Spinal cord stimulation attenuates dorsal horn neuronal hyperexcitability in a rat model of mononeuropathy

The mechanisms underlying the relief of neuropathic pain of peripheral origin by spinal cord stimulation (SCS) are poorly understood. The present study was designed to investigate the effects of SCS on evoked and spontaneous discharges in dorsal horn neurons in intact and in nerve-injured rats subjected to partial sciatic nerve ligation according to Seltzer et al. (1990). Tactile sensitivity in the hind paw was assessed in behavioral tests using von Frey filaments. The presence of 'allodynia' was defined as a withdrawal response to a filament of 10 g or less. Under halothane/oxygen anesthesia the effects of SCS (50 Hz, 0.2 ms, 80-620 microA, 5 min.) on mechanically evoked (brush and innocuous press on the hind paw) responses and spontaneous discharges were investigated in wide-dynamic range (WDR) neurons in three groups of animals: (1) rats that displayed 'allodynia' after nerve ligation (2) rats without signs of 'allodynia' after surgery and (3) control, intact rats. A significantly increased frequency of spontaneous discharge and of responsiveness to brush and press was found in the group of allodynic, as compared with non-allodynic and control rats. The majority (63%) of the investigated neurons in these animals displayed afterdischarge in response to press stimulation. SCS induced a significant depression of both the principal response and the afterdischarge in allodynic rats: the discharge during brush stimulation was reduced to 86 +/- 8.2% and during press to 77.4 +/- 4.5% as compared with the prestimulation value. These depressive effects on evoked responses in allodynic rats outlasted SCS by 10.5 +/- 1.7 min during which time the responses gradually recovered. The frequency of spontaneous discharge was markedly decreased in approximately one third of the neurons, whereas in another third it was increased. In non-allodynic and control rats, SCS had no significant depressive effects on the evoked responses and spontaneous discharge. The results suggest that SCS may provide a suppressive action on dorsal horn neuronal hyperexcitability associated with signs of peripheral neuropathy. The suppressive effect of SCS on tactile allodynia, as previously observed in behavioral experiments, presumably corresponds to a normalization of the excitability of WDR cells in response to innocuous stimuli.