UNASSIGNED: This study sought to determine the feasibility of collecting physiologic data in thoracic surgery residents and whether it would correlate with burnout and burnout with performance.
UNASSIGNED: This was a prospective study of thoracic surgery residents over a 5-month period. Participants were evaluated with a wearable biometric device (heart rate variability and sleep) and the Maslach Burnout Inventory. Resident performance was quantified using Accreditation Council for Graduate Medical Education Milestones (scale, 1-5) normalized to program-designated targets (3 for postgraduate year 6 or lower residents and 4 for postgraduate year 7 residents).
UNASSIGNED: The cohort consisted of 71% female participants (5/7) with 86% of residents having 1 or more children. High levels of emotional exhaustion (median, 30 [interquartile range, 20-36], where >26 is high) and high levels of depersonalization (median, 16 [interquartile range, 14-22], where >12 is high) were common, but personal accomplishment was also uniformly high (median, 43 [interquartile range, 41-46], where >38 is high). There was a significant correlation between heart rate variability and emotional exhaustion (r(12) = 0.65, P = .01) but not depersonalization (P = .28) or personal accomplishment (P = .24). Depersonalization and personal accomplishment did not correlate with resident performance (P = .12 and P = .75, respectively); however, increased emotional exhaustion showed a significant correlation with higher resident performance during periods when burnout was reported (r(6) = 0.76, P = .047).
UNASSIGNED: Dynamic measurement of resting heart rate variability may offer an objective measure of burnout in thoracic surgery residents. Thoracic surgery residents who report high levels of burnout in this cohort maintained the ability to meet program-designated milestones at or above the level expected of their postgraduate year.

UNASSIGNED: Sleep disordered breathing (SDB) may trigger nocturnal cardiac arrhythmias (NCA) in patients with heart failure with reduced ejection fraction (HFrEF). The NCA ancillary study of the ADVENT-HF trial will test whether, in HFrEF-patients with SDB, peak-flow-triggered adaptive servo-ventilation (ASVpf) reduces NCA. To this end, accurate scoring of NCA from polysomnography (PSG) is required.
UNASSIGNED: To develop a method to detect NCA accurately from a single-lead electrocardiogram (ECG) recorded during PSG and assess inter-observer agreement for NCA detection.
UNASSIGNED: Quality assurance of ECG analysis included training of the investigators, development of standardized technical quality, guideline-conforming semi-automated NCA-scoring via Holter-ECG software and implementation of an arrhythmia adjudication committee. To assess inter-observer agreement, the ECG was analysed by two independent investigators and compared for agreement on premature ventricular complexes (PVC) /h, premature atrial complexes/h (PAC) as well as for other NCA in 62 patients from two centers of the ADVENT-HF trial.
UNASSIGNED: The intraclass correlation coefficients for PVC/h and PAC/h were excellent: 0.99 (95%- confidence interval [CI]: 0.99-0.99) and 0.99 (95%-CI: 0.97-0.99), respectively. No clinically relevant difference in inter-observer classification of other NCA was found. The detection of non-sustained ventricular tachycardia (18% versus 19%) and atrial fibrillation (10% versus 11%) was similar between the two investigators. No sustained ventricular tachycardia was detected.
UNASSIGNED: These findings indicate that our methods are very reliable for scoring NCAs and are adequate to apply for the entire PSG data set of the ADVENT-HF trial.

This virtual workshop was convened by the National Heart, Lung, and Blood Institute, in partnership with the Office of Strategic Coordination of the Office of the National Institutes of Health Director, and held September 2 to 3, 2020. The intent was to assemble a multidisciplinary group of experts in basic, translational, and clinical research in neuroscience and cardiopulmonary disorders to identify knowledge gaps, guide future research efforts, and foster multidisciplinary collaborations pertaining to autonomic neural mechanisms of cardiopulmonary regulation. The group critically evaluated the current state of knowledge of the roles that the autonomic nervous system plays in regulation of cardiopulmonary function in health and in pathophysiology of arrhythmias, heart failure, sleep and circadian dysfunction, and breathing disorders. Opportunities to leverage the Common Fund\'s SPARC (Stimulating Peripheral Activity to Relieve Conditions) program were characterized as related to nonpharmacologic neuromodulation and device-based therapies. Common themes discussed include knowledge gaps, research priorities, and approaches to develop novel predictive markers of autonomic dysfunction. Approaches to precisely target neural pathophysiological mechanisms to herald new therapies for arrhythmias, heart failure, sleep and circadian rhythm physiology, and breathing disorders were also detailed.

UNASSIGNED: To describe the change in sleep duration during inpatient rehabilitation and to determine if sleep quality and sleep duration is associated with functional disability for individuals after stroke. It was hypothesized that participants who experienced optimal sleep during inpatient rehabilitation would have greater functional ability at discharge.
UNASSIGNED: Longitudinal observation study.
UNASSIGNED: Inpatient rehabilitation unit at a large, urban hospital.
UNASSIGNED: Thirty-seven individuals with acute stroke (N=37; mean age, 62.5±11.8y, male=20, female=17) were recruited from September 2018 to September 2019. Participants were invited to participate in the study by clinical personnel associated with their usual care as they were admitted to inpatient rehabilitation.
UNASSIGNED: Not applicable.
UNASSIGNED: Participants were asked to wear an actigraph for the duration of their rehabilitation program to assess sleep. The first 3 nights of actigraphy data were averaged to obtain total sleep time (TST) and sleep efficiency (SE) at admission, and the last 3 nights were averaged for TST and SE at discharge. Functional disability (primary outcome was FIM) at admission and discharge was gathered from the participants\' medical records. One-way analysis of variance and chi-square analyses assessed for group differences, and regression modeling was used to determine if sleep was associated with functional ability at discharge.
UNASSIGNED: Sixteen participants (43%) were categorized as \"good sleepers\" and 21 (57%) were \"poor sleepers\" based on their TST at admission. Of the poor sleepers, 14 participants (66%) remained short duration sleepers (<7h at admission and discharge). Sleep outcomes did not significantly predict FIM score at discharge.
UNASSIGNED: Most participants had less than optimal sleep duration during inpatient rehabilitation. Efforts may be warranted to optimize sleep during inpatient rehabilitation.

Non-invasive brain tissue stimulation with a magnetic coil provides several irreplaceable advantages over that with an implanted electrode, in altering neural activities under pathological situations. We reviewed clinical cases that utilized time-varying magnetic fields for the treatment of epilepsy, and the safety issues related to this practice. Animal models have been developed to foster understanding of the cellular/molecular mechanisms underlying magnetic control of epileptic activity. These mechanisms include (but are not limited to) (1) direct membrane polarization by the magnetic field, (2) depolarization blockade by the deactivation of ion channels, (3) alteration in synaptic transmission, and (4) interruption of ephaptic interaction and cellular synchronization. Clinical translation of this technology could be improved through the advancement of magnetic design, optimization of stimulation protocols, and evaluation of the long-term safety. Cellular and molecular studies focusing on the mechanisms of magnetic stimulation are of great value in facilitating this translation.

Most preclinical sleep studies are conducted in nocturnal rodents that have fragmented sleep in comparison to humans who are primarily diurnal, typically with a consolidated sleep period. Consequently, we sought to define basal sleep characteristics, sleep/wake architecture and electroencephalographic (EEG) activity in a diurnal non-human primate (NHP) to evaluate the utility of this species for pharmacological manipulation of the sleep/wake cycle. Adult, 9-11 y.o. male cynomolgus macaques (n = 6) were implanted with telemetry transmitters to record EEG and electromyogram (EMG) activity and Acticals to assess locomotor activity under baseline conditions and following injections either with vehicle or the caffeine (CAF; 10 mg/kg, i.m.) prior to the 12 h dark phase. EEG/EMG recordings (12-36 h in duration) were analyzed for sleep/wake states and EEG spectral composition. Macaques exhibited a sleep state distribution and architecture similar to previous NHP and human sleep studies. Acute administration of CAF prior to light offset enhanced wakefulness nearly 4-fold during the dark phase with consequent reductions in both NREM and REM sleep, decreased slow wave activity during wakefulness, and increased higher EEG frequency activity during NREM sleep. Despite the large increase in wakefulness and profound reduction in sleep during the dark phase, no sleep rebound was observed during the 24 h light and dark phases following caffeine administration. Cynomolgus macaques show sleep characteristics, EEG spectral structure, and respond to CAF in a similar manner to humans. Consequently, monitoring EEG/EMG by telemetry in this species may be useful both for basic sleep/wake studies and for pre-clinical assessments of drug-induced effects on sleep/wake.

BACKGROUND: The Glasgow Coma Scale (GCS) score is the primary method of assessing consciousness after traumatic brain injury (TBI), and the clinical standard for classifying TBI severity. There is scant literature discerning the influence of circadian rhythms or emergency department (ED) arrival hour on this important clinical tool.
METHODS: Retrospective cohort analysis of adult patients suffering blunt TBI using the National Sample Program of the National Trauma Data Bank, years 2003-2006. ED arrival GCS score was characterized by midday (10 a.m.-4 p.m.) and midnight (12 a.m.-6 a.m.) cohorts (N=24548). Proportions and standard errors are reported for descriptive data. Multivariable regressions using odds ratios (OR), mean differences (B), and their associated 95% confidence intervals [CI] were performed to assess associations between ED arrival hour and GCS score. Statistical significance was assessed at p<0.05.
RESULTS: Patients were 42.48±0.13-years-old and 69.5% male. GCS score was 12.68±0.13 (77.2% mild, 5.2% moderate, 17.6% severe-TBI). Overall, patients were injured primarily via motor vehicle accidents (52.2%) and falls (24.2%), and 85.7% were admitted to hospital (33.5% ICU). Injury severity score did not differ between day and nighttime admissions.Nighttime admissions associated with decreased systemic comorbidities (p<0.001) and increased likelihood of alcohol abuse and drug intoxication (p<0.001). GCS score demonstrated circadian rhythmicity with peak at 12 p.m. (13.03±0.08) and nadir at 4am (12.12±0.12). Midnight patients demonstrated lower GCS (12 a.m.-6 a.m.: 12.23±0.04; 10 a.m.-4 p.m.: 12.95±0.03, p<0.001). Multivariable regression adjusted for demographic and injury factors confirmed that midnight-hours independently associated with decreased GCS (B=-0.29 [-0.40, -0.19]).In patients who did not die in ED or go directly to surgery (N=21862), midnight-hours (multivariable OR 1.73 [1.30-2.31]) associated with increased likelihood of ICU admission; increasing GCS score (per-unit OR 0.82 [0.80-0.83]) associated with decreased odds. Notably, the interaction factor ED GCS score*ED arrival hour independently demonstrated OR 0.96 [0.94-0.98], suggesting that the influence of GCS score on ICU admission odds is less important at night than during the day.
CONCLUSIONS: Nighttime TBI patients present with decreased GCS scores and are admitted to ICU at higher rates, yet have fewer prior comorbidities and similar systemic injuries. The interaction between nighttime hours and decreased GCS score on ICU admissions has important implications for clinical assessment/triage.

BACKGROUND: Acute and chronic insomnia can exacerbate type 2 diabetes mellitus (T2DM). We investigated suvorexant (an anti-insomnia drug that targets the orexin system) effects on sleep architecture and glucose metabolism in T2DM patients with insomnia.
METHODS: This 7 day open-label, single-arm, intervention trial included 18 subjects with T2DM and insomnia. After 1 day acclimatization, daily glucose levels, sleep architecture, and autonomic nervous function were evaluated by continuous glucose monitoring (CGM), single-channel electroencephalography, and accelerometry, respectively.
RESULTS: Suvorexant treatment for 3 days significantly increased total sleep time and sleep efficiency, with partial suppression of sympathetic nerve activity. CGM-measured 24 h mean glucose level decreased significantly from 157.7 ± 22.9 to 152.3 ± 17.8 mg/dL, especially in the early glucose surge after the midnight nadir (from 28.3 ± 15.0 to 18.2 ± 9.9 mg/dL), and until supper with a significant improvement in homeostasis model assessment of insulin resistance from 4.0 ± 2.8 to 2.9 ± 1.6, respectively.
CONCLUSIONS: Suvorexant treatment for insomnia of subjects with T2DM significantly improved CGM-measured daily glycemic control, which was associated with changes in sympathomimetic tone and/or improved insulin sensitivity. The amelioration of insomnia may therefore be a target for improving glycemic control in T2DM patients with insomnia.

To clarify the effects of sleep on cortical irritability in benign adult familial myoclonus epilepsy (BAFME), we retrospectively compared epileptiform discharges of electroencephalographies (EEGs) between awake and sleep periods in 5 patients (mean age: 49.6 ± 20.3 years). We also analyzed polysomnography (PSG) of 1 patient. Epileptiform discharges were significantly more frequent during the awake period (1.3 ± 1.2/min) than those during light sleep stages (0.02 ± 0.04/min) (P < 0.05). Regarding PSG analysis, epileptiform discharges were also reduced during all sleep stages compared to those during awake periods. Our study suggests a relative reduction in cortical irritability during sleep in BAFME.

The neuropeptides orexin and melanin-concentrating hormone (MCH), as well as the neurotransmitters GABA (γ-Aminobutyric acid) and glutamate are chief modulators of the sleep-wake states in the posterior hypothalamus. To investigate co-expression of vesicular GABA transporter (VGAT, a marker of GABA neurons) and the vesicular glutamate transporter-2 (VGLUT2, a marker of glutamate neurons) in orexin and MCH neurons, we generated two transgenic mouse lines. One line selectively expressed the reporter gene EYFP in VGAT+ neurons, whereas the other line expressed reporter gene tdTomato in VGLUT2+ neurons. Co-localization between these genetic reporters and orexin or MCH immunofluorescent tags was determined using 3D computer reconstructions of Z stacks that were acquired using a multiphoton laser confocal microscope. Our results demonstrated that MCH neurons expressed neither VGAT nor VGLUT2, suggesting MCH neurons are a separate cluster of cells from VGAT+ GABAergic neurons and VGLUT2+ glutamatergic neurons. Moreover, most orexin neurons expressed VGLUT2, indicating these neurons are glutamatergic. Our data suggested that in the posterior hypothalamus there are four major distinct groups of neurons: VGAT+, orexin+/VGLUT2+, orexin-/VGLUT2+, and MCH neurons. This study facilitated our understanding of the role of these neurotransmitters and neuropeptides in relation to sleep/wake regulation.