Chronic sleep deficiency and its impact on pain perception in healthy females.

Acute sleep deprivation in experimental studies has been shown to induce pain hypersensitivity in females. However, the impact of natural sleep deficiency and fluctuations across the week on pain perception remains unclear. A sleep-monitoring headband and self-reports were utilized to assess objective and subjective sleep in longer (> 6 hr) and short sleepers (< 6 hr). Pain sensitivity measures including heat, cold, pressure pain thresholds, pain inhibition (conditioned pain modulation) and facilitation (tonic pain summation) were assessed on Mondays and Fridays. Forty-one healthy young (23.9 ± 0.74 years) women participated. Short sleepers slept on average 2 hr less than longer sleepers (297.9 ± 8.2 min versus 418.5 ± 10.9 min) and experienced impaired pain inhibitory response (mean = -21.14 ± 7.9°C versus mean = 15.39 ± 9.5°C; p = 0.005). However, no effect was observed in pain thresholds and pain summation (p > 0.05). Furthermore, pain modulatory responses differed between Mondays and Fridays. Chronic sleep deficiency (< 6 hr) compromises pain responses, notably on Mondays. Maintaining a consistent sleep pattern with sufficient sleep (> 6 hr) throughout the week may protect against pain sensitization and the development of chronic pain in females. Further research is needed, especially in patients with chronic pain.

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.

Sex predicts post-concussion symptom reporting, independently of fatigue and subjective sleep disturbance, in premorbidly healthy adults after mild traumatic brain injury.

The relationship between sex and post-concussion symptom (PCS) reporting after mild traumatic brain injury (mTBI) is not well understood. Subjective sleep disturbance and fatigue impact PCS reporting after mTBI and show sex differences in the normal population. This study investigated whether sex had a relationship with PCS reporting after mTBI, independently of self-reported sleep disturbance and fatigue. Ninety-two premorbidly healthy adults in the post-acute period after mTBI completed the Rivermead Post-Concussion Symptoms Questionnaire, the Pittsburgh Sleep Quality Index, the Multidimensional Fatigue Inventory and measures of depression, anxiety and post-traumatic stress symptomatology. Females (n = 23) demonstrated higher levels of fatigue (p = .019) and greater psychological distress (p = .001) than males (n = 69), but equivalent levels of sleep disturbance (p = .946). Bootstrapping analyses were undertaken because PCS responses were not normally distributed. Female sex predicted greater PCS reporting (p = .001), independently of subjective sleep disturbance, fatigue, psychological distress and litigation status. The current findings support and extend previous work showing premorbidly healthy females are at higher risk of experiencing elevated PCS after mTBI than males in the post-acute period after mTBI. It may be beneficial for clinicians to be particularly sensitive to increased symptom reporting after mTBI in females, irrespective of sleep quality, fatigue or psychological status.

An observational study of the association between sleep disturbance, fatigue and cognition in the post-acute period after mild traumatic brain injury in prospectively studied premorbidly healthy adults.

The literature examining the relationship between sleep disturbance, fatigue, and cognition in premorbidly healthy civilian adults after mTBI is very limited. The current study aimed to investigate the relationships of sleep disturbance and fatigue with cognition while controlling for psychological distress and age. Using a prospective observational design, we assessed 60 premorbidly healthy individuals approximately 8 weeks after mTBI. Participants were assessed with the Pittsburgh Sleep Quality Index and the Multidimensional Fatigue Inventory as well as measures of speed of information processing, attention, memory, and executive function; depression and anxiety were also assessed. Findings revealed associations between sleep disturbance and cognition (r2 = .586, p < .001) as well as between fatigue and cognition (r2 = .390, p < .01), independent of the impact of psychological status and age. Associations were evident in the domains of processing speed, attention, and memory, but were most consistently apparent on measures of executive function. Greater sleep disturbance was most consistently associated with poorer cognitive function. Unexpectedly, higher levels of fatigue were associated with better cognitive function, which may be explained by the coping hypothesis. Given sleep interventions have been shown to improve sleep disturbance, these findings suggest that sleep intervention may also result in improved cognition after mTBI.

A randomised controlled trial of nasal decongestant to treat obstructive sleep apnoea in people with cervical spinal cord injury.

STUDY DESIGN: Prospective, double-blind, randomised, placebo-controlled, cross-over trial of nasal decongestion in tetraplegia. OBJECTIVES: Tetraplegia is complicated by severe, predominantly obstructive, sleep apnoea. First-line therapy for obstructive sleep apnoea is nasal continuous positive airway pressure, but this is poorly tolerated. High nasal resistance associated with unopposed parasympathetic activation of the upper airway contributes to poor adherence. This preliminary study tested whether reducing nasal decongestion improved sleep. SETTING: Participants' homes in Melbourne and Sydney, Australia. METHODS: Two sleep studies were performed in participants' homes separated by 1 week. Participants were given a nasal spray (0.5 mL of 5% phenylephrine or placebo) in random order and posterior nasal resistance measured immediately. Outcomes included sleep apnoea severity, perceived nasal congestion, sleep quality and oxygenation during sleep. RESULTS: Twelve middle-aged (average (SD) 52 (12) years) overweight (body mass index 25.3 (6.7) kg/m2) men (C4-6, AIS A and B) participated. Nasal resistance was reduced following administration of phenylephrine (p = 0.02; mean between treatment group difference -5.20: 95% confidence interval -9.09, -1.32 cmH2O/L/s). No differences were observed in the apnoea hypopnoea index (p = 0.15; -6.37: -33.3, 20.6 events/h), total sleep time (p = 0.49; -1.33: -51.8, 49.1 min), REM sleep% (p = 0.50; 2.37: -5.6, 10.3), arousal index (p = 0.76; 1.15: -17.45, 19.75), 4% oxygen desaturation index (p = 0.88; 0.63: -23.5, 24.7 events/h), or the percentage of mouth breathing events (p = 0.4; -8.07: -29.2, 13.0) between treatments. The apnoea hypopnoea index did differ between groups, however, all except one participant had proportionally more hypopnoeas than apnoeas during sleep after decongestion. CONCLUSIONS: These preliminary data found that phenylephrine acutely reduced nasal resistance but did not significantly change sleep-disordered breathing severity.

Genioglossus reflex responses to negative upper airway pressure are altered in people with tetraplegia and obstructive sleep apnoea.

KEY POINTS: Protective reflexes in the throat area (upper airway) are crucial for breathing. Impairment of these reflexes can cause breathing problems during sleep such as obstructive sleep apnoea (OSA). OSA is very common in people with spinal cord injury for unknown reasons. This study shows major changes in protective reflexes that serve to keep the upper airway open in response to suction pressures in people with tetraplegia and OSA. These results help us understand why OSA is so common in people with tetraplegia and provide new insight into how protective upper airway reflexes work more broadly. ABSTRACT: More than 60% of people with tetraplegia have obstructive sleep apnoea (OSA). However, the specific causes are unknown. Genioglossus, the largest upper-airway dilator muscle, is important in maintaining upper-airway patency. Impaired genioglossus muscle function following spinal cord injury may contribute to OSA. This study aimed to determine if genioglossus reflex responses to negative upper-airway pressure are altered in people with OSA and tetraplegia compared to non-neurologically impaired able-bodied individuals with OSA. Genioglossus reflex responses measured via intramuscular electrodes to ∼60 brief (250 ms) pulses of negative upper-airway pressure (∼-15 cmH2 O at the mask) were compared between 13 participants (2 females) with tetraplegia plus OSA and 9 able-bodied controls (2 females) matched for age and OSA severity. The initial short-latency excitatory reflex response was absent in 6/13 people with tetraplegia and 1/9 controls. Genioglossus reflex inhibition in the absence of excitation was observed in three people with tetraplegia and none of the controls. When the excitatory response was present, it was significantly delayed in the tetraplegia group compared to able-bodied controls: excitation onset latency (mean ± SD) was 32 ± 16 vs. 18 ± 9 ms, P = 0.045; peak excitation latency was 48 ± 17 vs. 33 ± 8 ms, P = 0.038. However, when present, amplitude of the excitation response was not different between groups, 195 ± 26 vs. 219 ± 98% at baseline, P = 0.55. There are major differences in genioglossus reflex morphology and timing in response to rapid changes in airway pressure in people with tetraplegia and OSA. Altered genioglossus function may contribute to the increased risk of OSA in people with tetraplegia. The precise mechanisms mediating these differences are unknown.

Obstructive sleep apnoea pathogenesis from mild to severe: Is it all the same?

Obstructive sleep apnoea (OSA) is a common disorder caused by not only an impaired upper airway anatomy (i.e. anatomically narrow/collapsible airway), but also by several non-anatomical factors. In this review, we summarise what is known about how each of the pathological factors that cause OSA vary according to disease severity as measured by the apnoea-hypopnoea index. Our synthesis of the available literature indicates that most of the key factors that cause OSA vary with disease severity. However, there is substantial heterogeneity such that the relative contribution of each of these traits varies both between patients and within different severities of disease. These differences likely contribute to variable efficacy of many non-continuous positive airway pressure treatments and inconsistencies in responses with regard to different OSA severities at baseline.

Common drive to the upper airway muscle genioglossus during inspiratory loading.

Common drive is thought to constitute a central mechanism by which the efficiency of a motor neuron pool is increased. This study tested the hypothesis that common drive to the upper airway muscle genioglossus (GG) would increase with increased respiratory drive in response to an inspiratory load. Respiration, GG electromyographic (EMG) activity, single-motor unit activity, and coherence in the 0-5 Hz range between pairs of GG motor units were assessed for the 30 s before an inspiratory load, the first and second 30 s of the load, and the 30 s after the load. Twelve of twenty young, healthy male subjects provided usable data, yielding 77 pairs of motor units: 2 Inspiratory Phasic, 39 Inspiratory Tonic, 15 Expiratory Tonic, and 21 Tonic. Respiratory and GG inspiratory activity significantly increased during the loads and returned to preload levels during the postload periods (all showed significant quadratic functions over load trials, P < 0.05). As hypothesized, common drive increased during the load in inspiratory modulated motor units to a greater extent than in expiratory/tonic motor units (significant load × discharge pattern interaction, P < 0.05). Furthermore, this effect persisted during the postload period. In conclusion, common drive to inspiratory modulated motor units was elevated in response to increased respiratory drive. The postload elevation in common drive was suggestive of a poststimulus activation effect.

Crossed motor innervation of the base of human tongue.

Muscle fibers of the genioglossus (GG) form the bulk of the muscle mass at the base of the tongue. The motor control of the tongue is critical for vocalization, feeding, and breathing. Our goal was to assess the patterns of motor innervation of GG single motor units (SMUs) in humans. Simultaneous monopolar recordings were obtained from four sites in the base of the tongue bilaterally at two antero-posterior levels from 16 resting, awake, healthy adult males, who wore a face mask with airway pressure and airflow sensors. We analyzed 69 data segments in which at least one lead contained large action potentials generated by an SMU. Such potentials served as triggers for spike-triggered averaging (STA) of signals recorded from the other three sites. Spontaneous activity of the SMUs was classified as inspiratory modulated, expiratory modulated, or tonic. Consistent with the antero-posterior orientation of GG fibers, 44 STAs (77%) recorded ipsilateral to the trigger yielded sharp action potentials with a median amplitude of 52 µV [interquartile range (IQR): 25-190] that were time shifted relative to the trigger by about 1 ms. Notably, 48% of recordings on the side opposite to the trigger also yielded sharp action potentials. Of those, 17 (29%) had a median amplitude of 63 µV (IQR: 39-96), and most were generated by tonic SMUs. Thus a considerable proportion of GG muscle fibers receive a crossed motor innervation. Crossed innervation may help ensure symmetry and stability of tongue position and movements under normal conditions and following injury or degenerative changes affecting the tongue.

Adult obstructive sleep apnoea.

Obstructive sleep apnoea is an increasingly common disorder of repeated upper airway collapse during sleep, leading to oxygen desaturation and disrupted sleep. Features include snoring, witnessed apnoeas, and sleepiness. Pathogenesis varies; predisposing factors include small upper airway lumen, unstable respiratory control, low arousal threshold, small lung volume, and dysfunctional upper airway dilator muscles. Risk factors include obesity, male sex, age, menopause, fluid retention, adenotonsillar hypertrophy, and smoking. Obstructive sleep apnoea causes sleepiness, road traffic accidents, and probably systemic hypertension. It has also been linked to myocardial infarction, congestive heart failure, stroke, and diabetes mellitus though not definitively. Continuous positive airway pressure is the treatment of choice, with adherence of 60-70%. Bi-level positive airway pressure or adaptive servo-ventilation can be used for patients who are intolerant to continuous positive airway pressure. Other treatments include dental devices, surgery, and weight loss.

Enhanced upper-airway muscle responsiveness is a distinct feature of overweight/obese individuals without sleep apnea.

RATIONALE: Body habitus is a major determinant of obstructive sleep apnea (OSA). However, many individuals do not have OSA despite being overweight/obese (body mass index > 25 kg/m(2)) for reasons that are not fully elucidated. OBJECTIVES: To determine the key physiologic traits (upper-airway anatomy/collapsibility, upper-airway muscle responsiveness, chemoreflex control of ventilation, arousability from sleep) responsible for the absence of OSA in overweight/obese individuals. METHODS: We compared key physiologic traits in 18 overweight/obese subjects without apnea (apnea-hypopnea index < 15 events per hour) with 25 overweight/obese matched patients with OSA (apnea-hypopnea index ≥ 15 events per hour) and 11 normal-weight nonapneic control subjects. Traits were measured by repeatedly lowering continuous positive airway pressure to subtherapeutic levels for 3 minutes during non-REM sleep. MEASUREMENTS AND MAIN RESULTS: Overweight/obese subjects without apnea exhibited a less collapsible airway than overweight/obese patients with apnea (critical closing pressure: -3.7 ± 1.9 vs. 0.6 ± 1.2 cm H2O; P = 0.003; mean ± 95% confidence interval), but a more collapsible airway relative to normal-weight control subjects (-8.8 ± 3.1 cm H2O; P < 0.001). Notably, overweight/obese subjects without apnea exhibited a threefold greater upper-airway muscle responsiveness than both overweight/obese patients with apnea (Δgenioglossus EMG/Δepiglottic pressure: -0.49 [-0.22 to -0.79] vs. -0.15 [-0.09 to -0.22] %max/cm H2O; P = 0.008; mean [95% confidence interval]) and normal-weight control subjects (-0.16 [-0.04 to -0.30] %max/cm H2O; P = 0.02). Loop gain was elevated (more negative) in both overweight/obese groups and normal-weight control subjects (P = 0.02). Model-based analysis demonstrated that overweight/obese individuals without apnea rely on both more favorable anatomy and collapsibility and enhanced upper-airway dilator muscle responses to avoid OSA. CONCLUSIONS: Overweight/obese individuals without apnea have a moderately compromised upper-airway structure that is mitigated by highly responsive upper-airway dilator muscles to avoid OSA. Elucidating the mechanisms underlying enhanced muscle responses in this population may provide clues for novel OSA interventions.

Defining phenotypic causes of obstructive sleep apnea. Identification of novel therapeutic targets.

RATIONALE: The pathophysiologic causes of obstructive sleep apnea (OSA) likely vary among patients but have not been well characterized. OBJECTIVES: To define carefully the proportion of key anatomic and nonanatomic contributions in a relatively large cohort of patients with OSA and control subjects to identify pathophysiologic targets for future novel therapies for OSA. METHODS: Seventy-five men and women with and without OSA aged 20-65 years were studied on three separate nights. Initially, the apnea-hypopnea index was determined by polysomnography followed by determination of anatomic (passive critical closing pressure of the upper airway [Pcrit]) and nonanatomic (genioglossus muscle responsiveness, arousal threshold, and respiratory control stability; loop gain) contributions to OSA. MEASUREMENTS AND MAIN RESULTS: Pathophysiologic traits varied substantially among participants. A total of 36% of patients with OSA had minimal genioglossus muscle responsiveness during sleep, 37% had a low arousal threshold, and 36% had high loop gain. A total of 28% had multiple nonanatomic features. Although overall the upper airway was more collapsible in patients with OSA (Pcrit, 0.3 [-1.5 to 1.9] vs. -6.2 [-12.4 to -3.6] cm H2O; P <0.01), 19% had a relatively noncollapsible upper airway similar to many of the control subjects (Pcrit, -2 to -5 cm H2O). In these patients, loop gain was almost twice as high as patients with a Pcrit greater than -2 cm H2O (-5.9 [-8.8 to -4.5] vs. -3.2 [-4.8 to -2.4] dimensionless; P = 0.01). A three-point scale for weighting the relative contribution of the traits is proposed. It suggests that nonanatomic features play an important role in 56% of patients with OSA. CONCLUSIONS: This study confirms that OSA is a heterogeneous disorder. Although Pcrit-anatomy is an important determinant, abnormalities in nonanatomic traits are also present in most patients with OSA.

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.

Neurogenic changes in the upper airway of patients with obstructive sleep apnea.

RATIONALE: Controversy persists regarding the presence and importance of hypoglossal nerve dysfunction in obstructive sleep apnea (OSA). OBJECTIVES: We assessed quantitative parameters related to motor unit potential (MUP) morphology derived from electromyographic (EMG) signals in patients with OSA versus control subjects and hypothesized that signs of neurogenic remodeling would be present in the patients with OSA. METHODS: Participants underwent diagnostic sleep studies to obtain apnea-hypopnea indices. Muscle activity was detected with 50-mm concentric needle electrodes. The concentric needle was positioned at more than 10 independent sites per subject, after the local anatomy of the upper airway musculature was examined by ultrasonography. All activity was quantified with subjects awake, during supine eupneic breathing while wearing a nasal mask connected to a pneumotachograph. Genioglossus EMG signals were analyzed offline by automated software (DQEMG), which extracted motor unit potential trains (MUPTs) contributed by individual motor units from the composite EMG signals. Quantitative measurements of MUP templates, including duration, peak-to-peak amplitude, area, area-to-amplitude ratio, and size index, were compared between the untreated patients with OSA and healthy control subjects. MEASUREMENTS AND MAIN RESULTS: A total of 1,655 MUPTs from patients with OSA (n = 17; AHI, 55 ± 6/h) and control subjects (n = 14; AHI, 4 ± 1/h) were extracted from the genioglossus muscle EMG signals. MUP peak-to-peak amplitudes in the patients with OSA were not different compared with the control subjects (397.5 ± 9.0 vs. 382.5 ± 10.0 µV). However, the MUPs of the patients with OSA were longer in duration (11.5 ± 0.1 vs. 10.3 ± 0.1 ms; P < 0.001) and had a larger size index (4.09 ± 0.02 vs. 3.92 ± 0.02; P < 0.001) compared with control subjects. CONCLUSIONS: These results confirm and quantify the extent and existence of structural neural remodeling in OSA.

Fatigue and Sleep in Airline Cabin Crew: A Scoping Review.

Airline cabin crew operate in dynamic work environments that are continuously changing, from unpredictable shift work hours to travelling through multiple time zones. These likely impact cabin crews' overall health and may affect their performance on safety-related tasks. Research on this population has been limited; therefore, the aim was to summarise the relevant literature regarding fatigue, sleepiness and mental health of cabin crew. This review followed the PRISMA-ScR guidelines and conducted a systematic search utilising five databases. The initial search identified 1223 studies, and through vigorous screening processes, 27 studies were selected for this review. Over half of the selected studies focused on international or long-haul flights, and a large proportion of the sample participants were women. Findings suggested a high prevalence of fatigue and sleepiness as well as unsatisfactory sleep quality with elevated susceptibility to sleep disorders. Factors identified with health outcomes were associated with flight operations (e.g., rosters) and individual differences (e.g., age and coping strategies). Regarding mental health, cabin crews are potentially at a greater risk for depression and anxiety compared to the general public. This review draws attention to the importance of using a standardised approach, such as validated measures for fair and consistent inferences.

The impact of sleep disturbance on pain perception: A systematic review examining the moderating effect of sex and age.

Females have increased pain sensitivity and are more vulnerable to chronic pain conditions. Sleep disturbances are comorbid with chronic pain and exacerbate pain symptoms. Different types of sleep disturbance affect pain perception distinctly, but it is not clear if these effects are equal in men and women. This systematic review investigated potential differences in how sleep disturbance affects pain in males and females. We searched EBSCO, MEDLINE, Psych INFO, Science Direct, and Web of Science from January 2001 to November 2022 and found 38 studies with 978 participants. Separate random-effects models were used to estimate the pooled effect sizes based on standardized mean differences (SMDs) of experimental sleep disturbance paradigms on various pain outcomes. Sex moderated the effect of sleep disturbance on pain facilitation (SMD = 0.13; 95%CI: 0.004 to 0.022; p=.009) and pain inhibition (SMD = 0.033; 95%CI: 0.011 to 0.054; p=.005), with increased facilitation and decreased inhibition in females, but the opposite effect in males. Further, age moderated the effects of total sleep deprivation (SMD = -0.194; 95%CI -0.328 to -0.060; p=.008) on pain sensitivity and fragmented sleep (SMD = -0.110; 95%CI: 0.148 to -0.072; p<.001) on pain threshold. While the moderating effect of sex and age on the sleep-pain relationship was small, these factors need to be considered in future sleep-pain research.

A randomized controlled trial of a multi-dimensional intervention to improve CPAP use and self-efficacy.

OBJECTIVES: To assess the utility of a tailored intervention program to improve continuous positive airway pressure (CPAP) use and self-efficacy in individuals with obstructive sleep apnea (OSA). METHODS: 81 participants (mean age 52.1 ± 11.6 years; 35 females) with OSA were randomized to either a multi-dimensional intervention (PSY CPAP, n = 38) or treatment as usual (TAU CPAP, n = 43). The intervention included a psychoeducation session prior to CPAP initiation, a booster psychoeducation session in the first weeks of commencing CPAP, follow-up phone calls on days 1 and 7, and a review appointment on day 14. CPAP use was compared between the PSY CPAP and TAU CPAP groups at 1 week, 1 month, and 4 months. Self-efficacy scores (risk perception, outcome expectancies, and CPAP self-efficacy) were compared between groups following the initial psychoeducation session and again at 1 month and 4 months. RESULTS: CPAP use was higher in the PSY CPAP group compared to the TAU CPAP group for all time points (p = .02). Outcome expectancies improved significantly over time in PSY CPAP participants (p = .007). Change in risk perception was associated with CPAP use at 1 week (p = .02) for PSY CPAP participants. However, risk perception did not mediate the effect between group and CPAP use at 1 week. CONCLUSIONS: Interventions designed to increase self-efficacy and administered prior to CPAP initiation, repeated in the early stages of CPAP therapy, and combined with a comprehensive follow-up regime are likely to improve CPAP use. Sustained improvement in CPAP use is the ultimate goal but remains to be investigated.

Sleep and day-to-day PTSD symptom variability: an ecological momentary assessment and actigraphy monitored study in trauma-exposed young adults.

BACKGROUND: Disrupted sleep and post-traumatic stress disorder (PTSD) are bi-directionally linked and have been found to mutually reinforce each other on a day-to-day basis. However, most of the previous research has focused on subjective measures of sleep only. OBJECTIVE: Here, we investigated the temporal relationship between sleep and PTSD symptoms using both subjective (sleep diary) and objective measures of sleep (actigraphy). METHODS: Forty-one non-treatment seeking, trauma exposed young adults (age M = 24.68, SD = 8.15) with a range of PTSD symptom severities (PTSS, 0-53 on PCL-5) were recruited. Participants completed two surveys per day over four weeks to measure day-time PTSD symptoms (i.e. PTSS and number of intrusions) and night-time sleep subjectively, while wearing an actigraphy watch to measure sleep objectively. RESULTS: Linear mixed models revealed that subjectively reported sleep disruptions were associated with elevated next-day PTSS and increasing number of intrusive memories both within and between participants. Similar results were found for daytime PTSD symptoms on night-time sleep. However, these associations were not found using objective sleep data. Exploratory moderator analyses including sex (male vs. female) found that these associations differed in strength between sexes but were generally in the same direction. DISCUSSION: These results were in line with our hypothesis with regards to the sleep diary (subjective sleep), but not actigraphy (objective sleep). Several factors which have implications on both PTSD and sleep, such as the COVID-19 pandemic and/ or sleep-state misperception, may be potential reasons behind those discrepancies. However, this study had limited power and needs to be replicated in larger samples. Nonetheless, these results add to the current literature about the bi-directional relationship between sleep and PTSD and have clinical implications for treatment strategies.

Elevated day-time PTSD symptom severity (PTSS) and more frequent intrusive memories were generally associated with subjectively reported disruptions in sleep and vice versa, but not with objective measures of sleep.While longer subjective sleep duration predicted reductions in PTSS and shorter sleep onset latency predicted reduced numbers of intrusions the next day, reduced daytime PTSS was only associated with reductions in distress associated with nightmares during the following night.Exploratory analyses showed that sex (men vs. women) moderated the bi-directional relationships between night-time sleep and day-time PTSD symptoms with longer sleep onset latency and lower sleep efficiency being related to worse PTSD symptoms the next day in women, but was not associated with men.