Spinal Cord Stimulation
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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.
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]
Spinal cord stimulation can be used to treat a variety of diseases that result in chronic pain. The most commonly treated diagnoses include failed back surgery syndrome (FBSS; 33%), complex regional pain syndrome type I (45%) and type II (4%), neuropathy (10%), visceral pain (5%), and peripheral vascular disease (3%). [16]
FDA-approved indications include the following:
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, 17, 18] In general, these diagnostic entities include radiculopathy or polyradiculopathies due to epidural fibrosis, arachnoiditis, and intrinsic nerve root damage, or radiculitis. [13] 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.
Treatable causes of neuropathy must be excluded through appropriate diagnostic evaluation, including blood work, electrodiagnostic studies, and nerve biopsy, if necessary.
A 2006 study demonstrated good relief in 15 of 19 patients with lower extremity pain due to MS. [18]
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, 17, 18]
The following disorders have approved indications, but reduced probability of a beneficial response: [13, 17, 18, 19, 20]
Axial pain due to FBSS
Postherpetic neuralgia
Post-thoracotomy pain
Phantom limb pain
Intercostal neuralgia
Spinal cord injuries with most varied motor and sensory deficit
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. [21, 22, 23]
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. [24]
Nerve root stimulation has been identified as potentially useful in gastrointestinal motility disorders, as well as genitourinary and sexual dysfunction. [25, 26, 27, 28] Also, isolated subcutaneous peripheral nerve stimulation of is under investigation for treatment of focal neuralgias, [29] especially occipital nerve stimulation for chronic migraine/headache. [30]
Spinal cord stimulation has also shown to improve locomotor behavior in Parkinson’s disease. [31] Patients demonstrate improvements in pain control, gait, and posture; without inducing paresthesia. Additionally, SCS may have beneficial effects on mental status in patients with PD, with improvement in emtional symptoms. [32]
Relative contraindications [13] 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:
Untreated infection
Implanted cardiac pacemaker were all or similar device
Coexisting additional major chronic pain condition
Anticoagulant or antiplatelet therapy
See the list below:
Ongoing litigation
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, 33, 34] 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. [35]
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.
Cervical lead placement is effective in providing stimulation to the upper extremities. Entry point is typically in the upper thoracic spine, with advancement of the lead to the C2–3 level. [36] Relief of lower extremity pain is achieved with lead placement at the thoracic T7–12 levels. Advancement of leads to the T6–T9 levels can be used to target low back pain. Furthermore, lead placement in the mid- to upper thoracic spine, T4–5, is effective for targeting visceral pain and postherpetic neuralgia. [36]
Spinal cord stimulation systems are available as percutaneous leads or paddle electrodes. Both are commonly used, each with their own advantages and limitations. Both percutaneous leads and paddle electrodes are effective in controlling chronic pain. [37] Percutaneous leads are minimally invasive and can be placed by interventionists in an outpatient setting. However, percutaneous leads have a higher rate of migration and possible need for lead revision. Paddle electrodes are more invasive, requiring a laminectomy for placement. However, paddle electrodes can provide better coverage compared to percutaneous leads. Babu et al. compared outcomes of percutaneous leads to paddle electrodes for approximately 13,000 patients. Placement of paddle electrodes was associated with a slightly higher complication rate in the immediate postoperative period but had a significantly lower long-term re-operation rate. Long-term healthcare costs were similar between the two groups. [38]
The most common causes of complications in SCS are lead migration, pain over the implant site, and infection. [39] Over the past 10 years, better techniques in lead anchoring have decreased the incidence of lead migration. [36] To prevent wound infections, patients are typically given perioperative IV antibiotics and can be discharged home on an oral antibiotic, such as Keflex, for one-week duration. The rate of SCS-related infections is approximately 4.5%. [16] Patients with diabetes are at higher risk of SCS-related infection (9%). Infection typically requires hardware explant, followed by IV antibiotics for deep infections or oral antibiotics for superficial infections. Other complications include lead fracture, premature battery failure, and CSF leak from dural puncture. Serious adverse events, such as neurological injury are rare.
Persistent radicular pain after lumbosacral surgery can be managed either by reoperation or spinal cord stimulation. North et al. conducted a prospective, randomized clinical study that found SCS more effective in achieving pain control than reoperation as a treatment for persistent radicular pain after lumbosacral spine surgery. [40] The PROCESS study, a multi-center randomized clinical study, compared SCS in combination with conventional medical management in patients with FBSS and predominantly lower extremity radicular symptoms. [41] At 6-month follow-up, 48% of SCS patients achieved the primary outcome of >50% leg pain relief compared to only 9% of the medical management group. At 2-year follow-up, 42 out of 52 patients with SCS had less leg pain and improved functional capacity.
Patients with CRPS treated with SCS have demonstrated reduction in pain and allodynia with improvements in quality of life and limb function. [36] Kemler et al. found patients with CRPS who underwent SCS demonstrated a 2.4 fold reduction in pain on the visual analog scale compared to a 0.2 fold increase in pain for patients who received physical therapy alone at 6-month follow-up. [42] Long-term prospective data for spinal cord stimulation in CRPS indicates 63% of patients achieve long-term pain control. A 50% reduction in pain at 1 week post-implantation is associated with long-term success. [43] The best outcomes are demonstrated in CRPS type 1 in patients under 40 years of age and those who receive SCS within one year of diagnosis. [44]
SCS can be effective in patients with peripheral neuropathy secondary to diabetes. At 1-year follow-up, 63% of patients treated with SCS demonstrated a >50% reduction in lower extremity pain. Additionally, 60% of patients were weaned off analgesic medications. [45]
Postherpetic neuralgia is a chronic neuropathic pain syndrome that can occur following a herpes zoster eruption. [36] Spinal cord stimulation has been shown to be effective in the treatment of PHN, with 82% of patients experiencing a significant decrease in pain and improvement in quality of life. [46]
Spinal cord stimulation has shown benefit in chronic visceral pain resulting from mesenteric ischemic pain, esophageal dysmotility, gastroparesis, inflammatory bowel syndrome (IBS), chronic pancreatitis, familial Mediterranean fever, post-traumatic splenectomy, generalized chronic abdominal pain, postgastric bypass chronic epigastric pain, and chronic visceral pain resulting from post-surgical intra-abdominal adhesions. [36] Kapural et al. reported a study of SCS for chronic visceral abdominal pain. SCS resulted in 86% of patients achieving a >50% reduction in pain, along with a significant decrease in opioid requirements for pain control. [47] SCS has also shown benefit in chronic pancreatitis, with 80% of patients experiencing >50% reduction in pain at 1-year follow-up. [48]
Allodynia and painful cyanotic discoloration may be associated with the distal extremities Reynaud’s disease or ischemic peripheral vascular disease. SCS may result in decreased pain associated with ischemia. [36]
Direct stimulation of the dorsal root ganglion is an emerging treatment in the field of spinal cord stimulation. A DRG stimulator consists of electrical leads, which are threaded through the epidural space into the intervertebral foramen and directly overlie the dorsal root ganglion. Leads are then connected to an implanted battery through extension wiring. The main difference between DRG-SCS and traditional SCS lies in the type of fiber activation associated with the two types of stimulation. SCS involves stimulation of the dorsal columns resulting in broad electrical stimulation of multiple dermatomes. DRG stimulation is more precise, directly activating the cell bodies of the very neurons that innervate the painful regions. [49] DRG-SCS is as effective as traditional SCS in the treatment of pain due to failed back surgery syndrome, complex regional pain syndromes, and chronic postsurgical pain. [50] DRG can be particularly effective in treating pain in areas difficult to treat with traditional SCS, including focal distal distributions such as groin and foot. Additionally, DRG stimulation is associated with a lower rate of lead migration and positional side effects associated with traditional SCS. Liem et el. treated 51 patients with DRG-SCS. In their cohort, patients reported a 56% reduction in pain 12 months post-implantation, with 60% of patients reporting greater than 50% improvement in their pain. Pain localized to the back, legs, and feet was reduced by 42%, 62%, and 80%, respectively. Patients also demonstrated a significant improvement in quality of life. [49]
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Gaurav Gupta, MD Assistant Professor, Section Head, Endovascular and Cerebrovascular Neurosurgery, Fellowship Director, Endovascular Neurosurgery Fellowship (Site), Department of Surgery, Division of Neurosurgery, Rutgers Robert Wood Johnson Medical School
Gaurav Gupta, MD is a member of the following medical societies: American Academy of Neurology, American Association for the Advancement of Science, American Association of Neurological Surgeons, American College of Surgeons, American Heart Association, American Medical Association, Congress of Neurological Surgeons, Facial Pain Association, Society for Neuroscience, Society of NeuroInterventional Surgery
Disclosure: Nothing to disclose.
Arthur Carminucci, MD Resident Physician, Department of Neurological Surgery, Rutgers New Jersey Medical School
Disclosure: Nothing to disclose.
Kim J Burchiel, MD, FACS John Raaf Professor and Chairman, Department of Neurological Surgery, Professor, Department of Anesthesiology and Perioperative Medicine, Oregon Health and Science University School of Medicine; Attending Neurosurgeon, Section of Neurosurgery, Portland Veterans Affairs Medical Center; Attending Neurosurgeon, Shriners Hospital for Children
Kim J Burchiel, MD, FACS is a member of the following medical societies: American Academy of Pain Medicine, American Association of Neurological Surgeons, American College of Surgeons, American Pain Society, International Association for the Study of Pain, Oregon Medical Association, Society of Neurological Surgeons, Congress of Neurological Surgeons
Disclosure: Nothing to disclose.
Anthony H Wheeler, MD Department of Neurology, Bethany Medical Center
Anthony H Wheeler, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pain Medicine, North American Spine Society, North Carolina Medical Society
Disclosure: Received salary from Allergan, Inc. for speaking and teaching; Received none from Gralise for consulting.
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