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Spinal cord stimulation: Placement and management

Author
Anne Marie McKenzie-Brown, MD
Section Editor
Scott Fishman, MD
Deputy Editor
Marianna Crowley, MD

INTRODUCTION

Spinal cord stimulation (SCS) is a neuromodulation technique that is used to treat neuropathic and sympathetically mediated chronic pain. SCS involves percutaneous or surgical implantation of electrodes in the epidural space, with power supplied by an implanted battery.

This topic will discuss placement of spinal cord stimulators, management of anesthesia for spinal cord stimulator placement, and management of SCS for patients who undergo other surgical procedures. It does not address the technique for laminectomy and surgical lead placement. Evaluation of chronic pain, alternatives for therapy of chronic pain, and SCS for the treatment of specific conditions are discussed separately. (See "Evaluation of chronic pain in adults" and "Overview of the treatment of chronic non-cancer pain" and "Investigational therapies for treating symptoms of lower extremity peripheral artery disease", section on 'Spinal cord stimulation' and "Complex regional pain syndrome in adults: Prevention and management", section on 'Spinal cord stimulation'.)

MECHANISM OF ACTION

The complex mechanism of action of spinal cord stimulation (SCS) has not been fully elucidated and is probably multifactorial. The analgesia provided by SCS for neuropathic pain appears to differ from that provided for the relief of ischemic pain [1].

Neuropathic pain relief – SCS was originally thought to work through a gate control mechanism in the dorsal horn of the spinal cord. Thus, spinal cord stimulators were called dorsal column stimulators. According to gate control theory, the substantia gelatinosa in the dorsal horn was a functional "gate system" where pain was modulated. Small (painful A delta and C) nerve fibers and large (A beta) nerve fibers synapse at the "gate." Large fiber activation inhibited the painful small fibers, closing the "gate" and relieving pain [2].

The mechanism for pain relief with SCS is now known to be more complex. Relief of neuropathic pain by SCS is mediated in part by wide dynamic range (WDR) neuron suppression in the dorsal horn. This involves spinal gamma-aminobutyric acid (GABA) systems and their effect on excitatory amino acid (EAA) activity [3-5]. In addition, SCS appears to act at least partly through effects on the brain. Pain relief from SCS can often be realized for days or even weeks after the stimulation has been turned off, suggesting a more central mechanism of action [3,6]. 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 [7].

                     

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Literature review current through: Nov 2016. | This topic last updated: Tue Nov 01 00:00:00 GMT 2016.
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