Short-Term Effects of Social Exclusion at work and Worries on Sleep

The present study investigated short-term effects of daily social exclusion at work on various indicators of sleep quality and tested the mediating role of work-related worries using a time-based diary study with ambulatory assessments of sleep quality. Ninety full-time employees participated in a 2-week data collection. Multilevel analyses revealed that daily workplace social exclusion and work-related worries were positively related to sleep fragmentation in the following night. Daily social exclusion, however, was unrelated to sleep onset latency, sleep efficiency and self-reported sleep quality. Moreover, worries did not mediate the effect of social exclusion at work on sleep fragmentation. Theoretical and practical implications of the results are discussed.

Apnea and oxygen desaturations in children treated with opioids after adenotonsillectomy for obstructive sleep apnea syndrome: a prospective pilot study

Recent case reports have alerted the medical community of fatality in children receiving codeine after tonsillectomy and/or adenoidectomy for obstructive sleep apnea syndrome.

Effect of continuous positive airway pressure on day/night rhythm of prothrombotic markers in obstructive sleep apnea

Obstructive sleep apnea (OSA) has been associated with an increased risk of atherothrombotic events. A prothrombotic state might partially explain this link. This study investigated OSA patients' day/night rhythm of several prothrombotic markers and their potential changes with therapeutic continuous positive airway pressure (CPAP).

Thinner cortex in the frontal lobes in mentally disordered offenders

Antisocial and violent behaviour have been associated with both structural and functional brain abnormalities in the frontal and the temporal lobes. The aim of the present study was to assess cortical thickness in offenders undergoing forensic psychiatric assessments, one group with psychopathy (PSY, n=7) and one group with autism spectrum disorder (ASD, n=7) compared to each other as well as to a reference group consisting of healthy non-criminal subjects (RG, n=12). A second aim was to assess correlation between scores on a psychopathy checklist (PCL-SV) and cortical thickness. Magnetic resonance imaging (MRI) and surface-based cortical segmentation were used to calculate cortical thickness. Analyses used both regions of interest and statistical maps. When the two groups of offenders were compared, there were no differences in cortical thickness, but the PSY group had thinner cortex in the temporal lobes and in the whole right hemisphere compared to RG. There were no differences in cortical thickness between the ASD group and RG. Across subjects there was a negative correlation between PCL-SV scores and cortical thickness in the temporal lobes and the whole right hemisphere. The findings indicate that thinner cortex in the temporal lobes is present in psychopathic offenders and that these regions are important for the expression of psychopathy. However, whether thinner temporal cortex is a cause or a consequence of the antisocial behaviour is still unknown.

European guidelines on management of restless legs syndrome: report of a joint task force by the European Federation of Neurological Societies, the European Neurological Society and the European Sleep Research Society

Since the publication of the first European Federation of Neurological Societies (EFNS) guidelines in 2005 on the management of restless legs syndrome (RLS; also known as Willis-Ekbom disease), there have been major therapeutic advances in the field. Furthermore, the management of RLS is now a part of routine neurological practice in Europe. New drugs have also become available, and further randomized controlled trials have been undertaken. These guidelines were undertaken by the EFNS in collaboration with the European Neurological Society and the European Sleep Research Society.

Orexin receptor antagonism, a new sleep-enabling paradigm: a proof-of-concept clinical trial

The orexin system is a key regulator of sleep and wakefulness. In a multicenter, double-blind, randomized, placebo-controlled, two-way crossover study, 161 primary insomnia patients received either the dual orexin receptor antagonist almorexant, at 400, 200, 100, or 50 mg in consecutive stages, or placebo on treatment nights at 1-week intervals. The primary end point was sleep efficiency (SE) measured by polysomnography; secondary end points were objective latency to persistent sleep (LPS), wake after sleep onset (WASO), safety, and tolerability. Dose-dependent almorexant effects were observed on SE , LPS , and WASO . SE improved significantly after almorexant 400 mg vs. placebo (mean treatment effect 14.4%; P < 0.001). LPS (–18 min (P = 0.02)) and WASO (–54 min (P < 0.001)) decreased significantly at 400 mg vs. placebo. Adverse-event incidence was dose-related. Almorexant consistently and dose-dependently improved sleep variables. The orexin system may offer a new treatment approach for primary insomnia.

Ten novel mutations in the NR5A1 gene cause disordered sex development in 46,XY and ovarian insufficiency in 46,XX individuals

Steroidogenic factor-1 (SF-1/NR5A1) is a nuclear receptor that regulates adrenal and reproductive development and function. NR5A1 mutations have been detected in 46,XY individuals with disorders of sexual development (DSD) but apparently normal adrenal function and in 46,XX women with normal sexual development yet primary ovarian insufficiency (POI).

Sleep deprivation before stroke is neuroprotective: A pre-ischemic conditioning related to sleep rebound

BACKGROUND AND AIM: We have previously shown in a rat model of focal cerebral ischemia that sleep deprivation after stroke onset aggravates brain damage. Others reported that sleep deprivation prior to stroke is neuroprotective. The main aim of this study was to test the hypothesis that the neuroprotection may be related to an increase in sleep (sleep rebound) during the acute phase of stroke. METHODS: Male Sprague Dawley rats (n=36) were subjected to continuous polygraphic recordings for baseline, total sleep deprivation (TSD), and 24h after ischemia. TSD for 6h was performed by gentle handling and immediately followed by ischemia. Focal cerebral ischemia was induced by permanent occlusion of distal branches of the middle cerebral artery. Control experiments included ischemia without SD (nSD) and sham surgery with TSD (n=6/group). RESULTS: Shortly after stroke, the amount of slow wave sleep (SWS) and paradoxical sleep (PS) increased significantly (p<0.05) in the TSD/ischemia, resulting in an increase in the total sleep time by 30% compared to baseline, or by 20% compared with the nSD/ischemia group. The infarct volume decreased significantly by 50% in the TSD/ischemia compared to nSD group (p<0.02). Removal of sleep rebound by allowing TSD-rats sleep for 24h before ischemia eliminated the reduction in the infarct size. CONCLUSION PRESTROKE: Sleep deprivation results in sleep rebound and reduces brain damage. Sleep rebound may be causally related to the neuroprotection.