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Trends Neurosci. 2014 Jan;37(1):39-46. doi: 10.1016/j.tins.2013.10.003. Epub 2013 Nov 13.

The neuroimmune basis of fatigue.

Author information

1
The University of Texas MD Anderson Cancer Center, Division of Internal Medicine, Department of Symptom Research, Houston, TX 77030, USA. Electronic address: rdantzer@mdanderson.org.
2
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.
3
The University of Texas MD Anderson Cancer Center, Division of Internal Medicine, Department of Symptom Research, Houston, TX 77030, USA.
4
NutriNeuro, INRA, UMR 1286, University of Bordeaux 2, Bordeaux, France.

Abstract

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.

PMID:
24239063
PMCID:
PMC3889707
DOI:
10.1016/j.tins.2013.10.003
[Indexed for MEDLINE]
Free PMC Article

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