Investigation of Sleep

项目摘要/摘要：重症监护病房睡眠调查(ICU-睡眠) 睡眠不足是对ICU经历最常见的抱怨之一。重症监护室的睡眠往往是 轻度和非恢复性睡眠(相对于深度睡眠/恢复性睡眠)，严重支离破碎，分布不均 整个白天和黑夜，而不是合并到夜间。睡眠不足的患者患有 睡眠不足，一种注意力和记忆力受损的情况，以及认知减慢。ICU中的睡眠障碍 不仅来自光和噪音的污染，也来自于干扰大脑活动的药物 恢复性睡眠。睡眠不足也被认为是急性呼吸窘迫综合征的主要可改变的危险因素。 脑病，也称为神志不清。精神错乱是一种严重的精神错乱状态，影响高达80%的ICU 它是导致住院老年患者可预防的发病率和死亡率的六个主要原因之一。 许多在精神错乱中幸存下来的患者经历了长期的认知障碍和独立性丧失。 目前ICU中用于治疗睡眠问题的药物(如苯二氮类药物、抗精神病药物)不起作用 诱导自然睡眠，但不能防止精神错乱。相反，我们发现α2-肾上腺素能受体激动剂 右美托咪定可以诱导仿生睡眠，这是一种脑电模式的大脑状态 活动、脑血流和功能连接接近于恢复性睡眠。此外，最近的一次 对手术后患者的大型临床试验表明，小剂量的右美托咪定过夜给药 大大降低了精神错乱的风险。目前尚不清楚这种益处是否与改善睡眠有关，或者 在ICU期间睡眠更好的患者是否有更好的长期认知结果。我们的中央 假说是睡眠不足在很大程度上调节了短期和长期的认知损害 与危重疾病中的精神错乱有关。为了检验这一假设，我们的具体目标旨在 系统地确定1)预防性使用右美托咪定对睡眠质量的影响，2)最佳的治疗方法 给予右美托咪定(整夜VS仅在夜间开始)，2)睡眠剥夺对 短期认知功能和精神错乱，以及3)睡眠剥夺对长期认知功能的影响 危重疾病后的神经精神结局。在这些研究结束时，我们将扩大 我们在危重疾病中的睡眠生理学知识以及睡眠与精神错乱的关系；评估了一个新的 先发制人的治疗策略，以促进睡眠和防止精神错乱，并发展了对 睡眠如何影响危重疾病后的神经心理结果。因此，我们的研究将提供至关重要的 指导这位脆弱患者维持长期脑健康的个体化方法 人口。

PROJECT SUMMARY / ABSTRACT: Investigation of Sleep in the Intensive Care Unit (ICU-SLEEP) Sleep deprivation is among the most common complaints about the ICU experience. ICU sleep tends to be light and non-restorative (as opposed to deep / restorative sleep), severely fragmented, and distributed throughout the day and night rather than consolidated into nighttime hours. Sleep deprived patients suffer from sleep debt, a condition of impaired attention and memory, and cognitive slowing. Sleep disturbances in the ICU arise not only from light and noise pollution, but also from drugs that interfere with brain activity involved in restorative sleep. Sleep deprivation has also been suggested as a major modifiable risk factors for acute encephalopathy, also known as delirium. Delirium is an acute state of confusion that affects up to 80% of ICU patients, and is one of six leading causes of preventable morbidity and mortality in hospitalized elderly patients. Many patients who survive delirium experience long-term cognitive impairment and loss of independence. Current medications used in the ICU to treat sleep problems (e.g. benzodiazepines, antipsychotics) do not induce natural sleep and do not prevent delirium. In contrast, we have found that the α2-adrenoceptor agonist dexmedetomidine can induce biomimetic sleep, a brain state whose pattern of electroencephalogram (EEG) activity, cerebral blood flow, and functional connectivity approximates restorative sleep. Moreover, a recent large clinical trial in post-surgical patients suggests that low-dose dexmedetomidine given overnight substantially reduces the risk of delirium. It is unknown whether this benefit is linked to improved sleep, or whether patients with better sleep while in the ICU have better long-term cognitive outcomes. Our central hypothesis is that sleep deprivation substantially mediates both the short- and long-term cognitive impairments associated with delirium in critical illness. To test this hypothesis, our specific aims are designed to systematically determine 1) the impact of prophylactic dexmedetomidine on sleep quality, 2) the optimal way to give dexmedetomidine (all night vs at the beginning of the night only), 2) the impact of sleep deprivation on short-term cognitive function and delirium, and 3) the contribution of sleep deprivation to long-term neuropsychiatric outcome following critical illness. At the conclusion of these studies, we will have expanded our knowledge of sleep physiology in critical illness and relationship of sleep with delirium; evaluated a new preemptive therapeutic strategy to promote sleep and prevent delirium, and developed an understanding of how sleep impacts neuropsychological outcomes after critical illness. Our studies will thus will provide crucial guidance for individualized approaches to preserving long-term brain health in this vulnerable patient population.