![]() We first outline some physiological effects of SCS, then present evidence against previously hypothesized sites of action: dorsal columns and dorsal roots. ![]() Furthermore, we will focus on conventional stimulation therapy, given the half century of experience with this treatment modality compared to the limited data on new SCS algorithms, such as high frequency and burst stimulation (Linderoth and Foreman, 2017). Here, we focus on potential spinal sites of action-that is, what is happening at the site of therapy delivery-recognizing that supraspinal mechanisms also contribute to pain reduction (Bantli et al., 1975 Linderoth and Foreman, 1999). If, as in drug discovery, high quality mechanistic insights lead to improved therapies (Howick et al., 2010), it would be useful to understand the mechanisms of action of SCS in modulating neuropathic pain. Here, however, we suggest that it is our incomplete understanding of the mechanisms of SCS that has prevented further advancement. This stalling of clinical efficacy perhaps indicates that we have reached an absolute asymptote in the capacity of SCS therapy to improve quality of life. Furthermore, concomitant technological “advances”, including complex stimulator designs and treatment protocols, have not correlated with improvements in patient outcomes (Zhang et al., 2014). While the economics points towards cost‐effectiveness of SCS (Kumar and Rizvi, 2013), the price of SCS devices is increasing. The field of neuromodulation for chronic pain is rapidly expanding: in recent years, over 25,000 neurostimulators have been implanted annually in the United States alone (Prager, 2010). Since then, this use of electrical stimulation via leads placed in the spinal dorsal epidural space has become a valuable therapeutic tool for treating neuropathic pain. ![]() Spinal cord stimulation (SCS) was first reported as a treatment for pain a half‐century ago (Shealy, Taslitz et al., 1967).
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