Abstract
Hyperalgesia is characterized by a decrease in the threshold for eliciting pain, enhanced pain with suprathreshold stimuli, and even spontaneous pain in severe cases. It is termed primary hyperalgesia when occurring at the site of injury, and secondary hyperalgesia when elicited from regions outside the area of injury. While there is general agreement that primary hyperalgesia is largely dependent on peripheral sensitization of nociceptive nerve endings (for review see Meyer et al., 1985), there is long-standing controversy regarding the neural mechanisms underlying secondary hyperalgesia. Lewis (1935) explained secondary hyperalgesia through peripheral mechanisms involving release of algogenic substances which would spread through axon reflexes around injured tissue and render remote nociceptors hyperexcitable. Against this view, Hardy et al. (1950) produced indirect evidence suggesting that secondary hyperalgesia would be due to changes in signal processing in the central nervous system.
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References
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© 1991 Macmillan Publishers Limited
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Torebjörk, E. (1991). Hyperalgesia. In: Franzén, O., Westman, J. (eds) Information Processing in the Somatosensory System. Wenner-Gren Center International Symposium Series. Palgrave, London. https://doi.org/10.1007/978-1-349-11597-6_29
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DOI: https://doi.org/10.1007/978-1-349-11597-6_29
Publisher Name: Palgrave, London
Print ISBN: 978-1-349-11599-0
Online ISBN: 978-1-349-11597-6
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