Effects of sleep deprivation on neural functioning: an integrative review

Sleep deprivation has a broad variety of effects on human performance and neural functioning that manifest themselves at different levels of description. On a macroscopic level, sleep deprivation mainly affects executive functions, especially in novel tasks. Macroscopic and mesoscopic effects of sleep deprivation on brain activity include reduced cortical responsiveness to incoming stimuli, reflecting reduced attention. On a microscopic level, sleep deprivation is associated with increased levels of adenosine, a neuromodulator that has a general inhibitory effect on neural activity. The inhibition of cholinergic nuclei appears particularly relevant, as the associated decrease in cortical acetylcholine seems to cause effects of sleep deprivation on macroscopic brain activity. In general, however, the relationships between the neural effects of sleep deprivation across observation scales are poorly understood and uncovering these relationships should be a primary target in future research

Evidence for circadian influence on human slow wave sleep during daytime sleep episodes

The occurrence of slow wave sleep within spontaneously initiated daytime sleep episodes was studied to examine hypothesized associations with prior wakefulness and circadian factors. There was a strong relationship between measures of slow wave sleep and the proximity of sleep episodes to the maximum of body core temperature. Those sleep episodes that began within 4 hours of the maximum in body core temperature contained significantly more slow wave sleep than did all other daytime sleep periods, approximating proportions typical of nocturnal sleep. Multiple regression analysis revealed no relationship between measures of slow wave sleep and prior wakefulness. These findings are consistent with an hypothesized approximately-12-hour rhythm in the occurrence of slow wave sleep and they underscore the influence imposed on human sleep by the endogenous circadian timing system

Association between depressive symptoms and sleep neurophysiology in early adolescence

BACKGROUND: Depression is highly prevalent among adolescents, and depressive symptoms rise rapidly during early adolescence. Depression is often accompanied by subjective sleep complaints and alterations in sleep neurophysiology. In this study, we examine whether depressive symptoms, measured on a continuum, are associated with subjective and objective (sleep architecture and neurophysiology) measures of sleep in early adolescence. METHODS: High-density sleep EEG, actigraphy, and self-reported sleep were measured in 52 early adolescents (12.31 years; SD: 1.121; 25 female). Depressive symptoms were measured on a continuum using the Center for Epidemiological Studies Depression Scale (CES-D). The association between depressive symptoms and 2 weeks of actigraphy, self-reported sleep, sleep architecture, and sleep neurophysiology (slow wave activity and sigma power) was determined via multiple linear regression with factors age, sex, and pubertal status. RESULTS: Despite no association between polysomnography measures of sleep quality and depressive symptoms, individuals with more depressive symptoms manifested worse actigraphically measured sleep. Less sleep spindle activity, as reflected in nonrapid eye movement sleep sigma power, was associated with more depressive symptoms over a large cluster encompassing temporal, parietal, and occipital regions. Furthermore, worse subjectively reported sleep quality was also associated with less sigma power over these same areas. Puberty, age, and sex did not impact this association. CONCLUSIONS: Sleep spindles have been hypothesized to protect sleep against environmental disturbances. Thus, diminished spindle power may be a subtle sign of disrupted sleep and its association with depressive symptoms in early adolescence may signal vulnerability for depression

Multidetector-row computed tomography for evaluating the branching angle of the celiac artery: a descriptive study

<p>Abstract</p> <p>Background</p> <p>We performed this study in order to investigate the shape of the origin of the celiac artery in maximum intensity projection (MIP) using routine 64 multidetector-row computed tomography (MDCT) data in order to plan for the implantation of an intra-arterial hepatic port system.</p> <p>Methods</p> <p>A total of 1,104 patients with hepatocellular carcinoma were assessed with MDCT. In the definition of the branching angle, the anterior side of the abdominal aorta was considered the baseline, and the cranial and caudal sides were designated as 0 and 180 degrees, respectively. The angles between 0 and 90 degrees and between 90 and 180 degrees from the cranial side were considered upward and downward, respectively, and the branching angle of the celiac artery was classified every 30 degrees. The subclavian arterial route was used for the implantation of an intra-arterial hepatic port system in patients with branching angles of 150 degrees or more (sharp downward).</p> <p>Results</p> <p>The median branching angle was (median ± standard deviation) 135 ± 23 (range, 51–174) degrees. The branching was upward in 77 patients (7%) and downward in 1,027 patients (93%). The branching was downward with an angle of 120 to150 degrees in most patients (n = 613). The branching was sharply downward with an angle of 150 degrees or more in 177 patients (16%). A total of 10 patients were referred for interventional placement of an intra-arterial hepatic port system. The subclavian arterial route was used for implantation of an intra-arterial hepatic port system in 2 patients with sharp downward branching.</p> <p>Conclusions</p> <p>The branching angle of the celiac artery can be easily determined by the preparation of MIP images from routine MDCT data. MIP may provide useful information for the selection of the catheter insertion route in order to avoid a sharp branching angle of the celiac artery.</p