From disaster related stress causing insomnia, to poor air quality causing sleep related breathing problems, climate change poses a potentially serious threat to human sleep. We conducted a systematic review evaluating the relationship between climate change and human sleep in the PubMed, Scopus, and Cochrane databases from 1980 through 2017 following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Inclusion criteria included epidemiologic studies published in English that reported observational population data on human sleep and its relationship to climate change, temperature, extreme weather events and climate related disasters (e.g. hurricanes, floods, and wildfires). We excluded non-human studies, laboratory or experimental physiology studies, commentaries or letters, review articles, and articles on wind turbines. Using a systematic search strategy, 16 studies met the inclusion criteria. Six studies related to the effects of rising temperature, seven studies related to extreme weather events, and three studies related to floods or wildfires. Diminished total sleep times and sleep disruption were most commonly reported, especially among the most vulnerable populations including the elderly and low-income; however, the body of evidence was limited and further well-designed human studies are clearly needed. We present a conceptual framework for identifying the emerging threats of climate change and understanding their respective effects on human sleep.

The hypothermic response of rats to only brief ( approximately 2 h) hypoxia has been described previously. The present study analyzes the hypothermic response in rats, as well as level of activity (L(a)), to prolonged (63 h) hypoxia at rat thermoneutral temperature (29 degrees C). Mini Mitter transmitters were implanted in the abdomens of 10 adult Sprague-Dawley rats to continuously record body temperature (T(b)) and L(a). After habituation for 7 days to 29 degrees C and 12:12-h dark-light cycles, 48 h of baseline data were acquired from six control and four experimental rats. The mean T(b) for the group oscillated from a nocturnal peak of 38.4 +/- 0.18 degrees C (SD) to a diurnal nadir of 36.7 +/- 0.15 degrees C. Then the experimental group was switched to 10% O(2) in N(2). The immediate T(b) response, phase I, was a disappearance of circadian rhythm and a fall in T(b) to 36.3 +/- 0.52 degrees C. In phase II, T(b) increased to a peak of 38.7 +/- 0.64 degrees C. In phase III, T(b) gradually decreased. At reoxygenation at the end of the hypoxic period, phase IV, T(b) increased 1.1 +/- 0.25 degrees C. Before hypoxia, L(a) decreased 70% from its nocturnal peak to its diurnal nadir and was entrained with T(b). With hypoxia L(a) decreased in phase I to essential quiescence by phase II. L(a) had returned, but only to a low level in phase III, and was devoid of any circadian rhythm. L(a) resumed its circadian rhythm on reoxygenation. We conclude that 63 h of sustained hypoxia 1) completely disrupts the circadian rhythms of both T(b) and L(a) throughout the hypoxic exposure, 2) the hypoxia-induced changes in T(b) and L(a) are independent of each other and of the circadian clock, and 3) the T(b) response to hypoxia at thermoneutrality has several phases and includes both hypothermic and hyperthermic components.

The American Academy of Sleep Medicine (AASM) commissioned a Workgroup to develop quality measures for the care of patients with narcolepsy. Following a comprehensive literature search, 306 publications were found addressing quality care or measures. Strength of association was graded between proposed process measures and desired outcomes. Following the AASM process for quality measure development, we identifi ed three outcomes (including one outcome measure) and seven process measures. The fi rst desired outcome was to reduce excessive daytime sleepiness by employing two process measures: quantifying sleepiness and initiating treatment. The second outcome was to improve the accuracy of diagnosis by employing the two process measures: completing both a comprehensive sleep history and an objective sleep assessment. The third outcome was to reduce adverse events through three steps: ensuring treatment follow-up, documenting medical comorbidities, and documenting safety measures counseling. All narcolepsy measures described in this report were developed by the Narcolepsy Quality Measures Workgroup and approved by the AASM Quality Measures Task Force and the AASM Board of Directors. The AASM recommends the use of these measures as part of quality improvement programs that will enhance the ability to improve care for patients with narcolepsy. N arcolepsy is one of the most intriguing causes of excessive daytime sleepiness. Narcolepsy (with cataplexy) affects approximately 25-50 per 100,000 people in the US. 1 The prevalence of narcolepsy without cataplexy is higher still, yet the disorder remains under-recognized and under-diagnosed. Presently, narcolepsy treatment varies due to a heterogeneous presentation of symptoms and severity of disease among patients. Although narcolepsy is uncommon compared to other sleep disorders, the American Academy of Sleep Medicine (AASM) included it in the quality measure process because it is a disorder that generally results in signifi cant daily dysfunction when not appropriately treated. The quality measures described in this position paper include children and adolescents in the targeted patient population, as 40% to 50% of adult patients report onset of symptoms before age 15 years. 2,3 However, the Workgroup notes limitations in diagnostic testing and lack of level 1 evidence-based treatment studies in the pediatric population. Because of the paucity of clinical trials and FDA-approved treatments for narcolepsy for both pediatric and adult patients, the Workgroup believed that it was imperative to include off-label options in treatment plans.The International Classifi cation of Sleep Disorders, Third Edition (ICSD-3) was used as the narcolepsy diagnostic reference. The ICSD-3 subdivides narcolepsy into type 1 and 2, with type 1 characterized by excessive daytime sleepiness, hypocretin defi ciency syndrome, and signs of REM-sleep dissociation (e.g., cataplexy, hypnagogic and hypnopompic hallucinations, sleep paralysis) and type 2 characterized by excessive daytime sleepiness and ...