An experimental neuropathy of peripheral somatic nerve was produced in rats by placing loose ligatures around the common sciatic nerve in one hindleg. Pain sensation was measured by evoking the nocifensive flexion reflex with radiant heat directed to the plantar hindpaw. The latency of the reflex (paw-flick) was significantly shorter on the operated side at 5 days postoperatively and remained so for about 3 months. The amplitude and duration of the paw-flick from the operated side were also abnormal, being unusually large and prolonged. These data demonstrate that the neuropathy has produced the state of hyperalgesia. Other behavioral signs suggest that allodynia (the evocation of pain by normally innocuous stimuli) is also present. Thus, the animals habitually hold the effected leg in a slightly flexed position while standing, lying down, or sleeping; thereby avoiding touching the effected foot. Multiunit EMG recordings from the relevant flexor muscles confirmed that the reflex had a lower threshold and an abnormally long duration. Testing the pain threshold during the first 5 days postoperatively was complicated by the fact that the threshold for neurogenic inflammation was lowered. This phenomenon suggests that there is an abnormality in unmyelinated nociceptor function because these fibers are known to mediate neurogenic inflammation. Compound action potential (CAP) recordings from the effected nerves at various times during the presence of hyperalgesia showed grossly abnormal nerve conduction. Preliminary examination of the nerves after osmication confirmed that the nerves were severely demyelinated. Preliminary work indicates that there are also changes in the central nervous system. Fluoride resistant acid phosphatase is greatly reduced in lamina II. Substance P and calcitonin gene-related peptide are depleted in lamina V.
