Hypersensitisation of the pain transmission can occur at any level of the neuraxis. This can result in two phenomena: '''hyperalgesia''', where an exaggerated response to a noxious stimulus is experienced, and '''allodynia''', where a non-noxious stimulus (such as gentle touch) elicits a painful response.
** Type A and C peripheral nociceptors are sensitised due to inflammatory mediators released by tissue damage. This lowers the response threshold of the receptors, or a greater response to the same stimulus is produced. Both mechanisms may work in conjunction.
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* Centrally, giving '''central sensitisation'''.
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** The exictability of spinal nociceptive neurons is enhanced, giving a hypersensitive and hyperactice nociceptive transmission system.
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** Central sensitisation may be short-lived when it is associated with transient changes in neurotransmitter activity.
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** Central sensitisation may be long-lived when it is associated with phenotypic changes in central neurons.