Daytime continuous polysomnography predicts MSLT results in hypersomnias of central origin

In the diagnostic work‐up of hypersomnias of central origin, the complaint of excessive daytime sleepiness should be objectively confirmed by MSLT findings. Indeed, the features and diagnostic utility of spontaneous daytime sleep at 24 h continuous polysomnography (PSG) have never been investigated. We compared daytime PSG features to MSLT data in 98 consecutive patients presenting with excessive daytime sleepiness and with a final diagnosis of narcolepsy with cataplexy/hypocretin deficiency (n = 39), narcolepsy without cataplexy (n = 7), idiopathic hypersomnia without long sleep time (n = 19), and ‘hypersomnia’ with normal sleep latency at MSLT (n = 33). Daytime sleep time was significantly higher in narcolepsy‐cataplexy but similar in the other groups. Receiver operating characteristics (ROC) curves showed that the number of naps during daytime PSG predicted a mean sleep latency ≤8 min at MSLT with an area under the curve of 0.67 ± 0.05 (P = 0.005). The number of daytime sleep‐onset REM periods (SOREMPs) in spontaneous naps strikingly predicted the scheduled occurrence of two or more SOREMPs at MSLT, with an area under the ROC curve of 0.93 ± 0.03 (P < 10^?12). One spontaneous SOREMP during daytime had a sensitivity of 96% with specificity of 74%, whereas two SOREMPs had a sensitivity of 75%, with a specificity of 95% for a pathological REM sleep propensity at MSLT. The features of spontaneous daytime sleep well correlated with MSLT findings. Notably, the occurrence of multiple spontaneous SOREMPs during daytime clearly identified patients with narcolepsy, as well as during the MSLT.     

Case-control study of subjective and objective differences in sleep patterns in older adults with insomnia symptoms

Older adults have high prevalence rates of insomnia symptoms, yet it is unclear if these insomnia symptoms are associated with objective impairments in sleep. We hypothesized that insomnia complaints in older adults would be associated with objective differences in sleep compared with those without insomnia complaints. To test this hypothesis, we conducted a cross‐sectional study in which older adults with insomnia complaints (cases, n = 100) were compared with older adults without insomnia complaints (controls, n = 100) using dual‐night in‐lab nocturnal polysomnography, study questionnaires and 7 days of at‐home actigraphy and sleep diaries. Cases were noted to have reduced objective total sleep time compared with controls (25.8 ± 8.56 min, P = 0.003). This was largely due to increased wakefulness after sleep onset, and not increased sleep latency. When participants with sleep‐related breathing disorder or periodic limb movement disorder were excluded, the polysomnography total sleep time difference became even larger. Cases also had reduced slow‐wave sleep (5.10 ± 1.38 min versus 10.57 ± 2.29 min, effect size −0.29, P = 0.04). When comparing self‐reported sleep latency and sleep efficiency with objective polysomnographic findings, cases demonstrated low, but statistically significant correlations, while no such correlations were observed in controls. Cases tended to underestimate their sleep efficiency by 1.6% (±18.4%), while controls overestimated their sleep efficiency by 12.4% (±14.5%). In conclusion, we noted that older adults with insomnia complaints have significant differences in several objective sleep findings relative to controls, suggesting that insomnia complaints in older adults are associated with objective impairments in sleep.     

CBT for late‐life insomnia and the accuracy of sleep and wake perceptions: Results from a randomized‐controlled trial

Subjective and objective estimates of sleep are often discordant among individuals with insomnia who typically under‐report sleep time and over‐report wake time at night. This study examined the impact and durability of cognitive‐behavioural therapy for insomnia on improving the accuracy of sleep and wake perceptions in older adults, and tested whether changes in sleep quality were related to changes in the accuracy of sleep/wake perceptions. One‐hundred and fifty‐nine older veterans (97% male, mean age 72.2 years) who met diagnostic criteria for insomnia disorder were randomized to: (1) cognitive‐behavioural therapy for insomnia (n = 106); or (2) attention control (n = 53). Assessments were conducted at baseline, post‐treatment, 6‐months and 12‐months follow‐up. Sleep measures included objective (via wrist actigraphy) and subjective (via self‐report diary) total sleep time and total wake time, along with Pittsburgh Sleep Quality Index score. Discrepancy was computed as the difference between objective and subjective estimates of wake and sleep. Minutes of discrepancy were compared between groups across time, as were the relationships between Pittsburgh Sleep Quality Index scores and subsequent changes in discrepancy. Compared with controls, participants randomized to cognitive‐behavioural therapy for insomnia became more accurate (i.e. minutes discrepancy was reduced) in their perceptions of sleep/wake at post‐treatment, 6‐months and 12‐months follow‐up (p < .05). Improved Pittsburgh Sleep Quality Index scores at each study assessment preceded and predicted reduced discrepancy at the next study assessment (p < .05). Cognitive‐behavioural therapy for insomnia reduces sleep/wake discrepancy among older adults with insomnia. The reductions may be driven by improvements in sleep quality. Improving sleep quality appears to be a viable path to improving sleep perception and may contribute to the underlying effectiveness of cognitive‐behavioural therapy for insomnia.     

Comparison of actigraphy with polysomnography and sleep logs in depressed insomniacs

Actigraphy is increasingly used in the assessment and treatment of various clinical conditions, being a convenient and cost‐effective method of capturing bodily movements over long periods of time. This study examined the use of actigraphy in the measurement of sleep of patients with depression and insomnia. Fifty‐four patients diagnosed with a current major depressive episode and chronic insomnia underwent a baseline overnight study with concurrent actigraphic and polysomnography (PSG) monitoring, as well as subjective sleep diaries. Agreement between PSG, actigraphy and sleep diary measurements was evaluated using two‐tailed t‐tests, Pearson’s correlations and the Bland–Altman concordance technique. The only significant difference found between actigraphy and PSG was in latency to persistent sleep, in which actigraphy underestimated sleep latency relative to PSG (P < 0.05). There were moderate positive correlations between actigraphy and PSG for all variables. In contrast, significant differences were observed between sleep diaries and PSG for all sleep variables. Bland–Altman concordance diagrams also demonstrated that, while bias was limited between PSG and the other two measurement types, there were somewhat broad 95% limits of agreement for all sleep variables with both sleep diaries and actigraphy. In summary, actigraphic measurements of sleep more closely approximated those of PSG than did sleep diaries in this sample of depressed insomniacs.     

Is a polysomnographic recording prior to MSLT worth the effort?

Objective

It was recently proposed that polysomnography (PSG) may be replaced by actigraphy in order to obtain long-term sleep time prior to the multiple sleep latency test (MSLT). Polysomnography is used to assess sleep time and to detect and classify underlying sleep pathology. In the following article, the contribution of PSG to the diagnostic outcome of the MSLT is discussed.

Methods

MSLT referrals (n?=?81) with in-home polysomnography from the neurology (n?=?39, 23 women, 37 (±13) years) and pulmonary medicine (n?=?42, 20 women, 41 (±14) years) departments were analyzed. The diagnostic outcomes of the PSG and MSLT were examined.

Results

Median total sleep time prior to MSLT was 362 (range, 156–530) min. Sleep apnea (respiratory disturbance index >?15/h and >?30/h) was diagnosed in 21 and 19 patients, respectively. Periodic limb movements (PLM) were identified in 5 patients; 3 of these had a PLM arousal index >?5/h. Sleep onset REM (SOREM) was detected during PSG in 5 patients; 4 of these also had SOREM in the MSLT.

Conclusion

PSG combined with MSLT was found to improve diagnostic outcome and is highly useful for recognition of sleep-related pathology. Various sleep disorders remain undetected if ACT alone is used prior to MSLT procedures.     

Sleep hygiene and actigraphically evaluated sleep characteristics in children with ADHD and chronic sleep onset insomnia

In the present study we investigated sleep hygiene and actigraphically evaluated sleep in 74 medication‐naïve children, aged 6–12 years, with rigorously diagnosed attention‐deficit/hyperactivity disorder (ADHD) and chronic sleep onset insomnia (ADHD‐SOI) and 23 ADHD controls without insomnia (ADHD‐noSOI). Between‐group differences were analysed for lights out (sleep log), actigraphically evaluated sleep onset, sleep latency, total sleep duration, actual sleep time and sleep hygiene as measured with the Children's Sleep Hygiene Scale. We found a significant difference (P < 0.001) in mean (±SD) sleep onset between the ADHD‐SOI group (21:49 ± 0:56 h) and ADHD‐noSOI groups (20:41 ± 0:45 h). Sleep latency was significantly (P < 0.001) longer in ADHD‐SOI (00:53 ± 0:25 h) compared to ADHD‐noSOI (00:26 ± 0:25 h). The difference in total sleep duration between ADHD‐SOI (9:42 ± 0:44 h) and ADHD‐noSOI (10:09 ± 0:43 h) was not significantly different (P = 0.18). The group difference in actual sleep time was also not significant (8:43 ± 0:52 h in ADHD‐SOI versus 9:13 ± 1:16 h; P = 0.40). There was no significant difference (P = 0.17) in mean (±SD) total sleep hygiene score between the ADHD‐SOI (56.4 ± 10.5) and ADHD‐noSOI groups (53.0 ± 10.6). We conclude that there were differences in sleep onset and sleep latency in ADHD children with chronic SOI and those without insomnia; however, sleep hygiene practices were similar and did not relate to sleep characteristics.     

The exploratory power of sleep effort,dysfunctional beliefs and arousal for insomnia severity and polysomnography‐determined sleep

Differences between subjective sleep perception and sleep determined by polysomnography (PSG) are prevalent, particularly in patients with primary insomnia, indicating that the two measures are partially independent. To identify individualized treatment strategies, it is important to understand the potentially different mechanisms influencing subjective and PSG‐determined sleep. The aim of this study was to investigate to what extent three major components of insomnia models, i.e. sleep effort, dysfunctional beliefs and attitudes about sleep, and presleep arousal, are associated with subjective insomnia severity and PSG‐ determined sleep. A sample of 47 patients with primary insomnia according to DSM‐IV criteria and 52 good sleeper controls underwent 2 nights of PSG and completed the Glasgow Sleep Effort Scale, the Dysfunctional Beliefs and Attitudes about Sleep Scale, the Pre‐Sleep Arousal Scale and the Insomnia Severity Index. Regression analyses were conducted to investigate the impact of the three predictors on subjective insomnia severity and PSG‐ determined total sleep time. All analyses were adjusted for age, gender, depressive symptoms and group status. The results showed that subjective insomnia severity was associated positively with sleep effort. PSG‐determined total sleep time was associated negatively with somatic presleep arousal and dysfunctional beliefs and attitudes about sleep. This pattern of results provides testable hypotheses for prospective studies on the impact of distinct cognitive and somatic variables on subjective insomnia severity and PSG‐determined total sleep time.     

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.     

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.     

Relation between ambulatory actigraphy and laboratory polysomnography in insomnia practice and research

Actigraphy is increasingly used in practice and research studies because of its relative low cost and decreased subject burden. How multiple nights of at‐home actigraphy compare to one independent night of in‐laboratory polysomnography (PSG) has not been examined in people with insomnia. Using event markers (MARK) to set time in bed (TIB) compared to automatic program analysis (AUTO) has not been systematically evaluated. Subjects (n = 30) meeting DSM‐5 criteria for insomnia and in‐laboratory PSG sleep efficiency (SE) of <85% were studied. Subjects were free of psychiatric, sleep or circadian disorders, other chronic conditions and medications that effect sleep. Subjects had an in‐laboratory PSG, then were sent home for 7 nights with Philips Actiwatch Spectrum Plus. Data were analysed using Philips Actiware version 6. Using the mean of seven nights, TIB, total sleep time (TST), SE, sleep‐onset latency (SOL) and wake after sleep onset (WASO) were examined. Compared to PSG, AUTO showed longer TIB and TST and less WASO. MARK only differed from PSG with decreased WASO. Differences between the PSG night and the following night at home were found, with better sleep on the first night home. Actigraphy in people with insomnia over seven nights is a valid indicator of sleep compared to an independent in‐laboratory PSG. Event markers increased the validity of actigraphy, showing no difference in TIB, TST, SE and SOL. AUTO was representative of SE and SOL. Increased SE and TST without increased TIB suggests possible compensatory sleep the first at night home after in‐laboratory PSG.     

A randomized controlled trial of bedtime music for insomnia disorder

Music is often used as a self‐help tool to alleviate insomnia. To evaluate the effect of bedtime music listening as a strategy for improving insomnia, we conducted an assessor‐blinded randomized controlled trial. Fifty‐seven persons with insomnia disorder were included and randomized to music intervention (n = 19), audiobook control (n = 19) or a waitlist control group (n = 19). The primary outcome measure was the Insomnia Severity Index. In addition, we used polysomnography and actigraphy to evaluate objective measures of sleep, and assessed sleep quality and quality of life. The results showed no clear effect of music on insomnia symptoms as the group × time interaction only approached significance (effect size = 0.71, p = .06), though there was a significant improvement in insomnia severity within the music group. With regard to the secondary outcomes, we found a significant effect of the music intervention on perceived sleep improvement and quality of life, but no changes in the objective measures of sleep. In conclusion, music listening at bedtime appears to have a positive impact on sleep perception and quality of life, but no clear effect on insomnia severity. Music is safe and easy to administer, but further research is needed to assess the effect of music on different insomnia subtypes, and as an adjunctive or preventive intervention.     

Correlations among Epworth Sleepiness Scale scores, multiple sleep latency tests and psychological symptoms

The aim of this study was to identify factors other than objective sleep tendency associated with scores on the Epworth Sleepiness Scale (ESS). There were 225 subjects, of whom 40% had obstructive sleep apnoea (OSA), 16% had simple snoring, and 4.9% had snoring with sleep disruption (upper airway resistance syndrome); 9.3% had narcolepsy and 7.5% had hypersomnolence without REM sleep abnormalities; 12% had chronic fatigue syndrome; 7.5% had periodic limb movement disorder and 3% had diurnal rhythm disorders. ESS, the results of overnight polysomnography and multiple sleep latency test (MSLT) and SCL-90 as a measure of psychological symptoms were recorded. The ESS score and the mean sleep latency (MSL) were correlated (Spearman ö =−0.30, P <0.0001). The MSL was correlated with total sleep time (TST) and with sleep efficiency but not with apnoea/hypopnoea index. There was no association between the MSL and any aspect of SCL-90 scores, except a borderline significant association with the somatisation subscale. The ESS was correlated with TST but not with sleep efficiency or apnoea/hypopnoea index. The ESS was correlated with all subscales of the SCL-90 except psychoticism. An ESS≥10 had poor sensitivity and specificity as a predictor of MSL <10 min or MSL <5 min. We conclude that the MSLT and the ESS are not interchangeable. The ESS was influenced by psychological factors by which the MSL was not affected. The ESS cannot be used to demonstrate or exclude sleepiness as it is measured by MSLT.     

Toddler's self‐regulation strategies in a challenge context are nap‐dependent

Early childhood represents a time of developmental changes in both sleep and self‐regulation, a construct reflecting the ability to control one's behaviour, attention and emotions when challenged. Links between sleep and self‐regulation processes have been proposed, but experimental evidence with young children is lacking. In the current study, we tested the effects of acute sleep restriction (nap deprivation) on toddlers’ self‐regulation. Healthy children (n = 12; four males; aged 30–36 months (33.9 ± 1.7)) slept on a strict schedule (verified with actigraphy and sleep diaries) for 5 days before each of two afternoon assessments following a nap and a no‐nap condition (~11‐day protocol). Children were videotaped while attempting an unsolvable puzzle, and 10 mutually exclusive self‐regulation strategies were later coded. On average, children lost ~90 min of sleep on the no‐nap versus the nap day. Nap deprivation resulted in moderate‐to‐large effects on self‐regulation strategies, with decreases in scepticism (d = 0.77; 7% change), negative self‐appraisal (d = 0.92; 5% change) and increases in physical self‐soothing (d = 0.68; 10% change), focus on the puzzle piece that would not fit (perseveration; d = 0.50; 9% change) and insistence on completing the unsolvable puzzle (d = 0.91; 10% change). Results suggest that sleep serves an important role in the way that toddlers respond to challenging events in their daily lives. After losing daytime sleep, toddlers were less able to engage effectively in a difficult task and reverted to less mature self‐regulation strategies than when they were well rested. Over time, chronically missed sleep may impair young children's self‐regulation abilities, resulting in risk for social–emotional, behavioural and school problems.     

Pulse transit time as a surrogate measure of changes in systolic arterial pressure in children during sleep

Pulse transit time has been proposed as a surrogate measure of systolic arterial pressure, as it is dependent upon arterial stiffness. Past research has shown that pulse transit time has a significant inverse relationship to systolic arterial pressure in adults; however, studies in children are limited. This study aimed to explore the relationship between systolic arterial pressure and pulse transit time in children during sleep. Twenty‐five children (13.1 ± 1.6 years, 48% male) underwent overnight polysomnography (PSG) with a simultaneous recording of continuous systolic arterial pressure and photoplethysmography. Pulse transit time was calculated as the time delay between the R‐wave peak of the electrocardiogram (ECG) to the 50% point of the upstroke of the corresponding photoplethysmography waveform; 500 beats of simultaneous systolic arterial pressure and pulse transit time were analysed in each sleep stage for each child. Pulse transit time was normalized to each subject's mean wake pulse transit time. The ability of pulse transit time to predict systolic arterial pressure change was determined by linear mixed‐effects modelling. Significant negative correlations between pulse transit time and systolic arterial pressure were found for individual children for each sleep stage [mean correlations for cohort: non‐rapid eye movement (NREM) sleep 1 and 2 r = ?0.57, slow wave sleep (SWS) r = ?0.76, REM r = ?0.65, P < 0.01 for all]. Linear mixed‐model analysis demonstrated that changes in pulse transit time were a significant predictor of changes in systolic arterial pressure for each sleep stage (P < 0.001). The model of pulse transit time‐predicted systolic arterial pressure closely tracked actual systolic arterial pressure changes over time. This study demonstrated that pulse transit time was accurate in tracking systolic arterial pressure changes over time. Thus, the use of pulse transit time as a surrogate measure of changes in systolic arterial pressure in children is a valid, non‐invasive and inexpensive method with many potential applications.     

Internight sleep variability: its clinical significance and responsiveness to treatment in primary and comorbid insomnia

Although sleep diary and actigraphy data are usually collected daily for 1 or 2 weeks, traditional analytical approaches aggregate these data into mean values. Internight variability of sleep often accompanies insomnia. However, few studies have explored the relevance of this ‘construct’ in the context of diagnosis, clinical impact, treatment effects and/or whether having ‘variable sleep’ carries any prognostic significance. We explored these questions by conducting secondary analyses of data from a randomized clinical trial. The sample included primary (PI: n = 40) and comorbid insomnia (CMI: n = 41) sufferers receiving four biweekly sessions of cognitive–behavioural therapy (CBT) or sleep hygiene education. Using the within‐subject standard deviations of diary‐ and actigraphy‐derived measures collected for 2‐week periods [sleep onset latency (SOL), wake after sleep onset (WASO), total sleep time (TST) and sleep efficiency (SE)], we found that CMI sufferers displayed more variable self‐reported SOLs and SEs than PI sufferers. However, higher variability in diary and actigraphy‐derived measures was related to poorer sleep quality only within the PI group, as measured by the Pittsburgh Sleep Quality Index (PSQI). Within both groups, the variability of diary‐derived measures was reduced after CBT, but the variability of actigraphy‐derived measures remained unchanged. Interestingly, the variability of actigraphy measures at baseline was correlated with PSQI scores at 6‐month follow‐up. Higher SOL variability was associated with worse treatment outcomes within the PI group, whereas higher WASO variability was correlated with better treatment outcomes within the CMI group. Sleep variability differences across insomnia diagnoses, along with their distinctive correlates, suggest that mechanisms underlying the sleep disruption/complaint and treatment response in both patient groups are distinct. Further studies are warranted to support variability as a useful metric in insomnia studies.     

Calibrating actigraphy to improve sleep efficiency estimates

Actigraphy (ACT) can enhance treatment for insomnia by providing objective estimates of sleep efficiency; however, only two studies have assessed the accuracy of actigraphy‐based estimates of sleep efficiency (ACT‐SE) in sleep‐disordered samples studied at home. Both found poor correspondence with polysomnography‐based estimates (PSG‐SE). The current study tested that concordance in a third sample and piloted a method for improving ACT‐SE. Participants in one of four diagnostic categories (panic disorder, post‐traumatic stress disorder, comorbid post‐traumatic stress and panic disorder and controls without sleep complaints) underwent in‐home recording of sleep using concurrent ambulatory PSG and actigraphy. Precisely synchronized PSG and ACT recordings were obtained from 41 participants. Sleep efficiency was scored independently using conventional methods, and ACT‐SE/PSG‐SE concordance examined. Next, ACT data recorded initially at 0.5 Hz were resampled to 30‐s epochs and rescaled on a per‐participant basis to yield optimized concordance between PSG‐ and ACT‐based sleep efficiency estimates. Using standard scoring of ACT, the correlation between ACT‐SE and PSG‐SE across participants was statistically significant (r = 0.35, P < 0.025), although ACT‐SE failed to replicate a main effect of diagnosis. Individualized calibration of ACT against a night of PSG yielded a significantly higher correlation between ACT‐SE and PSG‐SE (r = 0.65, P < 0.001; z = 1.692, P = 0.0452, one‐tailed) and a significant main effect of diagnosis that was highly correspondent with the effect on PSG‐SE. ACT‐based estimates of sleep efficiency in sleep‐disordered patients tested at home can be improved significantly by calibration against a single night of concurrent PSG.     

Am I (hyper)aroused or anxious? Clinical significance of pre‐sleep somatic arousal in young adults

Self‐reported somatic arousal remains a challenging clinical construct, particularly because only a subset of patients report symptoms such as racing heart, palpitations or increased body temperature interfering with their sleep. It is unclear whether self‐reported somatic arousal is a marker of hyperarousal or co‐morbid clinical anxiety in individuals with insomnia. Participants included 196 young adults aged 20.2 ± 1.0 years old who were predominantly females (75%). About 39% of the sample reported subthreshold insomnia, and about 8% reported clinically significant insomnia, based on their Insomnia Severity Index. Participants completed the Pre‐Sleep Arousal Scale, Beck Anxiety Inventory, Beck Depression Inventory, Arousal Predisposition Scale, and Ford Insomnia Response to Stress Test. Multivariable stepwise regression assessed which factors were independently associated with pre‐sleep cognitive (Pre‐Sleep Arousal Scale‐Cognitive) and somatic (Pre‐Sleep Arousal Scale‐Somatic) arousal. Receiver‐operating characteristic analysis assessed the predictive value to identify clinically significant anxiety (Beck Anxiety Inventory ≥ 20), insomnia (Insomnia Severity Index ≥ 15) and arousability (Arousal Predisposition Scale ≥ 32). Beck Anxiety Inventory (β = 0.42) was the best single correlate of Pre‐Sleep Arousal Scale‐Somatic, while Insomnia Severity Index (β = 0.33) was of Pre‐Sleep Arousal Scale‐Cognitive. A Pre‐Sleep Arousal Scale‐Somatic score of 12 or more identified those with clinically significant anxiety with 65% specificity and 65% sensitivity, while a cut‐off score of 14 increased its sensitivity (86%). Self‐reported pre‐sleep somatic arousal may be an index of co‐morbid clinical anxiety in individuals with insomnia. These findings aid clinicians with assessment and treatment, particularly in the absence of clinical guidelines indicating when somatically focused relaxation techniques should be included as part of multicomponent cognitive behavioural treatment of insomnia.     

Does age worsen sleep‐dependent memory consolidation?

Slow wave sleep (SWS) is known to favour episodic memory consolidation. Given that ageing is associated with a reduction in SWS and episodic memory impairment, our aim was to investigate whether memory continues to benefit from sleep in older adults. Episodic memory consolidation was tested in 20 young (22.1 ± 1.7 years) and 20 older volunteers (68.9 ± 5.3 years) who performed a visuospatial two‐dimensional object‐location task. Retention capacities were evaluated after 12 h of wakefulness or 12 h of sleep. Performances before and after the interval allowed us to calculate a forgetting rate. Sleep architecture was measured by polysomnography (older adults = 410 min; young adults: 467 min). Our results showed that the beneficial effect of sleep on memory consolidation was reduced in older adults compared to young adults. In older adults, sleep did not enhance memory consolidation significantly compared to wakefulness. Sleep prevented young adults from forgetting (?0.10% ± 2.1), while the forgetting rate in older adults was still important after a period of sleep (16.60% ± 4.2; P = 0.05). The sleep architecture of older adults was characterized by a decrease in sleep efficiency (?12%; P < 0.05), in total cycle time (?137 min; P < 0.05), in percentage of total cycle time (?21%; P < 0.05) and in rapid eye movement time (?41 min; P < 0.05) compared to young adults. However, no difference in slow wave sleep was observed (?1%; not significant) and no correlation was found with performance. Age‐related changes in sleep parameters may have a negative impact on memory consolidation in older adults.     

Validity,potential clinical utility and comparison of a consumer activity tracker and a research‐grade activity tracker in insomnia disorder II: Outside the laboratory

Accurate assessment of sleep can be fundamental for monitoring, managing and evaluating treatment outcomes within diseases. A proliferation of consumer activity trackers gives easy access to objective sleep. We evaluated the performance of a commercial device (Fitbit Alta HR) relative to a research‐grade actigraph (Actiwatch Spectrum Pro) in measuring sleep before and after a cognitive behavioural intervention in insomnia disorder. Twenty‐five individuals with DSM‐5 insomnia disorder (M = 50.6 ± 15.9 years) wore Fitbit and Actiwatch and completed a sleep diary during an in‐laboratory polysomnogram, and for 1 week preceding and following seven weekly sessions of cognitive‐behavioural intervention for insomnia. Device performance was compared for sleep outcomes (total sleep time, sleep latency, sleep efficiency and wake after sleep onset). The analyses assessed (a) agreement between devices across days and pre‐ to post‐treatment, and (b) whether pre‐ to post‐treatment changes in sleep assessed by devices correlated with clinical measures of change. Devices generally did not significantly differ from each other on sleep variable estimates, either night to night, in response to sleep manipulation (pre‐ to post‐treatment) or in response to changes in environment (in the laboratory versus at home). Change in sleep measures across time from each device showed some correlation with common clinical measures of change in insomnia, but not insomnia diagnosis as a categorical variable. Overall, the Fitbit provides similar estimates of sleep outside the laboratory to a research grade actigraph. Despite the similarity between Fitbit and Actiwatch performance, the use of consumer technology is still in its infancy and caution should be taken in its interpretation.     

The effect of acute exposure to morphine on breathing variability and cardiopulmonary coupling in men with obstructive sleep apnea: A randomized controlled trial

Opioid‐related deaths from respiratory depression are increasing but there is only limited information on the effect of morphine on breathing during sleep. This study aimed to detect and quantify opioid‐induced cardiorespiratory pattern changes during sleep in obstructive sleep apnea (OSA) patients using novel automated methods and correlate these with conventional polysomnography (PSG) measures. Under a randomized double‐blind placebo‐controlled crossover design, 60 male OSA patients attended two one‐night visits to the sleep laboratory, at least a week apart. Either a 40‐mg controlled‐release oral morphine dose or placebo was administered. Breathing during sleep was measured by standard in‐laboratory PSG. We analysed the inter‐breath interval (IBI) from the PSG flow channel to quantify breathing irregularity. Cardiopulmonary coupling (CPC) was analysed using the PSG electrocardiogram (ECG) channel. Following the consumption of morphine, the 60 OSA patients had fewer breaths (p = .0006), a longer inter‐breath interval (p < .0001) and more irregular breathing with increased IBI coefficient of variation (CV) (p = .0015) compared to the placebo night. A higher CPC sleep quality index was found with morphine use. The change of key IBI and CPC parameters was significantly correlated with the change of key PSG sleep‐disordered breathing parameters. In conclusion, 40 mg controlled‐release morphine resulted in a longer breathing cycle and increased breathing irregularity but generally more stable sleep in OSA patients. The significant links between the IBI and CPC techniques and a range of PSG sleep‐disordered breathing parameters may suggest a practical value as surrogate overnight cardiorespiratory measurements, because both respiratory flow and ECG can be detected by small portable devices.