Investigating Correlates and Therapeutics of Fatigue

研究疲劳的相关性和治疗方法

• 批准号: 10255270
• 负责人: Leorey Saligan
• 金额: $ 26.23万
• 依托单位: NATIONAL INSTITUTE OF NURSING RESEARCH
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10255270
• 关键词: Astrocytes; Chronic Fatigue Syndrome; Clinical; Cytokine Gene; Depressed mood; Development; Drowsiness; Energy Metabolism; Etiology; Fatigue; Functional disorder; Gene Expression; Goals; IL8 gene; Individual; Inflammatory; Insulin-Like Growth Factor I; Interleukin-1 beta; Interleukin-6; Investigation; Mental Depression; Metabolism; Mood Disorders; Motor Neuron Disease; Multiple Sclerosis; Neurologic; Neurotransmitters; Norepinephrine; Pain; Parkinson Disease; Patient Self-Report; Pharmacotherapy; Physical activity; Plasma; Play; Population; Postpoliomyelitis Syndrome; Questionnaires; Role; Serotonin; Skeletal Muscle; Sleep; Standardization; Stress; Stroke; Symptoms; TNF gene; Therapeutic; comorbidity; cytokine; depressive symptoms; experience; fibromyalgia patients; healthy volunteer; hypothalamic-pituitary-adrenal axis; improved; multicatalytic endopeptidase complex; muscle strength; psychologic; theories

Fatigue is defined as a lack of energy and an overwhelming sense of tiredness that is distinguishable from sadness or weakness. Fatigue in the absence of psychological co-morbidities such as depression, has been associated with many neurological conditions, including multiple sclerosis, Parkinsons disease, motor neuron disease, stroke and post-polio syndromes. The pathophysiology of fatigue remains poorly understood. Dysregulation of pro-inflammatory cytokines (TNF alpha, IL-1 beta, IL-6), HPA axis dysfunction, disturbances of astroglia metabolism, and decreased levels of neurotransmitters (norepinephrine, serotonin) have all been proposed as mechanisms. The relationship between symptoms of depression and fatigue may be bidirectional, implying that these conditions have shared mechanisms. This association is evidenced by the fact that the cytokines associated with neurovegetative symptoms including fatigue are also associated with high rates of depression. Others argue against the shared mechanism hypothesis, as depressive symptoms may improve with pharmacotherapy, while symptoms of fatigue are resistive. Our investigation characterizes the symptoms of fatigue from different clinical populations (healthy volunteers, patients with fibromyalgia, chronic fatigue syndrome, and mood disorders) using standardized questionnaires and determine if physical activity, pain, depression, fatigue catastrophizing, stress, and daytime sleepiness play a role in their fatigue experience. This study will also examine the potential role of plasma cytokines, gene expression, and hypothalamic-pituitary-adrenal axis (HPA) functioning in symptoms of fatigue in these individuals. Information collected from this investigation will be useful to improve our understanding of the possible etiologic mechanisms of fatigue.

疲劳被定义为缺乏能量和压倒性的疲倦感，与悲伤或虚弱不同。在没有心理合并症（例如抑郁）的情况下，疲劳与许多神经系统疾病有关，包括多发性硬化症，帕金森氏病，运动神经元疾病，中风和后polio综合症。疲劳的病理生理学知之甚少。促炎性细胞因子（TNF Alpha，IL-1β，IL-6），HPA轴功能障碍，代谢障碍以及神经递质（Norepinepine）（去甲肾上腺素，羟色胺）的水平降低均已提议所有均已提出，所有均已提议所有均作为机械化。抑郁症状与疲劳之间的关系可能是双向的，这意味着这些疾病具有共同的机制。这种关联证明了这一事实是，与包括疲劳在内的神经疗法症状相关的细胞因子也与高抑郁率有关。其他人则反对共同的机制假设，因为药物治疗可能会改善抑郁症状，而疲劳症状是抵抗力的。我们的研究是使用标准化问卷调查的不同临床人群（健康志愿者，纤维肌痛，慢性疲劳综合症和情绪障碍）的疲劳症状的特征，并确定身体活动，疼痛，抑郁，抑郁症，疲劳灾难性，压力和白天在疲劳经历中起作用。这项研究还将检查血浆细胞因子，基因表达和下丘脑 - 垂体 - 肾上腺轴（HPA）在这些个体疲劳症状中起作用的潜在作用。从这项研究中收集的信息将有助于提高我们对疲劳可能的病因机制的理解。