Abstract
The intensity and severity of perceived pain does not correlate consistently with the degree of peripheral or central nervous system tissue damage or with the intensity of primary afferent or spinal nociceptive neurone activity. In this respect, the modulation of pain by emotion and context is now widely recognized. In particular, stress, fear and anxiety exert potent, but complex, modulatory influences on pain. Stress can either suppress pain (stress-induced analgesia) or exacerbate it (stress-induced hyperalgesia; SIH) depending on the nature, duration and intensity of the stressor. Herein, we review the methods and models used to study the phenomenon of SIH in rodents and humans and then present a detailed discussion of our current understanding of neural substrates and neurobiological mechanisms. The review provides perspectives and challenges for the current and future treatment of pain and the co-morbidity of pain with stress-related psychiatric disorders including anxiety and depression.
Parts of this text have previously been published in Olango and Finn (2013) and are reproduced by permission of the Royal Society of Chemistry.
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Funding from Science Foundation Ireland (10/IN.1/B2976 and 05/YI2/B686) and the Irish Research Council for Science, Engineering and Technology is gratefully acknowledged.
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Olango, W.M., Finn, D.P. (2014). Neurobiology of Stress-Induced Hyperalgesia. In: Taylor, B., Finn, D. (eds) Behavioral Neurobiology of Chronic Pain. Current Topics in Behavioral Neurosciences, vol 20. Springer, Berlin, Heidelberg. https://doi.org/10.1007/7854_2014_302
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