Tactile allodynia and thermal hyperalgesia, two robust signs of neuropathic pain associated
with experimental nerve injury, have been hypothesized to be mechanistically distinguished
based on (a) fiber types which may be involved in the afferent input,(b) participation of spinal
and supraspinal circuitry in these responses, and (c) sensitivity of these endpoints to
pharmacological agents. Here, the possibility that nerve-injury induced tactile allodynia and
thermal hyperalgesia may be mediated via different afferent fiber input was tested by …