Spinal cord stimulation analgesia

Abstract

T he use of neuromodulation by electrical stimulation of the peripheral or central nervous system for the treatment of pain has been around for a long time, beginning with the use of electric eels thousands of years ago. 7 Our modern understanding of the mechanisms of electrical stimulation for pain relief comes from the gate control theory, according to which the selective stimulation of nonnociceptive afferents (Ab) inhibits nociceptive afferents (A∂ and C) by the activation of inhibitory interneurons in the substantia gelatinosa of the posterior horns of the spinal cord. 10 Transcutaneous electrical nerve stimulation (TENS) was developed to trigger this endogenous analgesia by peripheral stimulation. The development of spinal cord stimulation (SCS) derives from the same basic mechanisms, but with a central stimulator. 13 Spinal cord stimulation consists of implantation of periepidural electrode in the posterior columns of the spinal cord at the spinal level of the dermatomes on which we want to produce the analgesic effect. The mechanism of function of SCS is based on the same neurophysiological postulate as TENS. However, unlike TENS, the fact that the stimulation is applied directly to the posterior horns of the spinal cord does not allow us to conclude on the specific neurophysiological mechanisms of this analgesia. The stimulation may recruit afferents from the periphery, afferents from the spinal cord to the higher centers, local neuron circuits, and even fibers of the anterior horns of the spinal cord. 6 Spinal cord stimulations have been used for different types of pain with moderate success; a little more than 50% of the patients achieve pain relief of approximately 50%. 16 We have to place these results in the context that SCS is commonly an end-of-the-road approach where conventional treatments have failed. It is suggested that patient selection is one of the burdens of SCS success. Most of the patient selection criteria are designed around exclusion criteria such as psychological problems, or inclusion criteria such as SCS trials with externalized electrodes to test for a good paresthesia and pain relief before the implant. 16,17 However, even when controlling for several factors such as pain location, history of surgery, initial level of pain, litigation/worker's compensation, age, gender, duration of pain, duration of follow-up, publication year, continent of data collection, study design, quality score, method of SCS lead implant, and type of SCS lead, the outcomes are still around 50% pain relief for 50% of the patients. 16 Probably the most important factor in predicting the efficacy of SCS and in selecting patients who are the best responders is to try to establish a relation between the mechanisms of SCS analgesia and identification of the neurophysiological mechanisms implicated in a specific chronic pain condition. For instance, the use of spinal (nociceptive reflexes-RIII) and cortical activity (somatosensory-evoked potentials [SEP]) permitted investigators to demonstrate that reduced RIII...

Spinal cord stimulation reduces cardiac pain through microglial deactivation in rats with chronic myocardial ischemia

“…Spinal cord stimulation (SCS) is an alternative therapeutic approach that has been clinically utilized for decades to treat patients with CMI, providing an improvement in intractable angina symptoms ( 8 , 9 ). SCS owes its inception to the classical ‘gate-control’ theory, in which the selective stimulation of non-nociceptive afferent fibers (Aβ) inhibits nociceptive afferent fibers (Aδ and C) through the activation of inhibitory interneurons in the substantia gelatinosa of the spinal dorsal horns ( 10 ). Although this mechanism may explain the immediate and short-term action of SCS, it does not readily account for the prolonged analgesic effect, which may reflect a potential anti-central sensitization mechanism by SCS in neuropathic pain.…”

Gabapentin, Concomitant Prescription of Opioids, and Benzodiazepines among Kidney Transplant Recipients

“…3 While opioids are effective analgesics, use for the treatment of neuropathic pain is appropriately limited because of the risks associated with opioids. 4 Studies have found that high-level opioid use in the first year after transplant was associated with a two-fold elevated risk of mortality and 68% higher risk of all-cause graft failure risk over the subsequent year. 5 Furthermore, chronic opioid use leads to a higher risk of mortality and dependency.…”