HF SCS does not generate action potentials to the dorsal horn as is seen in paresthesia-based SCS, and does not appear to involve supraspinal mechanisms. As examples, conventional and burst SCS have different effects on the dorsal horn, the gracile nucleus in the dorsal column, and the brain, and pain relief from burst SCS does not appear to involve GABAergic systems. The mechanism of action for paresthesia-free forms of SCS (ie, burst, HF SCS) may be different from conventional SCS, and is the subject of ongoing research. Cortical inhibition by paresthesia-based SCS has also been demonstrated via amplitude reduction in somatosensory evoked potentials (SSEP) monitoring. An electroencephalographic (EEG) study of patients with chronic lower extremity neuropathic pain found that long-term SCS influenced both pain thresholds and cortical signaling, further evidence of a more central mechanism of analgesia. Pain relief from SCS can often be realized for days or even weeks after the stimulation has been turned off, which underscores the importance of supraspinal mechanisms of action. Supraspinal mechanisms of SCS occur via descending inhibitory pathways and are also thought to contribute significantly to the effects of SCS. Relief of neuropathic pain by paresthesia-based SCS is mediated in part by wide dynamic range neuron suppression in the dorsal horn of the spinal cord, through A-beta mediated inhibitory factors involving gamma-aminobutyric acid (GABA), cholinergic, and other transmitter systems. Much of what is known comes from laboratory and animal studies. The mechanism for pain relief with conventional SCS is now known to be more complex, involving both spinal and supraspinal mechanisms. Paresthesias are generated via depolarization of A-beta fibers. Small (painful A-delta and C) nerve fibers and large (A-beta) nerve fibers synapse at the "gate." Large A-beta fiber activation inhibited the painful small fibers, closing the "gate" and relieving pain. According to gate control theory, the substantia gelatinosa in the dorsal horn was a functional "gate system" where pain was modulated. Thus, spinal cord stimulators were called dorsal column stimulators. Neuropathic pain relief – SCS was originally thought to work through a gate control mechanism in the dorsal horn of the spinal cord.(See 'Implantable pulse generators' below.) Knowledge about the mechanisms underlying pain relief from the newer SCS technologies, such as high-frequency (HF), burst, and most recently, closed loop evoked compound action potential (ECAP) stimulation, is evolving. The mechanisms described below pertain to conventional or standard SCS. MECHANISM OF ACTION - The complex mechanism of action of SCS has not been fully elucidated and is multifactorial, involving neuromodulation of dysregulated pain pathways. (See "Approach to the management of chronic non-cancer pain in adults".).(See "Complex regional pain syndrome in adults: Treatment, prognosis, and prevention", section on 'Spinal cord and peripheral nerve stimulation'.).
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