Spinal Cord Stimulation
- Author: Anthony H Wheeler, MD; Chief Editor: Kim J Burchiel, MD, FACS more...
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. 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. 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.
The image below depicts cross-section anatomy of spinal cord.
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.
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.
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. 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. 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]
FDA-approved indications include the following:
Failed back surgery syndrome (FBSS)
The application of SCS for FBSS is indicated by first excluding the presence of a causative lesion that can be treated surgically or by other nonoperative therapies. Treatment of neuropathic pain symptoms due to FBSS is more likely to respond favorably.[13, 16, 17] In general, these diagnostic entities include radiculopathy or polyradiculopathies due to epidural fibrosis, arachnoiditis, and intrinsic nerve root damage, or radiculitis. The differential diagnosis must exclude transient metabolic processes, such as diabetes, infectious etiologies, entrapment neuropathies, and potential referred or radiating pain often associated with arthropathy (zygapophysial and sacroiliac joints), visceral pathology, or myofascial disorders.
Chronic painful peripheral neuropathy or plexopathy
Treatable causes of neuropathy must be excluded through appropriate diagnostic evaluation, including blood work, electrodiagnostic studies, and nerve biopsy, if necessary.
Multiple sclerosis (MS)
A 2006 study demonstrated good relief in 15 of 19 patients with lower extremity pain due to MS.
Complex regional pain syndromes (CRPS) I and II
Of course, the goals in treating CRPS are reducing pain, improving function and blocking trophic changes that are associated with autonomic dysfunction. Patients should be diagnosed correctly, respond to sympathetic blockade (at least for diagnostic purposes), and demonstrate significant pain intensity (>5/10 on a visual analogue scale), along with physical findings that are diagnostic of this disorder.[13, 16, 17]
Other approved disorders
The following disorders have approved indications, but reduced probability of a beneficial response:[13, 16, 17, 18, 19]
Axial pain due to FBSS
Phantom limb pain
Spinal cord injuries with most varied motor and sensory deficit
Off-label applications undergoing investigation
Although peripheral vascular disease, end stage (PVD), and refractory angina have shown strong literature support for SCS treatment efficacy, these indications are not yet FDA-approved. SCS has a profound effect on sympathetic vascular tone and promotes local blood flow and ischemic ulcer healing in patients with PVD. Due to the nature of pain and disability associated with these disorders, many US insurers now cover SCS treatment for this indication.[20, 21, 22]
The treatment of axial and other musculoskeletal pain syndromes show some support in the literature when epidural placed SCS is coupled with subcutaneous peripheral nerve field stimulation.
Nerve root stimulation has been identified as potentially useful in gastrointestinal motility disorders, as well as genitourinary and sexual dysfunction.[24, 25, 26, 27] Also, isolated subcutaneous peripheral nerve stimulation of is under investigation for treatment of focal neuralgias, especially occipital nerve stimulation for chronic migraine/headache.
Relative contraindications include the following:
See the list below:
Previous spinal surgery with epidural scarring
Severe spondylolisthesis with stenosis
Scoliosis that creates difficulty with lead steering
See the list below:
Implanted cardiac pacemaker were all or similar device
Coexisting additional major chronic pain condition
Anticoagulant or antiplatelet therapy
See the list below:
Operant factors (secondary gain)
Occupational discord or reduced functional capacity
Psychogenic factors that suggests a somatoform pain disorder
Significant psychological characteristics, including unstable axis I or II comorbidities
Absolute contraindications[13, 30, 31] include the following:
See the list below:
Previous dorsal root entry zone surgery or disruption
Critical central canal stenosis
Serious neurological deficit with surgically correctable pathology
Anatomical spine instability or deformity at risk for progression
See the list below:
Demand-type cardiac pacemakers
Need for future MRI studies or possible cardioverter defibrillators
Pregnant or pediatric patients
Coagulopathy, immunosuppression, or any medical condition that compromises surgical benefit over risk
Ongoing requirement for therapeutic diathermy
See the list below:
Theft detectors and metal detection devices
Operation of dangerous equipment or machinery
See the list below:
Severe cognitive impairment that interferes with evaluation or operation of the device
Unacceptable living situation or social environment
Active substance abuse
Numerous patient-characteristics must be scrutinized when evaluating candidates for SCS. Evidence of aberrant opioid-related drug use that suggests abuse or diversion should be considered when patients demonstrate behaviors such as unapproved dose escalation, lost prescriptions, frequent requests for early refills, and obtaining medications from multiple physicians.
Some Axis II diagnoses, perhaps, most obviously borderline or sociopathic personality disorders, and Axis I disorders, such as the presence of psychoses, often lead to treatment failure. Untreated mood disorders, anxiety/panic disorders, post-traumatic stress disorders, and somatization disorders may lead to errant surgical decisions and unsatisfactory outcomes. Medical conditions that have been reported to carry a higher risk for secondary morbidity or poor outcome include the presence of coagulopathy, implantable site or systemic infection, morbid obesity, diabetes, progressive arthropathy, and deteriorating neurological status. Certain patient characteristics that are generally regarded as predictors of favorable SCS outcomes include the cognitive abilities to understand the procedure, risks, and expectations of SCS treatment.
Disease-specific entities that have demonstrated a high probability of successful pain reduction are most often seen with SCS treatment of chronic neuropathic pain, complex regional pain syndromes, refractory angina pectoris, or painful ischemic disorders. Disease states with a low probability of successful pain reduction that should be avoided include neuropathic pain due to spinal cord injury, central nervous system pain, or nerve root avulsion. Other disorders, such as postherpetic neuralgia, axial low back pain, and phantom limb pain present an unknown probability of pain reduction.
Furthermore, countless quality of life issues partner with chronic neuropathic pain. Reduced pain using SCS can prompt pain treatment physicians to eliminate polypharmacy or taper specific medications that cause cognitive dysfunction or blunt mental alertness and to avoid present or future adverse medication-related side effects. SCS may facilitate return to work or other life functions. These are additional influences that are considered when deciding upon whether a trial of SCS is indicated.
SCS implantation can lead to complications that are either technical or medical in causation. Technical complications are related to lead-failure, device malfunction, current leakage, and poor programming. Lead migration, breakage or disconnections are the most common adverse technical events. SCS system problems may be related to premature or unexpected battery failure or inability to recharge the battery. Inadequate battery charging may be caused by procedure-related depth of implantation, large tissue folds, or postoperative weight gain. Implantable pulse generator (IPG) and other device-related failures occur less commonly.
Medical or clinical complications can be divided into direct or indirect influences. Direct trauma to the neuraxis can occur during the procedure or result from subsequent epidural scarring, hematoma, and/or infection. Dural puncture may lead to CSF hygroma or low-pressure headache, and at worst, meningitis. Wound trauma may cause increased pain from nerve or tissue injury. Of course, implant-site wound or device-related infections should be constant considerations. A perforated viscus may result from tunneling. Local anesthetic toxicity can be caused by poor monitoring, individual sensitivity, or unintended injection placements that are intravascular or subarachnoid. A subarachnoid block can result in myelopathy and death. Device rejection has been reported. Longitudinal follow-up and monitoring are the most critical postoperative commitments.
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