For more than a century, electricity has been used for the neuromodulation of pain pathways. Spinal cord stimulation (SCS) has been used for the treatment of a variety of pain conditions over the past 40 years, with a primary indication for new or persistent back and leg pain after spine surgery, failed back surgery syndrome, chronic regional pain syndrome (CRPS), and chronic radiculopathy, as well as treating many other refractory neuropathic pain conditions.1 

During the past 10–15 years, there have been no true evidence-based advances in spinal neuromodulation technology, only minor improvements on pulse generator programming, software enhancements and the addition of magnetic resonance imaging compatibility. The mechanisms by which SCS relieves pain have yet to be fully elucidated. The gate control theory published by Melzack and Wall2 in 1965 is the basic premise for SCS. Recent studies and animal models showed evidence that SCS stimulates dorsal horn neurotransmitter pain modulators including serotonin, norepinephrine, γ-aminobutyric acid, and acetylcholine. The technology also modulates hyperexcitable/sensitized dorsal horn wide-dynamic range neurons implicated in neuropathic pain states. Some more recent studies also showed SCS to antidromically stimulate the peripheral release of vasodilatory neurotransmitters including calcitonin gene-related peptide and nitric oxide.2 

Only in more recent years, high-frequency (HF; 1–10 kHZ) SCS and dorsal root ganglion stimulation (DRGS) have emerged as modified techniques, devised to avoid some of the undesirable effects associated with traditional SCS. These novel platforms also overcome limitations such as the inability to derive the correct combination of pulse width, frequency, and amplitude of the electrical waveform needed to address the individual’s pain or positional/postural effects due to shifts in the relative distance between the stimulating electrodes and the dorsal column. 

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