Journal
TRENDS IN NEUROSCIENCES
Volume 37, Issue 1, Pages 39-46Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2013.10.003
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Funding
- National Institute of Neurological Diseases and Stroke of the National Institutes of Health [RO1NS073939, RO1NS074999]
- MD Anderson Cancer Center research funds
- STARS award of the University Cif Texas System
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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.
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