829 Chronic sleep deprivation in a 75-year-old female leading to micro-sleeps with atonia causing increased falls

Introduction Each year, 3 million older people are treated in emergency departments for fall-related injuries. These falls can lead to serious injuries and expensive health care costs. Some have looked into the relationship between chronic sleep disturbances and falls linking chronic sleep deprivation or excessive sleep to falling. Here, we present a unique case of chronic sleep deprivation causing sleep attacks or micro-sleeps with atonia causing falls. Report of case(s) We present a 75-year-old F with a history of increased daily falls up to 4x per day that began 3 years ago. She denies any triggering events, auras, frequent tripping, loss of balance or weakness. Reportedly, she will be walking along then suddenly falls. She is aware that she is falling yet feels as though she cannot prevent/stop the fall or break her fall. No one has witnessed her fall, but is frequently found lying on the floor. She has never sustained a serious injury as a result of her falls. She has an 8 year history of restless legs syndrome treated with ropinirole and a 10 year history of obstructive sleep apnea (OSA) treated with CPAP. Her general bedtime is 2200 and wake-time is 0400 with an average 3–4 hrs of quality sleep per night for many years. She endorses severe daytime hypersomnolence and chronic hypoxemia on 3L home oxygen. We hypothesized her falls were secondary to sleep attacks or micro-sleeps where she enters REM sleep and develops atonia. Nocturnal sleep study followed by MSLT showed severe OSA with severe, persistent daytime sleeping with REM sleep and atonia. She had a mean sleep latency of 2 minutes with 1 sleep-onset REM period. We started NIPPV with supplemental oxygen treatment, and within 4 months her daytime hypersomnolence resolved, exercise intolerance improved, saturations improved to 89–90% on room air, and has <1 fall per day. Conclusion Here, we presented a unique case of a 75 yo F with recurrent falls secondary to chronic sleep deprivation causing micro-sleeps involving REM sleep and atonia. She was treated with NIPPV which improved her oxygenation and reduced her number of falls to <1 per day. Support (if any):

Sleep modulates alcohol toxicity in Drosophila

Study ObjectivesAlcohol abuse is a significant public health problem, particularly in populations in which sleep deprivation is common as such as shift workers and aged individuals. Although research demonstrates the effect of alcohol on sleep, little is known about the role of sleep in alcohol sensitivity and toxicity. We investigated sleep as a factor modulating alcohol toxicity using Drosophila melanogaster, a model system ideal for studies of sleep, alcohol and aging.MethodsFollowing 24 hours of sleep deprivation using mechanical stimulation, Drosophila were exposed to binge-like alcohol exposures. Behavioral sensitivity, tolerance, and mortality were assessed. The effects of chronic sleep deprivation on alcohol toxicity were investigated using a short sleep mutant insomniac. Pharmacological induction of sleep for prior to alcohol exposure was accomplished using a GABAA-receptor agonist, 4,5,6,7-tetrahydroisoxazolo(5,4-c)pyridin-3-ol (THIP) to determine if increased sleep mitigated the effects of alcohol toxicity on middle-aged flies and flies with environmentally disrupted circadian clocks mimicking groups more vulnerable to the effects of alcohol.ResultsAcute sleep deprivation increased alcohol-induced mortality following alcohol exposure. However, sleep deprivation had no effect on alcohol absorbance or clearance. Sleep deprivation also abolished functional tolerance measured 24 hours after the initial alcohol exposure, although tolerance at 4 h was observed. Pharmacologically increasing sleep prior to alcohol exposure decreased alcohol-induced mortality.ConclusionsSleep quantity prior to alcohol exposure affects alcohol toxicity with decreased sleep increasing alcohol toxicity and dampened 24-hour alcohol tolerance. In contrast, increased sleep mitigated alcohol-induced mortality even in vulnerable groups such as aging flies and those with circadian dysfunction.Statement of significanceWith the growing incidence of sleep deprivation and sleep disorders across adolescents and adults, it is important to understand the role of sleep in alcohol toxicity to develop future therapies for prevention and treatment of alcohol-induced pathologies. Using Drosophila melanogaster, an established model for both sleep and alcohol research, we found that acute and chronic sleep deprivation increased alcohol toxicity and eliminated long-term functional alcohol tolerance. In contrast, increased sleep prior to binge-like alcohol exposure mitigated alcohol-induced mortality even in vulnerable groups with higher susceptibility to alcohol toxicity.