Mechanisms underlying the prolonged activation of the genioglossus following arousal from sleep.

STUDY OBJECTIVES: Transient arousal from sleep has been shown to elicit a prolonged increase in genioglossus muscle activity that persists following the return to sleep and which may protect against subsequent airway collapse. We hypothesized that this increased genioglossal activity following return to sleep after an arousal is due to persistent firing of inspiratory-modulated motor units (MUs) that are recruited during the arousal. METHODS: Thirty-four healthy participants were studied overnight while wearing a nasal mask with pneumotachograph to measure ventilation and with 4 intramuscular genioglossus EMG electrodes. During stable N2 and N3 sleep, auditory tones were played to induce brief (3-15s) AASM arousals. Ventilation and genioglossus MUs were quantified before the tone, during the arousal and for 10 breaths after the return to sleep. RESULTS: A total of 1089 auditory tones were played and gave rise to 239 MUs recorded across arousal and the return to sleep in 20 participants (aged 23 ±â€…4.2 years and BMI 22.5 ±â€…2.2 kg/m2). Ventilation was elevated above baseline during arousal and the first post-arousal breath (p < .001). Genioglossal activity was elevated for five breaths following the return to sleep, due to increased firing rate and recruitment of inspiratory modulated MUs, as well as a small increase in tonic MU firing frequency. CONCLUSIONS: The sustained increase in genioglossal activity that occurs on return to sleep after arousal is primarily a result of persistent activity of inspiratory-modulated MUs, with a slight contribution from tonic units. Harnessing genioglossal activation following arousal may potentially be useful for preventing obstructive respiratory events.

The influence of alcohol on genioglossus single motor units in men and women during wakefulness.

NEW FINDINGS: What is the central question of this study? How does alcohol intake, which worsens obstructive sleep apnoea, alter motor control of the genioglossus muscle, an upper airway dilator, in healthy awake human volunteers, and does alcohol alter genioglossus muscle afterdischarge? What is the main finding and its importance? Alcohol consumption had a very minor effect on the activity of the genioglossus in healthy young individuals studied during wakefulness and did not alter afterdischarge, leaving open the possibility that alcohol worsens obstructive sleep apnoea via other mechanisms. ABSTRACT: Alcohol worsens obstructive sleep apnoea (OSA). This effect is thought to be due to alcohol's depressant effect on upper airway dilator muscles such as the genioglossus, but how alcohol reduces genioglossal activity is unknown. The aim of this study was to investigate the effect of alcohol consumption on genioglossus muscle single motor units (MUs). Sixteen healthy individuals were studied on two occasions (alcohol: breath alcohol concentration ∼0.07% and placebo). They were instrumented with a nasal mask, four intramuscular genioglossal EMG electrodes, and an ear oximeter. They were exposed to 8-12 hypoxia trials (45-60 s of 10% O2 followed by one breath of 100% O2 ) while awake. MUs were sorted according to their firing patterns and quantified during baseline, hypoxia and recovery. For the alcohol and placebo conditions, global muscle activity (mean ± SD peak inspiratory EMG = 119.3 ± 44.1 and 126.5 ± 51.9 µV, respectively, P = 0.53) and total number of MUs recorded at baseline (68 and 67, respectively) were similar. Likewise, the peak discharge frequency did not differ between conditions (21.2 ± 4.28 vs. 22.4 ± 4.08 Hz, P = 0.09). There was no difference between conditions in the number (101 vs. 88, respectively) and distribution of MU classes during hypoxia, and afterdischarge duration was also similar. In this study, alcohol had a very minor effect on genioglossal activity and afterdischarge in these otherwise healthy young individuals studied while awake. If similar effects are observed during sleep, it would suggest that the worsening of OSA following alcohol may be related to increased upper airway resistance/nasal congestion or arousal threshold changes.

Learning from stakeholders to inform good practice guidance on consent to research in intensive care units: a mixed-methods study.

OBJECTIVES: Obtaining informed consent from patients in intensive care units (ICUs) prior to enrolment in a study is practically and ethically complex. Decisions about the participation of critically ill patients in research often involve substitute decision makers (SDMs), such as a patient's relatives or doctors. We explored the perspectives of different stakeholder groups towards these consent procedures. DESIGN AND METHODS: Mixed-methods study comprising surveys completed by ICU patients, their relatives and healthcare practitioners in 14 English ICUs, followed by qualitative interviews with a subset of survey participants. Empirical bioethics informed the analysis and synthesis of the data. Survey data were analysed using descriptive statistics of Likert responses, and analysis of interview data was informed by thematic reflective approaches. RESULTS: Analysis included 1409 survey responses (ICU patients n=333, relatives n=488, healthcare practitioners n=588) and 60 interviews (ICU patients n=13, relatives n=30, healthcare practitioners n=17). Most agreed with relatives acting as SDMs based on the perception that relatives often know the patient well enough to reflect their views. While the practice of doctors serving as SDMs was supported by most survey respondents, a quarter (25%) disagreed. Views were more positive at interview and shifted markedly depending on particularities of the study. Participants also wanted reassurance that patient care was prioritised over research recruitment. Findings lend support for adaptations to consent procedures, including collaborative decision-making to correct misunderstandings of the implications of research for that patient. This empirical evidence is used to develop good practice guidance that is to be published separately. CONCLUSIONS: Participants largely supported existing consent procedures, but their perspectives on these consent procedures depended on their perceptions of what the research involved and the safeguards in place. Findings point to the importance of explaining clearly what safeguards are in place to protect the patient.

Understanding Sleepiness and Fatigue in Cabin Crew Using COVID-19 to Dissociate Causative Factors.

OBJECTIVES: Airline cabin crew experience high levels of fatigue and sleepiness. Whether these are solely related to their work schedules/jetlag or are in part related to individual factors is unknown. The COVID-19 pandemic has significantly disrupted the aviation industry and many cabin crew have been grounded. This provides a unique opportunity to assess the causes of fatigue and sleepiness in this population.METHODS: An online anonymous survey was distributed in April-June 2020 to cabin crew who were 1) flying, 2) grounded but doing alternative work, and 3) grounded, not working, or unemployed. The survey measured fatigue, sleepiness, and mental health. It also screened their risk for insomnia, depression, and shift work disorder and assessed drug and caffeine use.RESULTS: Collected were 409 valid responses: 45 currently flying; 35 grounded but doing alternate work; and 329 not working. On average, all three groups experienced normal levels of fatigue and sleepiness. The risk for major depressive disorder was 27.4%, with 59.5% of individuals reporting abnormal levels of anxiety. Caffeine intake and the use of drugs and alcohol to facilitate sleep were common, although not different between those currently flying vs. grounded.CONCLUSIONS: With reduced workloads or not flying, cabin crew reported lowered fatigue and sleepiness compared to prepandemic findings, along with reduced risk for major depressive disorder. However, a high occurrence of negative emotional states were reported, potentially related to the uncertainty surrounding the pandemic. This study suggests fatigue and sleepiness is primarily related to airline operational rather than personal variables.Wen CC-Y, Nicholas CL, Howard ME, Trinder J, Jordan AS. Understanding sleepiness and fatigue in cabin crew using COVID-19 to dissociate causative factors. Aerosp Med Hum Perform. 2022; 93(1):50-53.

Aspirin as a Treatment for ARDS: A Randomized, Placebo-Controlled Clinical Trial.

BACKGROUND: There is no pharmacologic treatment for ARDS. Platelets play an important role in the pathophysiology of ARDS. Preclinical, observational, and clinically relevant models of ARDS indicate aspirin as a potential therapeutic option. RESEARCH QUESTION: Is enteral aspirin (75 mg, once daily) safe and effective in improving surrogate outcomes in adult patients with ARDS? STUDY DESIGN AND METHODS: This randomized, double-blind (patient and investigator), allocation-concealed, placebo-controlled phase 2 trial was conducted in five UK ICUs. Patients fulfilling the Berlin definition of ARDS were randomly assigned at a 1:1 ratio to receive enteral aspirin (75 mg) or placebo, for a maximum of 14 days, using a computer-generated randomization schedule, with variable block size, stratified by vasopressor requirement. The primary end point was oxygenation index (OI) on day 7. Secondary outcomes included safety parameters and other respiratory physiological markers. Analyses were by intention to treat. RESULTS: The trial was stopped early, due to slow recruitment, after 49 of a planned 60 patients were recruited. Twenty-four patients were allocated to aspirin and 25 to placebo. There was no significant difference in day 7 OI [aspirin group: unadjusted mean, 54.4 (SD 26.8); placebo group: 42.4 (SD 25); mean difference, 12.0; 95% CI, -6.1 to 30.1; P = .19]. Aspirin did not significantly impact the secondary outcomes. There was no difference in the number of adverse events between the groups (13 in each; OR, 1.04; 95% CI, 0.56-1.94; P = .56). INTERPRETATION: Aspirin was well tolerated but did not improve OI or other physiological outcomes; a larger trial is not feasible in its current design. TRIAL REGISTRATION: ClinicalTrials.gov; No.: NCT02326350; URL: www. CLINICALTRIALS: gov.

Feasibility of conservative fluid administration and deresuscitation compared with usual care in critical illness: the Role of Active Deresuscitation After Resuscitation-2 (RADAR-2) randomised clinical trial.

PURPOSE: Fluid overload is common in critical illness and is associated with mortality. This study investigated the feasibility of a randomised trial comparing conservative fluid administration and deresuscitation (active removal of accumulated fluid using diuretics or ultrafiltration) with usual care in critical illness. METHODS: Open-label, parallel-group, allocation-concealed randomised clinical feasibility trial. Mechanically ventilated adult patients expected to require critical care beyond the next calendar day were enrolled between 24 and 48 h following admission to the intensive care unit (ICU). Patients were randomised to either a 2-stage fluid strategy comprising conservative fluid administration and, if fluid overload was present, active deresuscitation, or usual care. The primary endpoint was fluid balance in the 24 h up to the start of study day 3. Secondary endpoints included cumulative fluid balance, mortality, and duration of mechanical ventilation. RESULTS: One hundred and eighty patients were randomised. After withdrawal of 1 patient, 89 patients assigned to the intervention were compared with 90 patients assigned to the usual care group. The mean plus standard deviation (SD) 24-h fluid balance up to study day 3 was lower in the intervention group (- 840 ± 1746 mL) than the usual care group (+ 130 ± 1401 mL; P < 0.01). Cumulative fluid balance was lower in the intervention group at days 3 and 5. Overall, clinical outcomes did not differ significantly between the two groups, although the point estimate for 30-day mortality favoured the usual care group [intervention arm: 19 of 90 (21.6%) versus usual care: 14 of 89 (15.6%), P = 0.32]. Baseline imbalances between groups and lack of statistical power limit interpretation of clinical outcomes. CONCLUSIONS: A strategy of conservative fluid administration and active deresuscitation is feasible, reduces fluid balance compared with usual care, and may cause benefit or harm. In view of wide variations in contemporary clinical practice, large, adequately powered trials investigating the clinical effectiveness of conservative fluid strategies in critically ill patients are warranted.

After-discharge in the upper airway muscle genioglossus following brief hypoxia.

STUDY OBJECTIVES: Genioglossus (GG) after-discharge is thought to protect against pharyngeal collapse by minimizing periods of low upper airway muscle activity. How GG after-discharge occurs and which single motor units (SMUs) are responsible for the phenomenon are unknown. The aim of this study was to investigate genioglossal after-discharge. METHODS: During wakefulness, after-discharge was elicited 8-12 times in healthy individuals with brief isocapnic hypoxia (45-60 s of 10% O2 in N2) terminated by a single breath of 100% O2. GG SMUs were designated as firing solely, or at increased rate, during inspiration (Inspiratory phasic [IP] and inspiratory tonic [IT], respectively); solely, or at increased rate, during expiration (Expiratory phasic [EP] or expiratory tonic [ET], respectively) or firing constantly without respiratory modulation (Tonic). SMUs were quantified at baseline, the end of hypoxia, the hyperoxic breath, and the following eight normoxic breaths. RESULTS: A total of 210 SMUs were identified in 17 participants. GG muscle activity was elevated above baseline for seven breaths after hyperoxia (p < 0.001), indicating a strong after-discharge effect. After-discharge occurred due to persistent firing of IP and IT units that were recruited during hypoxia, with minimal changes in ET, EP, or Tonic SMUs. The firing frequency of units that were already active changed minimally during hypoxia or the afterdischarge period (p > 0.05). CONCLUSION: That genioglossal after-discharge is almost entirely due to persistent firing of previously silent inspiratory SMUs provides insight into the mechanisms responsible for the phenomenon and supports the hypothesis that the inspiratory and expiratory/tonic motor units within the muscle have idiosyncratic functions.

Health Risks and Potential Predictors of Fatigue and Sleepiness in Airline Cabin Crew.

BACKGROUND: Aviation pilots and cabin crew regularly undertake shift work, and may experience circadian disruption, restricted sleep, sleepiness and impaired health. Research on aviation fatigue and sleepiness has focused on pilots, with less being known about cabin crew. This study aimed to identify likely predictors of fatigue, sleepiness, shift work disorder (SWD) and depression in cabin crew. METHODS: An online anonymous survey was distributed to active cabin crew around the world. It measured sleepiness, fatigue, and screened for insomnia, depression and SWD. Information on individuals' habits and work schedules were collected. RESULTS: 930 valid responses were analysed. 63.5% of the sample had abnormal levels of fatigue and 46.9% experienced excessive daytime sleepiness. 68.0% were at risk for SWD, 57.7% screened positive for insomnia, and 40.0% for depression. Caffeine and use of alcohol and drugs for sleep were independently associated with insomnia and SWD (p < 0.05), whereas, type of route (international, domestic, both) and number of duty days per week predicted fatigue (p < 0.05). CONCLUSIONS: Cabin crew had a high prevalence of fatigue, sleepiness and elevated risk for SWD, insomnia and depression. Many cabin crew engaged in behaviours detrimental to good sleep hygiene, highlighting targets for future interventional studies.

Does Nasal Obstruction Induce Obstructive Sleep Apnea in Healthy Women?

PURPOSE: Obstructive sleep apnea (OSA) is less prevalent among women and is associated with different symptoms and consequences to OSA in men. The reasons for these differences are unknown and difficult to tease apart in clinical populations. If OSA could be temporarily induced in healthy men and women, the causes of some of these differences could be investigated. Nasal blocking has been used to induce OSA in healthy men but its effect in women has not been reported. PATIENTS AND METHODS: A total of 14 healthy individuals (10 women) underwent in-laboratory diagnostic sleep studies on two occasions separated by a week. On one occasion, the nasal passages were blocked, whereas on the other occasion, participants slept naturally. In both conditions, a full-face mask was used to monitor respiratory events. Participants' self-reported sleepiness, mood and performance on a motor learning task were assessed in the evening and morning of both sleep studies. Furthermore, endothelial function and self-reported sleep quality were assessed in the morning following each study. RESULTS: Nasal blockage induced OSA in healthy young (age=22±3 years) and slim (BMI=22.2±3.2 kg/m2) women (control AHI=2.0±2.6, blocked AHI=33.1±36.7 events/hr, p=0.02). One night of OSA was associated with poorer self-reported sleep quality (p<0.001) and increased self-reported snoring (p<0.04), choking and gasping during sleep (p<0.001) but was not associated with alterations in mood, neurocognitive or endothelial function on the following morning. CONCLUSION: Nasal blockage induces OSA in healthy, young, and normal weight women. However, whether the induced OSA is representative of naturally occurring OSA and the technique useful for future studies is unclear.

Sleep and stress in adolescents: the roles of pre-sleep arousal and coping during school and vacation.

STUDY OBJECTIVES: This study explored the relationship between stress and actigraphy-measured and self-reported sleep in adolescents during periods of restricted (school) and unrestricted (vacation) sleep opportunities. We further examined whether (1) cognitive pre-sleep arousal (PSA) mediated the relationship between stress and sleep onset latency (SOL), and (2) coping moderated the effect of stress on PSA. METHODS: Participants were 146 (77 females) adolescents (M = 16.2, SD = 1.0) recruited from the community. Actigraphy assessed daily sleep over the last week of a school-term and the following two-week vacation. The following self-report measures were administered during both school and vacation: the Pittsburgh Sleep Quality Index, Inventory of High-School Students Recent Life Experiences (stress), Pre-Sleep Arousal Scale, and the Brief COPE (coping). RESULTS: Path analyses showed that during both school and vacation, higher cognitive PSA mediated the relationship between higher stress and longer self-report SOL (p < 0.01). During vacation, higher PSA also mediated the relationship between higher stress and longer actigraphy SOL (p < 0.05). During vacation (but not school), problem-focused coping moderated the mediating effects of PSA (p < 0.05), such that more frequent use of coping was associated with weaker association between stress and cognitive PSA, and shorter actigraphy and self-report SOL. CONCLUSIONS: Cognitive PSA and coping may be two modifiable factors influencing how stress affects adolescents' sleep onset. Interventions that reduce cognitive arousal at bedtime may therefore shorten adolescents' sleep onset during both school and vacation. Further, the use of problem-focused coping strategies might be protective against the effects of stress on sleep onset, especially during vacation periods. STATEMENT OF SIGNIFICANCE: This paper expands the understanding of the stress-sleep association in adolescents by examining the mediating role of cognitive pre-sleep arousal and the moderating effects of coping. By examining these associations during both school and vacation periods, findings are likely to be applicable to both restricted and relatively unconstrained sleep conditions. Practically, our findings suggest that interventions directed towards the reduction of cognitive pre-sleep arousal may improve adolescents' sleep onset latency. Additionally, fostering healthy coping, especially problem-focused coping strategies such as problem solving, may mitigate the effects of stress on adolescents' sleep.

Genioglossus motor unit activity in supine and upright postures in obstructive sleep apnea.

This study investigated whether a change in posture affected the activity of the upper-airway dilator muscle genioglossus in participants with and without obstructive sleep apnea (OSA). During wakefulness, a monopolar needle electrode was used to record single motor unit activity in genioglossus in supine and upright positions to alter the gravitational load that causes narrowing of the upper airway. Activity from 472 motor units was recorded during quiet breathing in 17 males, nine of whom had OSA. The mean number of motor units for each participant was 11.8 (SD 3.4) in the upright and 16.0 (SD 4.2) in the supine posture. For respiratory-modulated motor units, there were no significant differences in discharge frequencies between healthy controls and participants with OSA. Within each breath, genioglossus activity increased through the recruitment of phasic motor units and an increase in firing rate, with an overall increase of ~6 Hz (50%) across both postures and participant groups. However, the supine posture did not lead to compensatory increases in the peak discharge frequencies of inspiratory and expiratory motor units, despite the increase in gravitational load on the upper airway. Posture also had no significant effect on the discharge frequency of motor units that showed no respiratory modulation during quiet breathing. We postulate that, in wakefulness, any increase in genioglossus activity to compensate for the gravitational effects on the upper airway is achieved primarily through the recruitment of additional motor units in both healthy controls and participants with OSA.

Genioglossus muscle responses to resistive loads in severe OSA patients and healthy control subjects.

This study aimed to determine whether there is impairment of genioglossus neuromuscular responses to small negative pressure respiratory stimuli, close to the conscious detection threshold, in obstructive sleep apnea (OSA). We compared genioglossus electromyogram (EMGgg) responses to midinspiratory resistive loads of varying intensity (≈1.2-6.2 cmH2O·L-1·s), delivered via a nasal mask, between 16 severe OSA and 17 control participants while the subjects were awake and in a seated upright position. We examined the relationship between stimulus intensity and peak EMGgg amplitude in a 200-ms poststimulus window and hypothesized that OSA patients would have an increased activation threshold and reduced sensitivity in the relationship between EMGgg activation and stimulus intensity. There was no significant difference between control and OSA participants in the threshold (P = 0.545) or the sensitivity (P = 0.482) of the EMGgg amplitude vs. stimulus intensity relationship, where change in epiglottic pressure relative to background epiglottic pressure represented stimulus intensity. These results do not support the hypothesis that deficits in neuromuscular response to negative upper airway pressure exist in OSA during wakefulness; however, the results are likely influenced by a counterintuitive and novel genioglossus muscle suppression response observed in a significant proportion of both OSA and healthy control participants. This suppression response may relate to the inhibition seen in inspiratory muscles such as the diaphragm in response to sudden-onset negative pressure, and its presence provides new insight into the upper airway neuromuscular response to the collapsing force of negative pressure.NEW & NOTEWORTHY Our study used a novel midinspiratory resistive load stimulus to study upper airway neuromuscular responses to negative pressure during wakefulness in obstructive sleep apnea (OSA). Although no differences were found between OSA and healthy groups, the study uncovered a novel and unexpected suppression of neuromuscular activity in a large proportion of both OSA and healthy participants. The unusual response provides new insight into the upper airway neuromuscular response to the collapsing force of negative pressure.

Changes in heart rate and blood pressure during nocturnal hot flashes associated with and without awakenings.

Hot flashes (HFs) are a hallmark of menopause in midlife women. They are beyond bothersome symptoms, having a profound impact on quality of life and wellbeing, and are a potential marker of cardiovascular (CV) disease risk. Here, we investigated the impact on CV functioning of single nocturnal HFs, considering whether or not they were accompanied by arousals or awakenings. We investigated changes in heart rate (HR, 542 HFs), blood pressure (BP, 261 HFs), and pre-ejection period (PEP, 168 HFs) across individual nocturnal physiological HF events in women in the menopausal transition or post-menopause (age: 50.7 ± 3.6 years) (n = 86 for HR, 45 for BP, 27 for PEP). HFs associated with arousals/awakenings (51.1%), were accompanied by an increase in systolic (SBP; ~6 mmHg) and diastolic (DBP; ~5 mmHg) BP and HR (~20% increase), sustained for several minutes. In contrast, HFs occurring in undisturbed sleep (28.6%) were accompanied by a drop in SBP and a marginal increase in HR, likely components of the heat dissipation response. All HFs were accompanied by decreased PEP, suggesting increased cardiac sympathetic activity, with a prolonged increase for HFs associated with sleep disruption. Older age predicted greater likelihood of HF-related sleep disturbance. HFs were less likely to wake a woman in rapid-eye-movement and slow-wave sleep. Findings show that HFs associated with sleep disruption, which are in the majority and more likely in older women, lead to increases in HR and BP, which could have long-term impact on nocturnal CV restoration in women with multiple HFs.

The effect of sex and body weight on lung volumes during sleep.

STUDY OBJECTIVES: Low lung volumes are thought to contribute to obstructive sleep apnea (OSA). OSA is worse in the supine versus lateral body position, men versus women, obese versus normal-weight (NW) individuals and REM versus NREM sleep. All of these conditions may be associated with low lung volumes. The aim was to measure FRC during wake, NREM, and REM in NW and overweight (OW) men and women while in the supine and lateral body positions. METHODS: Eighty-one healthy adults were instrumented for polysomnography, but with nasal pressure replaced with a sealed, non-vented mask connected to an N2 washout system. During wakefulness and sleep, repeated measurements of FRC were made in both supine and right lateral positions. RESULTS: Two hundred eighty-five FRC measures were obtained during sleep in 29 NW (body mass index [BMI] = 22 ± 0.3 kg/m2) and 29 OW (BMI = 29 ± 0.7 kg/m2) individuals. During wakefulness, FRC differed between BMI groups and positions (supine: OW = 58 ± 3 and NW = 68 ± 3% predicted; lateral OW = 71 ± 3, NW = 81 ± 3% predicted). FRC fell from wake to NREM sleep in all participants and in both positions by a similar amount. As a result, during NREM sleep FRC was lower in OW than NW individuals (supine 46 ± 3 and 56 ± 3% predicted, respectively). FRC during REM was similar to NREM and no sex differences were observed in any position or sleep stage. CONCLUSIONS: Reductions in FRC while supine and with increased body weight may contribute to worsened OSA in these conditions, but low lung volumes appear unlikely to explain the worsening of OSA in REM and in men versus women.

Evidence against a subcortical gate preventing conscious detection of respiratory load stimuli.

Respiratory related evoked potentials (RREP) were used to examine respiratory stimulus gating. RREPs produced by consciously detected vs. undetected loads, near the detection threshold, were compared. Participants (n = 17) were instrumented with EEG and a nasal mask connected to a loading manifold, which presented a range of mid-inspiratory resistive loads, plus a control, in a random block design. Participants were cued prior to the stimulus and signalled detection by a button press. There were statistically significant differences in peak-to-peak amplitude of the P1 RREP peak for detected (mean ± SD; 3.86 ± 1.45 µV; P = 0.020) and undetected loads (3.67 ± 1.27 µV; P = 0.002) vs. control (2.36 ± 0.81 µV), although baseline-to-peak differences were not significantly different. In contrast peak-to-peak P3 amplitude was significantly greater for detected (5.91 ± 1.54 µV; P < 0.001) but not undetected loads (3.33 ± 0.98 µV; P = 0.189) vs. control (3.69 ± 1.46 µV), with the same pattern observed for baseline-to-peak measurements. The P1 peak, thought to reflect arrival of somatosensory information, appeared to be present in response to both detected and undetected loads, but the later P3 peak, was present for detected loads only. This suggests that for sub-threshold loads sensory information may reach the cortex, arguing against a sub-cortical gating process.

Mechanisms underlying the association between insomnia, anxiety, and depression in adolescence: Implications for behavioral sleep interventions.

There is robust evidence of an association between insomnia, anxiety, and depression in adolescence. The aim of this review is to describe and synthesize potential mechanisms underlying this association and explore implications for the design of adolescent behavioral sleep interventions. Specifically, we examine whether insomnia symptoms are a mechanism for the development of internalizing symptoms in adolescence and whether sleep interventions are an effective treatment for both insomnia and internalizing symptoms in adolescence because they target the shared mechanisms underlying these disorders. Research using different methodologies points to the role of sequential, parallel, and interacting mechanisms. In this paper, we review a wide range of relevant biological (i.e., polymorphisms and dysregulation in serotonin, dopamine, and circadian clock genes; alterations in corticolimbic and mesolimbic brain circuits; cortisol reactivity to stress; inflammatory cytokine dysregulation; biased memory consolidation; changes in sleep architecture), psychological (i.e., cognitive inflexibility, interpretational biases, judgment biases, negative attribution styles, worry, rumination, biased attention to threat, dysfunctional beliefs and attitudes about sleep, misperception of sleep deficit), and social mechanisms (i.e., reduced and impaired social interactions, unhelpful parenting behaviors, family stress) and propose an integrative multilevel model of how these phenomena may interact to increase vulnerability to both insomnia and internalizing disorders. Several 'biopsychosocial' mechanisms hold promise as viable treatment targets for adolescent behavioral sleep interventions, which may reduce both insomnia and internalizing symptoms.

Factor structure and psychometric properties of the Pittsburgh Sleep Quality Index in community-based adolescents.

Study Objectives: The Pittsburgh Sleep Quality Index (PSQI) is a widely used self-report questionnaire that assesses general sleep quality. This study aimed to validate the single-factor scoring structure and related psychometric properties in the English language version of the PSQI in community-based adolescents. Methods: Participants were 889 (352 males, 39.6%) students (age M = 15.71 ± 1.57; 12.08-18.92 years) recruited from 14 Australian secondary schools. Participants completed the PSQI, Center for Epidemiological Studies-Depression (CES-D) scale, and Spence Children's Anxiety Scale (SCAS). Exploratory factor analysis (EFA) and confirmatory factor analysis (CFA) of PSQI component scores were performed on two independent random half-samples (i.e. cross-validation approach). The internal consistency of PSQI components and convergent validity of the PSQI global score with CES-D and SCAS total scores were also assessed. Results: EFA yielded a single-factor model. CFA of the single-factor model in a separate sample yielded acceptable model fit to the data after important relationships were modeled. Namely, modification indices suggested improved model fit by correlating residual scores of PSQI components of sleep duration and sleep efficiency, and sleep efficiency and sleep latency. Internal consistency was acceptable (Cronbach's α = 0.73). The PSQI global score had moderate-to-large positive correlations with CES-D (r = 0.58) and SCAS (r = 0.45) total scores, demonstrating good convergent validity with emotional problems as predicted. Conclusions: The findings validate the single-factor scoring structure of the PSQI in an adolescent sample and highlight important covariation between poor sleep duration, efficiency, and latency in this age group. Further validation studies are required to determine an appropriate PSQI clinical cut-off score for adolescents.

Dynamic coupling between the central and autonomic nervous systems during sleep: A review.

Sleep is characterized by coordinated cortical and cardiac oscillations reflecting communication between the central (CNS) and autonomic (ANS) nervous systems. Here, we review fluctuations in ANS activity in association with CNS-defined sleep stages and cycles, and with phasic cortical events during sleep (e.g., arousals, K-complexes). Recent novel analytic methods reveal a dynamic organization of integrated physiological networks during sleep and indicate how multiple factors (e.g., sleep structure, age, sleep disorders) affect "CNS-ANS coupling". However, these data are mostly correlational and there is a lack of clarity of the underlying physiology, making it challenging to interpret causality and direction of coupling. Experimental manipulations (e.g., evoking K-complexes or arousals) provide information on the precise temporal sequence of cortical-cardiac activity, and are useful for investigating physiological pathways underlying CNS-ANS coupling. With the emergence of new analytical approaches and a renewed interest in ANS and CNS communication during sleep, future work may reveal novel insights into sleep and cardiovascular interactions during health and disease, in which coupling could be adversely impacted.