Focal nerve inflammation induces neuronal signs consistent with symptoms of early complex regional pain syndromes.

Early forms of complex regional pain syndromes (CRPS) are characterized by severe pain and autonomic dysfunction in a limb, both of which seem out of proportion to the inciting event. While often caused by obvious nerve injury, the syndromes also occur following relatively trivial trauma. Persistent inflammation has been implicated in the etiology of CRPS. We hypothesized that inflammation of a nerve proximal to the symptoms could lead to neural changes consistent with clinical CRPS. Using a rat model of neuritis, the activity of sensory and autonomic neurons was recorded distal to the inflamed site using single fiber electrophysiological methods. In normal rats, no sensory neurons had ongoing activity. The discharge rate of sympathetic postganglionic neurons was 2.26+/-1.33 Hz (mean+/-SD). However, in rats with inflamed nerves, 27% of slowly conducting neurons had ongoing activity after 3-4 days, and 50% had such activity after 7-8 days. Other sensory neurons did not exhibit ongoing activity. Sympathetic postganglionic neurons had a significantly slower ongoing discharge rate during inflammation (1.96+/-1.19 Hz after 3-4 days, 1.48+/-1.23 Hz after 7-8 days). Additionally, none of the sympathetic axons in any group were mechanically sensitive. These findings support that focal nerve inflammation is sufficient to cause neuronal discharge changes that are consistent with clinical findings in early CRPS. Furthermore, the lack of axonal mechanical sensitivity in sympathetic axons rules out channels expressed in these neurons as possible mechano-electrical transducers.