Idea Transcript
Spinal Cord Stimulation Updated: Jan 07, 2015 Author: Anthony H Wheeler, MD; Chief Editor: Kim J Burchiel, MD, FACS more...
OVERVIEW
Background The knowledge that electricity could be used to treat pain dates as far back as observations by Scribonius that the pain of gout could be relieved by contact with torpedo fish. [1] Furthermore, multiple examples and proposed mechanisms exist that demonstrate the perception of pain is not strictly proportional to the intensity of the noxious neural stimulus. [2] One postulate that pioneered our view of the spinal cord’s role in the bias of nociception is attributed to the gate theory as hypothesized by Melzack and Wall in 1965. [3] The image below depicts cross-section anatomy of spinal cord.
Cross-section anatomy of spinal cord.
View Media Gallery See Pain Management: Concepts, Evaluation, and Therapeutic Options, a Critical Images slideshow, to help assess pain and establish efficacious treatment plans. Although the action of spinal cord stimulation (SCS) is ascribed to the direct inhibition of pain transmission in the dorsal horn, these theories do not fully explain the mechanisms by which SCS reduces pain. Before the complexity of the gate theory was realized, Dr. Norman Shealy, a Harvard-trained neurosurgeon at Case Western Reserve University, sought to show clinical support for this function by implanting the first unipolar SCS in 1967. [4] Recent research has provided some insight into how such neuromodulation affects pain. The mechanisms of action may differ depending on the type of pain targeted for treatment. For example, its effect on neuropathic pain may be secondary to stimulation-induced suppression of central excitability, whereas the beneficial effect of SCS on ischemic pain may be related to stimulation-induced inhibition of sympathetic nervous system influences and antidromic vasodilation, which increases blood flow and reduces oxygen demand. [5] The neurophysiologic mechanisms of SCS are not completely understood; however, some research suggests that its effects occur at local and supraspinal levels and also through dorsal horn interneuron and neurochemical mechanisms. [6, 7, 8] Experimental evidence supports a beneficial SCS effect at the dorsal horn level, whereby the hyperexcitability of wide-dynamic-range neurons is suppressed. Evidence exists for increased levels of gamma-amino butyric acid (GABA) release and serotonin, and perhaps, for reduced levels of some excitatory amino acids, such as glutamate and aspartame. [6, 7, 8] Despite our limited knowledge of the precise biological mechanisms responsible for the benefit of SCS, the estimated number of stimulators implanted each year has surpassed 20,000, and the annual revenue is in the excess of a half-billion dollars. [9, 10] However, after analysis of the medical literature, Boswell and colleagues concluded that evidence for the efficacy of SCS in the treatment of failed back surgery syndrome (FBSS) and complex regional pain syndrome (CRPS) was strong for short-term pain relief and moderate for long-term relief. [11] Also, a 20-year literature review found evidence that revealed long-term safety and efficacy of SCS in FBSS, CRPS, peripheral neuropathy, and severe ischemic limb pain secondary to peripheral vascular disease. [12] The primary purposes of SCS are to improve quality-of-life (QOL) and physical function by reducing the severity of pain and its associated characteristics [13, 14, 15]