older healthy volunteers (55.0±7.3 yr.). HF oscillations in RR of 8 cardiac denervated transplant recipients (HTR) determined mechanical effects of respiration on the sinoatrial node during sleep. Transition from wake to non-REM sleep increased RR in young and older subjects and increased the HF variability of RR in the young (p<0.05) but not in the older subjects. Older subjects disclosed a faster RR (p<0.01) and a lower HF variability (p<0.05) during non-REM sleep than the young subjects. Aging did not affect light and REM sleep but decreased deep sleep (stage IV) from 39±23 min to 6±6 min (p<0.001). Reduction in sleep stage IV with aging blunted the increase in RR and in RR HF variability during non-REM sleep (r>+0.55, p<0.05). Transition from wake to non-REM sleep doubled the markedly reduced HF variability of RR in the HTR (p<0.05). Conclusion: Disappearance of deep sleep with aging impairs nocturnal increase in cardiac vagal activity. Mechanical effects of changes in breathing pattern during sleep favor increases in HF oscillations of RR during non-REM sleep.

Effects of Aging and Cardiac Denervation on Heart Rate Variability During Sleep

Cardiac vagal predominance increases the RR interval and RR high-frequency (HF) variability during non-rapid eye movement (non-REM) sleep (stages I through IV) in young subjects. Aging suppresses deep sleep, but effects of age-related changes in sleep architecture on RR are unknown. Whether mechanical effects of changes in the breathing pattern on the sinus node during sleep affect RR variability is unclear. Polygraphic sleep recordings and RR and RR spectral profiles were determined in 8 young (22.5+/-3.3 years) and 8 older (55.0+/-7.3 years) healthy volunteers. HF oscillations in RR of 8 cardiac-denervated heart transplant recipients determined mechanical effects of respiration on the sinoatrial node during sleep. Transition from wakefulness to non-REM sleep increased the RR interval in young and older subjects and increased the HF variability of RR in the young (P:<0.05) but not in the older subjects. Older subjects disclosed a faster RR (P:<0.01) and a lower HF variability (P:<0.05) during non-REM sleep than the young subjects. Aging did not affect light and REM sleep but decreased deep sleep (stage IV) from 39+/-23 to 6+/-6 minutes (P:<0.001). Reduction in sleep stage IV with aging blunted the increase in RR and in RR HF variability during non-REM sleep (r>0.55, P:<0.05). Transition from wakefulness to non-REM sleep doubled the markedly reduced HF variability of RR in the heart transplant recipients (P:<0.05). Disappearance of deep sleep with aging impairs nocturnal increase in cardiac vagal activity. Mechanical effects of changes in breathing pattern during sleep favor increases in HF oscillations of the RR interval during non-REM sleep.

The Effects of Antidepressants on Sleep: A Review

Sleep disturbances are a frequent complication of depressive disorders and their treatment. Familiarity with the interaction among sleep, depression, and antidepressant medications may assist the clinician in selecting agents to suit the needs of individual patients. The authors review the current knowledge of changes in sleep architecture associated with particular antidepressant agents and with depressive illness, as well as the theoretical relevance of such changes to the antidepressant effect. Articles for review were found through a Medline search on the terms "polysomnography," "sleep," "antidepressants," and "insomnia" in English-language papers published from 1966 through March 2000. Additional articles were found in the reference lists of relevant papers.

Physical Exercise as an Adjunct Therapy in Sleep Apnea-An Open Trial.

BACKGROUND: The aim of this study was to determine in an open trial if physical exercise in sleep apnea patients is safe and/or influences respiratory disturbance index (RDI). METHODS: After being treated 3 months or more with nasal CPAP for moderate to severe sleep apnea syndrome, eleven patients (1 female, 10 male, mean age 52.2 years) began a six-month period of supervised physical exercise twice a week, 2 hours each time. Before and after this period a Polysomnography without CPAP was recorded, along with a bicycle exercise test with lactate profile, echocardiography, body-weight, and body-height measurement. RESULTS: No adverse effects or cardiopulmonary problems were observed. There was no significant change in body weight with physical training; no significant difference in either min SaO2 nor mean SaO2; and no significant improvement in fitness. No adverse cardiopulmonary effects or problems were observed. There was a decrease of the RDI from 32.8 to 23.6 (p < 0.05), without a significant change in the REM-sleep portion of total sleep time (TST), NREM sleep, or TST. CONCLUSIONS: A prescription for mild to moderate exercise is safe in the management of sleep apnea, and, even in the absence of a fitness improvement, there occurred a decrease in RDI without a change in sleep architecture.

Sleep changes during long-term treatment of depression with fluvoxamine--a home-based study.

The effects of antidepressants on sleep in depression have been extensively investigated, although to date there have been relatively few studies of newer drug classes such as specific serotonin reuptake inhibitors (SSRIs). All reported studies on SSRIs have been conducted in patients admitted to sleep laboratories and very few longitudinal studies have continued to measure sleep beyond 5 weeks of treatment. The growing trend towards outpatient and community care has highlighted the need for studies of sleep in depression in a more naturalistic setting, and during longer periods of treatment in line with recommended clinical practice. To establish if the changes in sleep architecture and continuity described during early treatment with SSRIs persist after 3 months, to relate these changes to clinical state, and to establish whether home recordings would yield similar results to previous laboratory studies. We have recorded objective sleep parameters in 12 depressed patients before and during 12-week treatment with an SSRI, fluvoxamine. All the sleep recordings were performed in the patients' own homes, using the Oxford Medilog system. At 12 weeks, 7/12 patients had responded (HAM-D decreased by > 50%). REM latency showed the expected increase early in treatment; this change was less obvious at weeks 3 and 12. Amount of REM sleep was decreased at day 2 and week 3, but returned to baseline by week 12. Slow wave sleep was slightly increased at day 2 and decreased at week 12. Of the sleep continuity measures, the only significant change was in sleep onset latency, which was increased at week 3; the other measures showed non-significant worsening at night 2 and week 3, but most were better than baseline by 12 weeks. Subjective sleep (the three sleep items on the HAM-D) showed a progressive improvement over time, especially in the responders. The effects of the SSRI fluvoxamine on objective sleep measures are in the direction predicted by its pharmacological actions and some persist for at least 12 weeks. In addition subjective appraisal of sleep is strongly affected by mood state. All patients found the home recording procedure acceptable and only minimally disruptive.

Alcohol and sleep disturbances

Despite an initial sedative effect, alcohol disrupts sleep persistently and should not be used as a sleeping aid. Nocturnal withdrawal symptoms may lead to an increased duration of wakefulness, and to tachycardia and sweating in the second half of the night. It is not known by which mechanism alcohol affects sleep; however, effects do not appear to depend on the stimulation of benzodiazepine receptors or the antagonism at adenosine receptors. Alcohol can exacerbate primary sleep disturbances such as sleep apnea and nocturnal myoclonus, and thereby contribute to excessive daytime sleepiness. The sleep of alcoholic patients is characterized by increased sleep latency, and reduced sleep efficiency, total sleep time, slow wave sleep and non-REM sleep. Even during abstinence, the changes in sleep architecture can persist for months or years, and might contribute to a relapse into alcoholism. The use of benzodiazepines or other hypnotics to treat alcohol-related sleep disturbances is not recommended.