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| Hyperalgesia Classification and external resources |
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| ICD-9 | 782.0 |
|---|---|
| DiseasesDB | 30788 |
| MeSH | D006930 |
Hyperalgesia is an increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves.
Types
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.
Causes
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 and chemokines).[1]
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.[2] 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.
References
- ^ Marchand, F., Perretti, M., & McMahon, S. B. (2005). Role of the immune system in chronic pain. Nature Reviews Neuroscience, 6, 521-532.
- ^ Ikeda, H., Stark, J., Fischer, H., Wagner, M., Drdla, R., Jäger, T., et al. (2006). Synaptic amplifier of inflammatory pain in the spinal dorsal horn. Science, 312, 1659-1662.
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- This page was last modified on 30 September 2008, at 13:33.
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