Overnight neuronal plasticity and adaptation to emotional distress.

Expressions such as 'sleep on it' refer to the resolution of distressing experiences across a night of sound sleep. Sleep is an active state during which the brain reorganizes the synaptic connections that form memories. This Perspective proposes a model of how sleep modifies emotional memory traces. Sleep-dependent reorganization occurs through neurophysiological events in neurochemical contexts that determine the fates of synapses to grow, to survive or to be pruned. We discuss how low levels of acetylcholine during non-rapid eye movement sleep and low levels of noradrenaline during rapid eye movement sleep provide a unique window of opportunity for plasticity in neuronal representations of emotional memories that resolves the associated distress. We integrate sleep-facilitated adaptation over three levels: experience and behaviour, neuronal circuits, and synaptic events. The model generates testable hypotheses for how failed sleep-dependent adaptation to emotional distress is key to mental disorders, notably disorders of anxiety, depression and post-traumatic stress with the common aetiology of insomnia.

Associations of 24-Hour Rest-Activity Rhythm Fragmentation, Cognitive Decline, and Postmortem Locus Coeruleus Hypopigmentation in Alzheimer's Disease.

OBJECTIVE: While studies suggested that locus coeruleus (LC) neurodegeneration contributes to sleep-wake dysregulation in Alzheimer's disease (AD), the association between LC integrity and circadian rest-activity patterns remains unknown. Here, we investigated the relationships between 24-hour rest-activity rhythms, cognitive trajectories, and autopsy-derived LC integrity in older adults with and without cortical AD neuropathology. METHODS: This retrospective study leveraged multi-modal data from participants of the longitudinal clinical-pathological Rush Memory and Aging Project. Indices of 24-hour rest-activity rhythm fragmentation (intradaily variability) and stability (interdaily stability) were extracted from annual actigraphic recordings, and cognitive trajectories were computed from annual cognitive evaluations. At autopsy, LC neurodegeneration was determined by the presence of hypopigmentation, and cortical AD neuropathology was assessed. Contributions of comorbid pathologies (Lewy bodies, cerebrovascular pathology) were evaluated. RESULTS: Among the 388 cases included in the study sample (age at death = 92.1 ± 5.9 years; 273 women), 98 (25.3%) displayed LC hypopigmentation, and 251 (64.7%) exhibited cortical AD neuropathology. Logistic regression models showed that higher rest-activity rhythm fragmentation, measured up to ~7.1 years before death, was associated with increased risk to display LC neurodegeneration at autopsy (odds ratio [OR] = 1.46, 95% confidence interval [CI95%]: 1.16-1.84, pBONF = 0.004), particularly in individuals with cortical AD neuropathology (OR = 1.56, CI95%: 1.15-2.15, pBONF = 0.03) and independently of comorbid pathologies. In addition, longitudinal increases in rest-activity rhythm fragmentation partially mediated the association between LC neurodegeneration and cognitive decline (estimate = -0.011, CI95%: -0.023--0.002, pBONF = 0.03). INTERPRETATION: These findings highlight the LC as a neurobiological correlate of sleep-wake dysregulation in AD, and further underscore the clinical relevance of monitoring rest-activity patterns for improved detection of at-risk individuals. ANN NEUROL 2024;95:653-664.

Cognitive, Behavioral, and Circadian Rhythm Interventions for Insomnia Alter Emotional Brain Responses.

BACKGROUND: The highest risk of depression is conveyed by insomnia. This risk can be mitigated by sleep interventions. Understanding brain mechanisms underlying increased emotional stability following insomnia treatment could provide insight relevant to the prevention of depression. Here, we investigated how different sleep interventions alter emotion-related brain activity in people with insomnia at high risk of developing depression. METHODS: Functional magnetic resonance imaging was used to assess how the amygdala response to emotional stimuli (negative facial expression) in 122 people with insomnia disorder differed from 36 control subjects and how the amygdala response changed after 6 weeks of either no treatment or internet-based circadian rhythm support (CRS), cognitive behavioral therapy for insomnia (CBT-I), or their combination (CBT-I+CRS). Effects on depression, insomnia and anxiety severity were followed up for 1 year. RESULTS: Only combined treatment (CBT-I+CRS) significantly increased the amygdala response, compared with no treatment, CBT-I, and CRS. Individual differences in the degree of response enhancement were associated with improvement of insomnia symptoms directly after treatment (r = -0.41, p = .021). Moreover, exclusively CBT-I+CRS enhanced responsiveness of the left insula, which occurred in proportion to the reduction in depressive symptom severity (r = -0.37, p = .042). CONCLUSIONS: This functional magnetic resonance imaging study on insomnia treatment, the largest to date, shows that a combined cognitive, behavioral, and circadian intervention enhances emotional brain responsiveness and might improve resilience in patients with insomnia who are at high risk of developing depression.

The first-night effect and the consistency of short sleep in insomnia disorder.

The nature and degree of objective sleep impairments in insomnia disorder remain unclear. This issue is complicated further by potential changes in sleep architecture on the first compared with subsequent nights in the laboratory. Evidence regarding differential first-night effects in people with insomnia disorder and controls is mixed. Here, we aimed to further characterize insomnia- and night-related differences in sleep architecture. A comprehensive set of 26 sleep variables was derived from two consecutive nights of polysomnography in 61 age-matched patients with insomnia and 61 good sleeper controls. People with insomnia expressed consistently poorer sleep than controls on several variables during both nights. While poorer sleep during the first night was observed in both groups, there were qualitative differences regarding the specific sleep variables expressing a first-night effect. Short sleep (total sleep time < 6 hr) was more likely during the first night and in insomnia, although approximately 40% of patients with insomnia presenting with short sleep on night 1 no longer met this criterion on night 2, which is important given the notion of short-sleeping insomnia as a robust subtype.

Identifying the insomnia-related psychological issues associated with hyperarousal: A network perspective.

Hyperarousal, recognized as a fundamental characteristic of insomnia for decades, has yielded limited evidence concerning its direct psychological associations. This study aimed to explore the psychological factors linked to hyperarousal within the framework of interrelated variables. Two independent samples, comprising n = 917 and n = 652 young adults, were included in the study. Employing the first dataset as a discovery sample and the second dataset as a replication sample, network analyses were conducted using 26 variables derived from 17 scales. The objective was to estimate the direct and indirect associations between psychological issues, including hyperarousal and insomnia. Additionally, linear regression analysis was employed to assess the convergence of findings obtained from the network analysis. Network analyses in both samples converged to reveal direct associations between insomnia severity and several psychological factors, including negative sleep beliefs, physical fatigue, insomnia response to stress, hyperarousal, self-reported depression, and mental fatigue. Notably, the nodes with relative importance within the network include trait anxiety, depressive rumination, hyperarousal, perfectionism sub-dimension of concern over mistakes, and private self-consciousness. Hyperarousal is one of the key factors linking insomnia with a variety of psychological issues, including emotion-related factors (rumination, perveived stress), sleep-related factors (dysfunctional sleep beliefs and attitudes, insomnia response to stress, fatigue, chronotype), and self-related factors (self-consciousness, perfectionism). The results suggest that forthcoming strategies for enhancing the treatment efficacy of insomnia could consider supplementary interventions that specifically address hyperarousal, other factors directly linked to insomnia, or the hub nodes within the network.

Are some children genetically predisposed to poor sleep? A polygenic risk study in the general population.

BACKGROUND: Twin studies show moderate heritability of sleep traits: 40% for insomnia symptoms and 46% for sleep duration. Genome-wide association studies (GWAS) have identified genetic variants involved in insomnia and sleep duration in adults, but it is unknown whether these variants affect sleep during early development. We assessed whether polygenic risk scores for insomnia (PRS-I) and sleep duration (PRS-SD) affect sleep throughout early childhood to adolescence. METHODS: We included 2,458 children of European ancestry (51% girls). Insomnia-related items of the Child Behavior Checklist were reported by mothers at child's age 1.5, 3, and 6 years. At 10-15 years, the Sleep Disturbance Scale for Children and actigraphy were assessed in a subsample (N = 975). Standardized PRS-I and PRS-SD (higher scores indicate genetic susceptibility for insomnia and longer sleep duration, respectively) were computed at multiple p-value thresholds based on largest GWAS to date. RESULTS: Children with higher PRS-I had more insomnia-related sleep problems between 1.5 and 15 years (BPRS-I < 0.001 = .09, 95% CI: 0.05; 0.14). PRS-SD was not associated with mother-reported sleep problems. A higher PRS-SD was in turn associated with longer actigraphically estimated sleep duration (BPRS-SD < 5e08 = .05, 95% CI: 0.001; 0.09) and more wake after sleep onset (BPRS-SD < 0.005 = .25, 95% CI: 0.04; 0.47) at 10-15 years, but these associations did not survive multiple testing correction. CONCLUSIONS: Children who are genetically predisposed to insomnia have more insomnia-like sleep problems, whereas those who are genetically predisposed to longer sleep have longer sleep duration, but are also more awake during the night in adolescence. This indicates that polygenic risk for sleep traits, based on GWAS in adults, affects sleep already in children.

Network analysis of sleep bruxism in the EPISONO adult general population.

Sleep bruxism (SB) has been associated with biological and psychosocial factors. The assessment of SB includes self-report, clinical evaluation, and polysomnography. This study aimed to investigate the associations of self-reported SB with other sleep disorders and demographic, psychological, and lifestyle factors in the adult general population, and to investigate whether self-reported SB and polysomnographically (PSG) confirmed SB provide similar outcomes in terms of their associated factors. We recruited 915 adults from the general population in Sao Paulo, Brazil. All participants underwent a one-night PSG recording and answered questions about sex, age, BMI, insomnia, OSA risk, anxiety, depression, average caffeine consumption, smoking frequency, and alcohol consumption frequency. We investigated the link between SB and the other variables in univariate, multivariate, and network models, and we repeated each model once with self-reported SB and once with PSG-confirmed SB. Self-reported SB was only significantly associated with sex (p = 0.042), anxiety (p = 0.002), and depression (p = 0.03) in the univariate analysis, and was associated with insomnia in the univariate (p < 0.001) and multivariate (ß = 1.054, 95%CI 1.018-1.092, p = 0.003) analyses. Network analysis showed that self-reported SB had a direct positive edge to insomnia, while PSG-confirmed SB was not significantly associated with any of the other variables. Thus, sleep bruxism was positively associated with insomnia only when self-reported, while PSG-confirmed SB was not associated with any of the included factors.

The European Insomnia Guideline: An update on the diagnosis and treatment of insomnia 2023.

Progress in the field of insomnia since 2017 necessitated this update of the European Insomnia Guideline. Recommendations for the diagnostic procedure for insomnia and its comorbidities are: clinical interview (encompassing sleep and medical history); the use of sleep questionnaires and diaries (and physical examination and additional measures where indicated) (A). Actigraphy is not recommended for the routine evaluation of insomnia (C), but may be useful for differential-diagnostic purposes (A). Polysomnography should be used to evaluate other sleep disorders if suspected (i.e. periodic limb movement disorder, sleep-related breathing disorders, etc.), treatment-resistant insomnia (A) and for other indications (B). Cognitive-behavioural therapy for insomnia is recommended as the first-line treatment for chronic insomnia in adults of any age (including patients with comorbidities), either applied in-person or digitally (A). When cognitive-behavioural therapy for insomnia is not sufficiently effective, a pharmacological intervention can be offered (A). Benzodiazepines (A), benzodiazepine receptor agonists (A), daridorexant (A) and low-dose sedating antidepressants (B) can be used for the short-term treatment of insomnia (≤ 4 weeks). Longer-term treatment with these substances may be initiated in some cases, considering advantages and disadvantages (B). Orexin receptor antagonists can be used for periods of up to 3 months or longer in some cases (A). Prolonged-release melatonin can be used for up to 3 months in patients ≥ 55 years (B). Antihistaminergic drugs, antipsychotics, fast-release melatonin, ramelteon and phytotherapeutics are not recommended for insomnia treatment (A). Light therapy and exercise interventions may be useful as adjunct therapies to cognitive-behavioural therapy for insomnia (B).

The role of brain white matter in depression resilience and response to sleep interventions.

Insomnia poses a high risk for depression. Brain mechanisms of sleep and mood improvement following cognitive behavioural therapy for insomnia remain elusive. This longitudinal study evaluated whether (i) individual differences in baseline brain white matter microstructure predict improvements and (ii) intervention affects brain white matter microstructure. People meeting the Diagnostic and Statistical Manual of Mental Disorders-5 criteria for Insomnia Disorder (n = 117) participated in a randomized controlled trial comparing 6 weeks of no treatment with therapist-guided digital cognitive behavioural therapy for insomnia, circadian rhythm support or their combination (cognitive behavioural therapy for insomnia + circadian rhythm support). Insomnia Severity Index and Inventory of Depressive Symptomatology-Self Report were assessed at baseline and followed up at Weeks 7, 26, 39 and 52. Diffusion-weighted magnetic resonance images were acquired at baseline and Week 7. Skeletonized white matter tracts, fractional anisotropy and mean diffusivity were quantified both tract-wise and voxel-wise using tract-based spatial statistics. Analyses used linear and mixed effect models while correcting for multiple testing using false discovery rate and Bonferroni for correlated endpoint measures. Our results show the following: (i) tract-wise lower fractional anisotropy in the left retrolenticular part of the internal capsule at baseline predicted both worse progression of depressive symptoms in untreated participants and more improvement in treated participants (fractional anisotropy × any intervention, PFDR = 0.053, Pcorr = 0.045). (ii) Only the cognitive behavioural therapy for insomnia + circadian rhythm support intervention induced a trend-level mean diffusivity decrease in the right superior corona radiata (PFDR = 0.128, Pcorr = 0.108), and individuals with a stronger mean diffusivity decrease showed a stronger alleviation of insomnia (R = 0.20, P = 0.035). In summary, individual differences in risk and treatment-supported resilience of depression involve white matter microstructure. Future studies could target the role of the left retrolenticular part of the internal capsule and right superior corona radiata and the brain areas they connect.

A Longitudinal Study of Stress During Pregnancy, Children's Sleep and Polygenic Risk for Poor Sleep in the General Pediatric Population.

Early life stress is robustly associated with poor sleep across life. Preliminary studies suggest that these associations may begin already in utero. Here, we study the longitudinal associations of prenatal psychosocial stress with sleep across childhood, and assess whether prenatal stress interacts with genetic liability for poor sleep.The study is embedded in the Generation R population-based birth cohort. Caregivers reported on prenatal psychosocial stress (life events, contextual, parental or interpersonal stressors) and on children's sleep at ages 2 months, 1.5, 2, 3 and 6 years. The study sample consisted of 4,930 children; polygenic risk scores for sleep traits were available in 2,063.Prenatal stress was consistently associated with more sleep problems across assessments. Effect sizes ranged from small (B = 0.21, 95%CI: 0.14;0.27) at 2 months to medium (B = 0.45, 95%CI: 0.38;0.53) at 2 years. Prenatal stress was moreover associated with shorter sleep duration at 2 months (Bhrs = -0.22, 95%CI: -0.32;-0.12) and at 2 years (Bhrs = -0.04, 95%CI -0.07; -0.001), but not at 3 years (Bhrs = 0.02, 95%CI: -0.02;0.06). Prenatal negative life events interacted with polygenic risk for insomnia to exacerbate sleep problems at 6 years (Binteraction = 0.07, 95%CI: 0.02;0.13).Psychosocial stress during pregnancy has negative associations with children's sleep that persist across childhood, and are exacerbated by genetic liability for insomnia. Associations with sleep duration were more pronounced in infancy and seem to attenuate with age. These findings highlight the role of the prenatal environment for developing sleep regulation, and could inform early intervention programs targeting sleep in children from high-risk pregnancies.

Are sleep-related beliefs and behaviours dysfunctional in people with insomnia after acquired brain injury? A cross-sectional study.

Inappropriate sleep-related beliefs and behaviours are considered key maladaptive mechanisms in the development and maintenance of insomnia in the otherwise healthy population. The aim of this study was to evaluate critically the role of sleep-related beliefs and behaviours in insomnia after acquired brain injury. Cross-sectional data of 51 outpatients with insomnia disorder and acquired brain injury were used to evaluate associations of the insomnia severity index with the dysfunctional beliefs and attitudes about sleep scale and sleep-related behaviours questionnaire. Seven (44%) of the dysfunctional beliefs and attitudes about sleep scale items and 10 (31%) of the sleep-related behaviours questionnaire items correlated significantly with insomnia severity. Ten experts were consulted on whether they considered the questionnaire items maladaptive or accurately reflecting coping with conditions experienced by people with acquired brain injury. Although multiple linear regression showed that the total scores of the questionnaires explained a significant part of interindividual differences in insomnia severity (R2 = 0.27, F(2,48) = 8.72, p < 0.01), the experts unanimously rated only four (25%) of the dysfunctional beliefs and attitudes about sleep scale items as dysfunctional beliefs and three (9%) of the sleep-related behaviours questionnaire items as safety behaviours. In people with brain injury, sleep related beliefs and behaviours may also play a role in insomnia, especially a diminished perception of control and worry about sleep. However, more than half of the questionnaire items on sleep-related beliefs and behaviours may not be considered inappropriate and maladaptive for the acquired brain injury population, and may reflect adequate observations and efforts in coping with consequences of the brain damage.

Pupillometry to differentiate idiopathic hypersomnia from narcolepsy type 1.

Idiopathic hypersomnia is poorly diagnosed in the absence of biomarkers to distinguish it from other central hypersomnia subtypes. Given that light plays a main role in the regulation of sleep and wake, we explored the retinal melanopsin-based pupil response in patients with idiopathic hypersomnia and narcolepsy type 1, and healthy subjects. Twenty-seven patients with narcolepsy type 1 (women 59%, 36 ± 11.5 years old), 36 patients with idiopathic hypersomnia (women 83%, 27.2 ± 7.2 years old) with long total sleep time (> 11/24 hr), and 43 controls (women 58%, 30.6 ± 9.3 years old) were included in this study. All underwent a pupillometry protocol to assess pupil diameter, and the relative post-illumination pupil response to assess melanopsin-driven pupil responses in the light non-visual input pathway. Differences between groups were assessed using logistic regressions adjusted on age and sex. We found that patients with narcolepsy type 1 had a smaller baseline pupil diameter as compared with idiopathic hypersomnia and controls (p < 0.05). In addition, both narcolepsy type 1 and idiopathic hypersomnia groups had a smaller relative post-illumination pupil response (respectively, 31.6 ± 13.9% and 33.2 ± 9.9%) as compared with controls (38.7 ± 9.7%), suggesting a reduced melanopsin-mediated pupil response in both types of central hypersomnia (p < 0.01). Both narcolepsy type 1 and idiopathic hypersomnia showed a smaller melanopsin-mediated pupil response, and narcolepsy type 1, unlike idiopathic hypersomnia, also displayed a smaller basal pupil diameter. Importantly, we found that the basal pupil size permitted to well discriminate idiopathic hypersomnia from narcolepsy type 1 with a specificity = 66.67% and a sensitivity = 72.22%. Pupillometry may aid to multi-feature differentiation of central hypersomnia subtypes.

From childhood trauma to hyperarousal in adults: The mediating effect of maladaptive shame coping and insomnia.

Introduction: A new line of insomnia research focuses on the developmental trajectories from early live stress to insomnia in adulthood. Adverse childhood experiences (ACE's) might create a vulnerability for later maladaptive coping with distress, as seen in chronic hyperarousal or insomnia. In an functional magnetic resonance imaging (fMRI) study, failure to dissociate the neurobiological components of shame from autobiographical shameful memories in insomnia was reflected by continued activation of the dorsal anterior cingulate cortex (dACC), which may be a result of maladaptive coping in the wake of ACE's. Following up on that study, the current pilot study explores the relation between ACE's, shame coping-styles, adult insomnia, hyperarousal, and neurobiology of autobiographical memory. Methods: We used existing data (N = 57) from individuals with insomnia (N = 27) and controls (N = 30), and asked these participants to complete the childhood trauma questionnaire (CTQ). Two structural equation models were used to test the hypotheses that shame-coping styles and insomnia symptom severity mediate the association between ACE's and (1) self-rated hyperarousal symptoms and (2) dACC activation to recall of autobiographical memories. Results: For the association between ACE's and hyperarousal, there was a significant mediation of shame-coping style (p < 0.05). This model also indicated worse shame coping with more ACE's (p < 0.05) and worse insomnia symptoms with more ACES's (p < 0.05), but no association between shame coping and insomnia symptoms (p = 0.154). In contrast, dACC activation to recall of autobiographical memories could only be explained by its direct association with ACE's (p < 0.05), albeit that in this model more ACE's were also associated with worse insomnia symptoms. Discussion: These findings could have an implication for the approach of treatment for insomnia. It could be focused more on trauma and emotional processing instead of conventional sleep interventions. Future studies are recommended to investigate the relationship mechanism between childhood trauma and insomnia, with additional factors of attachment styles, personality, and temperament.

A blended eHealth intervention for insomnia following acquired brain injury: a randomised controlled trial.

The high prevalence and severe consequences of poor sleep following acquired brain injury emphasises the need for an effective treatment. However, treatment studies are scarce. The present study evaluates the efficacy of blended online cognitive behavioural therapy for insomnia (eCBT-I) developed specifically for people with acquired brain injury. In a multicentre prospective, open-label, blinded end-point randomised clinical trial, 52 participants with insomnia and a history of a stroke or traumatic brain injury were randomised to 6 weeks of guided eCBT-I or treatment as usual, with a 6-week follow-up. The primary outcome measure was the change in insomnia severity between baseline and after treatment, measured with the Insomnia Severity Index. Results showed that insomnia severity improved significantly more with eCBT-I than with treatment as usual compared to baseline, both at post-treatment (mean [SEM] 4.0 [1.3] insomnia severity index points stronger decrease, d = 0.96, p < 0.003) and at follow-up (mean [SEM] 3.2 [1.5] insomnia severity index points, d = -0.78, p < 0.03). In conclusion, our randomised clinical trial shows that blended CBT is an effective treatment for insomnia, and feasible for people with acquired brain injury, regardless of cognitive and psychiatric complaints. Online treatment has major advantages in terms of availability and cost and may contribute to the successful implementation of insomnia treatment for people with acquired brain injuries.

Actigraphy in studies on insomnia: Worth the effort?

In the past decades, actigraphy has emerged as a promising, cost-effective, and easy-to-use tool for ambulatory sleep recording. Polysomnography (PSG) validation studies showed that actigraphic sleep estimates fare relatively well in healthy sleepers. Additionally, round-the-clock actigraphy recording has been used to study circadian rhythms in various populations. To this date, however, there is little evidence that the diagnosis, monitoring, or treatment of insomnia can significantly benefit from actigraphy recordings. Using a case-control design, we therefore critically examined whether mean or within-subject variability of actigraphy sleep estimates or circadian patterns add to the understanding of sleep complaints in insomnia. We acquired actigraphy recordings and sleep diaries of 37 controls and 167 patients with varying degrees of insomnia severity for up to 9 consecutive days in their home environment. Additionally, the participants spent one night in the laboratory, where actigraphy was recorded alongside PSG to check whether sleep, in principle, is well estimated. Despite moderate to strong agreement between actigraphy and PSG sleep scoring in the laboratory, ambulatory actigraphic estimates of average sleep and circadian rhythm variables failed to successfully differentiate patients with insomnia from controls in the home environment. Only total sleep time differed between the groups. Additionally, within-subject variability of sleep efficiency and wake after sleep onset was higher in patients. Insomnia research may therefore benefit from shifting attention from average sleep variables to day-to-day variability or from the development of non-motor home-assessed indicators of sleep quality.

Functional connectivity correlates of attentional networks in insomnia disorder: A pilot study.

Insomnia disorder has been associated with poor executive functioning. Functional imaging studies of executive functioning in insomnia are scarce and inconclusive. Because the Attentional Network Test relies on well-defined cortical networks and sensitively distinguishes different aspects of executive function, it might reveal brain functional alterations in relatively small samples of patients. The current pilot study assessed functional connectivity during the Attentional Network Test performed using magnetic resonance imaging in 12 participants with insomnia and 13 self-defined good sleepers. ANCOVAs were used to evaluate group differences in performance and functional connectivity in the regions of interest representing the attentional networks (i.e. alerting, orienting and executive control) at p < 0.05, uncorrected. During the orienting part, participants with insomnia showed weaker connectivity of the precentral gyrus with the superior parietal lobe (false discovery rate-corrected), while they showed stronger connectivity between premotor and visual regions. Individual differences in connectivity between premotor and visual regions correlated inversely with reaction time. Reaction times suggested more efficient executive control in participants with insomnia compared with good sleepers. During the executive control part, participants with insomnia showed stronger connectivity of thalamic parts of the arousal circuit with the middle frontal and the occipital gyri. Conversely, connectivity between the inferior and superior frontal gyri was weaker. Participants with insomnia seem to recruit more cortical resources in visuo-motor regions to orient attention than good sleepers do, and seem to have enhanced executive control that relates to stronger connectivity of arousal-related thalamic areas. This latter result should be treated with caution and requires confirmation.

Can people with poststroke insomnia benefit from blended cognitive behavioral therapy? A single case experimental design.

PURPOSE: Sleep is essential for our overall health and wellbeing. Unfortunately, stroke often induces insomnia, which has been shown to impede rehabilitation and recovery of function. Cognitive behavioral therapy for insomnia (CBT-I) is the treatment of choice for insomnia in the general population and is efficacious both when delivered face-to-face or online. The primary aim of this study was to evaluate efficacy of blended CBT-I (eCBT-I) in five poststroke participants with insomnia according to DSM-5 criteria. METHODS: A randomized multiple baseline design was used to evaluate improvements in total sleep time, sleep onset latency, sleep efficiency, nocturnal awakenings and sleep quality. The intervention included six weeks of eCBT-I combined with two face-to-face sessions. RESULTS: All participants completed the intervention. One participant stopped using the diary, while the other four completed it fully. All five sleep diary measures improved, significantly so for nocturnal awakenings. Moreover, after completion of the treatment, four out of five participants no longer fulfilled DSM-5 criteria for insomnia disorder. CONCLUSIONS: This is the first study to show that blended CBT-I is potentially effective in participants with post-stroke insomnia. The findings justify extension to a randomized controlled trial.

Genetic risk for insomnia is associated with objective sleep measures in young and healthy good sleepers.

Insomnia disorder (ID) is the second most common neuropsychiatric disorder. Its socioeconomic burden is enormous while diagnosis and treatment are difficult. A novel approach that reveals associations between insomnia genetic propensity and sleep phenotypes in youth may help understand the core of the disease isolated from comorbidities and pave the way for new treatments. We obtained quantitative nocturnal sleep electroencephalogram (EEG) features in 456 participants (18-31y, 49 women). Sleep EEG was recorded during a baseline night following at least 7 days of regular sleep times. We then assessed daytime sleep onset latency in a subsample of N = 359 men exposed to manipulations affecting sleep pressure. We sampled saliva or blood for polygenic risk score (PRS) determination. The PRS for ID was computed based on genome-wide common single nucleotide polymorphism assessments. Participants also completed a battery of behavioral and cognitive tests. The analyses revealed that the PRS for ID was negatively associated with cumulated EEG power in the delta (0.5-4 Hz) and theta (4-8 Hz) bands across rapid eye movement (REM) and non-REM sleep (p ≤ .0026; ß ≥ -0.13) controlling for age, sex and BMI. The PRS for ID was also negatively associated with daytime likelihood of falling asleep (ß = -0.19, p = .0009). Other explorations for associations with non-baseline-nights, cognitive measures, and mood did not yield significant results. These results propose that the need or the ability to fall asleep and to generate slow brain activity during sleep may constitute the core sleep-related risk factors for developing ID.