Acute total sleep deprivation decreases brain activation in the fronto-parietal attention network (prefrontal cortex and intraparietal sulcus) and in the salience network (insula and medial frontal cortex). Increased thalamic activation after sleep deprivation may reflect a complex interaction between the de-arousing effects of sleep loss and the arousing effects of task performance on thalamic activity.
Shorter sleep duration may impair insulin sensitivity and beta-cell function in nondiabetic white men, possibly contributing to later type 2 diabetes and cardiovascular disease.
The current findings demonstrate that total sleep deprivation and chronic circadian misalignment modulate cortisol levels and that chronic circadian misalignment increases plasma concentrations of pro- and anti-inflammatory proteins.
Sleep deprivation has been associated with altered feeding patterns. This study reports the relationship between sleep deprivation, caloric consumption, and connectivity in affected regions of the brain. Human subjects were sleep deprived for one night, compared to the control group (normal sleep), sleep deprived individuals consumed more food during the extra wake period, and in the recovery period consumed similar total calories but with significantly more fat and less carbohydrate composition than controls. Functional MRI scanning revealed connectivity differences between the dorsal anterior cingulate cortex (dACC) and multiple regions of the brain, with the pathways between the dACC and putamen and dACC and insula being most highly correlated with increased fat and decreased carbohydrate consumption. Based on what is known of these pathways the authors suggest a connectivity mechanism by which attentiveness and reward centers (insula and putamen) interact with homeostatic-stress centers (dACC) to explain the increased consumption of fat after sleep deprivation.
Patients with Angelman’s syndrome (AS) have imprinting of the paternal allele of the unbiquitin ligase encoded by the Ube3a gene and sleep disturbances inclusive of short sleep duration and increased sleep latency. The authors of this work link Ube3a to modulation of circadian rhythms through the accumulation of the molecular clock protein BMAL1 in a mouse model of AS. AS mice have lengthened endogenous circadian period lengths (which is rescued ex-vivo by unsilencing the paternal allele), and entrain faster to advances in light than wild-type controls. Additionally AS mice have an increased body weight with a higher fat composition than controls. These data provide mechanistic detail to the link between altered metabolism and circadian disruption not only in AS but more broadly as well.
The authors perform a meta-analysis to explore the safety of sedation provided by anesthesiologists or non-anesthesiologists to patients undergoing gastrointestinal endoscopic procedures. No differences were detected between the incidence of desaturation or in the need of airway intervention between both groups. Satisfaction of gastroenterologists and patients was in favor of anesthesiologists. Important limitations like no control for hemodynamics or other aspects like recovery could be studied based on the data collected. Their conclusions might raise some debate in a topic that is controversial by nature.
Dexmedetomidine activates mechanisms of similar nature to those activated for natural sleep induction after sleep deprivation. Using animal models including those with a selective knockdown of 2A adrenergic receptors of the locus ceruleus, the study demonstrates that to induce its sedative effect dexmedetomidine engages neuronal systems involved in natural sleep pathways, which are different to the mechanisms involved in the induction of general anesthesia.
In this article, the authors evaluate the elusive link between delirium and sleep deprivation in 223 medical ICU patients over a 201 day period. Patient were also assessed for delirium on a regular basis. Using the Richards-Campbell Sleep Questionnaire, daily perceived sleep quality ratings were measured. Delirium was measured twice a day with the Confusion Assessment Method tool (CAM) for the ICU. In this study, perceived sleep quality was similar in ICU patients who developed delirium and those who did not. Additionally, perceived sleep quality was unrelated to delirium transition. This is another piece of work that fails to establish a link between delirium and sleep deprivation.
In this review, from one of the nation’s centers for evaluating sleep in the ICU, Dr. Pisani and colleagues offer a concise update on developments in critical care medicine pertaining to sleep. Specifically, the authors provide a very nice discussion on circadian rhythm in critical illness and a good review of potentially modifiable disruptors to sleep such as noise, patient care activities and light. Additionally, the authors give very helpful descriptions with different methods of analysis of EEG enabling the reading to better understand EEG interpretation for sleep evaluation in ICU patients. Overall this is a welcomed addition to the growing body of review articles focusing on sleep in the ICU.
In the article, the researchers evaluate sleep in the ICU after initiating a multimodal approach to improving sleep. The investigators enrolled 12 patients who were admitted in a neurological ICU. Sleep promoting interventions such as environmental light (eye mask) and noise reduction (headphones) were implemented as well as prescribing melatonin. Unfortunately, for many patients, EEG recordings could not be interpreted. In those patients who recordings could be obtained, the authors found no difference between intervention and non-intervention groups.