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Insomnia is common in children with autism. Cognitive behavioral treatment for childhood insomnia may improve sleep and functioning in children with autism and their parents, but delivery involving multiple office visits limits accessibility. This single-arm pilot study tested telehealth delivery of eight-session cognitive behavioral treatment for childhood insomnia in 17 children (6-12 years) with autism spectrum disorder and insomnia and their parent(s). Treatment integrity was assessed each session ("delivery," by therapist; "receipt," participant understanding; and "enactment," home practice). Treatment satisfaction was assessed after treatment. Children and parents wore actigraphs and completed electronic diaries for 2 weeks, children completed 5-min Holter Monitoring (assessed heart rate variability, physiological arousal indicator), and parents completed Aberrant Behavior Checklist before and after 1 month. Average integrity scores were high (98%, "delivery"; 93%, "receipt"; and 82%, "enactment"). Parents found cognitive behavioral treatment for childhood insomnia helpful, age-appropriate, and autism-friendly. Paired-samples t-tests (family-wise error controlled) indicated telehealth cognitive behavioral treatment for childhood insomnia improved child and parent sleep ("objective" and "subjective") and functioning (child--decreased irritability, lethargy, stereotypy, hyperactivity; parent--decreased fatigue). At 1 month, inappropriate speech also decreased, but hyperactivity was no longer decreased. Other gains were maintained. Most children demonstrated reduced arousal following treatment. This pilot shows telehealth cognitive behavioral treatment for childhood insomnia is feasible and may improve child and parent sleep, child behavior and arousal, and parent fatigue. A randomized controlled trial of telehealth cognitive behavioral treatment for childhood insomnia for children with autism is needed.

How suitable are federal housing policies and slum upgrading programs for those living in young land occupations? Scholars rarely ask this question because research and policy target well-established settlements that have acquired tenure security. In contrast, young land occupations are highly vulnerable, emergent settlements threatened with eviction and are not sufficiently visible to attract government and scholarly attention. Through a multiyear collaboration with activists, social movements, nonprofits, and residents of young land occupations in São Paulo, Brazil, this participatory action research elucidates who occupies these locations and why, where they come from, and the housing struggles they face. A survey administered to 906 households depicts land occupiers as uniformly very poor and vulnerable, unlike the low- to modest-income dwellers of consolidated informal settlements. An assessment of existing social housing programs emphasizes the need to develop housing assistance and upgrading programs specifically targeting the socioeconomic conditions of land occupiers, thus proactively supporting them. [ABSTRACT FROM AUTHOR]

Phosphodiesterase 2 (PDE2) is an enzyme responsible for hydrolysis of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) to restrict intracellular signalling of these second messenger molecules. This study investigated how PDE2 inhibitor Bay 60-7550 affects the dysregulated glucocorticoid signalling in neuronal cells and regulates depressive behaviours after chronic stress in mice. We found that exposure of hippocampal neurons to corticosterone resulted in time- and concentration-dependent increases in PDE2 expression. These intriguing findings were confirmed in the hippocampal cell line HT-22. After corticosterone exposure for 24 h, HT-22 cells showed a concentration-dependent increase in mRNA levels for PDE2 subtypes, PDE2A1 and 2A3, as well as for the total PDE2A protein expression. Bay 60-7550 was found to reverse the cell lesion induced by corticosterone (50 [im). This neuroprotective effect was blocked by pretreatment with protein kinase G inhibitor KT5823, but not protein kinase A inhibitor H89, suggesting the involvement of cGMP-dependent signalling. Although Bay 60-7550 treatment for 24 h did not change the levels of phosphorylated mitogen-activated protein kinases ERK1/2 (pERK) and phosphorylated cAMP response element-binding protein (pCREB), it down-regulated pERK at 2 h and up-regulated a CREB co-activator, CREB-binding protein, at 24 h. Both of these effects were blocked by KT 5823. Furthermore, Bay 60-7550 reversed corticosterone-induced down-regulation of brain-derived neurotrophic factor protein levels 24 h after corticosterone exposure. In behavioural testing, Bay 60-7550 produced antidepressant-like effects and reduced corticosterone levels in stressed mice, further supporting the involvement of a PDE2-dependent pathway in mediating Bay 60-7550's effect during stress hormone insults. [ABSTRACT FROM AUTHOR]

Fatigue is associated with numerous harmful physical and mental health outcomes. Despite the established relationship between sleep and fatigue, research examining sleep variability within a person (i.e. intraindividual variability; IIV) and fatigue is limited. In addition, the associations between child and parent sleep regarding parent fatigue have not been explicitly explored, which could be relevant for parents of autistic children with increased sleep disturbance likelihood. The current study used two weeks of objective sleep (actigraphy) and subjective fatigue data from 81 parents and their children to explore associations among child sleep IIV, parent sleep IIV, and parent average daily fatigue, including evaluating evidence for mediation. Sleep IIV was estimated using a validated Bayesian model. Linear regression analyses indicated that greater parent total sleep time IIV predicted significantly higher fatigue levels. Child sleep IIV was unrelated to parent sleep IIV and fatigue, unsupportive of hypothesized mediation. Similarly, post hoc analyses examining child sleep averages, parent total sleep time IIV, and average parent fatigue were insignificant. Findings cautiously support the uniqueness of total sleep time IIV within parental sleep’s relationship with fatigue, independent of child sleep. Objective sleep IIV should continue to be examined in addition to average levels.Fatigue is associated with numerous harmful physical and mental health outcomes. Despite research indicating a relationship between fatigue and sleep, there has been a limited focus on how the variability of a person’s sleep may be associated with fatigue. In addition, previous studies have not explicitly explored relationships among child sleep, parent sleep, and parent fatigue. Increasing knowledge about this area of research could be particularly relevant for families with autistic children with an increased likelihood of sleep disturbances. The current study used two weeks of objective sleep (actigraphy) data and subjective ratings of parent fatigue from 81 parents and their autistic children to examine associations among child and parent within-person sleep variability regarding average parent fatigue levels. Evidence was assessed for the role of parent sleep variability in hypothesized connections between child sleep variability and parent fatigue. We found that only greater variability in parents’ total sleep time was associated with higher levels of parents’ average daily fatigue rating over the two weeks. Child sleep variability was not significantly associated with parent sleep variability or average daily fatigue. In addition, average levels of child sleep were unrelated to parent total sleep time variability and fatigue. Although cautious interpretation is required, findings support the idea that variability in total sleep time may be a unique aspect of parental sleep’s association with fatigue, independent of child sleep. In addition, sleep variability could be important to consider when examining sleep in addition to average levels of parameters like total sleep time. [ABSTRACT FROM AUTHOR]

Study Objectives: Brain regions involved in insomnia and chronic pain are overlapping and diffuse. The interactive role of physiological arousal in associations between insomnia symptoms and neural regions is unknown. This preliminary study examined whether arousal interacted with sleep in associations with gray matter volume of frontal (dorsolateral prefrontal cortex, anterior cingulate cortex) and temporal (right/left hippocampus) regions in adults with chronic widespread pain and insomnia complaints., Methods: Forty-seven adults with chronic widespread pain and insomnia (mean age = 46.00, standard deviation = 13.88, 89% women) completed 14 daily diaries measuring sleep onset latency (SOL), wake time after sleep onset, and total sleep time (TST), as well as Holter monitor assessments of heart rate variability (measuring physiological arousal), and magnetic resonance imaging. Multiple regressions examined whether average SOL, wake time after sleep onset, or TST were independently or interactively (with arousal/heart rate variability) associated with dorsolateral prefrontal cortex, anterior cingulate cortex, and left/right hippocampus gray matter volumes., Results: Shorter TST was associated with lower right hippocampus volume. TST also interacted with arousal in its association with right hippocampal volume, Specifically, shorter TST was associated with lower volume at highest and average arousal levels. SOL interacted with arousal in its association with anterior cingulate cortex volume, such that, among individuals with lowest arousal, longer SOL was associated with lower volume., Conclusions: Preliminary findings highlight the interactive roles of physiological arousal and insomnia symptoms in associations with neural structure in chronic widespread pain and insomnia. Individuals with the highest physiological arousal may be particularly vulnerable to the impact of shorter TST on hippocampal volume loss. Reducing SOL may only impact anterior cingulate cortex volume in those with lower physiological arousal., Citation: Curtis AF, Nair N, Hayse B, et al. Preliminary investigation of the interactive role of physiological arousal and insomnia complaints in gray matter volume alterations in chronic widespread pain. J Clin Sleep Med. 2024;20(2):293-302., (© 2024 American Academy of Sleep Medicine.)