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Results for “Sleep-Wake Transition Disorders”

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PubMed2001

How accurately does wrist actigraphy identify the states of sleep and wakefulness?

STUDY OBJECTIVES: Because sleep and wakefulness differ from each other by the amount of body movement, it has been claimed that the two states can be accurately distinguished by wrist actigraphy. Our objective was to test this claim in lengthy polysomnographic (psg) and actigraphic (acf) samples that included night and day components. DESIGN: Fourteen healthy young (21-35 years) and old (70-72 years) men and women lived in a laboratory without temporal cues for 7 days. Each subject continuously wore sleep-recording electrodes as well as 2 wrist-movement recorders. Act measurements were converted to predictions of sleep and wakefulness by simple-threshold and multiple-regression methods. Psg served as the gold standard for calculation of predictive values (PV, the probability that an act prediction is correct by psg criteria). SETTING: N/A. PARTICIPANTS: N/A. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: The 7-day act recordings showed clear circadian cycles of high and low activity that respectively corresponded to subjective days, when subjects were wakeful, and subjective nights when they slept. Lower act levels corresponded to deeper states of psg sleep. Logistic regression on a 20-minute moving average of act gave the highest overall PV's. Nevertheless, the mean PV for sleep (PVS) was only 62.2% in complete, day + night samples. PVS was 86.6% in night samples. Act successfully predicted wakefulness during subjective nights (PVW = 89.6) and accurately measured circadian period length and the extent of sleep-wake consolidation, but it overestimated sleep rate and sleep efficiency. Act systematically decreased before sleep onset and increased before awakening, but reliable transitions among joint psg/act states (the Markov-1 property) were not demonstrated. CONCLUSIONS: Low PV's and overestimation of sleep currently disqualify actigraphy as an accurate sleep-wake indicator. Actigraphy may, however, by useful for measuring circadian period and sleep-wake consolidation and has face validity as a measure of rest/activity.

Adult↗

PubMed2004

Twenty-four-hour disruption of the sleep-wake cycle and sleep-onset REM-like episodes in a rat model of African trypanosomiasis.

STUDY OBJECTIVES: Patients with human African trypanosomiasis (sleeping sickness) due to the inoculation of Trypanosoma brucei gambiense or rhodesiense show a major disruption of the 24-hour sleep-wake distribution, accompanied by the occurrence of sleep-onset rapid-eye-movement (REM) sleep episodes, proportional to the severity of the illness. Although animal models of human African trypanosomiasis have been developed to understand the pathogenic mechanisms leading to immune alterations, the development of an animal model featuring the alterations of endogenous biologic rhythms remains a necessity. ANIMALS: Sprague-Dawley rats (N = 10) entrained to a 12:12-hour dark-light regimen. INTERVENTIONS: Rats were infected with Trypanosoma brucei brucei AnTat 1.1E and instrumented with electrocorticographic and electromyographic electrodes. Polysomnography was recorded continuously from 2 days before infection until the animal's death. MEASUREMENTS AND RESULTS: The analysis of the spontaneous sleep-wake architecture revealed an increased proportion of slow-wave sleep (SWS) and a decreased amount of wakefulness 2 days before death. Considerable sleep fragmentation was observed in the infected rats, with numerous changes in sleep-wake stages and an increased number of episodes of wakefulness and SWS. Infected rats presented a fragmented pattern of SWS and a marked reduction in the mean paradoxical-sleep (PS) latency, resulting in a considerable disruption of the PS-SWS sequences. Abnormal transitions, particularly the appearance of sleep-onset REM episodes, marked the disruption of the internal sleep structure. The electrocorticogram traces were modified during SWS, with the occurrence of abnormal hypersynchronic slow waves and a disappearance of spindles. CONCLUSION: The Trypanosoma brucei brucei-infected rat is a good model of the syndrome seen in human African trypanosomiasis, ie, the 24-hour disruption of the sleep-wake cycle and the occurrence of sleep-onset REM-like sleep episodes.

Animals↗

PubMed2004

Low-dose repeated caffeine administration for circadian-phase-dependent performance degradation during extended wakefulness.

OBJECTIVE: To investigate whether the effectiveness of a novel high-frequency low-dose caffeine regimen in counteracting the deterioration of performance during extended wakefulness is related to its interaction with homeostatic or circadian signals modulating performance and sleep propensity. DESIGN: Double-blind, placebo-controlled, parallel-group design in a 29-day forced desynchrony paradigm in which the period of the sleep-wake cycle was scheduled to be 42.85 hours, i.e., far removed from the circadian range. This design allowed for separate estimation of the sleep homeostatic, circadian, and caffeine contributions to performance deficits or improvements. SETTING: Private suite of a general clinical research center, in the absence of time of day information. PARTICIPANTS: Sixteen healthy normal-sleeping men (aged 18-30 years) INTERVENTIONS: Caffeine (0.3 mg per kg per hour) or placebo was administered hourly during the 28.57-hour wake episodes. RESULTS: Plasma caffeine concentrations rose in an exponential saturating manner during wakefulness. Rising caffeine levels markedly attenuated wake-dependent deterioration of a number of measures of cognitive performance, particularly at the circadian performance nadir. Moreover, caffeine enhanced the ability of subjects to remain consistently awake for extended periods, holding subjects back from completing the full transition to sleep, but at the expense of increasing subjective sleepiness. CONCLUSIONS: High-frequency low-dose caffeine administration is effective in countering the detrimental performance effects of extended wakefulness. These data are in accordance with the hypothesis that adenosine is a mediator of performance decrements associated with extended wakefulness and may lead to new strategies to use caffeine in situations in which neurobehavioral functioning is affected by sleep loss.

Adolescent↗

PubMed2004

What keeps us awake: the neuropharmacology of stimulants and wakefulness-promoting medications.

Numerous studies dissecting the basic mechanisms that control sleep regulation have led to considerable improvement in our knowledge of sleep disorders. It is now well accepted that transitions between sleep and wakefulness are regulated by complex neurobiologic mechanisms, which, ultimately, can be delineated as oscillations between two opponent processes, one promoting sleep and the other promoting wakefulness. The role of several neurotransmitter or neuromodulator systems, including noradrenergic, serotonergic, cholinergic, adenosinergic, and histaminergic systems and, more recently, the hypocretin/orexin and dopamine systems, has been clearly established. Amphetamine-like stimulants are known to increase wakefulness by blocking dopamine reuptake, by stimulating dopamine release, or by both mechanisms. Modafinil may increase wakefulness through activation of noradrenergic and dopaminergic systems, possibly through interaction with the hypocretin/orexin system. Caffeine inhibits adenosinergic receptors, which in turn can produce activation via interaction with GABAergic and dopaminergic neurotransmission. Nicotine enhances acetylcholine neurotransmission in the basal forebrain and dopamine release. Understanding the exact role of the hypocretin/orexin and dopamine systems in the physiology and pharmacology of sleep-wake regulation may reveal new insights into current and future wakefulness-promoting drugs.

Amphetamine↗

PubMed1996

Circadian rhythm, sleep, and epilepsy.

This review article: (1) describes the circadian distribution of ictal and interictal events; (2) differentiates transitional arousal, non-rapid eye movement and rapid eye movement sleep components and their substrates; (3) suggests the means by which the neural generators of these seizure-prone vs. seizure-resistant sleep and arousal states modulate the timing of different seizure manifestations; (4) considers clinical and mechanistic findings for the reciprocal effects of seizures and antiepileptic drugs upon the sleep-wake cycle; and (5) assesses clinical and basic mechanisms of sleep deprivation effects upon seizures.

Anticonvulsants↗

PubMed2004

Effects of hypocretin2-saporin and antidopamine-beta-hydroxylase-saporin neurotoxic lesions of the dorsolateral pons on sleep and muscle tone.

The hypocretin neurons have been implicated in regulating sleep-wake states as they are lost in patients with the sleep disorder narcolepsy. Hypocretin (HCRT) neurons are located only in the perifornical region of the posterior hypothalamus and heavily innervate pontine brainstem neurons, such as the locus coeruleus (LC), which have traditionally been implicated in promoting arousal. It is not known how the hypocretin innervation of the pons regulates sleep-wake states as pontine lesions have never been shown to increase sleep. It is likely that in previous studies specific neurons were not lesioned. Therefore, in this study, we applied saporin-based neurotoxins to the dorsolateral pons and monitored sleep in rats. Anti-dopamine-beta-hydroxylase-saporin killed the LC neurons but sleep was affected only during a two hour light-dark transition period. Application of hypocretin2-saporin killed fewer LC neurons relative to other adjacent neurons. This occurred because the LC neurons possess the hypocretin receptor 1 but the ligand hypocretin 2 binds to this receptor with less affinity relative to the hypocretin receptor 2. The hypocretin2-saporin lesioned rats compared to controls had increased sleep during the dark period and displayed increased limb movements during REM sleep. None of the lesioned rats had sleep onset REM sleep periods or cataplexy. We conclude that the hypocretin innervation to the pons functions to awaken the animal when the lights turn off (via its innervation of the LC), sustains arousal and represses sleep during the rest of the night (via a wider innervation of other pontine neurons), and modulates muscle tone.

Animals↗

PubMed1995

Paroxysmal microarousals in amygdala-kindled kittens: could they be subclinical seizures?

Amygdala-kindled kittens exhibit frequent epileptiform EEG transients, often in conjunction with phasic arousal events of sleep [k-complexes, pontogeniculo-occipital (PGO) waves, and/or sleep spindles]. In this study, paroxysmal microarousals occurred throughout the sleep-wake cycle after kindling, but were most frequent during seizure-prone states of slow-wave sleep (SWS) and the transition into rapid-eye-movement sleep (REM). Their incidence correlated with interictal sleep fragmentation as well as onset of spontaneous convulsions. Results could reflect transsynaptic kindling effects on brainstem and forebrain arousal mechanisms with which amygdala is reciprocally connected. Increased discharge rates of neural generators for normal EEG and behavioral arousal could disrupt sleep at some times and recruit epileptic neurons in the kindled focus to precipitate seizures at others. Alternatively, epileptiform EEG paroxysms were accompanied by subtle behavioral stereotypes (a head nod, limb elevation, eye twitch, lip smack, or a combination of these). Behavioral correlates were elements of partial kindled seizures, suggesting that paroxysmal microarousals may be subclinical seizures. Whether or not the microarousals are true seizures, our findings may link ictal onset and interictal sleep disorders to a subclinical paroxysmal arousal disorder and suggest a common epileptic mechanism.

Amygdala↗

PubMed1998

Melatonin effects on sleep, mood, and cognition in elderly with mild cognitive impairment.

The effects of immediate-release melatonin on circadian rest-activity profiles, cognition, and mood were investigated in ten elderly individuals with self-reported sleep-wake disturbances. Melatonin (6 mg), administered 2 hr before habitual bedtime, enhanced the rest-activity rhythm and improved sleep quality as observed in a reduction in sleep onset latency and in the number of transitions from sleep to wakefulness. However, total sleep time was not significantly increased nor was wake within sleep significantly reduced. The ability to remember previously learned items improved along with a significant reduction in depressed moods. No side effects or contraindications were reported by any of our participants during the 10 day trials. These data suggest that melatonin can safely improve some aspects of sleep, memory, and mood in the elderly in short-term use.

Affect↗

PubMed2004

Are sleep problems under-recognised in general practice?

AIMS: To evaluate the frequency of sleep problems in Australian children aged 4.5-16.5 years, and to determine whether the frequency of sleep problems on questionnaire predicts the reporting of sleep problems at consultation. METHODS: Parents of 361 children (aged 4.5-16.5 years) attending their general practitioner for "sick" visits were asked to assess their child's sleep over the previous six months using the Sleep Disturbance Scale for Children, from which six sleep "disorder" factors and a total sleep problem score were obtained. RESULTS: The percentage of children with a total sleep problem score indicative of clinical significance (T score >70 or >95th centile) was 24.6% (89/361). Despite this high frequency, parents only addressed sleep problems in 4.1% (13/317) of cases and reported that GPs discussed sleep problems in 7.9% (25/317) of cases. Of the 79 children who reported total sleep problem T scores in the clinical range, only 13.9% (11/79) discussed sleep with their general practitioner within the previous 12 months. Regression analyses revealed an age related decrease in problems with sleep-wake transition and sleep related obstructive breathing; sleep hyperhydrosis, initiating and maintaining sleep, and excessive daytime sleepiness did not significantly decrease with age. No significant gender differences were observed. CONCLUSIONS: Results suggest that chronic sleep problems in Australian children are significantly under-reported by parents during general practice consultations despite a relatively high frequency across all age groups. Given the impact on children and families, there is a need for increased awareness of children's sleep problems in the community and for these to be more actively addressed at consultation.

Adolescent↗

PubMed1986

Mobile long-term EEG monitoring in generalized seizure disorders of different etiology.

Eighteen EEG long-term recordings were carried out in patients with generalized fits of different etiologies using a mobile 4-channel monitoring system in order to observe individual patterns of epileptic activity. In patients with idiopathic tonic-clonic seizures (A) no connection of frequency of spike-wave bursts with the sleep-wakefulness cycle was observed. In patients suffering from fits of organic nature (B) a peak of paroxysms was obtained in the hours before sleep onset, whereas in patients with absence seizures (C) a maximum was found in the morning hours after awakening. In patients with idiopathic fits (tonic-clonic and absence seizures) the minimum of bursts was observed in REM sleep, whereas stage 0 (tonic-clonic) and stage 1 (absence) were most prone to discharges. Patients with secondary generalized epilepsy had most spike-wave bursts in deep sleep. In the absence seizure group the transitional periods within the light non-REM-sleep stages were more susceptible to paroxysms than the retained stages. In patients with idiopathic grand mal seizures, the highest frequency of paroxysmal discharges was found during time spent awake in the night when retained over a longer period of time. The group including cases with attacks of organic nature did not show any preference to shifting times or preservation episodes of sleep stages.

Adolescent↗

PubMed2002

Sleep structure correlates of continuous positive airway pressure variations during application of an autotitrating continuous positive airway pressure machine in patients with obstructive sleep apnea syndrome.

STUDY OBJECTIVES: To evaluate the relationship between sleep structure and continuous positive airway pressure (CPAP) delivered by an automatic CPAP (auto-CPAP) machine in patients with obstructive sleep apnea syndrome (OSAS). DESIGN: Nocturnal polysomnography was performed during CPAP administration by an auto-CPAP machine (Autoset Clinical 1; ResMed; Sydney, Australia). SETTING: Sleep-disorders center in a research institute. PATIENTS: Fifteen subjects with newly diagnosed OSAS deserving home CPAP treatment. MEASUREMENTS AND RESULTS: During the night, in most cases, the lowest CPAP level was recorded during a prolonged nonrapid eye movement (NREM) sleep period uninterrupted by arousals, whereas the highest level during wake-sleep transitions or NREM sleep fragmented by arousals. In four subjects, rapid eye movement sleep was always associated with increasing CPAP. Sleep efficiency was negatively correlated with CPAP variability, evaluated as the SD of the mean nocturnal CPAP level averaged epoch by epoch (r = 0.63, p < 0.02). Eighty-eight percent of rapid CPAP augmentations (increases by at least 2 cm H(2)O in less-than-or-equal 2 min) were observed during sleep-wake transitions or after arousals/awakenings (Ar/Aw); 63% of such Ar/Aw were not preceded by any detectable respiratory abnormality. CONCLUSIONS: CPAP levels and variations during auto-CPAP application may be mainly related to sleep continuity and efficiency. The recording of a highly variable pressure during auto-CPAP administration in an unattended environment must raise the question whether the patient's sleep quality was acceptable. A poor sleep quality during an autotitration night could lead to an undesirable overestimation of the CPAP level needed for use with fixed-level CPAP machines.

Adult↗

PubMed2000

Sleep-wake state and memory function.

Facility of memory formation and retrieval is affected by sleep-wake state. This paper discusses memory function while individuals are awake, but sleepy, at the transitions in state (i.e., wake to sleep and sleep to wake), and in REM and NREM sleep. The basal state of arousal at the time of memory function seems to be critical and the sleepy state, state transitions, and NREM sleep seem to define a continuum of arousal with respect to memory function. While different memory systems have been described, the effect of sleep-wake state on memory systems appears to be non-specific. Finally there is a shift in neurobiology from the NREM to REM state and memory function also appears to change in REM sleep.

Disorders of Excessive Somnolence↗

PubMedDate not supplied

Peculiarities of human sleep in the case of double alternation of "sleep-waking" cycles.

The dynamics of sleep was studied in seven healthy subjects in two schedules, differing in the magnitude of the sleep intervals and their distribution over the 24 hour period. The first series provided for the use of two four-hour sleep intervals, the second six- and two-hour intervals. The investigations showed that the transition to a new schedule was accompanied by substantial qualitative and quantitative sleep disturbances, followed by a restoration of sleep as the subjects adapted. Less pronounced sleep disorders and more rapid restoration were observed in the schedule with nonuniform distribution of the intervals; more pronounced sleep disorders and a slowed restoration of sleep were observed on the schedule with two four-hour intervals.

Adult↗