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Illness-induced hyperalgesia: Mediators, mechanisms and implications

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Part of the book series: Progress in Inflammation Research ((PIR))

Abstract

The focus of this chapter will be different from the others in this book as it takes a more holistic view of the organism. Such a view examines hyperalgesia from an adaptive perspective and makes the argument that exaggeration of pain is a natural and normal consequence of immune activation. During illness, infection, and injury, activated immune cells release substances that signal the brain, triggering a constellation of coordinated responses designed to enhance survival (for review, see Ref [1, 2]). Hyperalgesia will be argued to be simply one component of this brain-mediated illness response. There has been increasing recognition that the immune system is involved in the regulation of many diverse phenomena to which it has not previously thought to be relevant [2], and here we will argue that pain is such a phenomenon.

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Watkins, L.R., Maier, S.F. (1999). Illness-induced hyperalgesia: Mediators, mechanisms and implications. In: Watkins, L.R., Maier, S.F. (eds) Cytokines and Pain. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8749-6_3

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  • DOI: https://doi.org/10.1007/978-3-0348-8749-6_3

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