The excessive sensitivity to pain
Hyperalgesia pertains to the excessive sensitivity to pain. It is often associated with damaged nerve cells, such as nociceptors (i.e. sensory receptors responsible for detecting or responding to pain).
Hyperalgesia may also be induced by platelet-activating factor associated with inflammatory response of the body. The immune cells interact with the peripheral nervous system resulting in the release of cytokines and chemokines.1
Hyperalgesia may be experienced in focal areas or may be diffuse, i.e. affecting the body. It may be primary or secondary. A primary hyperalgesia is a type of hyperalgesia in which the pain sensitivity occurs directly in the damaged tissues. A secondary hyperalgesia is one in which the pain sensitivity occurs in surrounding undamaged tissues.
An example of hyperalgesia is opioid-induced hyperalgesia. Opioid treatments of chronic pain followed by opioid withdrawals may lead to hyperalgesia. The discontinuation of pain treatment may extremely activate the pain pathways in the nervous system.
Word origin: Greek hupér (“over”) + Greek algesis (pain)
1 Marchand F, Perretti M, McMahon SB (July 2005). “Role of the immune system in chronic pain”. Nat. Rev. Neurosci. 6 (7): 521–32.