The University of Texas MD Anderson Cancer Center, Division of Internal Medicine, Department of Symptom Research, Houston, TX 77030, USA.
The University of Texas MD Anderson Cancer Center, Division of Internal Medicine, Department of Symptom Research, Houston, TX 77030, USA; University Medical Center, Laboratory of Neuroimmunology of Developmental Origin of Disease, Utrecht, The Netherlands.
Trends Neurosci. 2014 Jan;37(1):39-46. doi: 10.1016/j.tins.2013.10.003. Epub 2013 Nov 13.
The exact nature and pathophysiology of fatigue remain largely elusive despite its high prevalence in physically ill patients. Studies on the relationship between the immune system and the central nervous system provide a new perspective on the mechanisms of fatigue. Inflammatory mediators that are released by activated innate immune cells at the periphery and in the central nervous system alter the metabolism and activity of neurotransmitters, generate neurotoxic compounds, decrease neurotrophic factors, and profoundly disturb the neuronal environment. The resulting alterations in fronto-striatal networks together with the activation of insula by inflammatory interoceptive stimuli underlie the many dimensions of fatigue including reduced incentive motivation, decreased behavioral flexibility, uncertainty about usefulness of actions, and awareness of fatigue.
尽管疲劳在身体不适的患者中非常普遍，但它的确切性质和病理生理学仍然很大程度上难以捉摸。免疫系统和中枢神经系统之间关系的研究为疲劳机制提供了新的视角。外周和中枢神经系统中激活的固有免疫细胞释放的炎症介质会改变神经递质的代谢和活性，产生神经毒性化合物，减少神经营养因子，并严重扰乱神经元环境。由此导致的额-纹状体网络改变，以及炎症内感受刺激对脑岛的激活，是疲劳的许多方面的基础，包括减少激励动机、降低行为灵活性、对行为有用性的不确定性以及对疲劳的感知。
