Spinal cord stimulation was developed as a therapeutic modality based on the gate-control theory in which activation of afferent A fibers is postulated to attenuate spinal pain transmission.

Because the electrical field of epidural stimulation may spread to nearby tissues via highly conductive cerebrospinal fluid, many action sites for spinal cord stimulation–induced pain relief may exist, but they have not been clearly defined. The class and number of nerve fibers that are activated under each circumstance are also unknown. 4,5It is unclear how paresthesia intensity correlates with the motor threshold. For example, bipolar stimulation that induces paresthesia that covers the painful areas is commonly used in patients, whereas monopolar stimulation at 60–90% of muscle twitching intensity ( i.e. , motor threshold) is often employed in experimental animals. Differences in lead design, stimulation mode, and intensity-selecting criteria also present barriers to correlating previous findings in experimental animals with mechanisms underlying therapeutic effects in patients. 1–3Yet, the biologic basis for the effectiveness of spinal cord stimulation in treating neuropathic pain is unclear. SPINAL cord stimulation is an effective neuromodulatory technique for managing a variety of chronic pain conditions, particularly neuropathic pain, which is often refractory to current pharmacotherapies. Therefore, stimulation of putative spinal substrates at A-fiber intensities with parameters similar to those used by patients with spinal cord stimulators attenuated established WDR neuronal hyperexcitability in the neuropathic condition and counteracted activity-dependent increase in neuronal excitability (i.e., windup). It is noteworthy that dorsal column stimulation blocked windup of WDR neuronal response to repetitive intracutaneous electrical stimulation (0.5 Hz) in nerve-injured and sham-operated rats, whereas dorsal root stimulation inhibited windup only in sham-operated rats. Conditioning stimulation also significantly attenuated WDR neuronal responses to mechanical stimuli in nerve-injured rats and inhibited the C-component of the neuronal response to graded intracutaneous electrical stimuli applied to the receptive field in nerve-injured and sham-operated rats. Within 15 min of the dorsal column or root conditioning stimulation, the spontaneous activity rate of WDR neurons was significantly reduced in nerve-injured rats.

Dorsal column electrical stimulation