Pain International Association for the Study of Pain

vidence for a role of the immune system in neuropathy and neuropathic pain is increasing.1 It is now estimated that half of all clinical cases of neuropathic pain are associated with infection or inflammation of peripheral nerves rather than with nerve trauma.2 Animal models have now been developed to explore the nociceptive impact of immune activation in and around nerve trunks, dorsal root ganglia (DRG), and dorsal roots. Such models reveal that immune activation at any of these sites is hyperalgesic, and that the immune system actively participates in creating and maintaining neuropathic pain of diverse etiologies. This issue of Pain: Clinical Updates is a brief survey of the immune system’s involvement in hyperalgesia (pain amplification). The roles of the immune system in pain will be illustrated using examples of trauma to or inflammation of peripheral nerves, antibody attack upon peripheral nerves, and immune attack upon the blood supply to peripheral nerves or upon DRG and spinal roots.