Subjective–objective sleep discrepancy among older adults: associations with insomnia diagnosis and insomnia treatment

Discrepancy between subjective and objective measures of sleep is associated with insomnia and increasing age. Cognitive behavioural therapy for insomnia improves sleep quality and decreases subjective–objective sleep discrepancy. This study describes differences between older adults with insomnia and controls in sleep discrepancy, and tests the hypothesis that reduced sleep discrepancy following cognitive behavioural therapy for insomnia correlates with the magnitude of symptom improvement reported by older adults with insomnia. Participants were 63 adults >60 years of age with insomnia, and 51 controls. At baseline, participants completed sleep diaries for 7 days while wearing wrist actigraphs. After receiving cognitive behavioural therapy for insomnia, insomnia patients repeated this sleep assessment. Sleep discrepancy variables were calculated by subtracting actigraphic sleep onset latency and wake after sleep onset from respective self‐reported estimates, pre‐ and post‐treatment. Mean level and night‐to‐night variability in sleep discrepancy were investigated. Baseline sleep discrepancies were compared between groups. Pre–post‐treatment changes in Insomnia Severity Index score and sleep discrepancy variables were investigated within older adults with insomnia. Sleep discrepancy was significantly greater and more variable across nights in older adults with insomnia than controls, P ≤ 0.001 for all. Treatment with cognitive behavioural therapy for insomnia was associated with significant reduction in the Insomnia Severity Index score that correlated with changes in mean level and night‐to‐night variability in wake after sleep onset discrepancy, P < 0.001 for all. Study of sleep discrepancy patterns may guide more targeted treatments for late‐life insomnia.     

Sleep characteristics as predictor variables of stress systems markers in insomnia disorder

This study investigates the extent to which sleep characteristics serve as predictor variables for inflammatory, hypothalamic–pituitary–adrenal and autonomic systems markers. Twenty‐nine participants with a diagnosis of insomnia disorder based on the Diagnostic Statistical Manual of Mental Disorders, Fifth Edition (age 25.3 ± 1.6 years, insomnia duration 6.6 ± 0.8 years) and 19 healthy control sleepers (age 25.4 ± 1.4 years) underwent a 2‐week at‐home evaluation keeping a sleep diary and wearing an actigraph, followed by a visit to the Research Center to measure blood pressure, and collect blood and urine samples. The actigraphy‐ and diary‐based variables of sleep duration, sleep‐onset latency, wake after sleep onset and sleep fragmentation/number of night‐time awakenings were averaged and entered as dependent variables in regression analyses. Composite scores were calculated for the autonomic (blood pressure, norepinephrine), inflammatory (monocyte counts, interleukin‐6, C‐reactive protein) and hypothalamic–pituitary–adrenal systems (cortisol), and used as predictor variables in regression models. Compared with controls, individuals with insomnia had a shorter sleep duration (P < 0.05), and a higher hypothalamic–pituitary–adrenal and inflammatory composite score (P < 0.05). The higher inflammatory score was mainly due to higher circulating monocytes (P < 0.05), rather than differences in interleukin‐6 or C‐reactive protein. In persistent insomnia disorder, cortisol is upregulated and associated with actigraphy‐ and diary‐based wake after sleep onset, suggesting that wake after sleep onset may serve as a marker to identify individuals at increased risks for disorders associated with a hyperactive hypothalamic–pituitary–adrenal system. The absence of autonomic and pro‐inflammatory changes (interleukin‐6, C‐reactive protein), despite a substantial decrease in actigraphic sleep duration, may relate to a higher resilience to the adverse biological consequences of insomnia in this young age group.     

Cognitive performance in DSWPD patients upon awakening from habitual sleep compared with forced conventional sleep

Difficult early morning awakening is one of the defining symptoms of delayed sleep–wake phase disorder. It is accompanied by low cognitive arousal and drowsiness resulting in difficulty concentrating and focusing attention upon awakening. We designed the current study to quantitate cognitive performance (i.e. omissions, commissions, reaction time [average and variability]) and cognitive domains (i.e. focused attention, sustained attention, impulsivity and vigilance) with Conners’ Continuous Performance Test II during both habitual and conventional (00:00–07:00 hr) sleep–wake schedule in young adult patients with delayed sleep–wake phase disorder (n = 20, mean age = 24.8 years, SD = 3.0) and controls (n = 16, mean age = 24.4 years, SD = 3.4). Conners’ Continuous Performance Test II was administered after awakening and in the afternoon during both habitual and conventional conditions. In‐laboratory polysomnography was performed for 2 nights. We assessed sleep, tiredness, chronotype and depression using questionnaires. Saliva was sampled for dim light melatonin onset measurements. Repeated‐measures ANOVAs were applied for the Conners’ Continuous Performance Test II measures with group (patient/control), time (afternoon/morning) and condition (habitual/conventional schedule) as fixed factors. Patients with delayed sleep–wake phase disorder had reduced reaction times, especially in the morning, greater response speed variability, and made more omission and commission errors compared with controls. Patients with delayed sleep–wake phase disorder also had reduced focused attention, especially upon forced early awakening. The short total sleep time of patients with delayed sleep–wake phase disorder could not statistically explain this outcome. In conclusion, we observed a state‐dependent reduced ability to focus attention upon early morning awakening in patients with delayed sleep–wake phase disorder. Patients also had more omissions, longer reaction time and increased RT variability after habitual sleep, suggesting a possible small cognitive trait dysfunction in delayed sleep–wake phase disorder.     

The subjective–objective mismatch in sleep perception among those with insomnia and sleep apnea

The diagnosis and management of insomnia relies primarily on clinical history. However, patient self‐report of sleep–wake times may not agree with objective measurements. We hypothesized that those with shallow or fragmented sleep would under‐report sleep quantity, and that this might account for some of the mismatch. We compared objective and subjective sleep–wake times for 277 patients who underwent diagnostic polysomnography. The group included those with insomnia symptoms (n = 92), obstructive sleep apnea (n = 66) or both (n = 119). Mismatch of wake duration was context dependent: all three groups overestimated sleep latency but underestimated wakefulness after sleep onset. The insomnia group underestimated total sleep time by a median of 81 min. However, contrary to our hypothesis, measures of fragmentation (N1, arousal index, sleep efficiency, etc.) did not correlate with the subjective sleep duration estimates. To unmask a potential relationship between sleep architecture and subjective duration, we tested three hypotheses: N1 is perceived as wake; sleep bouts under 10 min are perceived as wake; or N1 and N2 are perceived in a weighted fashion. None of these hypotheses exposed a match between subjective and objective sleep duration. We show only modest performance of a Naïve Bayes Classifier algorithm for predicting mismatch using clinical and polysomnographic variables. Subjective–objective mismatch is common in patients reporting insomnia symptoms. We conclude that mismatch was not attributable to commonly measured polysomnographic measures of fragmentation. Further insight is needed into the complex relationships between subjective perception of sleep and conventional, objective measurements.     

Dysmenorrhea,the Menstrual Cycle,and Sleep

This study examined the relationship between dysmenorrhea and insomnia, as well as variability in sleep across the menstrual cycle. Participants were 89 women, ages 18 to 24 (M = 18.63, SD = 0.93), who completed daily surveys for five weeks. On the second day of menses, they completed a questionnaire regarding dysmenorrhea. Participants having insomnia rated their dysmenorrhea as being more severe and causing more interference with daily activities than did participants without insomnia. Insomnia severity was directly associated with dysmenorrhea severity and interference. Sleep onset latency was longer and sleep efficiency was lower in participants with severe dysmenorrhea than in those with mild dysmenorrhea. Further, participants with mild dysmenorrhea reported significantly better sleep quality than did those having moderate or severe dysmenorrhea. Additionally, wake time after sleep onset was shortest and number of awakenings was lowest around the time of ovulation. Future research should examine whether treating dysmenorrhea or insomnia alone results in improvements in the other condition.     

Impact of sleep inertia on visual selective attention for rare targets and the influence of chronotype

Sleep inertia is affected by circadian phase, with worse performance upon awakening from sleep during the biological night than biological day. Visual search/selective visual attention performance is known to be sensitive to sleep inertia and circadian phase. Individual differences exist in the circadian timing of habitual wake time, which may contribute to individual differences in sleep inertia. Because later chronotypes awaken at an earlier circadian phase, we hypothesized that later chronotypes would have worse visual search performance during sleep inertia than earlier chronotypes if awakened at habitual wake time. We analysed performance from 18 healthy participants [five females (22.1 ± 3.7 years; mean ± SD)] at ~1, 10, 20, 30, 40 and 60 min following electroencephalogram‐verified awakening from an 8 h in‐laboratory sleep opportunity. Cognitive throughput and reaction times of correct responses were impaired by sleep inertia and took ~10–30 min to improve after awakening. Regardless whether chronotype was defined by dim light melatonin onset or mid‐sleep clock hour on free days, derived from the Munich ChronoType Questionnaire, the duration of sleep inertia for cognitive throughput and reaction times was longer for later chronotypes (n = 7) compared with earlier chronotypes (n = 7). Specifically, performance for earlier chronotypes showed significant improvement within ~10–20 min after awakening, whereas performance for later chronotypes took ~30 min or longer to show significant improvement (P < 0.05). Findings have implications for decision making immediately upon awakening from sleep, and are consistent with circadian theory suggesting that sleep inertia contributes to longer‐lasting impairments in morning performance in later chronotypes.     

Discrepancies in sleep diary and actigraphy assessments in adults with fibromyalgia: Associations with opioid dose and age

Sleep diary and actigraphy assessments of insomnia symptoms in patients with fibromyalgia (FM) are often discrepant. We examined whether opioid dose and age interact in predicting magnitude or direction of discrepancies. Participants (N = 199, M = 51.5 years, SD = 11.7) with FM and insomnia completed 14 days of diaries and actigraphy. Multiple regressions determined whether average opioid dose and its interaction with age predicted magnitude or direction of diary/actigraphy discrepancies in sleep onset latency (SOL), wake after sleep onset (WASO) and sleep efficiency (SE), controlling for sex, use of sleep medication, evening pain and total sleep time. Higher opioid dose predicted greater magnitude of discrepancy in SOL and SE. Opioid dose interacted with age to predict direction but not magnitude of discrepancy in SOL and SE. Specifically, higher opioid use was associated with better subjective (shorter SOL, higher SE) than objective reports of sleep among younger adults, and longer subjective than objectively measured SOL among older adults. Opioid dose did not predict magnitude or direction of WASO discrepancies. In FM, a higher opioid dose increases diary/actigraphy SOL and SE discrepancies, and direction of discrepancies may depend on age. We speculate that increased opioid use combined with age‐related factors, such as slow wave sleep disruption, increased awakenings and/or cognitive decline, may impact perceived sleep.     

Subjective–objective sleep discrepancy in patients with insomnia during and after cognitive behavioural therapy: An actigraphy study

Although patients with insomnia often show a discrepancy between self‐reported and objective sleep parameters, the role of and change in this phenomenon during treatment remain unclear. The present study aimed to assess the effect of cognitive behavioural therapy for insomnia on subjective and objective sleep discrepancy of total sleep time, sleep‐onset latency and wake after sleep onset. The total sleep time discrepancy was also assessed across the entire therapy. The second aim was to examine the treatment outcome of two insomnia groups differing in sleep perception. Thirty‐six adults with insomnia (mean age = 46.7 years, SD = 13.9; 22 females) were enrolled in the final analyses. Patients underwent a 6‐week group cognitive behavioural therapy for insomnia programme. Sleep diary and actigraphy measurements were obtained during the therapy. Patients who underestimated total sleep time (n = 16; underestimating group) were compared with patients who accurately perceived or overestimated total sleep time (n = 20; accurate/overestimating group). After cognitive behavioural therapy for insomnia, a significant decrease of total sleep time and sleep‐onset latency discrepancy was observed without a change in wake after sleep onset discrepancy in the total sample. Only the underestimating group reported decreased sleep‐onset latency discrepancy after the treatment, whereas total sleep time discrepancy significantly changed in both groups. The underestimating group showed a significant decrease of total sleep time discrepancy from Week 1 to Week 2 when the sleep restriction was implemented, whereas the accurate/overestimating group showed the first significant change at Week 4. In conclusion, both groups differing in sleep perception responded similarly to cognitive behavioural therapy for insomnia, although different In conclusion, both groups differing in sleep perception responded similarly to cognitive behavioural therapy for insomnia, although different therapeutic components could play important roles in each group. components could play important roles in each group.     

Sleep patterns and insomnia among adolescents: a population‐based study

The aim of the current study was to examine sleep patterns and rates of insomnia in a population‐based study of adolescents aged 16–19 years. Gender differences in sleep patterns and insomnia, as well as a comparison of insomnia rates according to DSM‐IV, DSM‐V and quantitative criteria for insomnia (Behav. Res. Ther., 41 , 2003, 427), were explored. We used a large population‐based study in Hordaland county in Norway, conducted in 2012. The sample included 10 220 adolescents aged 16–18 years (54% girls). Self‐reported sleep measurements included bedtime, rise time, time in bed, sleep duration, sleep efficiency, sleep onset latency, wake after sleep onset, rate and frequency and duration of difficulties initiating and maintaining sleep and rate and frequency of tiredness and sleepiness. The adolescents reported short sleep duration on weekdays (mean 6:25 hours), resulting in a sleep deficiency of about 2 h. A majority of the adolescents (65%) reported sleep onset latency exceeding 30 min. Girls reported longer sleep onset latency and a higher rate of insomnia than boys, while boys reported later bedtimes and a larger weekday–weekend discrepancy on several sleep parameters. Insomnia prevalence rates ranged from a total prevalence of 23.8 (DSM‐IV criteria), 18.5 (DSM‐V criteria) and 13.6% (quantitative criteria for insomnia). We conclude that short sleep duration, long sleep onset latency and insomnia were prevalent in adolescents. This warrants attention as a public health concern in this age group.     

Self‐administered acupressure for insomnia disorder: a pilot randomized controlled trial

Self‐administered acupressure has potential as a low‐cost alternative treatment for insomnia. To evaluate the short‐term effects of self‐administered acupressure for alleviating insomnia, a pilot randomized controlled trial was conducted. Thirty‐one subjects (mean age: 53.2 years; 77.4% female) with insomnia disorder were recruited from a community. The participants were randomized to receive two lessons on either self‐administered acupressure or sleep hygiene education. The subjects in the self‐administered acupressure group (n = 15) were taught to practise self‐administered acupressure daily for 4 weeks. The subjects in the comparison group (n = 16) were advised to follow sleep hygiene education. The primary outcome was the Insomnia Severity Index (ISI). Other measures included a sleep diary, Hospital Anxiety and Depression Scale and Short‐form Six‐Dimension. The subjects in the self‐administered acupressure group had a significantly lower ISI score than the subjects in the sleep hygiene education group at week 8 (effect size = 0.56, P = 0.03). However, this observed group difference did not reach a statistically significant level after Bonferroni correction. With regard to the secondary outcomes, moderate between‐group effect sizes were observed in sleep onset latency and wake after sleep onset based on the sleep diary, although the differences were not significant. The adherence to self‐administered acupressure practice was satisfactory, with 92.3% of the subjects who completed the lessons still practising acupressure at week 8. In conclusion, self‐administered acupressure taught in a short training course may be a feasible approach to improve insomnia. Further fully powered confirmatory trials are warranted.     

Nocturnal cardiac autonomic profile in young primary insomniacs and good sleepers

We investigated cardiac vagal and sympathetic activity in 13 young primary insomniacs (PI; 24.4 ± 1.6 years) and 14 good sleepers (GS; 23.3 ± 2.5 years) during nocturnal sleep. Pre-ejection period (PEP; inversely related to beta-adrenergic sympathetic activity), interval between consecutive R-waves (RR), and vagal-related indices of time- and frequency-domain heart rate variability were computed during pre-sleep wakefulness and undisturbed arousal-free sleep stages (N2, SWS, REM) as well as across the whole night irrespective of the presence of disruptive sleep events (e.g. sleep arousals/awakenings) and/or sleep stage transitions. Groups exhibited a similar vagal activity throughout each undisturbed sleep stage as well as considering the whole night, with a higher modulation during sleep compared to prior wakefulness. However, PEP was constantly shorter (higher sympathetic activity) during pre-sleep wakefulness and each sleep stage in PI compared to GS. Moreover, pre-sleep RR intervals were positively associated with sleep efficiency and negatively associated with wake after sleep onset in PI. Altogether our findings indicated a dysfunctional sympathetic activity but a normal parasympathetic modulation before and during sleep in young adults with insomnia.     

The effect on sleep of being on‐call: an experimental field study

The aim of this study was to: (i) gain more insight into the relationship between being on‐call and sleep and (ii) investigate the role of stress in this relationship. Data were collected by means of an experimental field study with a within‐subject design (two conditions, random order). Ninety‐six students participated during two consecutive nights: a reference night and a simulated on‐call night without an actual call. Participants were told they could be called at any time during the on‐call night. In the case of a call, participants had to perform online tasks for approximately 30 min. Self‐reported sleep quality and the extent to which participants experienced stress during the on‐call period were assessed by means of short questionnaires. Actigraphy was used to obtain objective sleep measures. Results for actigraphy data revealed no significant within‐person differences between conditions. However, participants reported longer sleep onset latencies, more awakenings and more wake after sleep onset during the on‐call night than during the reference night. They also reported more sleep problems and a lower overall sleep quality, and felt less recuperated after the on‐call night. Perceived stress moderated the relationship between being on‐call, on one hand, and the number of awakenings, wake after sleep onset, sleep problems and overall sleep quality, on the other hand. Results show that, even in the absence of an actual call, sleep during on‐call nights is of lower quality and has less restorative value – especially when being on‐call is experienced as stressful.     

Cardiac autonomic activity during daytime nap in young adults

The current study investigated both sympathetic and vagal autonomic patterns during a daytime sleep in 25 healthy adults (23.2 ± 2.4 years). Pre‐ejection period (PEP; related inversely to beta‐adrenergic sympathetic activity), the interval between consecutive R‐waves (RR) and frequency‐domain heart rate variability (HRV) were computed during pre‐nap wakefulness and undisturbed sleep stages. Results showed sleep‐related changes in RR and HRV measures, whereas PEP decreased significantly from pre‐nap to sleep, showing no differences across sleep stages. Moreover, pre‐nap PEP and HFnu (the normalized unit of the high‐frequency component of HRV) were associated negatively with sleep latency and wake after sleep onset. These results indicate a marked autonomic output reduction during daytime sleep, with different stage‐dependent fluctuations for sympathetic and vagal activity. Importantly, pre‐nap autonomic activity seems to modulate subsequent sleep quality.     

Slow oscillating transcranial direct current stimulation during sleep has a sleep‐stabilizing effect in chronic insomnia: a pilot study

Recent evidence suggests that lack of slow‐wave activity may play a fundamental role in the pathogenesis of insomnia. Pharmacological approaches and brain stimulation techniques have recently offered solutions for increasing slow‐wave activity during sleep. We used slow (0.75 Hz) oscillatory transcranial direct current stimulation during stage 2 of non‐rapid eye movement sleeping insomnia patients for resonating their brain waves to the frequency of sleep slow‐wave. Six patients diagnosed with either sleep maintenance or non‐restorative sleep insomnia entered the study. After 1 night of adaptation and 1 night of baseline polysomnography, patients randomly received sham or real stimulation on the third and fourth night of the experiment. Our preliminary results show that after termination of stimulations (sham or real), slow oscillatory transcranial direct current stimulation increased the duration of stage 3 of non‐rapid eye movement sleep by 33 ± 26 min (P = 0.026), and decreased stage 1 of non‐rapid eye movement sleep duration by 22 ± 17.7 min (P = 0.028), compared with sham. Slow oscillatory transcranial direct current stimulation decreased stage 1 of non‐rapid eye movement sleep and wake time after sleep‐onset durations, together, by 55.4 ± 51 min (P = 0.045). Slow oscillatory transcranial direct current stimulation also increased sleep efficiency by 9 ± 7% (P = 0.026), and probability of transition from stage 2 to stage 3 of non‐rapid eye movement sleep by 20 ± 17.8% (P = 0.04). Meanwhile, slow oscillatory transcranial direct current stimulation decreased transitions from stage 2 of non‐rapid eye movement sleep to wake by 12 ± 6.7% (P = 0.007). Our preliminary results suggest a sleep‐stabilizing role for the intervention, which may mimic the effect of sleep slow‐wave‐enhancing drugs.     

EEG predictors of dreaming outside of REM sleep

The stream of human consciousness persists during sleep, albeit in altered form. Disconnected from external input, the mind and brain remain active, at times creating the bizarre sequences of thought and imagery that comprise “dreaming.” Yet despite substantial effort toward understanding this unique state of consciousness, no reliable neurophysiological indicator of dreaming has been discovered. Here, we identified electroencephalographic (EEG) correlates of dreaming using a within‐subjects design to characterize the EEG preceding awakenings from sleep onset, REM (rapid eye movement) sleep, and N2 (NREM Stage 2) sleep from which participants were asked to report their mental experience. During the transition into sleep, compared to periods during which participants reported thinking, emergence of dream imagery was associated with increased absolute power below 7 Hz. During later N2, dreaming conversely occurred during periods of decreased relative power below 1 Hz, accompanied by an increase in relative power above 4 Hz. No EEG predictors of dreaming were identified during REM. These observations suggest an inverted‐U relationship between dreaming and the prevalence of low‐frequency EEG rhythms, such that dreaming first emerges in concert with EEG slowing during the sleep‐wake transition, but then disappears as high‐amplitude slow oscillations come to dominate the recording during later N2 sleep.     

Sleep inertia,sleep homeostatic and circadian influences on higher‐order cognitive functions

Sleep inertia, sleep homeostatic and circadian processes modulate cognition, including reaction time, memory, mood and alertness. How these processes influence higher‐order cognitive functions is not well known. Six participants completed a 73‐day‐long study that included two 14‐day‐long 28‐h forced desynchrony protocols to examine separate and interacting influences of sleep inertia, sleep homeostasis and circadian phase on higher‐order cognitive functions of inhibitory control and selective visual attention. Cognitive performance for most measures was impaired immediately after scheduled awakening and improved during the first ~2–4 h of wakefulness (decreasing sleep inertia); worsened thereafter until scheduled bedtime (increasing sleep homeostasis); and was worst at ~60° and best at ~240° (circadian modulation, with worst and best phases corresponding to ~09:00 and ~21:00 hours, respectively, in individuals with a habitual wake time of 07:00 hours). The relative influences of sleep inertia, sleep homeostasis and circadian phase depended on the specific higher‐order cognitive function task examined. Inhibitory control appeared to be modulated most strongly by circadian phase, whereas selective visual attention for a spatial‐configuration search task was modulated most strongly by sleep inertia. These findings demonstrate that some higher‐order cognitive processes are differentially sensitive to different sleep–wake regulatory processes. Differential modulation of cognitive functions by different sleep–wake regulatory processes has important implications for understanding mechanisms contributing to performance impairments during adverse circadian phases, sleep deprivation and/or upon awakening from sleep.     

Cardiovascular autonomic dysfunction in insomnia patients with objective short sleep duration

Two phenotypes have been proposed: insomnia with objective near‐normal sleep duration, related to increased psychological symptoms, and insomnia with objective short sleep duration, associated with cardiometabolic morbidity. Reduced heart rate variability has also been implicated in the pathophysiology of cardiometabolic disease; however, there are little data on whether cardiovascular function differs between patients with objective short sleep duration and near‐normal sleep duration. Participants (M_age = 49.9 ± 11.3 years; 62.8% female) were 180 adults with chronic insomnia (M_duration = 15.7 ± 13.6). Objective sleep duration was based on total sleep time averaged across two consecutive nights of polysomnography and subjective sleep duration was based on 2‐week sleep diaries. The sample was divided into two groups, with sleep duration shorter (polysomnography‐total sleep time: n = 46; sleep diary: n = 95) or equal/longer (polysomnography‐total sleep time: n = 134; sleep diary: n = 85) than 6 hr. Electrocardiogram data derived from polysomnography were used to obtain heart rate and heart rate variability during stage 2 (N2) and rapid eye movement sleep. Heart rate variability measures included absolute and normalized high‐frequency component, an index of parasympathetic activation, and the ratio of low‐ to high‐frequency (LF/HF ratio), an index of sympathovagal balance. After controlling for covariates (e.g., co‐morbidity), patients with objective short sleep duration had reduced high‐frequency (p < .05) and elevated low‐frequency/high‐frequency ratio (p = .036) and heart rate (p = .051) compared with patients with near‐normal sleep duration. No differences were observed between phenotypes when subjective sleep duration was used. Insomnia patients with objective short sleep duration showed significantly dampened parasympathetic activation and increased sympathovagal imbalance relative to their counterparts with near‐normal sleep duration. These findings highlight the importance of treating insomnia, as treatment may reduce the risk of cardiovascular disease.     

Validity,potential clinical utility,and comparison of consumer and research‐grade activity trackers in Insomnia Disorder I: In‐lab validation against polysomnography

Consumer activity trackers claiming to measure sleep/wake patterns are ubiquitous within clinical and consumer settings. However, validation of these devices in sleep disorder populations are lacking. We examined 1 night of sleep in 42 individuals with insomnia (mean = 49.14 ± 17.54 years) using polysomnography, a wrist actigraph (Actiwatch Spectrum Pro: AWS) and a consumer activity tracker (Fitbit Alta HR: FBA). Epoch‐by‐epoch analysis and Bland?Altman methods evaluated each device against polysomnography for sleep/wake detection, total sleep time, sleep efficiency, wake after sleep onset and sleep latency. FBA sleep stage classification of light sleep (N1 + N2), deep sleep (N3) and rapid eye movement was also compared with polysomnography. Compared with polysomnography, both activity trackers displayed high accuracy (81.12% versus 82.80%, AWS and FBA respectively; ns) and sensitivity (sleep detection; 96.66% versus 96.04%, respectively; ns) but low specificity (wake detection; 39.09% versus 44.76%, respectively; p = .037). Both trackers overestimated total sleep time and sleep efficiency, and underestimated sleep latency and wake after sleep onset. FBA demonstrated sleep stage sensitivity and specificity, respectively, of 79.39% and 58.77% (light), 49.04% and 95.54% (deep), 65.97% and 91.53% (rapid eye movement). Both devices were more accurate in detecting sleep than wake, with equivalent sensitivity, but statistically different specificity. FBA provided equivalent estimates as AWS for all traditional actigraphy sleep parameters. FBA also showed high specificity when identifying N3, and rapid eye movement, though sensitivity was modest. Thus, it underestimates these sleep stages and overestimates light sleep, demonstrating more shallow sleep than actually obtained. Whether FBA could serve as a low‐cost substitute for actigraphy in insomnia requires further investigation.     

Association between objective sleep measures and cognitive performance: a cross-sectional analysis in the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil) study

Sleep disturbances often co-exist, which challenges our understanding of their potential impact on cognition. We explored the cross-sectional associations of insomnia and objective measures of sleep with cognitive performance in the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil) study stratified by middle-aged and older adults. Participants aged ≥55 years underwent cognitive evaluations, polygraphy for 1 night, and actigraphy for 7 days. Insomnia was evaluated using the Clinical Interview Scheduled Revised. Obstructive sleep apnea (OSA) and short sleep duration (SSD) were defined by an apnea–hypopnea index (AHI) of ≥15 events/h and <6 h/ night, respectively. In 703 participants (mean [SD] age 62 [6] years, 44% men), cognition was evaluated using a 10-word list, verbal fluency, and trail-making tests. The frequencies of insomnia, SSD, and OSA were 11%, 24%, and 33%, respectively. In all, 4% had comorbid OSA and insomnia, and 11% had both OSA and SSD. Higher wake after sleep onset (β = −0.004, 95% confidence interval [CI] −0.008, −0.001) and the number of awakenings (β = −0.006, 95% CI −0.012, −0.001) were associated with worse verbal fluency performance. Compared to those without insomnia, older participants with insomnia had worse global performance (β = −0.354, 95% CI −0.671, −0.038). Insomnia was an effect modifier in the associations between AHI and executive function performance (p for the interaction between insomnia and AHI = 0.004) and between oxygen saturation <90% and memory performance (p for the interaction between insomnia and oxygen saturation = 0.02). Although some associations between sleep measures and cognition were significant, they should be considered with caution due to the large sample size and multiple testing performed in this study.     

Dynamic daily associations between insomnia symptoms and alcohol use in adults with chronic pain

Individuals with chronic pain are at risk for sleep disruption and heavy alcohol use, yet the daily associations between these behaviours are not well characterized. This study aimed to determine the extent to which alcohol use affects insomnia symptoms and vice versa in adults reporting symptoms of chronic pain. Participants were 73 individuals (93% women) reporting alcohol use in addition to symptoms of insomnia and chronic pain. They completed daily diaries assessing insomnia symptoms and alcohol use for 14 days. Multilevel modelling was used to evaluate the bidirectional associations between alcohol use and insomnia symptoms at the daily level. Consistent with laboratory‐based research, alcohol use was associated with decreased sleep‐onset latency the same night but increased sleep‐onset latency 2 nights later. Specifically, for every alcoholic drink consumed, time to sleep onset decreased by 5.0 min in the same night but increased by 4.3 min 2 nights later. Alcohol use was not significantly associated with subsequent wake after sleep onset or total sleep time, and insomnia symptoms were not significantly associated with subsequent alcohol use. To our knowledge, these data provide the first evidence that alcohol use negatively affects insomnia symptoms up to 2 days post‐consumption in patients reporting symptoms of insomnia and chronic pain. Findings suggest that one drink will have minimal impact on sleep, but heavier drinking (e.g. four–five drinks) may have a clinically significant impact (16–25‐min increase in sleep‐onset latency). Future studies may assess alcohol use as a point of intervention within this population.