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5 Articles in Volume 5, Issue #4
Chronic Pain and Cannabinoids
Lumbar Back Belts in the Workplace
Pain from Muscular Dysfunction
Spinal Cord Stimulation
Ziconotide for Chronic Severe Pain

Spinal Cord Stimulation

An overview and case study of spinal cord (dorsal column) stimulation in a spine-centered/orthopaedic clinical practice setting.
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Since the first published paper on spinal cord stimulation (SCS) (or dorsal column neuromodulation) by Dr. Shealy in 1967, there have been a cumulative total of well over 2500 articles, presentations, symposia, and abstracts on the topic of neuroaugmentation.1,2 The long-term results of SCS published in the 1970’s were disappointing, yet still provided promising outcomes.3-6 Most of the studies published in the 1970’s and early 1980’s demonstrated success rates of approximately 40%.7 As with many novel instrumentation devices, initial problems included poorly designed hardware, inadequate patient selection criteria, and suboptimal surgical technique. The hardware typically consisted of a single or dual electrode system that were implanted epidurally. They provided a small electrical field and thus were unable to consistently stimulate the spinal cord. In addition, these systems were implanted via laminectomy or laminotomy with the patient under general anesthesia, thus eliminating the possibility of surgeon-patient interaction. The electrodes were commonly implanted in the high thoracic or lower cervical region for lumbar pain syndromes and patients were not consistently screened for psychological dysfunction, drug habituation, secondary-gain issues, pain topography, and quality of pain. All of these factors have considerable impact on the overall efficacy of SCS, as we have seen the advancements of this technology over the years.6,8-10

Significant advances in SCS have been made in recent years. These results and postoperative outcomes of the procedures have shifted to more positive outcomes in the field of neuroaugmentation; especially with respect to more pertinent and practical factors, such as, return to work, reduction in medication use, reduction in visual analog pain scores (VAS), and improvement activities in daily living (ADL). The hardware is more durable, more effective, more maneuverable, and provides more range of coverage for the affected area for which it is aimed. The devices can be implanted percutaneously under fluoroscopic guidance (especially for the trial leads placement), which allows operator-patient verbal interaction and more accurate positioning of SCS leads, for trial and eventual permanent placement. Still the vast majority of SCS placements have been for failed back surgery syndrome (FBSS), although this varies according to regional preference. Over three decades of experience have provided improved patient selection criteria; which is paramount in affecting a positive eventual outcome. The net result is an improved capability to control various chronic pain conditions, especially peripherally-referred more so than centrally-referred pain conditions.7 This article will discuss the pathophysiology and mechanism of action and clinical applications of SCS, procedural indications/contraindications/ potential complications of SCS, SCS patient selection criteria, and current clinical results and potential future trends in dorsal column neuromodulation.6,8-10

Pathophysiology of Pain

Pain is an uncomfortable sensation associated with an emotional response.11,12 The International Association for the Study of Pain (IASP) defined pain as “an unpleasant sensory and emotional experience associated with actual and potential tissue damage, or described in terms of such damage” (IASP, 1986).11 It may originate from stimulation of chemical, mechanical, or thermal receptors found in free nerve endings within injured tissue. This is known as afferent pain, and can occur in ligamentous or muscular injuries of the spine.3-161 Pain can also occur from direct injury to the peripheral nerve, which results in burning or shooting pain in the distribution of the affected nerve. This is called peripheral deafferentation (neuropathic) pain and is demonstrated in conditions such as complex regional pain syndrome, peripheral neuropathy, or radiculopathy.5,17,18 Central deafferent pain appears after injury to the central nervous system structures, such as the thalamus, that are responsible for the transmission of pain. Peripheral pain signals are transmitted by either thinly myelinated A-delta or umnyelinated C fibers. The A-delta fibers convey discrete, sharp, fast pain at approximately 15 m/sec, whereas the C fibers transmit vague, chronic, burning, slow pain at less than 1 m/sec.19,20

In 1965, Melzack and Wall published their “gate control” theory in which they hypothesized that a “gate” system existed for pain modulation located in the dorsal gray horn within the substantia gelatinosa (laminae 2 and 3).21 They proposed that excess tactile signals traveling along the large myelinated A-delta fibers closed the gate, which then inhibited the propagation of pain impulses along the poorly myelinated C fibers. Although the pain pathway is still not completely understood, researchers have uncovered important parts of the neuronal system. This includes descending inhibitory influences from the brain, which have been shown to suppress transmission of pain.9,22-24 There is also evidence of an endogenous system of opioids that modulate sensory input.25-27 Today, there is a better awareness that the pain experience is not just physiologic but is also influenced by culture, religion, and psychologial makeup.28-31 In order to provide appropriate treatment all of these factors must be taken into consideration when evaluating patients.6,8,9,10

Mechanism of Action of Spinal Cord Stimulation

Although the exact mechanism for pain control from SCS is not entirely understood, it is believed to result from direct or facilitated inhibition of pain transmission.2,4-6,21,32 There exist five mechanistic theories for SCS which should be noted: 1) Gate control theory— segmental, antidromic activation of A-beta efferents; 2) SCS blocks transmission in the spinothalamic tract; 3) SCS produces supraspinal pain inhibition; 4) SCS produces activation of central inhibitory mechanisms influencing sympathetic efferent neurons; 5) SCS activates putative neurotransmitters or neuromodulators.32

The gate control theory motivated Shealy, et al. in 1967 to apply SCS as a means to antidromically activate the tactile A-beta fibers through dorsal column stimulation.2 Shealy reasoned that sustained stimulation of the dorsal columns would keep the gate closed and provide continuous pain relief. While the theoretical model put forth by Melzack and Wall has been shown not to be precisely correct, pain gating or pain control has been shown to exist.4-6,21

Others believe that pain relief from SCS results from direct inhibition of pain pathways in the spinothalamic tracts and not secondary to selective large fiber stimulation.33 This theory has been supported by Hoppenstein, who showed that the posterolateral stimulation of the spinal cord provided effective contralateral pain relief with substantially less current than posterior stimulation.34

Last updated on: December 28, 2011
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