Sympathetic postganglionic fibers sprout in the dorsal root ganglion (DRG) after peripheral nerve injury. Therefore, one possible
contributing factor of sympathetic dependency of neuropathic pain is the extent of sympathetic sprouting in the DRG after
peripheral nerve injury. The present study compared the extent of sympathetic sprouting in the DRG as well as in the injured
peripheral nerve in three rat neuropathic pain models: (1) the chronic constriction injury model (CCI); (2) the partial sciatic
nerve ligation injury model (PSI); and (3) the segmental spinal nerve ligation injury model (SSI). All three methods of peripheral
nerve injury produced behavioral signs of ongoing and evoked pain with some differences in the magnitude of each pain component.
The density of sympathetic fibers in the DRG was significantly higher at all examined postoperative times than controls in
the SSI model, while it was somewhat higher than controls only at the last examined postoperative time (20 weeks) in the CCI
and PSI models. Therefore, data suggest that, although sympathetic changes in the DRG may contribute to neuropathic pain syndromes
in the SSI model, other mechanisms seem to be more important in the CCI and PSI models at early times following peripheral
nerve injury.
Key words Causalgia - Hyperalgesia - Mechanical allodynia - Peripheral nerve injury - Sympathetically maintained pain - Rat
Received: 14 October 1997 / Accepted: 9 December 1997