Characterizing Sleep in Adolescents and Adults with Autism Spectrum Disorders.

We studied 28 adolescents/young adults with autism spectrum disorders (ASD) and 13 age/sex matched individuals of typical development (TD). Structured sleep histories, validated questionnaires, actigraphy (4 weeks), and salivary cortisol and melatonin (4 days each) were collected. Compared to those with TD, adolescents/young adults with ASD had longer sleep latencies and more difficulty going to bed and falling asleep. Morning cortisol, evening cortisol, and the morning-evening difference in cortisol did not differ by diagnosis (ASD vs. TD). Dim light melatonin onsets (DLMOs) averaged across participants were not different for the ASD and TD participants. Average participant scores indicated aspects of poor sleep hygiene in both groups. Insomnia in ASD is multifactorial and not solely related to physiological factors.

Clinical practice guideline for the treatment of intrinsic circadian rhythm sleep-wake disorders: advanced sleep-wake phase disorder (aswpd), delayed sleep-wake phase disorder (dswpd), non-24-hour sleep-wake rhythm disorder (n24swd), and irregular sleep-wake rhythm disorder (iswrd): an update for 2015

A systematic literature review and meta-analyses (where appropriate) were performed and the GRADE approach was used to update the previous American Academy of Sleep Medicine Practice Parameters on the treatment of intrinsic circadian rhythm sleep-wake disorders. Available data allowed for positive endorsement (at a second-tier degree of confidence) of strategically timed melatonin (for the treatment of DSWPD, blind adults with N24SWD, and children/ adolescents with ISWRD and comorbid neurological disorders), and light therapy with or without accompanying behavioral interventions (adults with ASWPD, children/adolescents with DSWPD, and elderly with dementia). Recommendations against the use of melatonin and discrete sleep-promoting medications are provided for demented elderly patients, at a second- and first-tier degree of confidence, respectively. No recommendations were provided for remaining treatments/ populations, due to either insufficient or absent data. Areas where further research is needed are discussed.

The impact of a week of simulated night work on sleep, circadian phase, and performance.

AIMS: To investigate factors that may contribute to performance adaptation during permanent night work. METHODS: Fifteen healthy subjects participated in an adaptation and baseline night sleep, directly followed by seven simulated eight-hour night shifts (2300 to 0700 hours). At the end of each shift they were taken outside and exposed to natural light for 20 minutes. They then slept from approximately 0800 hours until they naturally awoke. RESULTS: There was a significant increase in mean performance on a visual psychomotor vigilance task across the week. Daytime sleep quality and quantity were not negatively affected. Total sleep time (TST) for each of the daytime sleeps was reduced, resulting in an average cumulative sleep debt of 3.53 hours prior to the final night shift. TST for each of the daytime sleep periods did not significantly differ from the baseline night, nor did TST significantly vary across the week. There was a significant decrease in wake time after sleep onset and sleep onset latency across the week; sleep efficiency showed a trend towards greater efficiency across the consecutive daytime sleeps. Hours of wakefulness prior to each simulated night shift significantly varied across the week. The melatonin profile significantly shifted across the week. CONCLUSIONS: Results suggest that under optimal conditions, the sleep debt that accumulates during consecutive night shifts is relatively small and does not exacerbate decrements in night-time performance resulting from other factors. When sleep loss is minimised, adaptation of performance during consecutive night shifts can occur in conjunction with circadian adaptation.

The effects of day-time exogenous melatonin administration on cardiac autonomic activity.

Melatonin has a functional role in the nocturnal regulation of sleep and thermoregulation. In addition to its action on peripheral receptors, melatonin may act by altering autonomic activity. To determine the effect of melatonin on cardiac autonomic activity, 5 mg of melatonin or placebo was orally administered to 12 young subjects at 14:00 hr, in a repeated measures design. Melatonin decreased sleep onset latency to Stage 2 sleep by 4.92+/-1.81 min (measured by Multiple Sleep Latency Tests), rectal temperature by 0.19+/-0.05 degrees C, and increased foot temperature by 0.74+/-0.45 degrees C (all P<0.05). Melatonin decreased heart rate by 3.66+/-1.68 beats/min (P<0.05) and pre-ejection period (measure of cardiac sympathetic activity) by 16.48+/-4.28 ms (P<0.05), but had no effect on respiratory sinus arrhythmia (measure of cardiac parasympathetic activity) (P>0.05). As the decrease in pre-ejection period is likely to have resulted from a decrease in blood pressure, these results do not confirm an effect of melatonin on cardiac sympathetic activity. However, the results do clearly indicate that melatonin is unlikely to drive the previously observed presleep increase in cardiac parasympathetic activity.

Effects of bright light and melatonin on sleep propensity, temperature, and cardiac activity at night.

Melatonin increases sleepiness, decreases core temperature, and increases peripheral temperature in humans. Melatonin may produce these effects by activating peripheral receptors or altering autonomic activity. The latter hypothesis was investigated in 16 supine subjects. Three conditions were created by using bright light and exogenous melatonin: normal endogenous, suppressed, and pharmacological melatonin levels. Data during wakefulness from 1.5 h before to 2.5 h after each subject's estimated melatonin onset (wake time + 14 h) were analyzed. Respiratory sinus arrhythmia (cardiac parasympathetic activity) and preejection period (cardiac sympathetic activity) did not vary among conditions. Pharmacological melatonin levels significantly decreased systolic blood pressure [5.75 +/- 1.65 (SE) mmHg] but did not significantly change heart rate. Suppressed melatonin significantly increased rectal temperature (0.27 +/- 0.06 degrees C), decreased foot temperature (1.98 +/- 0.70 degrees C), and increased sleep onset latency (5.53 +/- 1.87 min). Thus melatonin does not significantly alter cardiac autonomic activity and instead may bind to peripheral receptors in the vasculature and heart. Furthermore, increases in cardiac parasympathetic activity before normal nighttime sleep cannot be attributed to the concomitant increase in endogenous melatonin.

The relationship between slow-wave activity, body temperature, and cardiac activity during nighttime sleep.

STUDY OBJECTIVES: Recent work indicates that cardiac sympathetic activity is not influenced by the circadian system and instead decreases after sleep onset. However, little is known about the pattern of change in cardiac sympathetic activity during NREM/REM sleep cycles and whether this is associated with alterations in slow-wave activity (SWA). To address these questions, we examined SWA, cardiac sympathetic activity, heart rate and rectal and foot temperatures during the first three NREM/REM sleep cycles and during transitions between NREM and REM sleep. DESIGN: Subjects were required to maintain a constant sleep-wake cycle for at least a week and have at least one adaptation night, before their night of recording. SETTING: Individual temperature controlled bedrooms. PARTICIPANTS: 10 young healthy males and females. INTERVENTIONS: NA. MEASUREMENTS AND RESULTS: All variables showed the greatest change in the first NREM cycle. Specifically, SWA, sympathetic activity, heart rate and foot temperature increased while rectal temperature decreased. After the initial increase, cardiac sympathetic activity decreased across the sleep phase, in association with a decrease in heart rate. Cardiac sympathetic activity did not significantly alter across NREM-REM cycles. CONCLUSIONS: The results suggest that increases in heart rate and cardiac sympathetic activity early in the sleep period are, in part, a compensatory reaction to the concomitant thermoregulatory changes observed. These results also indicate that the effect of time asleep on cardiac sympathetic activity may be greater than the influence of sleep cycles. These results are discussed with reference to the recuperative value of naps.

Performance, sleep and circadian phase during a week of simulated night work.

The current study investigated changes in night-time performance, daytime sleep, and circadian phase during a week of simulated shift work. Fifteen young subjects participated in an adaptation and baseline night sleep, directly followed by seven night shifts. Subjects slept from approximately 0800 hr until they naturally awoke. Polysomnographic data was collected for each sleep period. Saliva samples were collected at half hourly intervals, from 2000 hr to bedtime. Each night, performance was tested at hourly intervals. Analysis indicated that there was a significant increase in mean performance across the week. In general, sleep was not negatively affected. Rather, sleep quality appeared to improve across the week. However, total sleep time (TST) for each day sleep was slightly reduced from baseline, resulting in a small cumulative sleep debt of 3.53 (SD = 5.62) hours. Finally, the melatonin profile shifted across the week, resulting in a mean phase delay of 5.5 hours. These findings indicate that when sleep loss is minimized and a circadian phase shift occurs, adaptation of performance can occur during several consecutive night shifts.

Daytime cardiac autonomic activity during one week of continuous night shift.

Shift workers encounter an increased risk of cardiovascular disease compared to their day working counterparts. To explore this phenomenon, the effects of one week of simulated night shift on cardiac sympathetic (SNS) and parasympathetic (PNS) activity were assessed. Ten (5m; 5f) healthy subjects aged 18-29 years attended an adaptation and baseline night before commencing one week of night shift (2300-0700 h). Sleep was recorded using a standard polysomnogram and circadian phase was tracked using salivary melatonin data. During sleep, heart rate (HR), cardiac PNS activity (RMSSD) and cardiac SNS activity (pre-ejection period) were recorded. Night shift did not influence seep quality, but reduced sleep duration by a mean of 52 +/- 29 min. One week of night shift evoked a small chronic sleep debt of 5 h 14 +/- 56 min and a cumulative circadian phase delay of 5 h +/- 14 min. Night shift had no significant effect on mean HR, but mean cardiac SNS activity during sleep was consistently higher and mean cardiac PNS activity during sleep declined gradually across the week. These results suggest that shiftwork has direct and unfavourable effects on cardiac autonomic activity and that this might be one mechanism via which shiftwork increases the risk of cardiovascular disease. It is postulated that sleep loss could be one mediator of the association between shiftwork and cardiovascular health.

Attenuation of sleep propensity, core hypothermia, and peripheral heat loss after temazepam tolerance.

If changes in thermoregulation mediate sleepiness induced by sedative/hypnotics, then a reduction in the soporific efficacy (tolerance) of these agents may be accompanied by a concomitant reduction in their thermoregulatory effects. We compared the thermoregulatory and soporific effects of acute temazepam (30 mg at 1400) in 11 young male subjects before and immediately after 7 consecutive days of temazepam (30 mg). Subjects lay supine (0800-2030), while foot (T(ft)) and rectal (T(c)) temperatures were recorded. Sleep onset latency (SOL) was measured hourly using 20-min multiple sleep latency tests. Relative to placebo, temazepam significantly reduced both T(c) and SOL (-0.31 degrees C and 14.1 min) while increasing T(ft) (3.39 degrees C). A significant tolerance developed after the week of temazepam, with a mean reduction in soporific efficacy of 4.0 +/- 0.8 min. This was accompanied by a concomitant attenuation in both T(c) (-0.16 degrees C) and T(ft) (1.44 degrees C). Furthermore, SOL was temporally related to T(ft) and the maximum rate of decline in T(c) before and after tolerance. Together, these results indicate that the thermoregulatory system may be functionally involved in the regulation of sleepiness.

Serotonin-2 receptors and human sleep: effect of a selective antagonist on EEG power spectra.

To investigate the effect on the sleep EEG, a 1-mg oral dose of SR 46349B, a novel 5-HT2 antagonist, was administered three hours before bedtime. The drug enhanced slow wave sleep (SWS) and reduced stage 2 without affecting subjective sleep quality. In nonREM sleep (NREMS) EEG slow-wave activity (SWA; power within 0.75-4.5 Hz) was increased and spindle frequency activity (SFA; power within 12.25-15 Hz) was decreased. The relative NREMS power spectrum showed a bimodal pattern with the main peak at 1.5 Hz and a secondary peak at 6 Hz. A regional analysis based on bipolar derivations along the antero-posterior axis revealed significant 'treatment' x 'derivation' interactions within the 9-16 Hz range. In enhancing SWA and attenuating SFA, the 5-HT2 receptor antagonist mimicked the effect of sleep deprivation, whereas the pattern of the NREMS spectrum differed.

Cardiac autonomic nervous system activity during presleep wakefulness and stage 2 NREM sleep.

Previous research has found that cardiac parasympathetic nervous system (PNS) activity increases and cardiac sympathetic nervous system (SNS) activity decreases during night-time sleep. This study aimed to examine in greater detail the time course of these changes in cardiac autonomic nervous system (ANS) activity. In the week prior to the experimental night, nine subjects maintained a constant sleep-wake schedule and experienced an adaptation night. Each subject's experimental night consisted of 2 h of presleep wakefulness, followed by a night of sleep, commencing at each subject's normal sleep onset time. One hundred and twenty beat blocks of presleep wakefulness and stable Stage 2 non-rapid eye movement (NREM) sleep across the night were selected. SNS activity was assessed using pre-ejection period, the amplitude of the T-wave in the ECG and the 0.1 Hz peak from the spectral analysis of the ECG. PNS activity was assessed using respiratory sinus arrhythmia (spectral analysis). Heart rate and respiratory rate were also measured. The results indicated a progressive decrease in SNS activity throughout sleep and a rise in PNS activity during the first half of the normal sleep period. The changes in PNS activity were similar, while the changes in SNS activity were altered, compared with a previous study in which stage of sleep was not controlled. This indicates a likely sleep stage influence on SNS activity, but not on cardiac PNS activity. These results are consistent with the concept of a primarily circadian, but not sleep, influence on PNS activity, and primarily a sleep, but not circadian, influence on SNS activity.

Cardiac activity during sleep onset.

Alterations in a number of measures of cardiac activity were examined during sleep onset in 6 participants over 3 experimental nights. Each sleep onset was divided into four consecutive phases: wakefulness, mixed alpha and theta activity, stage 2 NREM sleep with arousals, and stable stage 2 sleep. The variables measured were heart rate (HR), respiratory sinus arrhythmia (RSA), pre-ejection period (PEP) and T-wave amplitude (TWA). Respiration rate (RR) was also measured. HR and RR were lower in stable Stage 2 sleep compared with wakefulness, whereas PEP, TWA and RSA did not change significantly. During the second and third phases of sleep onset, HR decreased at each transition into sleep and increased following each spontaneous arousal. This increase resolved rapidly, with a return to sleep levels by 12 beats after the arousal. HR changes are discussed with reference to RSA, PEP, TWA and the concept of a waking reflex.

Sleep and circadian influences on cardiac autonomic nervous system activity.

To assess the separate contributions of the sleep and circadian systems to changes in cardiac autonomic nervous system (ANS) activity, 12 supine subjects participated in two 26-h constant routines, which were counterbalanced and separated by 1 wk. One routine did not permit sleep, whereas the second allowed the subjects to sleep during their normal sleep phase. Parasympathetic nervous system activity was assessed with respiratory sinus arrhythmia as measured from the spectral analysis of cardiac beat-to-beat intervals. Sympathetic nervous system activity was primarily assessed with the preejection period as estimated from impedance cardiography, although the 0.1-Hz peak from the spectral analysis of cardiac beat-to-beat intervals, the amplitude of the T wave in the electrocardiogram, and heart rate were also measured. Respiratory sinus arrhythymia showed a 24-h rhythm independent of sleep, whereas preejection period only showed a 24-h rhythm if sleep occurred. Thus the findings indicate that parasympathetic nervous system activity is mostly influenced by the circadian system, whereas sympathetic nervous system activity is mostly influenced by the sleep system.

Cardiac parasympathetic nervous system activity does not increase in anticipation of sleep.

Parasympathetic Nervous System (PNS) activity increases while Sympathetic Nervous System (SNS) activity remains relatively stable from wakefulness to NREM sleep. However, it is not clear whether these changes are specifically associated with NREM sleep, or whether they anticipate sleep onset. The latter may occur if ANS activity was influenced by the circadian system. This issue was investigated by conducting spectral analysis of heart beat-to-beat intervals (Periodogram method), collected from 20 healthy male and female subjects at three different times across 24 h; in the morning, just prior to normal sleep onset time, and in slow-wave sleep (SWS). Subjects were supine in all conditions and awake in the first two conditions. The high- and low-frequency peaks, reflecting PNS and SNS activity, respectively, were expressed as proportions of the total power. PNS activity decreased significantly from the morning (0.22) to the presleep period (0.19), before it increased to its maximum during SWS (0.33). In contrast, SNS activity was similar in each of the three conditions (0.07, 0.06, and 0.05 for morning, presleep and SWS, respectively). Thus there do not appear to be changes in PNS activity in anticipation of sleep, as would be predicted on the basis of a circadian influence on the PNS. Instead the increased PNS activity appears to be sleep dependent.

The nutritional status of children ages 0-5 years in Nkhotakota, Malawi.

A nutritional status survey of children aged 0-5 years was carried out in a lake shore district in Malawi. Anthropometric and clinical studies indicated a high overall prevalence (14%) of Protein-Calorie Malnutrition (PCM), particularly among the 1- to 1 1/2-year-olds. Few signs of vitamin deficiencies were seen but iron deficient anaemia was common at all ages, 68% being below the acceptable haemoglobin level. Sixty percent of children had malaria parasitaemia and 25% conjunctivitis. Under-five mortality was estimated to lie between 31 and 44%. Muslim children had a higher mortality and prevalence of PCM and fewer of their fathers had been to school. It is suspected that many cases of undernutrition go unrecognized because of uniform stunting occurs and ages are not known. It is recommended therefore that medical units use a local calendar, similar to that evolved for the survey, in order to estimate ages more accurately.

A field worker's guide to a nutritional status survey.

This guide has been prepared specifically for the medical worker in a developing country who has little experience for survey methodology and few outside sources on which to draw. All, or only portions of the guide, may be used as local needs dictate. It provides an outline of necessary preparations, sampling, field organization, measuring techniques and recording form. To aid the statistical treatment and presentation of the data, a sample recording form is given together with coding instructions and output table layout.