Multiple sclerosis and fatigue: A review on the contribution of inflammation and immune-mediated neurodegeneration.

TL;DR: A hierarchical Bayesian framework for interoception, homeostatic/allostatic control, and meta-cognition is outlined that connects fatigue and depression to the experience of chronic dyshomeostasis and proposes that the performance of interoceptive- allostatic circuitry is monitored by a metacognitive layer that updates beliefs about the brain's capacity to successfully regulate bodily states.

TL;DR: A neurobiological overview of interoception is presented and how interoceptive impairments at different levels relate to specific physical and mental health conditions, including sickness behaviors and fatigue, depression, eating disorders, autism, and anxiety are described.

TL;DR: An overview of contemporary pathophysiological theories of fatigue in MS is provided and it is discussed how the mechanisms they propose may become measurable with emerging technologies and thus lay a foundation for future personalised treatments.

TL;DR: This work proposes a model of an imbalance in energy availability and energy expenditure as a consequence of low-grade inflammation, and presents evidence for these metabolic pathways in models of persistent fatigue, focusing on chronic fatigue syndrome and cancer-related fatigue.

TL;DR: The data regarding the pathophysiological foundations of ‘psychosomatic’ symptoms and the implications that this has for conceptualization of what may more appropriately be termed physio‐somatic symptoms are reviewed.

TL;DR: It is concluded that the observed dysregulation in multiple sclerosis is more likely a secondary effect of the extent of brain damage rather than primarily involved in the pathogenesis of MS.

TL;DR: Investigation of whether intracerebroventricular administration of an interleukin-1 receptor antagonist (IL-1ra) would block behavioral effects of a stressor found it to block interference with escape learning and enhancement of fear conditioning normally produced by this treatment.

TL;DR: The data do not support a role for hypocortisolism in MS once the disease is established, and data from studies of experimental animals exposed to chronic inflammatory stress showed mild increased activation of the HPA axis with increased relative activity of AVP in the regulation of the pituitary-adrenal axis.