Does a neuroimmune interaction contribute to the genesis of painful peripheral neuropathies?

Painful peripheral neuropathies are precipitated by nerve injury from disea se or trauma, All such injuries will be accompanied by an inflammatory reac tion, a neuritis, that will mobilize the immune system. The role of the inf lammation itself is difficult to determine in the presence of structural da mage to the nerve. A method has been devised to produce a focal neuritis in the rat sciatic nerve that involves no more than trivial structural damage to the nerve, This experimental focal neuritis produces neuropathic pain s ensations (heat- and mechano-hyperalgesia, and cold- and mechano-allodynia) in the ipsilateral hind paw. The abnormal pain sensations begin in 1-2 day s and last for 4-6 days, with a subsequent return to normal. These results suggest that there is a neuroimmune interaction that occurs at the outset o f nerve injury (and perhaps episodically over time in slow developing condi tions like diabetic neuropathy) that produces neuropathic pain. The short d uration of the phenomena suggest that they may prime the system for more sl owly developing mechanisms of abnormal pain (e.g., ectopic discharge in axo tomized primary afferent neurons) that underlie the chronic phase of painfu l neuropathy.