Preclinically, stimulation intensity or amplitude is programmed at 66–90% of the intensity that generates regular muscle twitches in the animal. Tonic stimulation is applied with a frequency ranging from 40 to 80 Hz and a pulse width varying between 200 and 500 µs and at intensities which induce tingling sensations or paresthesias. is referred to as conventional or tonic stimulation. The stimulation paradigm introduced by Shealy et al. Initial long-term study results on closed-loop SCS systems hold promise for improvement of future SCS treatment. Mechanisms of stimulation of the DRG as well as those related to new SCS paradigms are now under investigation, where it seems that burst SCS not only stimulates sensory, discriminative aspects of pain (like Tonic SCS) but also emotional, affective, and motivational aspects of pain. Tonic SCS concurrently initiates neuropathic pain modulation through a supraspinal-spinal feedback loop and serotonergic descending fibers. Tonic SCS mainly acts via a segmental spinal mechanism where it induces GABA-release from inhibitory interneurons in the spinal dorsal horn. The aim of this review is to provide a brief overview of the main mechanisms behind the mode of action of the different SCS paradigms. Despite its clinical successes in a subset of chronic neuropathic pain syndromes, several limitations such as insufficient pain relief and uncomfortable paresthesias have led to the development of new targets, the dorsal root ganglion, and new stimulation waveforms, such as burst and high frequency. Tonic spinal cord stimulation (SCS) has been used as a treatment for chronic neuropathic pain ever since its discovery in late 1960s.
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