Abstract
Spinal cord stimulation (SCS) as an evidence-based interventional treatment has been used and approved for clinical use in a variety of pathological states including peripheral neuropathic pain; however, until now, it has not been used for the treatment of spinal cord injury- (SCI-) induced central neuropathic pain. This paper reviews the underlying mechanisms of SCS-induced analgesia and its clinical application in the management of peripheral and central neuropathic pain. Evidence from recent research publications indicates that nociceptive processing at peripheral and central sensory systems is thought to be modulated by SCS through (i) inhibition of the ascending nociceptive transmission by the release of analgesic neurotransmitters such as GABA and endocannabinoids at the spinal dorsal horn; (ii) facilitation of the descending inhibition by release of noradrenalin, dopamine, and serotonin acting on their receptors in the spinal cord; and (iii) activation of a variety of supraspinal brain areas related to pain perception and emotion. These insights into the mechanisms have resulted in the clinically approved use of SCS in peripheral neuropathic pain states like Complex Regional Pain Syndrome (CRPS) and Failed Back Surgery Syndrome (FBSS). However, the mechanisms underlying SCS-induced pain relief in central neuropathic pain are only partly understood, and more research is needed before this therapy can be implemented in SCI patients with central neuropathic pain.
Highlights
Electrostimulation for pain therapy emerged in the convergence of Pacemaker technology, the “Gate control” theory of pain, and pioneering clinical trials from 1950s to 1960s [1, 2]
While a growing number of studies showed that the motor system and the sympathetic system could be modulated by Spinal cord stimulation (SCS) to improve the locomotor function after SCI and alleviate angina pectoris [21, 22], in this review, we focus on the effects of conventional SCS on neuromodulation of peripheral and spinal cord injuryinduced central neuropathic pain
A recent functional magnetic resonance imaging (fMRI) study using the partial sciatic nerve ligation-induced PNP model in rats demonstrated that the higher centers of the pain perception system comprising the thalamus, somatosensory cortex, insular cortex, anterior cingulate cortex, limbic network, hippocampus, and nucleus accumbens were tuned by conventional SCS via interactions in multiple pain pathways, and even more brain areas like the raphe nuclei and caudate putamen were activated by an active recharge burst SCS [63]
Summary
Electrostimulation for pain therapy emerged in the convergence of Pacemaker technology, the “Gate control” theory of pain, and pioneering clinical trials from 1950s to 1960s [1, 2] According to this theory, the activation of lowthreshold nonnociceptive fibers closes the gate of the nociceptive signal input through the activation of inhibitory neurons in the spinal cord to suppress pain [1]. While a growing number of studies showed that the motor system and the sympathetic system could be modulated by SCS to improve the locomotor function after SCI and alleviate angina pectoris [21, 22], in this review, we focus on the effects of conventional SCS on neuromodulation of peripheral and spinal cord injuryinduced central neuropathic pain
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