is an increased sensitivity to pain
, which may be caused by damage to nociceptors
or peripheral nerves
Hyperalgesia can be experienced in focal, discrete areas, or as a more diffuse, body-wide form. Conditioning studies have established that it is possible to experience a learned
hyperalgesia of the latter, diffuse form. The focal form is typically associated with injury, and is divided into two subtypes:
- Primary hyperalgesia describes pain sensitivity that occurs directly in the damaged tissues.
- Secondary hyperalgesia describes pain sensitivity that occurs in surrounding undamaged tissues.
Hyperalgesia is induced by Platelet aggregating factor
(PAF) which comes about in an inflammatory
or an allergic
response. This seems to occur via immune cells interacting with the peripheral nervous system
and releasing pain-producing chemicals (cytokines
One unusual cause of focal hyperalgesia is platypus venom.
Long term opioid (e.g. heroin) users and those on opioid medications may experience hyperalgesia and experience pain out of proportion to physical findings.
Ikeda, Stark, Fischer, Wagner, Drdla, Jäger, et al. (2006) showed that stimulation of pain fibres in a pattern consistent with that from inflammation switched on a form of amplification in the spinal cord, long term potentiation. This occurred where the pain fibres contacted a pain pathway, the periaqueductal grey. Ikeda et al. argued that amplification in the spinal cord is another way of producing hyperalgesia.