Psychometric properties of an omnibus sleep problems questionnaire for school-aged children.

OBJECTIVE: There is a paucity of sleep questionnaires that have been psychometrically validated for use in school-aged children. Due to the limitation regarding the psychometric properties and the great variety in question design, there remains a need for a robust omnibus questionnaire that assesses sleep problems in community populations. This study aimed to develop such a questionnaire for school-aged children by assessing the construct validity and reliability of a questionnaire based on a combination of children's sleep domains from two frequently used and validated questionnaires (Habits Questionnaire and Sleep Disorders Scale for Children) and author devised questions. PATIENTS/METHODS: Parents of 1904 children aged 5-10 years (mean 7.7 ± 1.7 years) from 32 elementary schools in Adelaide, South Australia, completed the questionnaire. RESULTS: Principal axis factoring revealed six unique sub-scales--Sleep Routine, Bedtime Anxiety, Morning Tiredness, Night Arousals, Sleep Disordered Breathing, and Restless Sleep--containing a total of 26 items. Internal consistency for sub-scales were moderate to strong (range α = 0.6-0.8) and test-retest reliability was adequate (>0.4). T-score cut-offs were devised for age and sex. CONCLUSION: The new questionnaire provides a robust set of sleep problem sub-scales which can be used for assessment of sleep concerns in a community sample as well as provide for optimal analysis of associations with other measures of childhood daytime functioning such as neurocognition and behaviour.

Prevalence of snoring and associated factors in infancy.

INTRODUCTION: In children aged 3-12 years snoring is associated with significant neurocognitive and behavioural deficits; however, there are few studies that have considered both the prevalence of snoring in infants and associated factors that may influence the development of snoring. The goal of the present study was to examine sleep, snoring and associated factors in a community sample of 0-3 month olds. METHODS: Previously validated infant sleep and parent sleep questionnaires were completed by parents of 457 term infants aged 1-13.9 weeks old (mean age=4.6 weeks; SD=2.7; 45% males) during a home-based nurse visit. RESULTS: Approximately 9% of infants were reported to snore habitually (snoring ≥ 3 nights/week). Habitual snoring was significantly associated with exclusive formula feeding (OR: 28.87; p<.01), maternal concern about child's breathing during sleep (OR: 3.91; p=.01) and restless sleep ≥ 3 nights/week (OR: 17.76; p<.001). CONCLUSION: These results show that snoring is as common in infants as it is in older children. Given the known relationships between Sleep Disordered Breathing (SDB) and neurocognitive development, the effect of SDB developing early in childhood may have important consequences on future developmental outcomes.

Chasing the silver bullet: measuring driver fatigue using simple and complex tasks.

Driver fatigue remains a significant cause of motor-vehicle accidents worldwide. New technologies are increasingly utilised to improve road safety, but there are no effective on-road measures for fatigue. While simulated driving tasks are sensitive, and simple performance tasks have been used in industrial fatigue management systems (FMS) to quantify risk, little is known about the relationship between such measures. Establishing a simple, on-road measure of fatigue, as a fitness-to-drive tool, is an important issue for road safety and accident prevention, particularly as many fatigue related accidents are preventable. This study aimed to measure fatigue-related performance decrements using a simple task (reaction time - RT) and a complex task (driving simulation), and to determine the potential for a link between such measures, thus improving FMS success. Fifteen volunteer participants (7 m, 8 f) aged 22-56 years (mean 33.6 years), underwent 26 h of supervised wakefulness before an 8h recovery sleep opportunity. Participants were tested using a 30-min interactive driving simulation test, bracketed by a 10-min psychomotor vigilance task (PVT) at 4, 8, 18 and 24h of wakefulness, and following recovery sleep. Extended wakefulness caused significant decrements in PVT and driving performance. Although these measures are clearly linked, our analyses suggest that driving simulation cannot be replaced by a simple PVT. Further research is needed to closely examine links between performance measures, and to facilitate accurate management of fitness to drive, which requires more complex assessments of performance than RT alone.

Effects of moderate sleep deprivation and low-dose alcohol on driving simulator performance and perception in young men.

STUDY OBJECTIVE: To determine the combined effects of sleep restriction and low-dose alcohol on driving simulator performance, EEG, and subjective levels of sleepiness and performance in the mid-afternoon. DESIGN: Repeated measures with 4 experimental conditions. Normal sleep without alcohol, sleep restriction alone (4 hours) and sleep restriction in combination with 2 different low blood alcohol concentrations (0.025 g/dL and 0.035 g/dL). SETTING: Sleep Laboratory, Adelaide Institute for Sleep Health. PARTICIPANTS: Twenty-one healthy young men, aged 18-30 years, mean (+/-SD) = 22.5(+/-3.7) years, BMI = 25(+/-6.7) kg/m2; all had normal sleep patterns and were free of sleep disorders. MEASUREMENTS: Participants completed a 70-minute simulated driving session, commencing at 14:00. Driving parameters included steering deviation, braking reaction time, and number of collisions. Alpha and theta EEG activity and subjective driving performance and sleepiness were also measured throughout the driving task. RESULTS: All measures were significantly affected by time. Steering deviation increased significantly when sleep restriction was combined with the higher dose alcohol. This combination also resulted in a significant increase in alpha/theta EEG activity throughout the drive, as well as greater subjective sleepiness and negative driving performance ratings compared to control or sleep restriction alone. DISCUSSION: These data indicate that combining low-dose alcohol with moderate sleep restriction results in significant decrements to subjective alertness and performance as well as to some driving performance and EEG parameters. This highlights the potential risks of driving after consumption of low and legal doses of alcohol when also sleep restricted.

Peripheral heat loss: a predictor of the hypothermic response to melatonin administration in young and older women.

Core hypothermia following daytime melatonin administration typically displays significant interindividual variability. As this hypothermia has been associated with significant increases in skin temperature, the mechanism by which melatonin decreases core temperature may involve increasing peripheral heat loss. If so, the interindividual variability in this effect may reflect concomitant interindividual variability in heat loss capacity at the distal periphery. For six younger (mean +/- SEM: 23.4 +/- 0.3 years) and 10 older women (mean +/- SEM: 65.6 +/- 0.7 years), the maximum decrease in core body temperature following a 5-mg (p.o.) dose of melatonin was correlated with the capacity to lose heat. This was determined by the maximum increase in contralateral hand temperature following a mild positive thermal challenge (PTC). The regression analysis yielded a significant (p < 0.01) correlation of 0.80, suggesting that the individual magnitude of hypothermia following melatonin administration may reflect the capacity of an individual to dissipate heat at the distal periphery.

Thermoregulatory and soporific effects of very low dose melatonin injection.

The effect of a rapid increase in circulating melatonin on body temperatures and sleepiness was investigated in eight young adults at 1000. Melatonin administered intravenously at 10- and 30-microgram doses, but not 3 microgram, resulted in elevated plasma and saliva levels consistent with endogenous levels measured in adults at night. Melatonin at 10 and 30 microgram significantly attenuated the daytime increase in rectal core temperature (P < 0.05 for both). The mean maximum rectal core temperature differences between saline and melatonin treatment were 0.11 +/- 0.03 degreesC, 0.16 +/- 0.04 degreesC, and 0.18 +/- 0.04 degreesC after the 3-, 10-, and 30-microgram melatonin doses, respectively. All three doses significantly increased hand temperature compared with saline (P < 0. 05) within 30 min. The mean maximum hand temperature differences were 0.72 +/- 0.12 degreesC (3 microgram), 0.95 +/- 0.15 degreesC (10 microgram), and 0.65 +/- 0.11 degreesC (30 microgram). Foot temperature and subjective sleepiness measures did not change at any melatonin dose. The results suggest that daytime intravenous injection of melatonin to achieve normal nocturnal levels in young adults may produce significant thermoregulatory changes without soporific effects.

Daytime melatonin and temazepam in young adult humans: equivalent effects on sleep latency and body temperatures.

1. As changes in core body temperature are generally associated with concomitant changes in sleep propensity, it is possible that the effects of hypnotic/soporific agents may be related to changes in thermoregulation. Therefore, to increase our knowledge of the mechanisms by which these agents exert their soporific effects, we compared the thermoregulatory and soporific effects of temazepam (20 mg per os (p.o.)) with those of melatonin (5 mg p.o.) when administered at 14.00 h to 20 young healthy adults (13 male, 7 female; age, 23.5 +/- 0.4 years). 2. From 08.00 to 20.30 h, subjects lay in bed, and foot and rectal (Tc) temperatures were recorded. Sleep onset latency (SOL) was measured using 20 min multiple sleep latency tests, performed hourly from 11.00 to 20.00 h, during which time heart rate was recorded. 3. Compared with placebo, both melatonin and temazepam significantly reduced Tc (-0.17 +/- 0.02 and -0.15 +/- 0.03 C, respectively) and SOL (by 4.8 +/- 1.49 and 6.5 +/- 1.62 min, respectively). Although both treatments significantly increased heat loss, only melatonin demonstrated cardiac effects. Importantly, there was a temporal relationship between minimum SOL and the maximum rate of decline in Tc for both melatonin (r = 0.48) and temazepam (r = 0.44). 4. A possible role of thermoregulation in sleep initiation is suggested by the similar temporal relationship between Tc and SOL for two different classes of soporific agents.

Etiology and treatment of intrinsic circadian rhythm sleep disorders.

Some individuals experience an acute or chronic sleep disturbance, associated with a misalignment between the timing of their sleep and the sleep-wake cycle that is desired, or considered normal by society. It is estimated that 5-10% of insomniacs seeking treatment have this type of disorder, collectively called circadian rhythm sleep disorders. This paper reviews circadian rhythm sleep disorders of the intrinsic type, which include delayed sleep phase syndrome, advanced sleep phase syndrome, non-24-hour sleep-wake syndrome, and irregular sleep-wake pattern. For each disorder, we present data addressing its pathophysiology and potential treatments, including the use of behavioral measures and chronotherapy, bright light treatment and pharmacological treatments such as melatonin. We conclude by addressing some of the limitations and drawbacks of the various treatments.

Effect of sustained nocturnal transbuccal melatonin administration on sleep and temperature in elderly insomniacs.

Previous research has suggested a role for the pineal hormone melatonin in the control of the body's sleep-wake and thermoregulatory systems. In the elderly population, there have been reports of decreased nighttime secretion of melatonin and suggestions that this may, in turn, be responsible for the increased incidence of sleep disorders reported by this age group. On this basis, it has been suggested that augmented nocturnal melatonin levels may improve sleep quality in age-related sleep disorders. Following screening assessments, 12 elderly (> 55 years) subjects with sleep maintenance insomnia were treated with either 0.5 mg transbuccal melatonin or a placebo for two sessions of 4 consecutive nights, at least 3 days apart. Subjects self-selected lights-out times, and sleep was assessed using standard polysomnographic (PSG) measures. Body temperature was measured continually from 2100 to 0700 h, and sleep quality was assessed from PSG variables measured. Nightly urine samples were assayed for the melatonin metabolite 6-sulfatoxy-melatonin (aMT.6S). Compared to the placebo, transbuccal melatonin administration significantly increased mean nocturnal aMT.6S excretion (mean +/- SEM: 194.2 +/- 16.5 vs. 42.5 +/- 7.7 nmol). In addition, there was a significant reduction in core body temperature relative to the placebo condition (p < .05). However, sustained transbuccal melatonin treatment had no positive significant effect on any PSG measure of sleep quality. The results from the present study suggest that sustained nocturnal administration of melatonin, in the low pharmacological range, might be of limited clinical benefit in this subject population.

Changes in sleepiness and body temperature precede nocturnal sleep onset: evidence from a polysomnographic study in young men.

Recent research has shown a close temporal relationship between the nocturnal decrease in rectal core temperature and the initiation of sleep. However, there is not yet a clear temporal relationship between changes in peripheral and core temperatures and nocturnal sleep onset. We recorded body temperatures in 14 adult males (age +/- SEM = 22.1 +/- 0.6 y), who attended the sleep laboratory for an adaptation night and two counterbalanced experimental sessions. Subjects self-selected lights-out on one experimental night (the Habitual Sleep condition). To determine the relationship between body temperature changes and sleep onset, lights out was delayed until after 01.00 hours on the other experimental night (Delayed Sleep condition). Individual datasets in both conditions were expressed relative to the time of sleep onset in the Habitual Sleep condition only, so that they were aligned at identical clock times. Saliva samples confirmed that mean dim light melatonin onset (DLMO) occurred at 00.10 +/- 00.16 hours in the Delayed Sleep condition, which was after habitual sleep onset at 23.44 +/- 00.08 hours. Rectal core temperature (Tc) decreased significantly over time only in the Habitual Sleep condition (P < 0.01). For the 20 min before habitual sleep onset, Delayed Sleep Tc was on average 0.1 degree C higher than Tc in the Habitual Sleep condition (P < 0.01). The greater decline in Habitual Sleep Tc was associated with significantly increased peripheral hand and foot skin temperatures before sleep (both P < 0.05). Subjective sleepiness measures were higher in the Habitual Sleep onset condition from 150 min prior until sleep onset (P < 0.01). From these results it is reasonable to infer that a sequence of thermoregulatory and sleep propensity changes occur before, but are associated with habitual sleep onset, as the changes are significantly attenuated if sleep is delayed.

Effects of daytime melatonin infusion in young adults.

Daytime oral melatonin typically exerts soporific and thermoregulatory effects; however, it is not clear whether these effects reflect the normal physiological response to endogenous nocturnal melatonin production. We infused melatonin at doses that produced physiological and supraphysiological steady-state levels in 24 young adults during two daytime bed rest protocols. From 1000 to 1630, subjects were infused intravenously with saline or melatonin in counterbalanced order. Each group of eight subjects received melatonin (and saline) infusions at one dose rate: 0.04 microg . h-1 . kg body wt-1 (low), 0.08 microg . h-1 . kg-1 (medium), or 8.0 microg . h-1 . kg-1 (high). Low and medium melatonin infusions produced plasma and saliva levels within the normal nocturnal range observed in young adults. These levels were not associated with any changes in rectal, hand, forehead, or tympanic temperatures or with subjective sleepiness. High melatonin produced supraphysiological plasma and saliva levels and was associated with a significant attenuation in the daytime increase in rectal temperature, significantly increased hand temperature, and greater sleepiness. It is not yet clear whether the thermoregulatory and soporific effects of daytime supraphysiological melatonin administration are equivalent to the physiological responses to endogenous melatonin.

Integrating the actions of melatonin on human physiology.

Melatonin has a diverse range of physiological effects in humans. Reported effects include modulation of the sleep-wake, thermoregulatory, cognitive, cardiovascular and immune systems. While integrating these broad-ranging effects is difficult when current paradigms are used, the diverse effects of melatonin on human physiology may be better understood by shifting our theoretical perspective. Traditionally, research has treated melatonin as a classical hormone for which a defined effect in physiological systems and a mechanism of action can be elucidated. In this article, we suggest that it may be more appropriate to view melatonin as an evolutionally stable timing signal to which each species has adapted the timing of physiological processes. From this perspective, it appears that the physiological role of melatonin in humans falls into two categories. The first relates to the self-regulation of circadian timing by the suprachiasmatic nucleus-pineal complex. The second relates to the promotion of restorative or anabolic physiological processes. In humans, elevated melatonin levels have been associated with reduced core temperature, increased heat loss, decreased cardiovascular output, reduced alertness and enhanced immune responsiveness. Taken together, these changes suggest that melatonin may increase the propensity for physiological processes promoting nocturnal sleep or processes that occur during the sleep period.

Effect of atenolol on nocturnal sleep and temperature in young men: reversal by pharmacological doses of melatonin.

To examine the physiological role of melatonin in sleep, nocturnal melatonin secretion was suppressed using 100 mg oral atenolol in two studies. In Study 1, nocturnal sleep was recorded in 8 young men over 4 nights. Subjects received atenolol on one of the last 2 nights and showed significantly increased total wake time (TWT) and wakefulness after sleep onset (WASO), as well as decreased REM sleep and slow-wave sleep (SWS). When melatonin (total 5 mg) was given after atenolol on the other night, the changes in TWT, WASO, REM, and SWS were reversed. In Study 2, sleep onset latencies (SOL) and core temperature (Tc) of 10 young men were measured for 3 nonconsecutive nights. In a cross-over design, atenolol given on one night significantly suppressed urinary 6-sulphatoxymelatonin (6s-aMT) production and increased hourly measures of Tc and SOL relative to baseline night values. Oral melatonin (3 mg), administered after atenolol, reversed the changes in Tc and SOL. These results suggest that endogenous melatonin may assist in the maintenance of normal sleep architecture (Study 1) and also increase nocturnal sleep propensity by hypothermic effects (Study 2).

Leukocyte subpopulations in the rat corpus luteum during pregnancy and pseudopregnancy.

Leukocytes including monocyte/macrophages, granulocytes, and T lymphocytes were localized in the corpus luteum (CL) of pregnant and pseudopregnant rats using monoclonal antibodies reactive with lineage-specific antigens. Neutrophilic granulocytes and monocytes/macrophages were found to be the most abundant leukocyte populations in the CL during both pregnancy and pseudopregnancy. The density of neutrophilic granulocytes (MCA 149-reactive cells) increased approximately 2-fold after mating, to peak on Day 9 of pseudopregnancy (214 +/- 13 positive cells/0.125 mm2 grid area) and Day 10 of pregnancy (216 +/- 12/grid area), and then declined in later stages of CL life. In pregnant rats, monocytes/macrophages positive for the monoclonal antibody ED1 were most numerous during early CL life when they were approximately 6-fold more plentiful than at luteolysis (153 +/- 14/grid area at Day 5 vs. 25 +/- 2 at 2 days postpartum). In pseudopregnant rats, the density of ED1-positive cells declined approximately 5-fold during the life span of the CL (124 +/- 17/grid area at Day 2 vs. 20 +/- 2 at Day 13) prior to a second, somewhat lesser peak at luteal regression (84 +/- 12 at Day 15). Fewer monocyte/macrophages within the CL were found to express antigen reactive with the monoclonal antibody ED2, which is characteristically a marker for tissue-macrophages (7% of the density of ED1-positive cells at Day 5 in the pregnant group and 13% at Day 2 in the pseudopregnant group); and while there was an approximately 60% reduction in the number of ED2-positive cells during pregnancy, these cells were found not to fluctuate significantly in number over the course of CL life in pseudopregnant animals.(ABSTRACT TRUNCATED AT 250 WORDS)