Sleep disturbance and impulsivity are key components of mood vulnerability in bipolar disorder (BD), but few studies have assessed the association between these two symptoms among patients with BD.

Forty-seven euthymic patients with bipolar I disorder (BDI) or bipolar II disorder (BDII) and 58 age- and sex-matched healthy controls were enrolled in this cross-sectional study. Trait impulsivity was measured using the Barratt Impulsiveness Scale Version 11 (BIS-11), which yielded 3 second-order factors: attention, motor, and non-planning. Subjective sleep quality was assessed using the self-reported Pittsburgh Sleep Quality Index (PSQI). General linear models (GLMs) were used to assess the associations between subjective poor sleep and trait impulsivity with multiple testing corrections.

Patients with BD scored higher in BIS-11 and PSQI than healthy controls. PSQI total scores positively correlated with BIS-11 total scores, while sleep disturbance and daytime dysfunction were associated with attentional impulsiveness after controlling for covariates. Participants with higher PSQI total scores (>10) had higher scores in BIS-11 total, attention, and non-planning than those with low PSQI scores (≤5).

These findings support the hypothesis that poor sleep quality might lead to impulsivity and add to the growing evidence that improving sleep quality may be a therapeutic target for patients with BD.

Pre-diagnostic stages of psychotic illnesses, including ‘clinical high risk’ (CHR), are marked by sleep disturbances. These sleep disturbances appear to represent a key aspect in the etiology and maintenance of psychotic disorders. We aimed to examine the relationship between self-reported sleep dysfunction and attenuated psychotic symptoms (APS) on a day-to-day basis.

Seventy-six CHR young people completed the Experience Sampling Methodology (ESM) component of the European Union Gene-Environment Interaction Study, collected through PsyMate® devices, prompting sleep and symptom questionnaires 10 times daily for 6 days. Bayesian multilevel mixed linear regression analyses were performed on time-variant ESM data using the brms package in R. We investigated the day-to-day associations between sleep and psychotic experiences bidirectionally on an item level. Sleep items included sleep onset latency, fragmentation, and quality. Psychosis items assessed a range of perceptual, cognitive, and bizarre thought content common in the CHR population.

Two of the seven psychosis variables were unidirectionally predicted by previous night's number of awakenings: every unit increase in number of nightly awakenings predicted a 0.27 and 0.28 unit increase in feeling unreal or paranoid the next day, respectively. No other sleep variables credibly predicted next-day psychotic symptoms or vice-versa.

In this study, the relationship between sleep disturbance and APS appears specific to the item in question. However, some APS, including perceptual disturbances, had low levels of endorsement amongst this sample. Nonetheless, these results provide evidence for a unidirectional relationship between sleep and some APS in this population.

Depression is a highly recurrent disorder, with more than 50% of those affected experiencing a subsequent episode. Although there is relatively little stability in symptoms across episodes, some evidence indicates that suicidal ideation may be an exception. However, these findings warrant replication, especially over longer periods and across multiple episodes.

To assess the relative stability of suicidal ideation in comparison with other non-core depressive symptoms across episodes.

We examined 490 individuals with current major depressive disorder (MDD) at baseline and at least one subsequent episode during 9-year follow-up within the Netherlands Study of Depression and Anxiety (NESDA). The Inventory of Depressive Symptomatology (IDS) was used to assess DSM-5 non-core MDD symptoms (fatigue, appetite/weight change, sleep disturbance, psychomotor disturbance, concentration difficulties, worthlessness/guilt, suicidal ideation) at baseline and 2-, 4-, 6- and 9-year follow-up. We examined consistency in symptom presentation (i.e. whether the symptom met the diagnostic threshold, based on a binary categorisation of the IDS) using kappa (κ) and percentage agreement, and stability in symptom severity using Spearman correlation, based on the continuous IDS scores.

Out of all non-core depressive symptoms, insomnia appeared the most stable across episodes (r = 0.55–0.69, κ = 0.31–0.47) and weight decrease the least stable (r = 0.03–0.33, κ = 0.06–0.19). For suicidal ideation, correlations across episodes ranged from r = 0.36 to r = 0.55 and consistency ranged from κ = 0.28 to κ = 0.49.

Suicidal ideation is moderately stable in recurrent depression over 9 years. Contrary to prior reports, however, it does not exhibit substantially more stability than most other non-core symptoms of depression.

Insomnia and disturbed sleep are more common in autistic adults compared with non-autistic adults, contributing to significant social, psychological and health burdens. However, sleep intervention research for autistic adults is lacking.

The aim of the study was to implement an acceptance and commitment therapy group insomnia intervention (ACT-i) tailored for autistic adults to examine its impact on insomnia and co-occurring mental health symptoms.

Eight individuals (6 male, 2 female) aged between 18 and 70 years, with a clinical diagnosis of autism spectrum disorder, and scores ranging from 9 to 26 on the Insomnia Severity Index (ISI) participated in the trial. Participants were assigned to one of two intervention groups (4 per group) within a multiple baseline over time design for group. Participants completed questionnaires pre-intervention, post-intervention, and at 2-month follow-up, actigraphy 1 week prior to intervention and 1 week post-intervention, and a daily sleep diary from baseline to 1 week post-intervention, and 1 week at follow-up.

At a group level there were significant improvements in ISI (λ2=10.17, p=.006) and HADS-A (anxiety) (λ2=8.40, p=.015) scores across the three time points. Clinically reliable improvement occurred for ISI scores (n=5) and HADS-A scores (n=4) following intervention. Client satisfaction indicated that ACT-i was an acceptable intervention to the participants (median 4 out of 5).

This pilot study with eight autistic adults indicates that ACT-i is both an efficacious and acceptable intervention for reducing self-reported insomnia and anxiety symptoms in autistic adults.

There is growing evidence that sexual minority men (e.g., gay, bisexual) experience lower sleep quality when compared to their heterosexual peers. Minority stress (e.g., discrimination, victimization) may account for these differences, however little is known about these relationships and how generalized anxiety may play a role in sleep disturbance.

Therefore, the aims of this study are to (a) understand the relationship between minority stress and sleep disturbance in a sample of sexual minority men, and (b) test whether these relationships are mediated by generalized anxiety.

In 2020, 241 sexual minority men were recruited across a south-eastern state in the USA. Participants were asked to respond to scales assessing perceived social stress, minority stress constructs (i.e., internalized homophobia, experiences of harassment, microaggressions), generalized anxiety, and sleep disturbance. Linear regressions were used to test the relationship between minority stress and sleep disturbance controlling for perceived social stress and to test mediation by generalized anxiety.

Two minority stress constructs (experiences of harassment, and microaggressions) and perceived social stress were found to have a positive relationship with sleep disturbance. Generalized anxiety symptoms fully mediated the relationship between minority stress and sleep disturbance.

Because sleep quality has a profound impact on health, findings from this study suggest the need for psychological intervention to improve sleep for sexual minority men. Given that generalized anxiety fully mediates the relationship between minority stress and sleep, targeted anxiety-based interventions have the potential to reduce sleep disturbance disparities between heterosexual and sexual minority men.

No significant relationships.

Despite its efficacy in treating comorbid insomnia and depression, cognitive behavioral therapy for insomnia (CBT-I) is limited in its accessibility and, in many countries, cultural compatibility. Smartphone-based treatment is a low-cost, convenient alternative modality. This study evaluated a self-help smartphone-based CBT-I in alleviating major depression and insomnia.

A parallel-group randomized, waitlist-controlled trial was conducted with 320 adults with major depression and insomnia. Participants were randomized to receive either a 6-week CBT-I via a smartphone application, proACT-S, or waitlist condition. The primary outcomes included depression severity, insomnia severity, and sleep quality. The secondary outcomes included anxiety severity, subjective health, and acceptability of treatment. Assessments were administered at baseline, post-intervention (week 6) follow-up, and week 12 follow-up. The waitlist group received treatment after the week 6 follow-up.

Intention to treat analysis was conducted with multilevel modeling. In all but one model, the interaction between treatment condition and time at week 6 follow-up was significant. Compared with the waitlist group, the treatment group had lower levels of depression [Center for Epidemiologic Studies Depression Scale (CES-D): Cohen's d = 0.86, 95% CI (−10.11 to −5.37)], insomnia [Insomnia Severity Index (ISI): Cohen's d = 1.00, 95% CI (−5.93 to −3.53)], and anxiety [Hospital Anxiety and Depression Scale – Anxiety subscale (HADS-A): Cohen's d = 0.83, 95% CI (−3.75 to −1.96)]. They also had better sleep quality [Pittsburgh Sleep Quality Index (PSQI): Cohen's d = 0.91, 95% CI (−3.34 to −1.83)]. No differences across any measures were found at week 12, after the waitlist control group received the treatment.

proACT-S is an efficacious sleep-focused self-help treatment for major depression and insomnia.

ClinicalTrials.gov, NCT04228146. Retrospectively registered on 14 January 2020. https://clinicaltrials.gov/ct2/show/NCT04228146

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.

Fibromyalgia (FM) is a chronic widespread pain syndrome. Although its mechanism remains relatively unknown, accelerated neurodegeneration in the brain has been reported in patients with FM. Sleep disturbance can increase the risk of neurocognitive disorders, which are associated with tau and beta-amyloid (Aβ) protein accumulation. We hypothesize neurodegeneration in patients with FM may be associated with sleep disturbance.

In this case-control study, we analyzed serum tau and Aβ levels and their association with symptom profiles for patients with FM, by recruiting 22 patients with FM and 22 age-matched healthy participants. The visual analog scale, Fibromyalgia Impact Questionnaire, pressure pain threshold test, Pittsburgh Sleep Quality Index (PSQI), Beck Depression Inventory-II, Beck Anxiety Inventory, and serum tau and beta-amyloid-42 (Aβ-42) levels were recorded. The Mann–Whitney test was conducted to compare questionnaire and protein level results between the groups. Pearson correlation test was conducted to investigate the correlation of questionnaire scores with tau and Aβ-42 levels in patients with FM. The significance level was set at P < .05.

Serum tau and Aβ-42 levels were significantly higher in patients with FM than in controls. A positive correlation between serum tau levels and PSQI scores was observed in patients with FM (r = 0.476, P = .025). We found that only sleep disturbance in patients with FM was significantly associated with higher serum tau levels among all symptom scores.

We suggest sleep disturbance may play a vital role in the pathomechanism of accelerated neurodegeneration in FM.

After reading this article you will be able to:

• • recognise the challenges faced by the large number of refugees worldwide

• • understand the relationship between PTSD, sleep disturbance and pain in refugees

• • broadly understand the evidence for psychological and pharmacological therapy for treating PTSD, sleep disturbance and pain in refugees.

None.

Bipolar disorder (BD) is associated with attentional and processing abnormalities. Such abnormalities are also seen in healthy subjects with sleep disruption. We hypothesised cognitive abnormalities in BD patients would be worse in those with objectively verified sleep abnormalities.

Forty-six BD patients and 42 controls had comprehensive sleep/circadian rhythm assessment over 21 days alongside mood questionnaires. Cognitive function was assessed with a range of tasks including Psychomotor Vigilance Test (PVT), Attention Network Task (ANT) and Digit Symbol Substitution Test (DSST). BD participants with normal and abnormal sleep were compared with age- and sex-matched controls.

BD patients had longer response times and made more lapses (responses >500 ms) than controls on the PVT (both p < 0.001). However, patients with normal sleep patterns did not differ from controls while those with sleep abnormalities did (p < 0.001). An identical pattern of effects were seen with the ANT response times, with the abnormality in bipolar abnormal sleepers related to the executive attentional network. Similarly, patients made fewer correct responses on the DSST compared with the controls (p < 0.001). Bipolar normal sleepers did not differ while those with abnormal sleep did (p < 0.001). All these differences were seen in bipolar abnormal sleepers who were euthymic (p < 0.01) and across the main abnormal sleep phenotypes.

We confirm impairment in attention and processing speed in BD. Rather than sleep abnormalities exacerbating such dysfunction, the impairments were confined to bipolar abnormal sleepers, consistent with sleep disturbance being the main driver of cognitive dysfunction.

Sleep disturbance is common on in-patient psychiatry wards. This study explored subjective and objective patterns of sleep disturbance and contributory environmental factors. Participants were recruited from mental health acute admission wards and had a range of subjective and objective assessments of sleep. Light intensity and noise levels were measured to characterise potential environmental causes for poor sleep.

We recruited 20 patients; 15% were high risk for obstructive sleep apnoea. Nineteen participants reported poor sleep quality on the Pittsburgh Sleep Quality Index, and 90% had significant sleep fragmentation with objective measures. Inside light levels were low (day <200 lux and night <10 lux). Night sound levels were 40–90 db.

Sleep disturbance was highly prevalent. Increased awareness of sleep disorders is needed. Modifiable environmental factors on the ward were implicated, therefore increased awareness and a change of approach to sleep disturbance in in-patient psychiatry is recommended.

None.

Sleep problems are a modifiable risk factor for suicidal thoughts and behaviors. Yet, sparse research has examined temporal relationships between sleep disturbance, suicidal ideation, and psychological factors implicated in suicide, such as entrapment. This is the first in-the-moment investigation of relationships between suicidal ideation, objective and subjective sleep parameters, and perceptions of entrapment.

Fifty-one participants with current suicidal ideation completed week-long ecological momentary assessments. An actigraph watch was worn for the duration of the study, which monitored total sleep time, sleep efficiency, and sleep latency. Daily sleep diaries captured subjective ratings of the same sleep parameters, with the addition of sleep quality. Suicidal ideation and entrapment were measured at six quasi-random time points each day. Multi-level random intercept models and moderation analyses were conducted to examine the links between sleep, entrapment, and suicidal ideation, adjusting for anxiety and depression severity.

Analyses revealed a unidirectional relationship whereby short sleep duration (both objective and subjective measures), and poor sleep quality, predicted the higher severity of next-day suicidal ideation. However, there was no significant association between daytime suicidal ideation and sleep the following night. Sleep quality moderated the relationship between pre-sleep entrapment and awakening levels of suicidal ideation.

This is the first study to report night-to-day relationships between sleep disturbance, suicidal ideation, and entrapment. Findings suggest that sleep quality may alter the strength of the relationship between pre-sleep entrapment and awakening suicidal ideation. Clinically, results underscore the importance of assessing and treating sleep disturbance when working with those experiencing suicidal ideation.

Alzheimer's disease (AD) is a neurodegenerative brain disease that causes cognitive impairment and dementia. Within the US, AD is the most common form of dementia in the elderly, affecting 1 in 10 people over the age of 65. Sleep disturbance has been called a “public health epidemic” and, like depression, is a prodromal symptom of AD but may also contribute to the risk of developing AD. It was hypothesized that sleep disturbance, depression, and the apolipoprotein E (APOE) genotype increase the likelihood of AD.

Utilizing data from the National Alzheimer's Coordinating Center, information from evaluations of 11,453 cognitively asymptomatic participants was analyzed. Survival analysis was used to explore the independent relationships between depression, sleep disturbance, and APOE genotypes with eventual AD diagnosis. Cox proportional hazard models were utilized to explore the main effects and synergistic effects of psychosocial factors as moderated by APOE genotypes.

This study reinforced the association between APOE and AD. The hazard of developing AD was eight times higher for those with recent depression and the Ɛ4 homozygote (HR = 8.15 [3.70–17.95]). Among Ɛ4 carriers with clinician-verified depression, the hazard was ten times that of the reference group (HR = 10.11 [4.43–23.09]). The hazard for Ɛ4 carriers reporting sleep disturbance was almost 7 times greater than the reference group (HR = 6.79 [2.38–19.37]).

Findings suggest that sleep disturbance, depression, and APOE Ɛ4 genotype are associated with AD during follow-up evaluations among a group of initially cognitively asymptomatic participants. This study contributes to the literature base exploring an increased hazard or risk of AD due to potential modifiable risk factors as well as genetic biomarkers, such as APOE.

We investigated the prevalence of sleep disturbance and psychological distress in lung cancer patients. We also examined the association between sleep disturbance and psychological distress, pain, fatigue, and quality of life in the same population.

Fifty lung cancer patients were evaluated. Sleep disturbance was assessed using the Athens Sleep Insomnia Scale (AIS) and psychological distress using the Hospital Anxiety and Depression Scale (HADS). Quality of life (QOL), pain, and fatigue were assessed employing the European Organization of Research and Treatment Quality of Life Questionnaire–Cancer 30 (EORTC QLQ–C30).

We observed that 56% of lung cancer patients had sleep disturbance (AIS score ≥6) and 60% had psychological distress (total HADS score ≥11). Patients with sleep disturbance had a HADS score of 14.6 ± 5.8, a fatigue score of 45.3 ± 22.0, and a pain score of 27.2 ± 26.2. In contrast, patients without sleep disturbance had a lower HADS score of 9.9 ± 8.1 (p < 0.05) and a higher fatigue score of 28.5 ± 18.0 (p < 0.01) and a pain score of 8.7 ± 15.8 (p < 0.01). In addition, we found a lower QOL in patients with sleep disturbance (46.3 ± 20.2) than in those without (65.2 ± 20.7) (p < 0.05). We also observed a significant correlation between the AIS, HADS, fatigue, QOL, and pain scores.

Lung cancer patients suffered from combined symptoms related to sleep. Sleeping pills improved sleep induction but were not sufficient to provide sleep quality and prevent daytime dysfunction. Daytime dysfunction was specifically associated with psychological distress. Additionally, the type of sleep disturbance was related to other patient factors, including whether or not they received chemotherapy.