Plasma adiponectin level and sleep structures in children with Prader–Willi syndrome

Adiponectin, an adipose tissue-derived hormone, has been negatively related to obstructive sleep apnea syndrome. Besides sleep apnea, children with Prader–Willi syndrome (PWS) may have excessive daytime sleepiness and rapid eye movement (REM) sleep abnormality. The aim of this study is to determine whether changes in sleep structures are related to plasma adiponectin levels in PWS. Correlations between adiponectin level and sleep variables were analyzed in 28 children with PWS and 18 controls. Overnight polysomnography was performed. The fasting plasma adiponectin levels were higher in the children with PWS than in the controls ( P  =   0.0006). In the PWS, Epworth sleepiness scale was significantly higher ( P  =   0.002); sleep latency ( P  =   0.003) and REM latency ( P  =   0.001) were significantly shortened; the apnea–hypopnea index (AHI) was significantly increased ( P  =   0.0001); and the duration of non-rapid eye movement (NREM) sleep stages 3 and 4 was decreased ( P  =   0.005). Multiple regression analysis revealed correlations between the adiponectin level and the total sleep time ( β  = 0.688, P  =   0.009), AHI ( β  = 1.274, P  =   0.010), REM latency ( β  = −0.637, P  =   0.021) and the percentage of NREM sleep ( β  = −7.648, P  =   0.002) in PWS. In children with PWS, higher plasma adiponectin levels were independently associated with several sleep variables, which was not observed in the control group. These results suggest a potential influence of elevated adiponectin level on the sleep structures in PWS.     

Differential effects of waking from non-rapid eye movement versus rapid eye movement sleep on cardiovascular activity

The occurrence of cardiovascular events increases in the morning, and while the mechanism responsible is yet to be determined, possible contributors include surges in sympathetic activity and concurrent rises in blood pressure (BP). This study tested the hypothesis that the increase in sympathetic dominance and the surge in BP were greater when waking spontaneously from Stage 2 sleep compared with waking from rapid eye movement (REM) sleep. Twenty healthy young adults had overnight polysomnography, including electrocardiogram measurements. Spectral analysis of heart rate variability (HRV) was conducted on 2-min blocks of stable data selected from the last 30 min of sleep and during 30 min of resting wakefulness (supine) immediately following sleep. Outputs included absolute low frequency (LF) and high frequency (HF) power, the LF/HF ratio, heart rate (HR) and BP. To investigate the effect of waking from Stage 2 or REM sleep on HRV and BP responses, two-way analyses of variance ( anova s) (Stage 2 versus REM) with repeated measures (sleep versus morning wakefulness) were performed. It was found that waking from Stage 2 sleep was associated with significant increases in HR ( P  = 0·002) and BP ( P  < 0·001), as well as a tendency towards an increase in the LF/HF ratio ( P  = 0·08), whereas measurements during REM sleep and subsequent wakefulness were similar ( P  > 0·05). The greater increase in BP and HR when waking from Stage 2 sleep compared with REM sleep suggests that in vulnerable populations, waking from Stage 2 sleep could be an adjunct risk factor of cardiovascular events during the morning period.     

Does age worsen sleep‐dependent memory consolidation?

Slow wave sleep (SWS) is known to favour episodic memory consolidation. Given that ageing is associated with a reduction in SWS and episodic memory impairment, our aim was to investigate whether memory continues to benefit from sleep in older adults. Episodic memory consolidation was tested in 20 young (22.1 ± 1.7 years) and 20 older volunteers (68.9 ± 5.3 years) who performed a visuospatial two‐dimensional object‐location task. Retention capacities were evaluated after 12 h of wakefulness or 12 h of sleep. Performances before and after the interval allowed us to calculate a forgetting rate. Sleep architecture was measured by polysomnography (older adults = 410 min; young adults: 467 min). Our results showed that the beneficial effect of sleep on memory consolidation was reduced in older adults compared to young adults. In older adults, sleep did not enhance memory consolidation significantly compared to wakefulness. Sleep prevented young adults from forgetting (?0.10% ± 2.1), while the forgetting rate in older adults was still important after a period of sleep (16.60% ± 4.2; P = 0.05). The sleep architecture of older adults was characterized by a decrease in sleep efficiency (?12%; P < 0.05), in total cycle time (?137 min; P < 0.05), in percentage of total cycle time (?21%; P < 0.05) and in rapid eye movement time (?41 min; P < 0.05) compared to young adults. However, no difference in slow wave sleep was observed (?1%; not significant) and no correlation was found with performance. Age‐related changes in sleep parameters may have a negative impact on memory consolidation in older adults.     

Inhibitory and excitatory intracortical circuits across the human sleep–wake cycle using paired-pulse transcranial magnetic stimulation

Studies using single-pulse transcranial magnetic stimulation (TMS) have shown that excitability of the corticospinal system is systematically reduced in natural human sleep as compared to wakefulness with significant differences between sleep stages. However, the underlying excitatory and inhibitory interactions on the corticospinal system across the sleep–wake cycle are poorly understood. Here, we specifically asked whether in the motor cortex short intracortical inhibition (SICI) and facilitation (ICF) can be elicited at all in sleep using the paired-pulse TMS protocol, and if so, how SICI and ICF vary across sleep stages. We studied 28 healthy subjects at interstimulus intervals of 3 ms (SICI) and 10 ms (ICF), respectively. Magnetic stimulation was performed over the hand area of the motor cortex using a focal coil and evoked motor potentials were recorded from the contralateral first dorsal interosseus muscle (1DI). Relevant data was obtained from 13 subjects (NREM 2: n = 7; NREM 3/4: n = 7; REM: n = 7). Results show that both SICI and ICF were present in NREM sleep. SICI was significantly enhanced in NREM 3/4 as compared to wakefulness and all other sleep stages whereas in NREM 2 neither SICI nor ICF differed from wakefulness. In REM sleep SICI was in the same range as in wakefulness, but ICF was entirely absent. These results in humans support the hypothesis derived from animal experiments which suggests that intracortical inhibitory mechanisms are involved in the control of neocortical pyramidal cells in NREM and REM sleep, but along different intraneuronal circuits. Further, our findings suggest that cortical mechanisms may additionally contribute to the inhibition of spinal motoneurones in REM sleep.     

Quantitative electroencephalography during rapid eye movement (REM) and non‐REM sleep in combat‐exposed veterans with and without post‐traumatic stress disorder

Sleep disturbances are a hallmark feature of post‐traumatic stress disorder (PTSD), and associated with poor clinical outcomes. Few studies have examined sleep quantitative electroencephalography (qEEG), a technique able to detect subtle differences that polysomnography does not capture. We hypothesized that greater high‐frequency qEEG would reflect ‘hyperarousal’ in combat veterans with PTSD (n = 16) compared to veterans without PTSD (n = 13). EEG power in traditional EEG frequency bands was computed for artifact‐free sleep epochs across an entire night. Correlations were performed between qEEG and ratings of PTSD symptoms and combat exposure. The groups did not differ significantly in whole‐night qEEG measures for either rapid eye movement (REM) or non‐REM (NREM) sleep. Non‐significant medium effect sizes suggest less REM beta (opposite to our hypothesis), less REM and NREM sigma and more NREM gamma in combat veterans with PTSD. Positive correlations were found between combat exposure and NREM beta (PTSD group only), and REM and NREM sigma (non‐PTSD group only). Results did not support global hyperarousal in PTSD as indexed by increased beta qEEG activity. The correlation of sigma activity with combat exposure in those without PTSD and the non‐significant trend towards less sigma activity during both REM and NREM sleep in combat veterans with PTSD suggests that differential information processing during sleep may characterize combat‐exposed military veterans with and without PTSD.     

Pulse transit time as a surrogate measure of changes in systolic arterial pressure in children during sleep

Pulse transit time has been proposed as a surrogate measure of systolic arterial pressure, as it is dependent upon arterial stiffness. Past research has shown that pulse transit time has a significant inverse relationship to systolic arterial pressure in adults; however, studies in children are limited. This study aimed to explore the relationship between systolic arterial pressure and pulse transit time in children during sleep. Twenty‐five children (13.1 ± 1.6 years, 48% male) underwent overnight polysomnography (PSG) with a simultaneous recording of continuous systolic arterial pressure and photoplethysmography. Pulse transit time was calculated as the time delay between the R‐wave peak of the electrocardiogram (ECG) to the 50% point of the upstroke of the corresponding photoplethysmography waveform; 500 beats of simultaneous systolic arterial pressure and pulse transit time were analysed in each sleep stage for each child. Pulse transit time was normalized to each subject's mean wake pulse transit time. The ability of pulse transit time to predict systolic arterial pressure change was determined by linear mixed‐effects modelling. Significant negative correlations between pulse transit time and systolic arterial pressure were found for individual children for each sleep stage [mean correlations for cohort: non‐rapid eye movement (NREM) sleep 1 and 2 r = ?0.57, slow wave sleep (SWS) r = ?0.76, REM r = ?0.65, P < 0.01 for all]. Linear mixed‐model analysis demonstrated that changes in pulse transit time were a significant predictor of changes in systolic arterial pressure for each sleep stage (P < 0.001). The model of pulse transit time‐predicted systolic arterial pressure closely tracked actual systolic arterial pressure changes over time. This study demonstrated that pulse transit time was accurate in tracking systolic arterial pressure changes over time. Thus, the use of pulse transit time as a surrogate measure of changes in systolic arterial pressure in children is a valid, non‐invasive and inexpensive method with many potential applications.     

Developmental changes in the sleep electroencephalogram of adolescent boys and girls

The sleep electroencephalogram (EEG) changes across adolescence; however, there are conflicting data as to whether EEG changes are regionally specific, are evident in non‐rapid eye movement (NREM) and rapid eye movement (REM) sleep, and whether there are sex differences. The present study seeks to resolve some of these issues in a combined cross‐sectional and longitudinal analysis of sleep EEG in adolescents. Thirty‐three healthy adolescents (18 boys, 15 girls; 11–14 years) were studied on two occasions 6–8 months apart. Cross‐sectional analysis of data from the initial visit revealed significantly less slow‐wave sleep, delta (0.3 to <4 Hz) and theta (4 to <8 Hz) power in both NREM and REM sleep with advancing age. The age–delta power relationship was significant at the occipital site, with age accounting for 26% of the variance. Longitudinal analysis revealed that NREM delta power declined significantly from the initial to follow‐up visit, in association with declining delta amplitude and incidence (P < 0.01), with the effect being greatest at the occipital site. REM delta power also declined over time in association with reduced amplitude (P < 0.01). There were longitudinal reductions in theta, alpha and sigma power in NREM and REM sleep evident at the occipital site at follow‐up (P < 0.01). No sex differences were apparent in the pattern of change with age for NREM or REM sleep. Declines in sleep EEG spectral power occur across adolescence in both boys and girls, particularly in the occipital derivation, and are not state‐specific, occurring in both NREM and REM sleep.     

Sleep–wake fluctuations and respiratory events during Cheyne–Stokes respiration in patients with heart failure

Fluctuations in sleep–wake state are thought to contribute to the respiratory instability of Cheyne–Stokes respiration in patients with heart failure by promoting the rhythmic occurrence of central apnea and ventilatory overshoot. There are no data, however, on the relationship between vigilance state and respiratory events. In this study we used a novel method to detect the occurrence of state transitions (time resolution: 0.25 s, minimum duration of state changes: 2 s) and to assess their time relationship with apnoeic events. We also evaluated whether end‐apnoeic arousals are associated with a ventilatory overshoot. A polysomnographic, daytime laboratory recording (25 min) was performed during Cheyne–Stokes respiration in 16 patients with heart failure. Automatic state classification included wakefulness and non‐rapid eye movement sleep stages 1–2. As a rule, wakefulness occurred during hyperpnoeic phases, and non‐rapid eye movement sleep occurred during apnoeic events. Ninety‐two percent of the observed central apneas (N = 272) were associated with a concurrent wakefulness → non‐rapid eye movement sleep → wakefulness transition. The delay between wakefulness → non‐rapid eye movement sleep transitions and apnea onset was ?0.3 [?3.1, 3.0] s [median (lower quartile, upper quartile); P = 0.99 testing the null hypothesis: median delay = 0], and the delay between non‐rapid eye movement sleep → wakefulness transitions and apnea termination was 0.2 [?0.5, 1.2] s (P = 0.7). A positive/negative delay indicates that the state transition occurred before/after the onset or termination of apnea. Non‐rapid eye movement sleep → wakefulness transitions synchronous with apnea termination were associated with a threefold increase in tidal volume and a twofold increase in ventilation (all P < 0.001), indicating ventilatory overshoot. These findings highlight that wakefulness → non‐rapid eye movement sleep → wakefulness transitions parallel apnoeic events during Cheyne–Stokes respiration in patients with heart failure. The relationships between state changes and respiratory events are consistent with the notion that state fluctuations promote ventilatory instability.     

A new quantitative automatic method for the measurement of non-rapid eye movement sleep electroencephalographic amplitude variability

The aim of this study was to arrange an automatic quantitative measure of the electroencephalographic (EEG) signal amplitude variability during non‐rapid eye movement (NREM) sleep, correlated with the visually extracted cyclic alternating pattern (CAP) parameters. Ninety‐eight polysomnographic EEG recordings of normal controls were used. A new algorithm based on the analysis of the EEG amplitude variability during NREM sleep was designed and applied to all recordings, which were also scored visually for CAP. All measurements obtained with the new algorithm correlated positively with corresponding CAP parameters. In particular, total CAP time correlated with total NREM variability time (r = 0.596; P < 1E‐07), light sleep CAP time with light sleep variability time (r = 0.597; P < 1E‐07) and slow wave sleep CAP time with slow wave sleep variability time (r = 0.809; P < 1E‐07). Only the duration of CAP A phases showed a low correlation with the duration of variability events. Finally, the age‐related modifications of CAP time and of NREM variability time were found to be very similar. The new method for the automatic analysis of NREM sleep amplitude variability presented here correlates significantly with visual CAP parameters; its application requires a minimum work time, compared to CAP analysis, and might be used in large studies involving numerous recordings in which NREM sleep EEG amplitude variability needs to be assessed.     

Pineal gland volume in primary insomnia and healthy controls: a magnetic resonance imaging study

Little is known about the relation between pineal volume and insomnia. Melatonin promotes sleep processes and, administered as a drug, it is suitable to improve primary and secondary sleep disorders in humans. Recent magnetic resonance imaging studies suggest that human plasma and saliva melatonin levels are partially determined by the pineal gland volume. This study compares the pineal volume in a group of patients with primary insomnia to a group of healthy people without sleep disturbance. Pineal gland volume (PGV) was measured on the basis of high‐resolution 3 Tesla MRI (T1‐magnetization prepared rapid gradient echo) in 23 patients and 27 controls, matched for age, gender and educational status. Volume measurements were performed conventionally by manual delineation of the pineal borders in multi‐planar reconstructed images. Pineal gland volume was significantly smaller (P < 0.001) in patients (48.9 ± 26.6 mm³) than in controls (79 ± 30.2 mm³). In patients PGV correlated negatively with age (r = ?0.532; P = 0.026). Adjusting for the effect of age, PGV and rapid eye movement (REM) latency showed a significant positive correlation (r_S = 0.711, P < 0.001) in patients. Pineal volume appears to be reduced in patients with primary insomnia compared to healthy controls. Further studies are needed to clarify whether low pineal volume is the basis or the consequence of functional sleep changes to elucidate the molecular pathology for the pineal volume loss in primary insomnia.     

Sleep state distribution of obstructive events in children: is obstructive sleep apnoea really a rapid eye movement sleep‐related condition?

Obstructive sleep apnoea (OSA) in children is commonly considered to occur predominantly in rapid eye movement (REM) sleep, but clinical experience suggests that this is not universally the case. We hypothesized that there would be a subgroup of children with OSA who have non‐REM (NREM) predominance of obstructive events and that these children share certain clinical characteristics. Thus, we aimed to compare the obstructive apnoea–hypopnoea index (OAHI) in REM versus NREM sleep and to assess factors influencing the distribution of events by sleep state. Polysomnography (PSG) recordings of 102 children aged 0–18 years with moderate to severe OSA (OAHI ≥5 h^?1) were reviewed. OAHI was calculated separately for REM and NREM sleep. A REM predominance index (RPI) was determined using log transformation [RPI = log (REM OAHI + 0.5) ? log (NREM OAHI + 0.5)] and compared with possible influencing factors using multiple linear regression. Analysis showed that obstructive events were more common in REM sleep (median REM OAHI 21.4 h^?1, median NREM OAHI 8.3 h^?1, P < 0.001). Mean RPI was significantly greater than zero (P = 0.003). However, a substantial minority of children (30.4%) had a higher NREM than REM OAHI. The factors that were related significantly to NREM predominance were older age (P = 0.02), higher arousal index (P < 0.001) and higher SpO₂ nadir (P < 0.001). Our findings demonstrate that while OSA is a REM sleep‐related problem in the majority of children, there is a significant subset of children with NREM predominance of obstructive events. This finding highlights the importance of considering sleep state distribution of events in studies of the pathophysiology and outcomes of OSA in childhood.     

Sleep duration is associated with white matter hyperintensity volume in older adults: the Northern Manhattan Study

Self‐reports of long or short sleep durations have indicated an association with cardiovascular morbidity and mortality, but there are limited data evaluating their association with white matter hyperintensity volume (WMHV), a marker of cerebral small vessel disease. We conducted a cross‐sectional analysis of self‐reported sleep duration to test for a correlation with white matter hyperintensities, measured by quantitative magnetic resonance imaging (MRI), in the Northern Manhattan Study. We used multivariable linear regression models to assess associations between both short (<6 h) and long (≥9 h) sleep durations and log‐transformed WMHV, adjusting for demographic, behavioural and vascular risk factors. A total of 1244 participants, mean age 70 ± 9 years, 61% women and 68% Hispanics were analysed with magnetic resonance brain imaging and self‐reported sleep duration. Short sleep was reported by 23% (n = 293) and long sleep by 10% (n = 121) of the sample. Long sleep (β = 0.178; P = 0.035), but not short sleep (β = ?0.053; P = 0.357), was associated with greater log‐WMHV in fully adjusted models. We observed an interaction between sleep duration, diabetes mellitus and log‐WMHV (P = 0.07). In fully adjusted models, stratified analysis showed that long sleep duration was associated with greater WMHV only in those with diabetes (β = 0.78; P = 0.0314), but not in those without diabetes (β = 0.022; P = 0.2), whereas short sleep was not associated with white matter hyperintensities in those with or without diabetes. In conclusion, long sleep duration was associated with a greater burden of white matter lesions in this stroke‐free urban sample. The association was seen mainly among those with diabetes mellitus.     

Does the Circadian Modulation of Dream Recall Modify with Age?

Study objectives:

The ultradian NREM-REM sleep cycle and the circadian modulation of REM sleep sum to generate dreaming. Here we investigated age-related changes in dream recall, number of dreams, and emotional domain characteristics of dreaming during both NREM and REM sleep.

Design:

Analysis of dream recall and sleep EEG (NREM/REM sleep) during a 40-h multiple nap protocol (150 min of wakefulness and 75 min of sleep) under constant routine conditions.

Setting:

Centre for Chronobiology, Psychiatric Hospital of the University of Basel, Basel, Switzerland.

Participants:

Seventeen young (20-31 years) and 15 older (57-74 years) healthy volunteers

Interventions:

N/A.

Measurements and Results:

Dream recall and number of dreams varied significantly across the circadian cycle and between age groups, with older subjects exhibiting fewer dreams (P < 0.05), particularly after naps scheduled during the biological day, closely associated with the circadian rhythm of REM sleep. No significant age differences were observed for the emotional domain of dream content.

Conclusions:

Since aging was associated with attenuated amplitude in the circadian modulation of REM sleep, our data suggest that the age-related decrease in dream recall can result from an attenuated circadian modulation of REM sleep.

Citation:

Chellappa SL; Möunch M; Blatter K; Knoblauch V; Cajochen C. Does the circadian modulation of dream recall modify with age? SLEEP 2009;32(9):1201-1209.     

Power spectrum analysis and heart rate variability in Stage 4 and REM sleep: evidence for state-specific changes in autonomic dominance

The present study investigated autonomic activity during NREM and REM sleep stages and wakefulness by spectral analysis of heart rate variability. The results demonstrated that NREM sleep in humans was characterized by a widely different autonomic activation pattern than REM sleep: high parasympathetic activity was found in NREM, while REM was characterized by attenuated vagal tone, and augmented sympathetic activity. The overall pattern during wakefulness showed an intermediate position between NREM and REM patterns; parasympathetic activity was lower than in NREM and higher than in REM, with an opposite trend for sympathetic activity.     

The effects of sleep deprivation in humans: topographical electroencephalogram changes in non‐rapid eye movement (NREM) sleep versus REM sleep

Studies on homeostatic aspects of sleep regulation have been focussed upon non‐rapid eye movement (NREM) sleep, and direct comparisons with regional changes in rapid eye movement (REM) sleep are sparse. To this end, evaluation of electroencephalogram (EEG) changes in recovery sleep after extended waking is the classical approach for increasing homeostatic need. Here, we studied a large sample of 40 healthy subjects, considering a full‐scalp EEG topography during baseline (BSL) and recovery sleep following 40 h of wakefulness (REC). In NREM sleep, the statistical maps of REC versus BSL differences revealed significant fronto‐central increases of power from 0.5 to 11 Hz and decreases from 13 to 15 Hz. In REM sleep, REC versus BSL differences pointed to significant fronto‐central increases in the 0.5–7 Hz and decreases in the 8–11 Hz bands. Moreover, the 12–15 Hz band showed a fronto‐parietal increase and that at 22–24 Hz exhibited a fronto‐central decrease. Hence, the 1–7 Hz range showed significant increases in both NREM sleep and REM sleep, with similar topography. The parallel change of NREM sleep and REM sleep EEG power is related, as confirmed by a correlational analysis, indicating that the increase in frequency of 2–7 Hz possibly subtends a state‐aspecific homeostatic response. On the contrary, sleep deprivation has opposite effects on alpha and sigma activity in both states. In particular, this analysis points to the presence of state‐specific homeostatic mechanisms for NREM sleep, limited to <2 Hz frequencies. In conclusion, REM sleep and NREM sleep seem to share some homeostatic mechanisms in response to sleep deprivation, as indicated mainly by the similar direction and topography of changes in low‐frequency activity.     

Neurofibromatosis type 1 (Nf1)‐mutant mice exhibit increased sleep fragmentation

Neurofibromatosis type 1 (NF1) is a neurodevelopmental disorder in which affected children and adults are at a higher risk of sleep disorders. In an effort to identify potential sleep disturbances in a small animal model, we used a previously reported Nf1 conditional knockout (Nf1^CKO) mouse strain. In contrast to Nf1 mutant flies, the distribution of vigilance states was intact in Nf1^CKO mice. However, Nf1^CKO mice exhibited increased non‐REM sleep (NREM)‐to‐wake and wake‐to‐NREM transitions. This sleep disruption was accompanied by decreased bout durations during awake and NREM sleep states under both light and dark conditions. Moreover, Nf1^CKO mice have higher percentage delta power during awake and NREM sleep states under all light conditions. Taken together, Nf1^CKO mice phenocopy some of the sleep disturbances observed in NF1 patients and provide a tractable platform to explore the molecular mechanisms governing sleep abnormalities in NF1.     

Is sleep‐related verbal memory consolidation impaired in sleepwalkers?

In order to evaluate verbal memory consolidation during sleep in subjects experiencing sleepwalking or sleep terror, 19 patients experiencing sleepwalking/sleep terror and 19 controls performed two verbal memory tasks (16‐word list from the Free and Cued Selective Reminding Test, and a 220‐ and 263‐word modified story recall test) in the evening, followed by nocturnal video polysomnography (n = 29) and morning recall (night‐time consolidation after 14 h, n = 38). The following morning, they were given a daytime learning task using the modified story recall test in reverse order, followed by an evening recall test after 9 h of wakefulness (daytime consolidation, n = 38). The patients experiencing sleepwalking/sleep terror exhibited more frequent awakenings during slow‐wave sleep and longer wakefulness after sleep onset than the controls. Despite this reduction in sleep quality among sleepwalking/sleep terror patients, they improved their scores on the verbal tests the morning after sleep compared with the previous evening (+16 ± 33%) equally well as the controls (+2 ± 13%). The performance of both groups worsened during the daytime in the absence of sleep (?16 ± 15% for the sleepwalking/sleep terror group and ?14 ± 11% for the control group). There was no significant correlation between the rate of memory consolidation and any of the sleep measures. Seven patients experiencing sleepwalking also sleep‐talked during slow‐wave sleep, but their sentences were unrelated to the tests or the list of words learned during the evening. In conclusion, the alteration of slow‐wave sleep during sleepwalking/sleep terror does not noticeably impact on sleep‐related verbal memory consolidation.     

Respiratory and body movements as indicators of sleep stage and wakefulness in infants and young children

Conventional polysomnographic (PSG) sleep staging to sleep staging based on a static-charge-sensitive bed (SCSB) recording in infants and young children was compared. The study consisted of whole-night clinical sleep studies in 22 children at 24 weeks (SD 24, range 1–79 weeks) of age. Most of the children presented with respiratory disturbances during sleep. From the SCSB record, sleep stages were differentiated according to regularity of breathing, presence of body movements, and most important, presence of high-frequency components of breathing (SCSB spikes). With both methods, three sleep/wake stages were distinguished: rapid eye movement (REM) sleep, non-rapid eye movement (NREM) sleep and wakefulness. The average inter-scorer reliability of the PSG sleep staging controlled in nine subjects was 88%. The average concordance between the two methods ranged from 82 to 85%, depending on the criteria used for scoring the SCSB. The mean sensitivity of the SCSB to detect NREM sleep ranged from 77 to 90% and the mean sensitivity to detect REM sleep ranged from 61 to 86%. The mean positive predictive value was 89–96% for NREM sleep and 54–67% for REM sleep. In conclusion, REM sleep is characterized by irregular breathing with superimposed fast respiratory movements. These changes are specific enough to allow distinction between episodes of NREM sleep, REM sleep and wakefulness with the non-invasive SCSB method in infants and young children. Incomplete concordance between PSG and SCSB score was most frequently observed during sleep stage transition periods, where the behavioural state and electrophysiological criteria disagreed. When combined with the PSG, the SCSB provides complementary information about the behavioural state of child.     

Low‐grade albuminuria in children with obstructive sleep apnea

Small urinary protein loss (low‐grade albuminuria or microalbuminuria) may reflect altered permeability of the glomerular filtration barrier. In the present study, it was hypothesized that children with obstructive sleep apnea have an increased risk of microalbuminuria compared with control subjects without sleep‐disordered breathing. Albumin‐to‐creatinine ratio was measured in morning spot urine specimens collected from consecutive children with or without snoring who were referred for polysomnography. Three groups were studied: (i) control subjects (no snoring, apnea–hypopnea index < 1 episode h^?1; n = 31); (ii) mild obstructive sleep apnea (snoring, apnea–hypopnea index = 1–5 episodes h^?1; n = 71); and (iii) moderate‐to‐severe obstructive sleep apnea (snoring, apnea–hypopnea index > 5 episodes?h^?1; n = 27). Indications for polysomnography in control subjects included nightmares, somnambulism and morning headaches. An albumin‐to‐creatinine ratio > median value in the control group (1.85 mg of albumin per g of creatinine) was defined as elevated. Logistic regression analysis revealed that children with moderate‐to‐severe obstructive sleep apnea, but not those with mild obstructive sleep apnea, had increased risk of elevated albumin‐to‐creatinine ratio relative to controls (reference) after adjustment for age, gender and presence of obesity: odds ratio 3.8 (95% confidence interval 1.1–12.6); P = 0.04 and 1.5 (0.6–3.7); P > 0.05, respectively. Oxygen desaturation of hemoglobin and respiratory arousal indices were significant predictors of albumin‐to‐creatinine ratio (r = 0.31, P = 0.01; and r = 0.43, P < 0.01, respectively). In conclusion, children with moderate‐to‐severe obstructive sleep apnea are at significantly higher risk of increased low‐grade excretion of albumin in the morning urine as compared with control subjects without obstructive sleep apnea. These findings may reflect altered permeability of the glomerular filtration barrier related to nocturnal hypoxemia and sympathetic activation which are induced by obstructive sleep apnea.