IntroductionUnderstanding how environmental interact challenges with genetic predispositions modulate health and wellbeing is an important area of biomedical research. Circadian rhythms play an important role in coordinating the multitude of cellular and tissue processes that organisms use to predict and adapt to regular changes in the environment, and robust circadian rhythms contribute to optimal physiological and behavioral responses to challenge. However, artificial lighting and modern round-the-clock lifestyles can disrupt the circadian system, leading to desynchronization of clocks throughout the brain and body. When coupled with genetic predispositions, circadian desynchronization may compound negative outcomes. Polymorphisms in the brain-derived neurotrophic (BDNF) gene contribute to variations in neurobehavioral responses in humans, including impacts on sleep, with the common Val66Met polymorphism linked to several negative outcomes.MethodsWe explored how the Val66Met polymorphism modulates the response to environmental circadian desynchronization (ECD) in a mouse model. ECD was induced by housing adult male mice in a 20 h light-dark cycle (LD10:10; 10 h light, 10 h dark). Sleep and circadian activity were recorded in homozygous (Met) mice and their wild-type (Val) littermates in a standard 24 h LD cycle (LD12:12), then again after 20, 40, and 60 days of ECD.ResultsWe found ECD significantly affected the sleep/wake timing in Val mice, however, Met mice maintained appropriate sleep timing after 20 days ECD, but not after 40 and 60 days of ECD. In addition, the rise in delta power at lights on was absent in Val mice but was maintained in Met mice. To elucidate the circadian and homeostatic contribution to disrupted sleep, mice were sleep deprived by gentle handling in LD12:12 and after 20 days in ECD. Following 6 h of sleep deprivation delta power was increased for both Val and Met mice in LD12:12 and ECD conditions. However, the time constant was significantly longer in the Val mice during ECD compared to LD12:12, suggesting a functioning but altered sleep homeostat.DiscussionThese data suggest the Val66Met mutation is associated with an ability to resist the effects of LD10:10, which may result in carriers suffering fewer negative impacts of ECD.

To facilitate awake endotracheal intubation, a blockade of the glossopharyngeal, superior laryngeal, and recurrent laryngeal nerves can be utilized. The peripheral blockade of nerves in the neck is most often used to facilitate awake endotracheal intubation for the patient with a difficult airway. Although topicalization with minimal-to-moderate sedation is often sufficient to perform an awake intubation, one should be knowledgeable of all the alternative methods should the need arise. This chapter focuses on the indications, relevant anatomy, and complications of these blocks. Also described is blockade of the cervical plexus, which is useful in facilitating surgery on more superficial neck structures.

Regional anesthesia for procedures involving the head can be easily achieved through the careful application of peripheral nerve blockade. Because the head has predictable surface and bony landmarks, the blocks can easily be placed pre- and intraoperatively to provide both regional anesthesia and postoperative analgesia with minimal complications. The peripheral blockade of nerves involving the head can provide perioperative anesthesia as well as management of both perioperative pain and chronic pain. The purpose of this chapter is to provide information and recommendations on how to best perform these blocks as well as describe their indications, complications, and relevant surrounding anatomy.