Can enhancing SWS improve daytime function in patients with CFS?
Can enhancing SWS improve daytime function in patients with CFS?
批准号:
MR/M501591/1
负责人:
David Nutt
金额:
$15.78万
依托单位:
依托单位国家:
英国
项目类别:
Research Grant
财政年份:
2014
资助国家:
英国
项目状态:
已结题
起止时间:
2014 至 --
中文摘要
睡眠障碍是慢性疲劳综合征(CFS)的核心症状,对白天的功能和生活质量有巨大的负面影响。过去10年的睡眠研究已经提供了证据,证明大脑的睡眠调节机制,特别是体内平衡,在慢性疲劳综合症中被破坏。睡眠内稳态机制受损导致夜间睡眠不足,白天嗜睡和疲劳,导致这些患者出现主观和客观认知障碍。本研究将汇集CFS、睡眠和精神药理学方面的专家,研究CFS体内平衡损害的本质及其对白天功能的影响。我们建议使用一种药物来增加深度恢复性睡眠(慢波睡眠),这是夜间自我平衡驱动睡眠的标志。我们将对慢性疲劳综合症患者进行单剂量激发试验,以确定这种短暂而安全的慢波睡眠药物增强(以及体内平衡机制)在多大程度上对白天功能障碍有显著的有益影响。我们将包括对困倦、警惕性、记忆力和主观幸福感的测量。如果我们的结果是积极的,这显然会给慢性疲劳综合症患者带来一些潜在的好处。首先,它将强调一个主要的生物功能,即睡眠-觉醒周期的稳态成分,在慢性疲劳综合症中受损的程度。其次,它将使我们能够专注于特定的重要大脑通路。第三,它将使我们能够评估患者的日常功能和生活质量在良好的夜间睡眠后可能得到改善的程度。第四,我们的结果将指导未来的主要研究项目,以更好地了解慢性疲劳综合症的潜在睡眠障碍。最后,提出的工作可能提出潜在的治疗干预措施。
英文摘要
Sleep disturbance is a core symptom of chronic fatigue syndrome (CFS) and has a huge negative impact on daytime function and quality of life. Studies of sleep in the past 10 years have provided evidence that brain mechanisms of sleep regulation, and in particular homeostasis, are disrupted in CFS. Impaired homeostatic mechanisms of sleep result in poor sleep at night and sleepiness and fatigue during the day, contributing to the subjective and objective cognitive impairment seen in these patients. This study will bring together experts in CFS, sleep and psychopharmacology, to study the nature of homeostatic impairment in CFS and its impact on daytime function. We propose to use a pharmacological agent which increases deep restorative sleep (slow wave sleep) which is a marker for homeostatic drive to sleep at night. We will perform a single-dose challenge test in patient with CFS, to ascertain the extent to which this brief and safe pharmacological enhancement of slow wave sleep (and thus of homeostatic mechanisms) will have a significant beneficial impact on daytime impairment. We will include measures of sleepiness, vigilance, memory and subjective well-being. If our results are positive, this will clearly have several potential benefits to CFS sufferers. First, it will underscore the extent to which a major biological function, namely the homeostatic component of the sleep-wake cycle, is impaired in CFS. Second, it will enable us to focus on a specific important brain pathway. Third, it will allow us to evaluate the extent to which patients' daily functions and quality of life are likely to improve following a good night's refreshing sleep. Fourth, our results would direct future major programmes of research into understanding better the underlying sleep disorder in CFS. Finally, the proposed work may suggest potential therapeutic interventions.
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