An experimental neuropathy was produced in the sciatic nerve of adult rats. The postoperative behavior of these rats indicated that hyperalgesia, allodynia and, perhaps, spontaneous pain and sympathetic dysfunction were produced. Hyperalgesic responses were evident on the second postoperative day and lasted for nearly three months. The hyperalgesia was revealed by a decrease in the threshold and in a marked exaggeration of the reflex's amplitude and duration. The presence of allodynia (pain evoked by normally inncouous stimuli) was inferred from the nocifensive responses evoked by standing on a chilled metal floor. The presence of spontaneous pain was suggested by a suppression appetite and from the appearance of apparently spontaneous withdrawal reflexes. The presence of sympathetic dysfunction was suggested by the finding of unusually warm or cool skin temperature on the affected hindpaw. Postmortem microscopic examination of the injured nerve revealed a near total loss of myelin at the site of the injury. By 1-2 days after nerve injury, nearly all myelinated fibers can conduct impulses in the nerve proximal to the injury, but they cannot conduct through the injury. Unmyelinated fibers, however, conduct impulses through the injured region in a normal manner. Immunocytochemistry and enzyme histochemistry show that the dorsal horn levels of fluoride-resistant acid phosphatase, substance P, and calcitonin gene-related peptide all decrease. An increase in dorsal horn levels of methionine enkephalin and dynorphin has been detected by day 20 and may occur earlier. Colchicine experiments show that this increase occurs within intrinsic spinal neurons.
