Duration Of Sleep Episodes Research Articles

Early Developmental Changes in Sleep in Infants: The Impact of Maternal Depression

This study evaluated whether sleep over the first 6 months of life was more disturbed in infants born to mothers who were depressed compared with infants from nondepressed mothers. Actigraphy was recorded for 7 consecutive days starting at 2 weeks postpartum and monthly thereafter until 6 months of age. Mothers completed daily sleep/wake diaries. Sleep data at 2 weeks and 6 months postpartum are presented here. The home environment. Eighteen healthy, full-term infants, 9 males and 9 females. Seven infants were born to women with no personal or family history of depression; 11 infants were born to women diagnosed with depression or with elevated levels of depression symptoms. N/A. Total sleep time, sleep latency, sleep efficiency, and number and duration of sleep episodes were computed for nocturnal and daytime sleep in each 24-hour block. Data were coded for risk group (1 = low risk, 2 = high risk), and repeated-measures multivariate analysis of variance contrasted changes in sleep measures at Week 2 and Week 24, between risk groups. The high-risk infants took longer to fall asleep, had lower sleep efficiencies, and had more sleep bouts in the nocturnal sleep period than did low-risk infants. These effects persisted at 6 months postpartum. Maternal depression is associated with significant sleep disturbance in infancy at 2 weeks postpartum that continues through 24 weeks. It remains to be determined if sleep disturbance in infancy confers a greater risk of developing early-onset depression in childhood.

Assessing sleepiness in the rat: a multiple sleep latencies test compared to polysomnographic measures of sleepiness

Sleepiness following 6 h of sleep deprivation (SD) was evaluated with a rat multiple sleep latencies test (rMSLT), and the findings were compared to conventional polysomnographic measures of sleepiness. The 6 h of SD was produced by automated activity wheels, and was terminated at either the end of the light period or at the beginning of the dark period. The rMSLT consisted of 5 min wakefulness induced by sensory stimulation followed by 25 min of freedom to sleep. This procedure was repeated every 30 min for 3 h and was designed to minimize the amount of sleep lost due to the testing procedure. In separate rats, 6 h SD was followed by undisturbed recovery, allowing evaluation of conventional polysomnographic measures of sleepiness. Sleep onset latencies were reduced following SD, with recovery in the light (baseline = 8 min, 3 s versus post-SD = 1 min, 17 s) and dark period (baseline = 14 min, 17 s versus 7 min, 7 s). Sleep onset latencies were not altered by varying the duration criterion for the first sleep bout (i.e., sleep bout length criteria of 10, 20, 30, or 60 s were compared). Polysomnographic variables (non-rapid eye movement sleep episode duration, delta power, and number of awakenings) also provided reliable indirect measures of sleepiness, regardless of whether the recovery sleep occurred in the light or dark period. Evaluation of effect size indicated that the rMSLT was a strong measure of sleepiness, and was influenced by homeostatic, circadian, and illumination factors. The rMSLT provided a simple, objective, robust and direct measure of sleepiness that was as effective as conventional polysomnographic measures of sleepiness.

Effects of adolescent ethanol exposure on sleep in adult rats

Although adolescent ethanol (EtOH) exposure has been associated with long-lasting changes in brain function, little is known as to whether EtOH exposure during adolescence alters sleep and cortical arousal. This study examined protracted alterations in sleep in adult rats exposed to EtOH during adolescence. Adolescent male Wistar rats were exposed to EtOH vapor for 12 h/day for 5 weeks. Cortical electroencephalograms were obtained during 4-h recording sessions after 5 weeks of withdrawal from EtOH. Adolescent EtOH exposure significantly reduced the mean duration of slow-wave sleep (SWS) episodes and the total amount of time spent in SWS in EtOH-exposed rats, compared to controls. Spectral analysis revealed that adolescent EtOH exposure significantly increased cortical peak frequencies during SWS in the 2–4, 4–6, and 6–8 Hz bands. Taken together, our findings suggest that chronic EtOH exposure in adolescent rats reduces measures of SWS, an effect also seen as part of normal aging. Although the cellular and molecular mechanisms mediating the consequences of EtOH exposure on the aging process are not known, the similarities between adolescent EtOH exposure and aging merits further investigation.

Homeostatic regulation of sleep in the white-crowned sparrow (Zonotrichia leucophrys gambelii)

BackgroundSleep is regulated by both a circadian and a homeostatic process. The homeostatic process reflects the duration of prior wakefulness: the longer one stays awake, the longer and/or more intense is subsequent sleep. In mammals, the best marker of the homeostatic sleep drive is slow wave activity (SWA), the electroencephalographic (EEG) power spectrum in the 0.5–4 Hz frequency range during non-rapid eye movement (NREM) sleep. In mammals, NREM sleep SWA is high at sleep onset, when sleep pressure is high, and decreases progressively to reach low levels in late sleep. Moreover, SWA increases further with sleep deprivation, when sleep also becomes less fragmented (the duration of sleep episodes increases, and the number of brief awakenings decreases). Although avian and mammalian sleep share several features, the evidence of a clear homeostatic response to sleep loss has been conflicting in the few avian species studied so far. The aim of the current study was therefore to ascertain whether established markers of sleep homeostasis in mammals are also present in the white-crowned sparrow (Zonotrichia leucophrys gambelii), a migratory songbird of the order Passeriformes. To accomplish this goal, we investigated amount of sleep, sleep time course, and measures of sleep intensity in 6 birds during baseline sleep and during recovery sleep following 6 hours of sleep deprivation.ResultsContinuous (24 hours) EEG and video recordings were used to measure baseline sleep and recovery sleep following short-term sleep deprivation. Sleep stages were scored visually based on 4-sec epochs. EEG power spectra (0.5–25 Hz) were calculated on consecutive 4-sec epochs. Four vigilance states were reliably distinguished based on behavior, visual inspection of the EEG, and spectral EEG analysis: Wakefulness (W), Drowsiness (D), slow wave sleep (SWS) and rapid-eye movement (REM) sleep. During baseline, SWA during D, SWS, and NREM sleep (defined as D and SWS combined) was highest at the beginning of the major sleep period and declined thereafter. Moreover, peak SWA in both SWS and NREM sleep increased significantly immediately following sleep deprivation relative to baseline.ConclusionAs in mammals, sleep deprivation in the white-crowned sparrow increases the intensity of sleep as measured by SWA.

Behavioral actions of urotensin-II

Urotensin-II (U-II) and urotensin-II-related peptide (URP) have been identified as the endogenous ligands of the orphan G-protein-coupled receptor GPR14 now renamed UT. The occurrence of U-II and URP in the central nervous system, and the widespread distribution of UT in the brain suggest that U-II and URP may play various behavioral activities. Studies conducted in rodents have shown that central administration of U-II stimulates locomotion, provokes anxiety- and depressive-like states, enhances feeding activity and increases the duration of paradoxical sleep episodes. These observations indicate that, besides the endocrine/paracrine activities of U-II and URP on cardiovascular and kidney functions, these peptides may act as neurotransmitters and/or neuromodulators to regulate various neurobiological activities.

Short light–dark cycles affect sleep in mice

Environmental light has a strong impact on human physiology and behaviour, including cognitive functioning and alertness. Previous studies have shown that short light-dark (LD) cycles influence sleep in the albino rat. Rapid eye movement (REM) sleep increases after the onset of darkness and increases after light onset. In the present study, we investigated whether light affects sleep in mice. To this purpose the electroencephalogram and electromyogram of nine adult male C57BL/6 mice was recorded under 12 : 12 h baseline LD conditions, followed by 24 h continuous darkness (DD) and 6 days with LD cycles of different durations (2 h, 30 min, 14 min, 10 min, 4 min and 2 min), presented in a randomized order. NREM sleep was evenly distributed over the light and dark intervals of all short LD cycles. REM sleep, however, was increased during the dark intervals of short (10-30 min) LD cycles. Analysis showed that in these LD cycles, the increment in REM sleep was maximal in the second minute after dark onset, where the percentage of epochs with REM sleep increased significantly to 175% of baseline values. This increase was attributable to an increase in REM sleep episode duration. The recorded responses show that sleep in mice is affected by photic stimulation. The results demonstrate that pigmented animals can show REM sleep induction after dark onset and indicate that light has significant effects on the regulation of sleep.

Sleep in Kcna2 knockout mice

BackgroundShaker codes for a Drosophila voltage-dependent potassium channel. Flies carrying Shaker null or hypomorphic mutations sleep 3–4 h/day instead of 8–14 h/day as their wild-type siblings do. Shaker-like channels are conserved across species but it is unknown whether they affect sleep in mammals. To address this issue, we studied sleep in Kcna2 knockout (KO) mice. Kcna2 codes for Kv1.2, the alpha subunit of a Shaker-like voltage-dependent potassium channel with high expression in the mammalian thalamocortical system.ResultsContinuous (24 h) electroencephalograph (EEG), electromyogram (EMG), and video recordings were used to measure sleep and waking in Kcna2 KO, heterozygous (HZ) and wild-type (WT) pups (P17) and HZ and WT adult mice (P67). Sleep stages were scored visually based on 4-s epochs. EEG power spectra (0–20 Hz) were calculated on consecutive 4-s epochs. KO pups die by P28 due to generalized seizures. At P17 seizures are either absent or very rare in KO pups (< 1% of the 24-h recording time), and abnormal EEG activity is only present during the seizure. KO pups have significantly less non-rapid eye movement (NREM) sleep (-23%) and significantly more waking (+21%) than HZ and WT siblings with no change in rapid eye movement (REM) sleep time. The decrease in NREM sleep is due to an increase in the number of waking episodes, with no change in number or duration of sleep episodes. Sleep patterns, daily amounts of sleep and waking, and the response to 6 h sleep deprivation are similar in HZ and WT adult mice.ConclusionKv1.2, a mammalian homologue of Shaker, regulates neuronal excitability and affects NREM sleep.

Knitting a Ravelled Sleave

For an activity in which we spend about a third of our lifetime, much about sleep remains enigmatic. Foltenyi et al . investigated the role of epidermal growth factor receptor (EGFR) signaling in regulating sleep in Drosophila melanogaster . Activation of fly EGFR ligands like Spitz depends on the transmembrane protein Star and on Rhomboid family (Rho) proteases. Using flies in which Rho and Star expression could be conditionally induced, the authors showed that their overexpression led to a dose-dependent increase in sleep. There was a transient increase in both the duration and number of sleep episodes, which was followed by a decrease and then a return to normal. Overexpression of a soluble form of Spitz, which does not require Rho processing, had similar effects. Overexpression of Rho and Star led to an increase in phosphorylation of extracellular signal-regulated kinase (ERK, a target of EGFR signaling) in the head that paralleled the temporal pattern of increased sleep, an increase that was blocked by coexpression of a dominant-negative EGFR mutant. Immunohistochemical analysis indicated that the increase in ERK phosphorylation was greatest in the tritocerebrum. Moreover, several lines of flies in which Rho activity in neurons projecting from the pars intercerebralis (PI, a region analogous to the vertebrate hypothalamus) to the tritocerebrum was inhibited with RNAi showed decreased sleep. This decrease involved brief sleep episodes in conjunction with an increase in the number of times that sleep was attempted--a pattern that could constitute a fly model of insomnia. The authors propose that the production of EGFR ligand by PI neurons leads to ERK activation in tritocerebrum neurons, thereby promoting sleep. Colwell provides thoughtful commentary. K. Foltenyi, R. J. Greenspan, J. W. Newport, Activation of EGFR and ERK by rhomboid signaling regulates the consolidation and maintenance of sleep in Drosophila . Nat. Neurosci . 10 , 1160-1167 (2007). [PubMed] C. S. Colwell, Soporific signaling: How flies sleep through the night. Nat. Neurosci . 10 , 1079-1080 (2007). [PubMed]

Sleep fragmentation elevates behavioral, electrographic and neurochemical measures of sleepiness

Sleep fragmentation, a feature of sleep apnea as well as other sleep and medical/psychiatric disorders, is thought to lead to excessive daytime sleepiness. A rodent model of sleep fragmentation was developed (termed sleep interruption, SI), where rats were awakened every 2 min by the movement of an automated treadmill for either 6 or 24 h of exposure. The sleep pattern of rats exposed to 24 h of SI resembled sleep of the apneic patient in the following ways: sleep was fragmented (up to 30 awakening/h), total rapid eye movement (REM) sleep time was greatly reduced, non-rapid eye movement (NREM) sleep episode duration was reduced (from 2 min, 5 s baseline to 58 s during SI), whereas the total amount of NREM sleep time per 24 h approached basal levels. Both 6 and 24 h of SI made rats more sleepy, as indicated by a reduced latency to fall asleep upon SI termination. Electrographic measures in the recovery sleep period following either 6 or 24 h of SI also indicated an elevation of homeostatic sleep drive; specifically, the average NREM episode duration increased (e.g. for 24 h SI, from 2 min, 5 s baseline to 3 min, 19 s following SI), as did the NREM delta power during recovery sleep. Basal forebrain (BF) levels of extracellular adenosine (AD) were also measured with microdialysis sample collection and high performance liquid chromatography detection, as previous work suggests that increasing concentrations of BF AD are related to sleepiness. BF AD levels were significantly elevated during SI, peaking at 220% of baseline during 30 h of SI exposure. These combined findings imply an elevation of the homeostatic sleep drive following either 6 or 24 h of SI, and BF AD levels appear to correlate more with sleepiness than with the cumulative amount of prior wakefulness, since total NREM sleep time declined only slightly. SI may be partially responsible for the symptom of daytime sleepiness observed in a number of clinical disorders, and this may be mediated by mechanisms involving BF AD.

Sedative and hypnotic activities of the ethanol fraction from Fructus Schisandrae in mice and rats

Fruits of Fructus Schisandrae have been used as medicine for the treatment for insomnia in traditional Chinese medicine. In the present research, the sedative and hypnotic activities of the ethanol fraction of Fructus Schisandrae fruit (SY3) were studied in mice and rats. In the open field test, SY3 (25, 50 and 100 mg/kg) significantly inhibited the motor activity of mice compared to the normal. Results also showed SY3 potentiated pentobarbital-induced sleep by not only increasing the number of falling asleep and prolonging sleeping time but also reducing sleep latency. Furthermore, sleep–wake stages of rats were evaluated by polytrophic recording for 3 h after treatment. The results demonstrated that SY3 at doses of 20, 40 and 80 mg/kg behaved remarkable action on sleep architecture of rats, which contain the increase of total sleeping time, the rate of deep slow wave sleep (SWS) and mean episode duration of deep SWS, and the decrease of the latency of deep SWS. Therefore, these results suggest that the ethanol fraction of Fructus Schisandrae fruit possesses potent sedative and hypnotic activity, which supported its therapeutic use for insomnia.

Hippocampal synaptic plasticity and spatial learning are impaired in a rat model of sleep fragmentation

Sleep fragmentation, a symptom in many clinical disorders, leads to cognitive impairments. To investigate the mechanisms by which sleep fragmentation results in memory impairments, rats were awakened once every 2 min via 30 s of slow movement on an automated treadmill. Within 1 h of this sleep interruption (SI) schedule, rats began to sleep in the 90-s periods without treadmill movement. Total non-rapid eye movement sleep (NREM) sleep time did not change over the 24 h of SI, although there was a significant decline in rapid eye movement sleep (REM) sleep and a corresponding increase in time spent awake. In the SI group, the mean duration of sleep episodes decreased and delta activity during periods of wake increased. Control rats either lived in the treadmill without movement (cage controls, CC), or had 10-min periods of movement followed by 30 min of non-movement allowing deep/continuous sleep (exercise controls, EC). EC did not differ from baseline in the total time spent in each vigilance state. Hippocampal long-term potentiation (LTP), a long-lasting change in synaptic efficacy thought to underlie declarative memory formation, was absent in rats exposed to 24 and 72 h SI. In contrast, LTP was normal in EC rats. However, long-term depression and paired-pulse facilitation were unaltered by 24 h SI. Twenty-four hour SI also impaired acquisition of spatial learning in the hippocampus-dependent water maze test. Twenty-four hour SI elevated plasma corticosterone (CORT) to levels previously shown to enhance LTP (125 ng/mL). The results suggest that sleep fragmentation negatively impacts spatial learning. Loss of N-methyl-D-aspartate (NMDA) receptor-dependent LTP in the hippocampal CA1 region may be one mechanism involved in this deficit.

Changes in sleep on chronic exposure to warm and cold ambient temperatures

Alterations in sleep induced by chronic exposure to mild changes in ambient temperature ( T a) were studied in male Wistar rats with chronically implanted electrodes for recording electrooculogram (EOG), electroencephalogram (EEG) and electromyogram (EMG), and a thermocouple to record the brain temperature ( T br). Changes in sleep–wakefulness (S–W) and T br on exposure to warm (30±1 °C) and cold (18±1 °C) T a for 4 weeks were studied in two groups of five rats each. Chronic heat exposure produced a persistent increase in sleep, primarily due to an increase in the durations of sleep episodes. A disproportionate increase in sleep during the dark period resulted in reduced circadian variation. The paradoxical sleep (PS)/total sleep time (TST) ratio also remained increased, during heat exposure. On chronic cold exposure, the sleep was decreased initially, but it recovered after 3 weeks, due to an increase in the frequency of slow wave sleep (SWS) episodes. The T br was not altered on exposure to warm T a, but it remained high throughout the 4 weeks of cold exposure. The increase in the amount of sleep, especially the PS with enhanced ambient temperature, may be considered as an adaptation to thermal load aimed at energy conservation. Though the increased wakefulness is suggested to enable the organism to optimize thermoregulation during acute cold stress, thermoregulation itself may be readjusted to ensure homeostatic restoration of sleep during chronic cold exposure.

Changes in sleep–wakefulness in the medial preoptic area lesioned rats: role of thermal preference

Changes in sleep–wakefulness (S–W) were studied in adult male Wistar rats, along with body temperature ( T b), locomotor activity (LMA) and thermal preference, after the lesion of the medial preoptic area (mPOA) with N-methyl-D-aspartic acid (NMDA). The sleep was decreased after the lesion of the mPOA, but there was recovery when the rats were given freedom to stay in an ambient temperature ( T amb) which they preferred. When given a choice between three T amb (24, 27 and 30 °C), the rats preferred 27 °C before the mPOA lesion, and 24 °C during the initial days after the lesion. There was a shift in the thermal preference to 30 °C, on the fourth week after the lesion, which coincided with the considerable recovery of sleep. The preference for higher T amb probably helped to improve sleep, as T amb of 30 °C is known to promote sleep. When the lesioned rats were not given the freedom to select the T amb, there was no recovery in sleep. The mPOA seems to be essential for increasing the durations of slow wave sleep (SWS) episodes, especially the light SWS (S1), as they remained shorter than the pre-lesion value, even when the rats were given freedom to stay in a preferred T amb. The homeostatic recovery of sleep, especially the night time sleep, resulted in the disruption of circadian sleep rhythm. But, the LMA, T b and thermal preference maintained their diurnal variation. T b and LMA were elevated after the mPOA lesion and they remained so till the end of the study.

Common scale-invariant patterns of sleep-wake transitions across mammalian species.

Although mammals of different species have different sleep patterns, brief sleep-wake transitions commonly are observed across species and appear to occur randomly throughout the sleeping period. The dynamical patterns and functions of these brief awakenings from sleep are not well understood, and they often are viewed as disruptions (random or pathologic) of the sleep process. In this article, we hypothesize that brief awakenings from sleep may reflect aspects of the endogenous sleep control mechanism and thus may exhibit certain robust dynamical patterns across species. We analyze sleep recordings from mice, rats, cats, and humans, and we compare the distributions of sleep and wake episode durations. For all four species, we find that durations of brief wake episodes during the sleep period exhibit a scale-free power-law behavior with an exponent alpha that remains the same for all species (alpha approximately equal to 2.2). In contrast, sleep episode durations for all four species follow exponential distributions with characteristic time scales, which change across species in relation to body mass and metabolic rate. Our findings suggest common dynamical features of brief awakenings and sleep durations across species and may provide insights into the dynamics of the neural circuits controlling sleep.

Sleep disturbances, pain and analgesia in adults hospitalized for burn injuries

Background and purpose Sleep disturbances are frequently reported in hospitalized patients. We have recently shown significant daily relationships between poor sleep and acute burn pain during the first week of hospitalization, where poor sleep leads to reports of higher pain intensity and in return, greater pain affects quality of sleep. This prospective study was designed to objectively evaluate sleep disturbances in hospitalized burn patients and further evaluate their relationships with pain intensity and administered medication. Patients and methods Sixteen non-ventilated burn patients wore an actigraph (Ambulatory Monitoring, Inc.) during hospitalization ( N of 24-h observations 164). Sleep measures included duration and fragmentation (# of awakenings, mean duration of awakenings, mean duration of sleep episodes (MDAW)). Pain intensity was assessed at rest (nighttime, morning, during the day) and following therapeutic procedures known to be painful (e.g. dressing changes). Results Although sleep duration was extremely variable, patients slept an average of 5.5 h a night with numerous awakenings. During the day, patients often took naps, bringing their total sleep time (TST) to 8 h. Regression analyses showed significant temporal relationships between sleep, pain and analgesic medication such that a night of poor sleep was followed by a significantly more painful day and higher analgesic intake. Further, high levels of pain and analgesic medication during the day were both significant predictors of poor sleep on the following night. Conclusions These results obtained with objective measures support previous findings that subjective sleep quality following burn injuries is poor, and strengthen the evidence of a relationship between sleep and sensitivity to pain. Nonetheless, further analyses are necessary to determine and dissociate the effects of pain intensity and analgesic medication on sleep.

Sleep homeostasis in Drosophila melanogaster.

The fruit fly Drosophila melanogaster is emerging as a promising model system for the genetic dissection of sleep. As in mammals, sleep in the fruit fly is a reversible state of reduced responsiveness to the external world and has been defined using an array of behavioral, pharmacologic, molecular, and electrophysiologic criteria. A central feature of mammalian sleep is its homeostatic regulation by the amount of previous wakefulness. Dissecting the mechanisms of homeostatic regulation is likely to provide key insights into the functions of sleep. Thus, it is important to establish to what extent sleep homeostasis is similar between mammals and flies. This study was designed to determine whether in flies, as in mammals, (1) sleep rebound is dependent on prior time awake; (2) sleep deprivation affects the intensity, in addition to the duration, of sleep rebound; (3) sleep loss impairs vigilance and performance; (4) the sleep homeostatic response is conserved among different wild-type lines, and between female and male flies of the same line. Motor activity of individual flies was recorded at 1-minute intervals using the infrared Drosophila Activity Monitoring System during 2 baseline days; during 6, 12, and 24 hours of sleep deprivation; and during 2 days of recovery. Sleep was defined as any period of uninterrupted behavioral immobility lasting > 5 minutes. Sleep continuity was measured by calculating the number of brief awakenings, the number and duration of sleep episodes, and a sleep continuity score. Vigilance before and after sleep deprivation was assessed by measuring the escape response triggered by 2 different aversive stimuli. Fly sleep research laboratory at UW-Madison. Adult flies of the Canton-S (CS) strain and 116 other wild-type lines (> or = 16 female and > or = 16 male flies per line). In wild-type CS flies, as in mammals, the amount of sleep recovered after sleep deprivation was dependent on prior time awake. Relative to baseline sleep, recovery sleep in CS flies was less fragmented, with longer sleep episodes, and was associated with a higher arousal threshold. Sleep deprivation in CS flies also reduced performance. Sleep duration and continuity increased after 24 hour of sleep deprivation in all the other wild-type lines tested. The sleep homeostatic response in fruit flies is a stable phenotype and shares most of, if not all, the major features of mammalian sleep homeostasis, thus supporting the use of Drosophila as a model system for the genetic dissection of sleep mechanisms and functions.

35 Sleep Characteristics of Young Alcohol Affected Children: A Quantitative and Qualitative Analysis

Fetal alcohol spectrum disorder refers to a group of phenotypic and behavioral anomalies associated with the use of alcohol in pregnancy, including growth retardation, craniofacial anomalies, and central nervous system involvement. Sleep disorders have been identified, but poorly described in fetal alcohol spectrum disorder. To quantitatively describe the sleep characteristics of children with fetal alcohol spectrum disorder, and to qualitatively describe the effects of sleep disruption on the affected child and their family. To develop appropriate sleep management strategies for children with fetal alcohol spectrum disorder and their families. A two part design was used. Nine children and their families were recruited from the Clinic for Alcohol and Drug Exposed Children at Children's Hospital in Winnipeg. Each study child was matched with a non-biologically related healthy control child in the same household. The first part of this research was a qualitative study of sleep using actigraphy to measure sleep disturbance. Actigraphic parameters were correlated with information from a pediatric sleep questionnaire designed for this study, and with a parent-maintained sleep log. The second part of the study consisted of a series of semi-structured interviews with the same families, with thematic analysis of the data. Actigraphic analysis showed significant differences in the mean duration of wake episodes (minutes, p=0.0072) and the mean duration of sleep episodes (minutes, p=0.0064). The differences in the number of wake episodes was also significant (p=0.0241) as was the number of sleep episodes (p=0.0214). These data support observably more restless sleep in alcohol affected children. Questionnaire analysis supports a significant degree of concern among families of these children, who identify disrupted and restless sleep patterns, along with daytime behavioral concerns including daytime fatigue and hyperactivity. Alcohol affected children were described as having five times as many sleep related behaviors as control children. Thematic analysis of the interviews supports a significant impact of sleep disruption in families caring for these children. Actigraphic analysis supports significantly disrupted sleep patterns in alcohol affected children, with frequent wakenings and greater restlessness in sleep. Families are more likely to identify sleep disruption in alcohol affected children, describing excessive movements in sleep with associated daytime fatigue and hyperactivity. While there is a significant impact of sleep disturbance and related behaviors on families caring for these children, appropriate management and understanding of these problems is important to support families who care for these children.

Sleep science 50 years after the discovery of REM sleep: contributions of the Italian Association of Sleep Medicine

Clinical and population health recommendations are derived from studies that include self-report. Differences in question wording and response scales may significantly affect responses. We conducted a methodological review assessing variation in event definition(s), context (i.e., work- versus free-day), and timeframe (e.g., “in the past 4 weeks”) of sleep timing/duration questions.We queried databases of sleep, medicine, epidemiology, and psychology studies for survey-based research and/or publications with sleep duration/timing questions. The text of these questions was thematically analyzed.We identified 53 surveys with sample sizes ranging from 93 to 1,185,106. For sleep duration questions, participants reported nocturnal sleep (24 of 44 questions), sleep in the past 24-hours (14/44), their major sleep episode (3/44), or answered unaided (3/44). For bedtime questions, participants reported time into bed (19/47), first attempt to sleep (16/40), or fall-asleep time (12/47). For wake-time questions, participants reported wake-up time (30/43), the time they “get up” (7/43), or their out-of-bed time (6/43). Context guidance appeared in 18/44 major sleep duration, 35/47 bedtime, and 34/43 wake-time questions. Timeframe was provided in 8/44 major sleep episode duration, 16/47 bedtime, and 10/43 wake-time questions. One question queried the method of awakening (e.g., by alarm clock), 18 questions assessed sleep latency, and 12 measured napping.There is variability in the event definition(s), context, and timeframe of questions relating to sleep. This work informs efforts at data harmonization for meta-analyses, provides options for question wording, and identifies potential questions for future surveys.

Measuring Daytime Drowsiness in Nursing Home Residents: The MSLT-NH

A standardized method of assessing daytime drowsiness in frail nursing home residents has not been previously available. We present here the development and test characteristics of an instrument to measure daytime drowsiness in nursing home residents with cognitive and functional impairment, the Multiple Sleep Latency Test-Nursing Home (MSLT-NH). In a standardized manner, the resident is tested three times in one day (at 9 a.m., 11 a.m., and 1 p.m.) to measure the amount of time until the subject falls asleep. The average sleep latency (minutes to fall asleep) is the measure of interest. We tested the MSLT-NH in 95 residents from six community nursing homes in the Los Angeles area (82% of subjects were female; 81% were white, mean age was 86.6 years and mean score on the Mini-Mental State Examination [MMSE] was 9.4). Interrater reliability of the MSLT-NH was quite good (correlations between raters ranged from 0.98 to 0.99; all p values were <.0001). Validity was assessed by comparing MSLT-NH results to simultaneous wrist activity estimation of sleep, and by comparing MSLT-NH findings to results from nighttime sleep estimation by wrist actigraphy the night prior to MSLT-NH. The percent agreement between MSLT-NH and wrist actigraph ranged from 77% to 79% MSLT-NH results were significantly associated with peak duration of nighttime sleep episodes the night prior to testing. The MSLT-NH was also quite acceptable for use in the NH setting. In conclusion, we have developed a promising measure of daytime drowsiness in NH residents. Further testing will help establish whether this test is a clinically useful measure of daytime drowsiness from medications or other conditions in the NH setting.

Sleep Patterns After Carbachol Delivery in the Ventral Oral Pontine Tegmentum of the Cat

This study examines dose-related effects on sleep produced by low-volume and low-dose carbachol microinjections in the ventral part of the cat nucleus reticularis pontis oralis. Carbachol microinjections (0.04, 0.08, 0.8 or 4 μg; volume 20 nl) in this location triggered paradoxical sleep with a very short dose-unrelated latency. The four carbachol doses effectively generated all the polygraphic and behavioral signs of paradoxical sleep when microinjected at any level within the ventral part of the nucleus reticularis pontis oralis (AP 0.5 to −3.5, L 0.5–3.5, V 3.5–5.0, on the Reinoso-Suárez atlas [ Topographischer Hirnatlas der Katze (1961) ; Merck, Darmstadt]). The dose-related increase of total paradoxical sleep time was due to the increase in both the duration and number of paradoxical sleep episodes. This paradoxical sleep increase was associated with a dose-related decrease in the amount of time spent in both slow wave sleep and drowsiness, but not with any decrease in total wakefulness. The lengthening of the latency to slow wave sleep onset was dose related. These results show that the ventral oral pontine tegmentum is a very sensitive site for the induction and maintenance of paradoxical sleep.