Sleep pattern alteration is a core feature of bipolar disorder (BD), often challenging to treat and affecting clinical outcomes. Suvorexant, a hypnotic agent that decreases wakefulness, has shown promising results in treating primary insomnia. To date, data on its use in BD are lacking. This study evaluated the efficacy and tolerability of adjunctive suvorexant for treatment-resistant insomnia in BD patients.

Thirty-six BD outpatients (19 BDI, 69.4% female, 48.9 [±15.2] years) were randomized for 1 week to double-blind suvorexant (10–20 mg/day) versus placebo. Then, all subjects who completed the randomized phase were offered open suvorexant for 3 months. Subjective total sleep time (sTST) and objective total sleep time (oTST) were assessed.

During the randomized control trial (RCT) phase, an overall increase in the oTST emerged, which was statistically significant for the Cole–Kripke algorithm (p = 0.035). The comparison between the suvorexant and placebo groups was limited by significant differences between measurements at baseline. During the open phase, no significant improvement was detected relative to either sTST and oTST. No adverse events nor major intolerances were reported.

Efficacy results are inconsistent. During the RCT phase, only a small increase in the objective oTST emerged, while during the open phase, no significant improvement was detected. While this is the first ever study of suvorexant in BD-related insomnia, the limitation of the small sample and the high rate of dropouts limits the generalizability of these findings. Larger studies are needed to assess suvorexant in treating BD-related insomnia.

Although the association between chronotype and mood disorders has been consistently reported, conversely, attempts to measure the association between chronotype and anxiety symptoms have generated inconsistent results. We aimed at evaluating whether chronotype (assessed through subjective and objective measures) is associated with lifetime mood and panic-agoraphobic spectrum symptoms in healthy controls (HCs) and in patients with bipolar disorder (BD).

Overall, 173 subjects, patients with BD in euthymic phase (n = 76) and HC (n = 97), were evaluated through the reduced Morningness–Eveningness Questionnaire (rMEQ), actigraphy monitoring and mood and panic-agoraphobic spectrum self-report (MOODS-SR and PAS-SR). The discrepancy between objective (actigraphic-based) versus subjective (rMEQ-based) circadian typology was estimated through the Circadian Classification Discrepancy Index (CCDI).

rMEQ-based evening chronotype (ET) was associated with higher scores in MOODS-SR depressive and rhythmicity and vegetative functions domains in HC and BD.Both ET and morning chronotypes (MT) were associated with higher PAS-SR scores in BD only. Actigraphic-based MT was associated with higher MOODS-SR depressive scores in HC. Likewise, the discrepancy between actigraphic-based and rMEQ-based circadian typology was associated with depressive symptoms in HC only.

Self-reported ET was consistently associated with mood symptoms, while associations with panic-agoraphobic symptoms only emerged in BD and involved both extreme chronotypes. The discrepancy between the preferred circadian typology (rMEQ-based) and the actual one (actigraphic-based) could contribute to depressive symptoms in HC. These results pave the way for interventional studies targeting circadian typology in an attempt to prevent or treat mental health disorders.

This study aimed to investigate changes in sleep parameters and self-perceived sleep quality in unilateral vestibular hypofunction participants after vestibular rehabilitation.

Forty-six unilateral vestibular hypofunction participants (before and after vestibular rehabilitation) along with a control group of 60 healthy patients underwent otoneurological examination, a one-week actigraphy sleep analysis and a series of self-report and performance measures.

After vestibular rehabilitation, unilateral vestibular hypofunction participants showed a significant score decrease in the Pittsburgh Sleep Quality Index, a self-rated reliable questionnaire depicting sleep quality during the last month, as well as a reduction in sleep onset latency and an increase in total sleep time, indicating an objective improvement in sleep quality as measured by actigraphy analysis. However, after vestibular rehabilitation, unilateral vestibular hypofunction participants still showed statistically significant differences with respect to the control group in both self-rated and objective measurements of sleep quality.

Vestibular rehabilitation may impact on sleep performance and chronotype behaviour, possibly by opposing long-term structural changes along neural pathways entangled in sleep activity because of the deafferentation of the vestibular nuclei.

This study was carried out to map psychosis spectrum disorder risk factors.

Our goal was to find what kind of instrumental methods may help to detect latent liabilities for schizophrenia and bipolar affective disorder

Using online questionnaires n=710 students were screened. Groups were formed based on the inclusion criteria: N = 25 people prone to mood swings, N = 30 people prone to odd experiences and delusive thinking, and a normal control group with N = 30 people. Personality, temperament, self-experiences, affectivity scales, and cognitive screening were conducted in addition to actigraphy coupled with a mobile application for detecting subjective experiences (EMA). Furthermore, instrumental examination of self-agency, testing time interval discrimination and (re)production, eye-tracking, EEG-microstates, and laboratory testing of inflammatory, immunologic and cardio-metabolic measures of allostatic load were applied.

Self-experience disorders: both risk groups showed significantly higher scores than the control group (CG). Self-agency: based on incorrectly attributed responses, the positive schizotypy risk factor (PSF) group differed from the CG (p = 0.003). Antisaccade study: the PSF group showed a difference from the CG (p = 0.002). Actigraphy: based on the distributions of diurnal cumulative activities, it distinguished those with a cyclothymic risk factor (CTF) from the CG (67% probability in the k-means clustering procedure).

Healthy students with a latent liability for schizotypy or bipolarity could be distinguished by some targeted laboratory methods. Susceptibility for bipolarity was indicated by actigraphic analyzes, and the risk for schizotypal development was indicated by deficiencies in the self-agency experience and by anti-saccadic eye movement disorders.

No significant relationships.

Sleep disturbances (SDs), such as insomnia or regular nightmares, are associated with multiple mental health disorders, most notably PTSD, where SDs are reported in up to 92% of cases. Examining the effect of changing sleep on psychological symptomology is essential to develop the evidence base on the contribution of sleep to mental resilience.

To examine the effect a short skills-based sleep intervention on psychological symptomology and actigraphy measured sleep.

A 4-session sleep skills training programme was used to treat active SDs in participants likely to have experienced occupation-associated trauma, namely military and first responders.

Nineteen participants were included in the study. Insomnia Severity Index (ISI) measured; difficulty sleeping, difficulty staying asleep, waking too early, sleep satisfaction, sleep interference on quality of life and total ISI insomnia score improved significantly post-treatment (M = 9.44, SE = 7.35, p <0.001). No significant difference was identified post-treatment for actigraphy-measured sleep. The severity of depression (M = 5.27, SE = 1.41, p = 0.002), anxiety (M = 5.07, SE = 1.66, p = 0.008), and PTSD symptoms among participants with likely PTSD, were significantly lower following treatment (M = 29.4, SE = 4.19, p = 0.002).

A short sleep skills intervention based on CBT-I was effective at reducing self-report insomnia symptoms and severity of psychological symptomology but failed to improve actigraphy sleep metrics. These findings highlight a differing contribution of night-time sleep and current insomnia symptoms to the severity of self-reported psychological symptomology.

No significant relationships.

Sleep problems are common in patients with substance use disorders (SUD) and have been related to poor treatment outcomes. Little is known about the sleep characteristics in patients with opioid and alcohol use disorders after detoxification program.

To compare sleep quantitative and qualitative characteristics between patients with opioid and alcohol use disorders.

This is a secondary data analysis of the longitudinal data from the observational study in St. Petersburg, Russia. The sample included 75 patients (22.7% female) who received detoxification treatment for alcohol (n=49) or opioid (n=26) withdrawal. Participants completed the Pittsburgh Sleep Quality Index (PSQI) and underwent daily wrist actigrahy.

Good internal consistency was demonstrated for self-report and actigraphy data (r=-0,405, p<0,01). Sleep duration and sleep onset latency were not different between alcohol and opioid groups (5.7 vs. 6.1 hours; 74 vs. 65 minutes, respectively) based on self-report data. The majority of the patients (57-100%) had sleep complaints and low quality of sleep after detoxification completion (at baseline). In both groups, the mean PSQI score had a tendency to decrease, representing better sleep quality, over the 1-week following detoxification program completion (from 12 at baseline to 10 at 1-week in alcohol group; from 13 to 12 in opioid group, p<0,001).

The findings show that sleep characteristics are similar in patients with different SUD and insomnia symptoms are prevalent after detoxification, suggesting the rationale for sleep assessment before hospital discharge. Despite the positive changes in sleep quality over 1-week abstinence, patients might benefit from the therapeutic sleep interventions.

This work was financially supported by a research grant from Russian Foundation for Basic Research, 18-013-00481.

In many countries, depressed individuals often first visit primary care settings for consultation, but a considerable number of clinically depressed patients remains unidentified. Introducing additional screening tools may facilitate the diagnostic process.

This study aims to examine whether Experience Sampling Method (ESM)-based measures of depressive affect and behaviors can discriminate depressed from non-depressed individuals. In addition, the added value of actigraphy-based measures was examined.

We used data from two samples to develop and validate prediction models. The development dataset included 14 days of ESM and continuous actigraphy of currently depressed (n=43) and non-depressed individuals (n=82). The validation dataset included 30 days of ESM and continuous actigraphy of currently depressed (n=27) and non-depressed individuals (n=27). Backward stepwise logistic regression analyses were applied to build the prediction models. The performance of the models was assessed with the goodness of fit indices, calibration curves, and discriminative ability (AUC, the area under the receiver operating characteristic curve).

In the development dataset, the discriminative ability was good for the actigraphy model (AUC=0.790) and excellent for the ESM (AUC=0.991) and combined-domains model (AUC=0.993). In the validation dataset, the discriminative ability was reasonable for the actigraphy model (AUC=0.648) and excellent for the ESM (AUC=0.891) and combined-domains model (AUC=0.892).

ESM is a good diagnostic predictor and is easy to calculate, and, therefore, holds promise for implementation in clinical practice. Actigraphy shows no added value to ESM as a diagnostic predictor, but might still be useful when active monitoring with ESM is not feasible.

No significant relationships.

In older populations disturbed 24-h activity rhythms, poor sleep, and depressive symptoms are often lingering and co-morbid, making treatment difficult. To improve insights into these commonly co-occurring problems, we assessed the bidirectional association of sleep and 24-h activity rhythms with depressive symptoms in middle-aged and elderly persons.

In 1734 participants (mean age: 62.3 ± 9.3 years, 55% women) from the prospective Rotterdam Study, 24-h activity rhythms and sleep were estimated with actigraphy (mean duration: 146 ± 19.6 h), sleep quality with the Pittsburgh Sleep Quality Index, and depressive symptoms with the Center for Epidemiological Studies Depression scale. Repeated measures were available for 947 participants (54%) over a median follow-up of 6 years (interquartile range = 5.6–6.3). Linear-mixed models were used to assess temporal associations of 24-h activity rhythms and sleep with depressive symptoms in both directions.

High 24-h activity rhythm fragmentation (IV) (B = 1.002, 95% confidence interval (CI) = 0.641–1.363), long time in bed (TIB) (B = 0.111, 95% CI = 0.053–0.169), low sleep efficiency (SE) (B = −0.015, 95% CI = −0.020 to −0.009), long sleep onset latency (SOL) (B = 0.009, 95% CI = 0.006–0.012), and low self-rated sleep quality (B = 0.112, 95% CI = 0.0992–0.124) at baseline were associated with increasing depressive symptoms over time. Conversely, more depressive symptoms at baseline were associated with an increasing 24-h activity rhythm fragmentation (B = 0.002, 95% CI = 0.001–0.003) and TIB (B = 0.009, 95% CI = 0.004–0.015), and a decreasing SE (B = −0.140, 95% CI = −0.196 to −0.084), SOL (B = 0.013, 95% CI = 0.008–0.018), and self-rated sleep quality (B = 0.193, 95% CI = 0.171–0.215) over time.

This study demonstrates a bidirectional association of 24-h activity rhythms, actigraphy-estimated sleep, and self-rated sleep quality with depressive symptoms over a time frame of multiple years in middle-aged and elderly persons.

Hypersomnolence has been considered a prominent feature of seasonal affective disorder (SAD) despite mixed research findings. In the largest multi-season study conducted to date, we aimed to clarify the nature and extent of hypersomnolence in SAD using multiple measurements during winter depressive episodes and summer remission.

Sleep measurements assessed in individuals with SAD and nonseasonal, never-depressed controls included actigraphy, daily sleep diaries, retrospective self-report questionnaires, and self-reported hypersomnia assessed via clinical interviews. To characterize hypersomnolence in SAD we (1) compared sleep between diagnostic groups and seasons, (2) examined correlates of self-reported hypersomnia in SAD, and (3) assessed agreement between commonly used measurement modalities.

In winter compared to summer, individuals with SAD (n = 64) reported sleeping 72 min longer based on clinical interviews (p < 0.001) and 23 min longer based on actigraphy (p = 0.011). Controls (n = 80) did not differ across seasons. There were no seasonal or group differences on total sleep time when assessed by sleep diaries or retrospective self-reports (p's > 0.05). Endorsement of winter hypersomnia in SAD participants was predicted by greater fatigue, total sleep time, time in bed, naps, and later sleep midpoints (p's < 0.05).

Despite a winter increase in total sleep time and year-round elevated daytime sleepiness, the average total sleep time (7 h) suggest hypersomnolence is a poor characterization of SAD. Importantly, self-reported hypersomnia captures multiple sleep disruptions, not solely lengthened sleep duration. We recommend using a multimodal assessment of hypersomnolence in mood disorders prior to sleep intervention.

Poor sleep is a modifiable risk factor for multiple disorders. Frontline treatments (e.g. cognitive-behavioral therapy for insomnia) have limitations, prompting a search for alternative approaches. Here, we compare manualized Mindfulness-Based Therapy for Insomnia (MBTI) with a Sleep Hygiene, Education, and Exercise Program (SHEEP) in improving subjective and objective sleep outcomes in older adults.

We conducted a single-site, parallel-arm trial, with blinded assessments collected at baseline, post-intervention and 6-months follow-up. We randomized 127 participants aged 50–80, with a Pittsburgh Sleep Quality Index (PSQI) score ⩾5, to either MBTI (n = 65) or SHEEP (n = 62), both 2 hr weekly group sessions lasting 8 weeks. Primary outcomes included PSQI and Insomnia Severity Index, and actigraphy- and polysomnography-measured sleep onset latency (SOL) and wake after sleep onset (WASO).

Intention-to-treat analysis showed reductions in insomnia severity in both groups [MBTI: Cohen's effect size d = −1.27, 95% confidence interval (CI) −1.61 to −0.89; SHEEP: d = −0.69, 95% CI −0.96 to −0.43], with significantly greater improvement in MBTI. Sleep quality improved equivalently in both groups (MBTI: d = −1.19; SHEEP: d = −1.02). No significant interaction effects were observed in objective sleep measures. However, only MBTI had reduced WASOactigraphy (MBTI: d = −0.30; SHEEP: d = 0.02), SOLactigraphy (MBTI: d = −0.25; SHEEP: d = −0.09), and WASOPSG (MBTI: d = −0.26; SHEEP (d = −0.18). There was no change in SOLPSG. No participants withdrew because of adverse effects.

MBTI is effective at improving subjective and objective sleep quality in older adults, and could be a valid alternative for persons who have failed or do not have access to standard frontline therapies.

Sleep problems are common among children with autism spectrum disorder (ASD) and can have a negative impact on the child’s behaviour and daytime functioning. The current pilot study examined objective measurements of child and parent sleep as factors associated with the stress, anxiety, depressive symptoms, social support and quality of life of parents of children with ASD.

Participants were nine children with ASD and their parents (nine mothers and three fathers). Participants wore an actigraph for 7 consecutive days and nights. Measures of sleep habits and quality were used to ascertain child and parent sleep. Measures of parenting stress, anxiety, depressive symptoms, quality of life and social support were collated.

Results indicated the emergence of high parental stress, anxiety and depressive symptoms. Significant correlations were observed between parent depressive symptoms, and both subjective sleep quality and child sleep disruptions.

The present study found that parental well-being is affected by child sleep problems.

To investigate the presence, nature and direction of the daily temporal association between depressive symptoms, cognitive performance and sleep in older individuals.

Single-subject study design in eight older adults with cognitive impairments and depressive symptoms.

For 63 consecutive days, depressive symptoms, working memory performance and night-time sleep duration were daily assessed with an electronic diary and actigraphy. The temporal associations of depressive symptoms, working memory and total sleep time were evaluated for each participant separately with time-series analysis (vector autoregressive modeling).

For seven out of eight participants we found a temporal association between depressive symptoms and/or sleep and/or working memory performance. More depressive symptoms were preceded by longer sleep duration in one person (r = 0.39; p < .001), by longer or shorter sleep duration than usual in one other person (B = 0.49; p < .001), by worse working memory in one person (B = −0.45; p = .007), and by better working memory performance in one other person (B = 0.35; p = .009). Worse working memory performance was preceded by longer sleep duration (r = −.35; p = .005) in one person, by shorter or longer sleep duration in three other persons (B = −0.76; p = .005, B = −0.61; p < .001; B = −0.34; p = .002), and by more depressive symptoms in one person (B = −0.25; p = .009).

The presence, nature and direction of the temporal associations between depressive symptoms, cognitive performance and sleep differed between individuals. Knowledge of personal temporal associations may be valuable for the development of personalized intervention strategies in order to maintain their health, quality of life, functional outcomes and independence.

Considering the heterogeneity of depression, distinct depressive symptom dimensions may be differentially associated with more objective actigraphy-based estimates of physical activity (PA), sleep and circadian rhythm (CR). We examined the association between PA, sleep, and CR assessed with actigraphy and symptom dimensions (i.e. mood/cognition, somatic/vegetative, sleep).

Fourteen-day actigraphy data of 359 participants were obtained from the Netherlands Study of Depression and Anxiety. PA, sleep, and CR estimates included gross motor activity (GMA), sleep duration (SD), sleep efficiency (SE), relative amplitude between daytime and night-time activity (RA) and sleep midpoint. The 30-item Inventory of Depressive Symptomatology was used to assess depressive symptoms, which were categorised in three depression dimensions: mood/cognition, somatic/vegetative, and sleep.

GMA and RA were negatively associated with higher score on all three symptom dimensions: mood/cognition (GMA: β = −0.155, p < 0.001; RA: β = −0.116, p = 0.002), somatic/vegetative (GMA: β = −0.165, p < 0.001; RA: β = −0.133, p < 0.001), sleep (GMA: β = −0.169, p < 0.001; RA: β = −0.190, p < 0.001). The association with sleep was more pronounced for two depression dimensions: longer SD was linked to somatic/vegetative (β = 0.115, p = 0.015) dimension and lower SE was linked to sleep (β = −0.101, p = 0.011) dimension.

As three symptom dimensions were associated with actigraphy-based low PA and dampened CR, these seem to be general indicators of depression. Sleep disturbances appeared more linked to the somatic/vegetative and sleep dimensions; the effectiveness of sleep interventions in patients reporting somatic/vegetative symptoms may be explored, as well as the potential of actigraphy to monitor treatment response to such interventions.

Sleep quantity and quality are associated with executive function (EF) in experimental studies, and in individuals with sleep disorders. With advancing age, sleep quantity and quality decline, as does the ability to perform EF tasks, suggesting that sleep disruption may contribute to age-related EF declines. This cross-sectional cohort study tested the hypothesis that poorer sleep quality (i.e., the frequency and duration of awakenings) and/or quantity may partly account for age-related EF deficits.

Community-dwelling older adults (N = 184) completed actigraphic sleep monitoring then a range of EF tasks. Two EF factors were extracted using exploratory structural equation modeling. Sleep variables did not mediate the relationship between age and EF factors. Post hoc moderated mediation analyses were conducted to test whether cognitive reserve compensates for sleep-related EF deficits, using years of education as a proxy measure of cognitive reserve.

We found a significant interaction between cognitive reserve and the number and frequency of awakenings, explaining a small (approximately 3%), but significant amount of variance in EF. Specifically, in individuals with fewer than 11 years of education, greater sleep disturbance was associated with poorer EF, but sleep did not impact EF in those with more education. There was no association between age and sleep quantity.

This study highlights the role of cognitive reserve in the sleep–EF relationship, suggesting individuals with greater cognitive reserve may be able to counter the impact of disturbed sleep on EF. Therefore, improving sleep may confer some protection against EF deficits in vulnerable older adults.

Despite its pivotal role in prophylaxis for bipolar-I-disorders (BD-I), variability in lithium (Li) response is poorly understood and only a third of patients show a good outcome. Converging research strands indicate that rest–activity rhythms can help characterize BD-I and might differentiate good responders (GR) and non-responders (NR).

Seventy outpatients with BD-I receiving Li prophylaxis were categorized as GR or NR according to the ratings on the retrospective assessment of response to lithium scale (Alda scale). Participants undertook 21 consecutive days of actigraphy monitoring of sleep quantity (SQ), sleep variability (SV) and circadian rhythmicity (CR).

Twenty-five individuals were categorized as GR (36%). After correcting statistical analysis to minimize false discoveries, four variables (intra-daily variability; median activity level; amplitude; and relative amplitude of activity) significantly differentiated GR from NR. The odds of being classified as a GR case were greatest for individuals showing more regular/stable CR (1.41; 95% confidence interval (CI) 1.08, 2.05; p < 0.04). Also, there was a trend for lower SV to be associated with GR (odds ratio: 0.56; 95% CI 0.31, 1.01; p < 0.06).

To our knowledge, this is the largest actigraphy study of rest–activity rhythms and Li response. Circadian markers associated with fragmentation, variability, amount and/or amplitude of day and night-time activity best-identified GR. However, associations were modest and future research must determine whether these objectively measured parameters, singly or together, represent robust treatment response biomarkers. Actigraphy may offer an adjunct to multi-platform approaches aimed at developing personalized treatments or stratification of individuals with BD-I into treatment-relevant subgroups.

Bipolar disorder (BD) is linked to circadian rhythm disruptions resulting in aberrant motor activity patterns. We aimed to explore whether motor activity alone, as assessed by longitudinal actigraphy, can be used to classify accurately BD patients and healthy controls (HCs) into their respective groups.

Ninety-day actigraphy records from 25 interepisode BD patients (ie, Montgomery–Asberg Depression Rating Scale (MADRS) and Young Mania Rating Scale (YMRS) < 15) and 25 sex- and age-matched HCs were used in order to identify latent actigraphic biomarkers capable of discriminating between BD patients and HCs. Mean values and time variations of a set of standard actigraphy features were analyzed and further validated using the random forest classifier.

Using all actigraphy features, this method correctly assigned 88% (sensitivity = 85%, specificity = 91%) of BD patients and HCs to their respective group. The classification success may be confounded by differences in employment between BD patients and HCs. When motor activity features resistant to the employment status were used (the strongest feature being time variation of intradaily variability, Cohen’s d = 1.33), 79% of the subjects (sensitivity = 76%, specificity = 81%) were correctly classified.

A machine-learning actigraphy-based model was capable of distinguishing between interepisode BD patients and HCs solely on the basis of motor activity. The classification remained valid even when features influenced by employment status were omitted. The findings suggest that temporal variability of actigraphic parameters may provide discriminative power for differentiating between BD patients and HCs while being less affected by employment status.

Both sleep and motor activity have a bidirectional relationship with depression. The existing literature on motor activity during therapeutic sleep deprivation in depressed patients is inconsistent and fragmentary. In the present study we measured motor activity continuously during 40 hours of sleep deprivation in depressed patients.

Thirty-four inpatients suffering from a major depression (DSM-IV) underwent sleep deprivation with a continuous waking period of 40 hours. Motor activity of the patients was continuously recorded using an actigraph on the non-dominant wrist. The effect of sleep deprivation was assessed by the Hamilton Depression Scale (six-item version), thus separating the group into responders and non-responders to sleep deprivation.

We found no significant differences in motor activity between responders and non-responders on the day before sleep deprivation. During the night, responders to sleep deprivation exhibited a higher motor activity and less periods of rest. On the day after sleep deprivation, responders exhibited a higher activity, too.

Motor activity levels differ between the two groups, thus giving more insight into possible mechanisms of action of the therapeutic sleep deprivation. We suggest that higher motor activity during the night prevents naps and leads to better response to sleep deprivation.