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Examine how changes in sleep duration, objectively measured by activity trackers, impact weight gain in incoming college freshman.Supplemental data for this article can be accessed online at https://doi.org/10.1080/07448481.2022.2032720.

To assess the efficacy of ramelteon in preventing delirium, an acute neuropsychiatric condition associated with increased morbidity and mortality, in the perioperative, ICU setting.Parallel-arm, randomized, double-blinded, placebo-controlled trial.Academic medical center in La Jolla, California.Patients greater than or equal to 18 years undergoing elective pulmonary thromboendarterectomy.Ramelteon 8 mg or matching placebo starting the night prior to surgery and for a maximum of six nights while in the ICU.Incident delirium was measured twice daily using the Confusion Assessment Method-ICU. The safety outcome was coma-free days assessed by the Richmond Agitation-Sedation Scale. One-hundred twenty participants were enrolled and analysis completed in 117. Delirium occurred in 22 of 58 patients allocated to placebo versus 19 of 59 allocated to ramelteon (relative risk, 0.8; 95% CI, 0.5-1.4; p = 0.516). Delirium duration, as assessed by the number of delirium-free days was also similar in both groups (placebo median 2 d [interquartile range, 2-3 d] vs ramelteon 3 d [2-5 d]; p = 0.181). Coma-free days was also similar between groups (placebo median 2 d [interquartile range, 1-3 d] vs ramelteon 3 d [2-4 d]; p = 0.210). We found no difference in ICU length of stay (median 4 d [interquartile range, 3-5 d] vs 4 d [3-6 d]; p = 0.349), or in-hospital mortality (four vs three deaths; relative risk ratio, 0.7; 95% CI, 0.2-3.2; p = 0.717), all placebo versus ramelteon, respectively.Ramelteon 8 mg did not prevent postoperative delirium in patients admitted for elective cardiac surgery.

Additional file 1. SPIRIT Checklist.

Additional file 2. Statistical Analysis Plan.

Delirium may lead to poor outcomes in hospitalized older adults, and sleep deprivation may contribute to its pathogenesis. Thus, we sought to measure sleep duration and fragmentation using wrist-worn actigraphy in older, hospitalized patients with and without delirium, and to determine if actigraphy-based parameters could be used to predict delirium prior to clinical recognition. We conducted a secondary analysis of data from a recent, randomized clinical trial aimed at preventing inpatient delirium. Participants (n = 70) were aged ≥ 65 years admitted to an internal medicine service. Delirium was defined by the Confusion Assessment Method, or altered mental status identified by a clinician. Sleep measurements were actigraphy-based, and included total sleep time, median sleep bout duration and other measures of sleep fragmentation. We found that total sleep duration was similar between patients with (n = 17) and without (n = 53) delirium (mean 384.9 ± SD 162.7 versus mean 456.6 ± SD 135.8 min; p = .081). Mean sleep bout times were shorter in delirious versus never-delirious patients (median 6.1 [interquartile range 4.3-8.9] versus 7.9 [interquartile range 5.7-11.3] min, p = .048). Patients with delirium had more short sleep bouts ( 10 min) and fewer longer sleep bouts ( 30 min) compared with those without delirium. Increased sleep fragmentation was present prior to the clinical recognition of delirium. Overall, delirium was associated with increased sleep fragmentation detected by actigraphy, and sleep fragmentation might be useful as a biomarker for delirium prediction in the future.

This cohort study examines sleep and demographic data from wearable activity tracking devices to assess for an association of sleep duration and variability with body mass index.

Sleep is a biological necessity, and adequate sleep is important for neurocognitive health and wellbeing. Family members of intensive care patients may lack adequate sleep either due to the ICU environment (lack of opportunities for sleep) or due to stress and anxiety (i.e., insomnia). Moreover, difficulty sleeping may persist after ICU discharge. In addition to reviewing the key literature, we propose a model for family education and engagement to optimize sleep for family members and patients in the ICU. This model may aid in family member engagement with clinicians and may ultimately alleviate symptoms of difficulty sleeping and post-intensive care syndrome in caregivers after the ICU.

Nicotine exposure in utero negatively affects neuronal growth, differentiation, and synaptogenesis. We used rhythmic brainstems slices and immunohistochemistry to determine how developmental nicotine exposure (DNE) alters inhibitory neurotransmission in two regions essential to normal breathing, the hypoglossal motor nucleus (XIIn), and preBotzinger complex (preBotC). We microinjected glycine or muscimol (GABAA agonist) into the XIIn or preBotC of rhythmic brainstem slices from neonatal rats while recording from XII nerve roots to obtain XII motoneuron population activity. Injection of glycine or muscimol into the XIIn reduced XII nerve burst amplitude, while injection into the preBotC altered nerve burst frequency. These responses were exaggerated in preparations from DNE animals. Quantitative immunohistochemistry revealed a significantly higher GABAA receptor density on XII motoneurons from DNE pups. There were no differences in GABAA receptor density in the preBotC, and there were no differences in glycine receptor expression in either region. Nicotine, in the absence of other chemicals in tobacco smoke, alters normal development of brainstem circuits that are critical for normal breathing. © 2015 Wiley Periodicals, Inc. Develop Neurobiol, 2015

At the American Thoracic Society Meeting in 2016, a post-graduate session focused on a number of current issues and ideas relevant to sleep in the critical care setting. The prevailing theme was encouraging physicians to consider sleep issues when caring for critically ill patients while recognizing how difficult this focus can be in practice. Emerging evidence shows the importance of sleep to mortality, cognition, and overall wellbeing. The necessities of quality sleep clearly carry over into the inpatient setting.

OBJECTIVE To compare ambient sound and light levels, including SLCs, in ICU and non-ICU environments. DESIGN Observational study. SETTING Tertiary-care hospital. MEASUREMENTS Sound measurements of 0.5 Hz were analyzed to provide average hourly sound levels, sound peaks, and SLCs =17.5 decibels (dB). For light data, measurements taken at 2-minute intervals provided average and maximum light levels. RESULTS The ICU rooms were louder than non-ICU wards; hourly averages ranged from 56.1 ± 1.3 dB to 60.3 ± 1.7 dB in the ICU, 47.3 ± 3.7 dB to 55.1 ± 3.7 dB on the telemetry floor, and 44.6 ± 2.1 dB to 53.7 ± 3.6 dB on the general ward. However, SLCs = 17.5 dB were not statistically different (ICU, 203.9 ± 28.8 times; non-ICU, 270.9 ± 39.5; P = 0.11). In both ICU and non-ICU wards, average daytime light levels were

Sleep disorders affect a substantial number of people worldwide and may be increasing in prevalence. Unfortunately, many of these disorders can go unrecognized and untreated in clinical practice. Although physicians understand that good sleep is essential to patient health, approaching the issue is often glossed over in the primary care setting. Importantly, recent data also suggest that sleep disorders are becoming increasingly recognized in developing nations. Here, we review the pertinent features and treatment of some of the major sleep disorders, including obstructive sleep apnea, central sleep apnea, insomnia, and others, that affect patient health. We aim to promote clinician and public awareness of various sleep disorders with the intent of increasing rates of recognition and treatment.

Developmental nicotine exposure (DNE) impacts central respiratory control in neonates born to smoking mothers. We previously showed that DNE enhances the respiratory motor response to bath application of AMPA to the brainstem, although it was unclear which brainstem respiratory neurons mediated these effects (Pilarski and Fregosi, 2009). Here we examine how DNE influences AMPA-type glutamatergic neurotransmission in the pre-Bötzinger complex (pre-BötC) and the hypoglossal motor nucleus (XIIMN), which are neuronal populations located in the medulla that are necessary for normal breathing. Using rhythmic brainstem slices from neonatal rats, we microinjected AMPA into the pre-BötC or the XIIMN while recording from XII nerve rootlets (XIIn) as an index of respiratory motor output. DNE increased the duration of tonic activity and reduced rhythmic burst amplitude after AMPA microinjection into the XIIMN. Also, DNE led to an increase in respiratory burst frequency after AMPA injection into the pre-BötC. Whole-cell patch-clamp recordings of XII motoneurons showed that DNE increased motoneuron excitability but did not change inward currents. Immunohistochemical studies indicate that DNE reduced the expression of glutamate receptor subunits 2 and 3 (GluR2/3) in the XIIMN and the pre-BötC. Our data show that DNE alters AMPAergic synaptic transmission in both the XIIMN and pre-BötC, although the mechanism by which this occurs is unclear. We suggest that the DNE-induced reduction in GluR2/3 may represent an attempt to compensate for increased cell excitability, consistent with mechanisms underlying homeostatic plasticity.

Purpose Studies suggest that melatonin may prevent delirium, a condition of acute brain dysfunction occurring in 20%-30% of hospitalized older adults that is associated with increased morbidity and mortality. We examined the effect of melatonin on delirium prevention in hospitalized older adults while measuring sleep parameters as a possible underlying mechanism. Methods This was a randomized clinical trial measuring the impact of 3 mg of melatonin nightly on incident delirium and both objective and subjective sleep in inpatients age ≥65 years, admitted to internal medicine wards (non-intensive care units). Delirium incidence was measured by bedside nurses using the confusion assessment method. Objective sleep measurements (nighttime sleep duration, total sleep time per 24 hours, and sleep fragmentation as determined by average sleep bout length) were obtained via actigraphy. Subjective sleep quality was measured using the Richards Campbell Sleep Questionnaire. Results Delirium occurred in 22.2% (8/36) of subjects who received melatonin vs in 9.1% (3/33) who received placebo (P = .19). Melatonin did not significantly change objective or subjective sleep measurements. Nighttime sleep duration and total sleep time did not differ between subjects who became delirious vs those who did not, but delirious subjects had more sleep fragmentation (sleep bout length 7.0 ± 3.0 vs 9.5 ± 5.3 min; P = .03). Conclusions Melatonin given as a nightly dose of 3 mg did not prevent delirium in non-intensive care unit hospitalized patients or improve subjective or objective sleep.

In a recent study (Huang YH et al. Respir Physiol Neurobiol 143: 1–8, 2004), we showed that prenatal nicotine exposure (PNE) increased the frequency of spontaneous apneic events on the first 2 days of life in unanesthetized neonatal rats. Here we test the hypothesis that PNE blunts chemoreceptor reflexes. Ventilatory responses to three levels each of hypoxia (inspired O2 fraction: 16, 12, and 10%) and hypercapnia (3, 6, and 9% inspired CO2 fraction, all in 50% O2, balance N2), and one level each of combined hypoxia-hypercapnia (H/H; 12% inspired O2 fraction/5% inspired CO2 fraction) and hyperoxia (50% O2, 50% N2) were recorded with head-out plethysmography in neonatal rats exposed to either nicotine ( N = 12) or physiological saline ( N = 12) in the prenatal period. Recordings were made on postnatal day 1 (P1), P3, P6, P9, P12, and P18, in each animal. The change in ventilation in response to hypoxia was blunted in PNE animals on P1 and P3, but there were no other treatment effects. Hyperoxia significantly depressed ventilation in both groups from P3–P18, but there were no significant treatment effects. The ventilatory response to 3, 6, and 9% inspired CO2 was significantly blunted in PNE animals at all ages studied, due exclusively to a blunted tidal volume response. PNE also blunted the ventilatory response to H/H at all ages, due primarily to blunting of the tidal volume response. PNE had no significant effect on body mass or metabolic rate, except that PNE animals had a slightly higher mass on P18 and a lower metabolic rate on P1. As shown by others, PNE has small and inconsistent effects on hypoxic ventilatory responses, but here we show that responses to hypercapnia and H/H are consistently blunted by PNE due to a diminished tidal volume response. The combination of reduced hypoxic and hypercapnic sensitivity over the first 3 days of life may define an especially vulnerable developmental period.