Continuing Education Activity

Spinal cord stimulation (SCS) is an established neuromodulation therapy for chronic, refractory pain and select ischemic conditions. By delivering targeted electrical impulses to the dorsal columns of the spinal cord, SCS modulates pain signal transmission and provides durable analgesia when conservative medical or surgical interventions fail. Robust evidence supports its use in failed back surgery syndrome, complex regional pain syndrome (CRPS), refractory angina, and peripheral ischemia, demonstrating significant improvements in pain relief, functional capacity, and quality of life. Cost-utility studies confirm that SCS is not only clinically effective but also economically advantageous compared with repeat surgery or long-term conventional medical management. Emerging technologies, such as closed-loop, evoked compound action potential (ECAP)-controlled systems, and subperception stimulation, further enhance precision, patient comfort, and long-term outcomes.

By participating in this course, clinicians gain a comprehensive understanding of SCS therapy, encompassing patient selection and preoperative evaluation, procedural techniques, and postoperative management. Learners will be equipped to identify appropriate candidates, interpret diagnostic imaging, and collaborate effectively with multidisciplinary teams to optimize patient outcomes. The course also reviews the latest evidence on clinical efficacy, cost-effectiveness, and emerging technologies, providing participants with the knowledge and skills to integrate SCS safely and effectively into contemporary pain management practice.

Objectives:

• Implement best practices for perioperative management, complication prevention, and postoperative follow-up to ensure durable analgesia.
• Differentiate between traditional, closed-loop, and subperception spinal cord stimulation technologies, as well as their respective clinical applications.
• Assess pain etiology, chronicity, functional impairment, and prior treatment failure to establish appropriateness for spinal cord stimulation referral.
• Collaborate with an interdisciplinary team, including pain specialists, surgeons, anesthesiologists, nurses, and device representatives, to ensure seamless care and optimize patient outcomes.

Introduction

Chronic neuropathic pain remains a challenging and often debilitating condition, affecting millions worldwide and significantly impairing quality of life and functional capacity. For patients with refractory pain unresponsive to pharmacologic therapy, physical rehabilitation, and less invasive interventions, neuromodulation has emerged as a pivotal therapeutic strategy. Spinal cord stimulation (SCS), first introduced in the late 1960s, uses pulsed electrical energy near the spinal cord to modulate pain signaling and provide durable analgesia.[1] Initially, this technique delivered pulsed energy in the intrathecal space. Still, modern neuromodulation now involves the implantation of leads within the epidural space, allowing more precise and sustained stimulation of the dorsal columns.[2] SCS represents part of a broader family of neurostimulation modalities—such as deep brain stimulation and peripheral nerve stimulation—that apply electrical energy to the central or peripheral nervous system to modify pathologic pain signaling.

The theoretical foundation of SCS originated from the gate control theory of pain proposed by Melzack and Wall, which posits that pain impulses provoked in the periphery and carried by small, slow-conducting C fibers and A-delta fibers can be interrupted by stimulating larger, fast-conducting A-beta fibers.[2] Because these afferent pathways converge at the substantia gelatinosa of the dorsal horn, activation of A-beta fibers effectively “closes the gate” to ascending noxious stimuli, thereby attenuating the perception of pain. This mechanism highlights the intricate interplay between multiple pain systems, each comprising integrative neuronal networks that convey both excitatory and inhibitory signals across nociceptors.[3] Nociceptors initially detect noxious thermal, chemical, or mechanical stimuli in the periphery and transmit this information to second-order neurons in the dorsal horn of the spinal cord. These signals are then relayed via projection neurons to higher centers in the brainstem and cortex, where the sensation and emotional context of pain are ultimately perceived and modulated.

Over the past 2 decades, rapid technological advancements, including the development of high-frequency stimulation, burst waveforms, and closed-loop feedback systems, have substantially expanded the clinical utility and efficacy of SCS. Indications now encompass complex regional pain syndrome, failed back surgery syndrome, peripheral neuropathies, ischemic limb pain, and painful diabetic neuropathy, among others. Randomized controlled trials and long-term observational studies have consistently demonstrated significant reductions in pain intensity, improvements in function and quality of life, and reductions in opioid utilization in appropriately selected patients.

Despite these advances, challenges persist in patient selection, optimizing stimulation parameters, and managing complications such as lead migration, infection, and hardware failure. Furthermore, the economic implications of SCS, as well as its integration into multidisciplinary pain management, remain areas of active investigation. This review provides a comprehensive overview of the current evidence, technological developments, clinical indications, outcomes, and future directions in spinal cord stimulation, with an emphasis on emerging therapies and strategies to optimize patient-centered care.

Anatomy and Physiology

Effective SCS depends on a detailed understanding of the spinal anatomy, neurophysiology of pain transmission, and the mechanisms by which neuromodulation alters these pathways. SCS systems are implanted in the epidural space, located between the dura mater and the vertebral canal’s inner wall. This space contains epidural fat, venous plexuses, and segmental arteries, providing a corridor for percutaneously introduced leads that deliver pulsed electrical energy to the dorsal columns. Initially, early SCS techniques employed pulsed energy in the intrathecal space; however, current practice involves placing leads in the dorsal epidural compartment for more controlled and sustained stimulation.[2]

Pain Pathways and Gate Control Theory

Peripheral pain is initiated by nociceptors, which detect noxious thermal, chemical, or mechanical stimuli. These signals are carried by unmyelinated C fibers and lightly myelinated A-delta fibers, both of which conduct slow, nociceptive pain impulses. In contrast, large, myelinated A-beta fibers conduct non-nociceptive sensations such as touch, pressure, and vibration. These fibers terminate in the dorsal horn, particularly in the substantia gelatinosa (lamina II), where they synapse on second-order neurons. These projection neurons then cross the midline and ascend via the anterolateral (spinothalamic) tract to higher centers. The primary integrative site is the thalamus, although other supraspinal structures contribute to the perception and modulation of pain. Upon arrival of these signals, the brain rapidly generates responses including somatic and autonomic reflexes, endocrine and emotional reactions, cortical awareness, feedback mechanisms that can amplify or dampen pain, and even the encoding of the painful event into memory.

The gate control theory of pain, proposed by Melzack and Wall, provided the original mechanistic framework for SCS. Both nociceptive (C and A-delta) and non-nociceptive (A-beta) fibers synapse on transmission cells and inhibitory interneurons in the dorsal horn. While all 3 fiber types can activate transmission cells, only the non-nociceptive A-beta fibers stimulate inhibitory interneurons, which release gamma-aminobutyric acid (GABA) and glycine to suppress transmission cell activity and “close the gate,” thereby reducing ascending pain signals.[4] Modern research, however, has demonstrated that the underlying mechanisms of SCS analgesia extend beyond the original gate control model and vary between different pain types. In neuropathic pain, SCS alters local neurochemistry by suppressing the hyperexcitability of wide-dynamic-range neurons, increasing the release of GABA and serotonin, and reducing excitatory cytokines such as glutamate and aspartate.[5] In ischemic pain, analgesia is thought to derive from altered sympathetic tone, restoring a favorable balance between oxygen supply and demand.[5]

Spinal Cord Anatomy and Vascular Supply

The spinal cord extends from the medulla to approximately the level of L1 in adults, terminating as the conus medullaris. Below this level, the spinal nerve roots elongate and descend as the cauda equina, floating freely in cerebrospinal fluid, making this region an ideal location for epidural access.[6] The cord is enveloped by 3 meningeal layers: the pia mater (innermost, adherent to the cord), the arachnoid mater, and the dura mater (outermost).

Accessing the epidural space requires navigating key vertebral structures. Each vertebra consists of a vertebral body anteriorly and a vertebral arch posteriorly. The arch comprises lateral pedicles joined by posterior laminae, a single spinous process, and 2 transverse processes. The intervertebral foramina, formed at the level of the pedicle, permit the exit of the spinal nerves. There are 7 cervical, 12 thoracic, and 5 lumbar vertebrae, followed by the fused sacrum and coccyx.[6] During epidural placement, the needle sequentially passes through the supraspinous ligament, the interspinous ligament, and the thick ligamentum flavum before entering the epidural space. Anterior and posterior longitudinal ligaments stabilize the vertebral bodies.[6]

The spinal cord’s arterial supply originates from the vertebral arteries in the cervical region and from intercostal and lumbar arteries in the thoracic and lumbar regions. These vessels form a pial plexus and give rise to anterior and posterior spinal arteries. The posterior spinal arteries anastomose extensively to protect the dorsal sensory columns, whereas a single anterior spinal artery supplies the ventral motor cord. A key contributor is the artery of Adamkiewicz, which most often enters through the L1 foramen and supplies the lower two-thirds of the cord. Inadvertent damage to this vessel during epidural access can result in catastrophic bilateral lower extremity paralysis.[6] Venous drainage occurs through the vertebral venous plexus, which empties into the azygos system and ultimately the superior vena cava. Increased intra-abdominal or thoracic pressure, such as in patients with masses or superior vena cava compression, can engorge these veins and increase the risk of accidental venous cannulation during epidural needle placement.[6]

Mechanisms of Spinal Cord Stimulation and Emerging Technologies

SCS leads are positioned over the dorsal columns, which carry the large A-beta fibers whose activation is central to neuromodulation. By stimulating these fibers, SCS promotes inhibitory interneuron activity, modulates descending pain control pathways from the periaqueductal gray and rostroventral medulla, and influences sympathetic outflow. In addition to classical paresthesia-based systems, modern devices incorporate high-frequency and burst stimulation, as well as closed-loop SCS (CL-SCS) technology. CL-SCS utilizes evoked compound action potentials to dynamically and automatically monitor spinal responses, adjusting stimulation intensity within a therapeutic window to accommodate physiologic changes such as coughing or posture shifts, without requiring manual reprogramming.[7] In summary, the interplay between spinal anatomy and pain physiology underlies the therapeutic effect of SCS. From precise epidural lead placement to the modulation of ascending and descending nociceptive pathways, successful neuromodulation relies on a comprehensive understanding of both the structural and neurochemical bases of pain.

Indications

Patient selection is often the most challenging step in determining whether to offer neurostimulation. Factors that may initially seem unrelated to treatment response, particularly social determinants of health, can significantly influence the likelihood of a positive outcome. Because SCS involves an implantable device, patients must be willing and able to participate actively in their care, including regular follow-up for reprogramming, wound management, and, in some cases, wireless recharging of the stimulator. Long-term success depends as much on patient engagement and adherence to these responsibilities as on the technical aspects of the procedure.

Beyond social considerations, certain clinical features correlate more strongly with the success of SCS. Complex regional pain syndrome (CRPS) is among the most predictive indications for favorable outcomes. A positive response to a sympathetic nerve block may also suggest potential benefit from stimulation therapy.[8] In a retrospective cohort of 318 patients, 255 of whom had CRPS, sympathetic blocks resulted in greater than 50% pain relief in 61% of patients with CRPS, with a typical duration of 1 to 4 weeks. However, the magnitude of block-related analgesia did not predict the success of subsequent SCS trials.[9] Level A evidence supports SCS for failed back surgery syndrome, also known as postlaminectomy syndrome, peripheral ischemia, peripheral neuropathy, and angina pectoris.[10] Nevertheless, dorsal column stimulation has demonstrated efficacy across a wide range of neuropathic and radicular pain syndromes, especially when pain is refractory to medications, physical therapy, psychotherapy, chiropractic interventions, and other procedural treatments.

Conversely, patient age, pain duration, intensity, or laterality do not appear to influence SCS outcomes significantly.[11] Moreover, contemporary evidence underscores the growing effectiveness of newer stimulation strategies. Results from a 2024 network meta-analysis showed that novel SCS approaches, including high-frequency and burst stimulation, outperformed conventional medical management at 6 months, yielding superior responder rates (odds ratio approximately 8.76 vs 3), greater reductions in both back and leg pain, higher EuroQol 5-Dimension quality-of-life scores, and more pronounced improvements in functional disability.[12] In summary, successful SCS therapy depends on careful patient selection that integrates social readiness and clinical indication, while recognizing that innovative stimulation technologies are broadening the range of patients who may benefit.

Contraindications

Because most available data on SCS come from small prospective or retrospective studies, formal evidence-based guidelines for contraindications remain limited. Nevertheless, as with other elective surgical procedures, standard perioperative contraindications apply. These include active infection at the surgical site, aberrant spinal anatomy that prevents safe epidural access, uncontrolled systemic illness, and uncontrolled bleeding diathesis. Patients receiving therapeutic anticoagulation typically require their medications to be held in accordance with guidelines from the American Society of Regional Anesthesia. If anticoagulation cannot be interrupted due to a life-threatening clotting disorder or imminent cardiac surgery, SCS placement is contraindicated.

Specific clinical and psychological features are associated with reduced success and may be considered relative contraindications. In a study of 36 patients with CRPS, mechanical allodynia, defined as pain elicited by light touch, was associated with significantly poorer outcomes: patients with mechanical allodynia experienced only a 31% reduction in pain, compared to an 81% reduction in those without allodynia.[13] Likewise, active psychiatric comorbidities such as depression, anxiety, somatization, and poor coping skills predict unfavorable results.[11] For this reason, a comprehensive psychological evaluation is a standard prerequisite before implantation. Notably, catastrophizing, or the tendency to perceive a situation as worse than it is, does not appear to impact SCS outcomes negatively.[14] SCS is also generally ineffective for specific pain syndromes, such as stump pain, phantom limb pain, and paraplegic pain, where evidence consistently shows little or no benefit.[10]

Equipment

Modern SCS systems consist of 3 primary components. The first is the electrodes or leads, which may be cylindrical (percutaneous) or paddle-shaped (surgical). Cylindrical leads can be placed percutaneously using an epidural needle and are easier to revise. In contrast, paddle leads require a laminotomy for implantation but are less prone to migration and can provide broader stimulation coverage. The second component is the implantable pulse generator (IPG)—the internal battery and electronic control unit that delivers electrical pulses to the leads. Finally, SCS systems typically include external charging and reprogramming equipment, comprising a wireless charger and a patient-operated remote control that allows for the adjustment of stimulation settings.

Although numerous companies manufacture neuromodulation devices, the majority of the SCS market is dominated by 3 primary manufacturers.[15] All leading companies now provide rechargeable IPGs designed to last up to 10 years, a significant advance that enables patients to use higher voltages without rapid battery depletion. Rechargeable systems also increase the range of available programming options and reduce the need for surgical generator replacement.

When selecting an SCS system, magnetic resonance imaging (MRI) compatibility is a key consideration because many patients will require advanced imaging during their lifetime. Each manufacturer offers devices with different levels of MRI conditionality, and the specific requirements must be reviewed before implantation to ensure the device is appropriate for the patient’s anticipated imaging needs. A 2025 comparative review of neuromodulation devices from 10 manufacturers reported that full-body MRI at 1.5 Tesla (T) is generally supported; however, only certain SCS systems allow scanning at 3.0 T. Device-specific limitations may include maximum spatial gradient fields (ranging from 1000–4000 Gauss/cm), specific absorption rate restrictions, and limits on active scan time duration.[16]

Personnel

Successful SCS trials and permanent implantations require coordinated collaboration among a specialized interprofessional team. Each member contributes distinct expertise to optimize patient safety, procedural efficiency, and device functionality. The operating clinician, typically a pain medicine specialist, neurosurgeon, or anesthesiologist with interventional training, is primarily responsible for performing the SCS trial and permanent placement. This clinician must understand the roles of all personnel in the procedure room, be fully credentialed to perform both trial and implantation, and ensure that the patient is thoroughly educated regarding the risks, benefits, and alternatives of SCS therapy.

The anesthesia clinician administers the minimum sedation necessary to maintain patient comfort and safety while enabling effective monitoring. Familiarity with procedural steps is essential to rapidly adjust anesthesia depth during intraoperative paresthesia mapping, when patient feedback is required to confirm appropriate lead positioning. The circulating nurse plays a critical role in maintaining procedural flow and patient safety. This includes understanding the equipment and steps necessary for SCS placement, verifying patient identity and surgical site, monitoring sterile technique, and assisting with patient transport and positioning.

A radiology technician operates the C-arm fluoroscopy unit, ensuring optimal imaging of the spinal anatomy while maintaining a sterile field. Precise imaging is essential for accurate epidural lead placement and minimizing complications. The surgical technician manages the surgical instruments and supports the sterile field. This includes anticipating the sequence of procedural steps, preparing and passing instruments, maintaining accurate needle and sponge counts, and helping to prevent breaks in sterility that could increase the risk of infection.

Finally, the device representative, a technical specialist employed by the device manufacturer, provides critical support for device-specific aspects of the procedure. The representative assists the operating provider in troubleshooting hardware or programming issues, facilitates paresthesia mapping, and educates the patient about device operation and long-term maintenance. This structured collaboration of providers, nurses, technical staff, and industry specialists is essential for a safe and effective SCS implantation, enabling precise device placement and optimal therapeutic outcomes.

Preparation

Thorough preparation is essential to optimize outcomes with spinal cord stimulation and should begin well in advance of the implantation date. The process typically starts with a pain evaluation with a clinician, during which the patient’s pain syndrome, medical history, and prior treatments are carefully reviewed. The goal is to determine whether the pain pattern is amenable to neuromodulation and to ensure that appropriate conservative therapies, such as pharmacologic management, physical therapy, and interventional procedures, have been exhausted. This consultation also establishes realistic expectations and provides patients with education regarding the potential benefits, risks, and responsibilities associated with long-term SCS management.

A psychological evaluation is a critical step in the candidate selection process. Active or untreated psychiatric conditions such as depression, anxiety, or somatization have been associated with poorer outcomes. A licensed mental health professional assesses for these conditions and evaluates coping strategies and readiness to participate in the demanding follow-up care required for successful SCS therapy.

Diagnostic imaging, ideally with MRI, helps map the epidural space and delineate the spinal anatomy at the intended level of lead placement. Imaging both guides the procedural approach and helps correlate pain distribution with structural findings, thereby refining the therapeutic plan. A trial stimulation is then performed. One or more temporary leads are inserted and connected to an external IPG, allowing the patient to experience SCS in real time. Success is typically defined as achieving at least a 50% reduction in pain and/or a 50% improvement in functional capacity, with confirmation of adequate coverage of all painful regions. If the trial is successful, the patient proceeds to permanent implantation, which involves reimplantation of one or more leads and the IPG. This staged process not only improves patient selection and satisfaction but also maximizes the likelihood of long-term pain relief and functional improvement.

Technique or Treatment

The technique associated with SCS is considered 1 of the most challenging procedures in interventional pain management. The implantation of the SCS device is divided into 2 steps: the trial and the permanent SCS implantation. Although the same or similar equipment is used for these procedures, the technique employed for each step changes significantly. The trial enables the patient to assess the effect of the SCS device on their specific pain pattern. Typically, patients return to the clinic within 10 days after the trial procedure has been completed. If they experience over 50% pain relief, an increase in activity level, and/or a decrease in medication use during this time, the trial is considered successful, and they can be scheduled for a permanent SCS procedure.[17][18]

Procedural Technique for SCS Placement

Both the trial and permanent spinal cord stimulator procedures are performed as sterile operations in the operating room under monitored sedation. To reduce the risk of infection, patients are instructed to shower with chlorhexidine the evening before or the morning of the procedure. For permanent implantation, preoperative antibiotics are administered to provide coverage against skin flora.

On the day of the procedure, the patient is positioned prone on the operating table. The back is prepped with an alcohol-based chlorhexidine scrub and then covered with sterile towels and a full surgical drape to maintain a sterile field. Access to the epidural space is typically achieved using a Tuohy needle, introduced under continuous fluoroscopic guidance. The needle is advanced at an angle of less than 45 degrees to facilitate the smooth passage of the SCS lead. A perpendicular approach should be avoided, as it requires excessive bending of the lead and may increase the risk of mechanical damage or malposition.

Once the epidural space is entered, the lead is carefully threaded through the posterior paramedian epidural space and advanced to the targeted vertebral level, providing optimal coverage of the patient’s pain distribution with paresthesia. This typically requires placement at the midthoracic level, most commonly between T8 and T10; however, final positioning is guided by intraoperative testing and the patient’s specific pain pattern. One or more leads may be placed to ensure adequate coverage before securing the hardware and completing the procedure.

Types of SCS Trials and Permanent Implantation Techniques

Two primary strategies are employed to assess patient response before permanent SCS implantation: the percutaneous lead trial and the permanent lead trial. The choice of trial depends on clinician preference, patient-specific factors, and long-term therapeutic goals.

• SCS percutaneous lead trial

  • The percutaneous trial is the most commonly performed approach. After the lead or leads are positioned within the epidural space at the desired spinal level, the epidural needle is withdrawn. The lead is then secured externally with a suture, surgical adhesive, or skin glue. The lead's externalized portion connects to an external pulse generator, which is likewise fixed to the skin with a suture or skin glue, a chlorhexidine patch, and a sterile dressing. Device programming is initiated intraoperatively and finalized in the recovery room before discharge.
  • Although a successful percutaneous trial requires a second procedure for permanent implantation, this approach is preferred because it avoids additional incisions and reduces postprocedural discomfort during the trial. Significantly, it is also associated with a lower risk of infection compared to a permanent trial approach.[19]
• Permanent SCS lead trial

  • In the permanent trial technique, once the leads are optimally positioned, a local anesthetic is infiltrated around the epidural needle. A midline incision is created through the skin to the supraspinous fascia, where the leads are anchored using a nonabsorbable suture and anchoring device. The anchoring device is placed as close to the fascia as possible, with the tip seated within the fascia to minimize lead bending, and secured with nonabsorbable suture.
  • Two methods are used to connect the leads to the IPG:

    • Extended midline approach 

      • The midline incision is enlarged, and a temporary extension wire is attached to the permanent lead to guide it to the skin surface.
    • Lateral pocket approach 

      • A subcutaneous pocket is created in the flank for IPG placement (less commonly in the posterior superior gluteal region, lower abdomen, or pectoral region). The permanent lead is tunneled from the midline incision to this pocket and connected to a temporary extension wire.
  • The permanent trial is more cost-effective because the same device is used if the trial is successful, and it ensures that the leads remain in their exact locations for the final implantation.[19]
• Permanent placement with paddle-type electrodes

  • Permanent SCS systems may also use paddle electrodes, which can be introduced percutaneously with a wide, flat introducer or surgically implanted via a laminotomy, thereby allowing direct placement of the paddle into the epidural space. Neurosurgeons typically perform this approach, and it is generally a permanent implantation method rather than a temporary trial.[20]
• Permanent percutaneous SCS implantation

  • For patients who underwent a permanent trial, final implantation involves reopening the IPG pocket incision on the day of implantation. The temporary lead extension is removed, and the permanent lead is connected to a new extension that attaches directly to the IPG.
  • For those who underwent a percutaneous trial, the permanent implantation follows the same procedural steps as the trial. The permanent lead is tunneled to a subcutaneous IPG pocket of the appropriate size, where it is connected to the IPG. The device is secured within the pocket, the incisions are closed with staples, and a sterile dressing is applied. Staples are typically removed in the clinic about 14 days postoperatively.[17]
  • A radiopaque template often guides pocket sizing to ensure accurate dimensions. The pocket location is typically selected for patient comfort and ease of access, typically above or below the beltline, on the side opposite the side where the patient sleeps, or on the side the patient can easily reach for reprogramming or recharging the IPG.

Complications

Complications associated with SCS span from correctable issues such as inappropriate paresthesia coverage to infection, lead migration, epidural hematoma, nerve injury, paralysis, and death. Luckily, the more devastating complications are exceedingly rare. The use of sterile technique and operating room conditions helps minimize the risk of infection. The risk of nerve injury and paralysis is mitigated by using continuous fluoroscopy throughout the procedure, providing both trajectory and depth views. More serious complications related to oversedation, anesthesia, airway compromise, and anaphylactic reactions can be lowered and managed by licensed anesthesia professionals.

The most common, not-easily correctable problem is infection. Over the years, with the implementation of rigorous quality-control measures, advances in techniques, and perioperative antibiotic guidelines, the incidence of disease has declined to between 3% and 5%, depending on the source.[21] The most common infection is Staphylococcus, accounting for 18% of cases. The most common site of infection is the IPG site (54%). In most cases, infection requires the explantation of the entire system, unless the contamination is confined to the superficial tissues.[22]

The most frequent complication overall is lead migration or breakage. This issue can be minimized by restricting activity for 1 to 2 months, during which the patient limits bending, lifting, and twisting until the leads have scarred in the appropriate location. As lead and anchor technology advances, the rate of revision due to lead migration continues to decline. Of note, the more rigid paddle leads are twice as likely to break as the percutaneous leads.[23]

Clinical Significance

SCS has emerged as a highly effective, evidence-based intervention for refractory and difficult-to-treat pain syndromes and certain ischemic conditions, providing durable analgesia, functional improvement, and enhanced quality of life when conventional medical or surgical therapies fail. Beyond efficacy, the cost-effectiveness of SCS is an important consideration, particularly in patients with chronic pain who often require prolonged care and multiple interventions.

Failed Back Surgery Syndrome: Level A Recommendation

FBSS is the most common indication for SCS in the United States. SCS is established to provide long-term pain relief, reduce opioid and other medication dependence, enhance functional capacity, improve quality of life, and increase the likelihood of returning to work, with fewer adverse events compared to repeat surgical interventions.[24] In a randomized study, North et al compared 27 FBSS individuals undergoing repeat laminectomy with those undergoing SCS. Pain relief of more than 50% was achieved in 47% of those with SCS versus 12% in the reoperation group, with higher opioid use in the latter.[25] Kumar et al randomized individuals with FBSS with neuropathic radicular pain to SCS or conventional medical management. At 6 months, 48% of those with SCS achieved greater than 50% pain relief, compared to 9% in the traditional medical management group, with superior improvements in back and leg pain, functional capacity, quality of life, and patient satisfaction. Benefits persisted at 24 months.[26]

SCS is also highly cost-effective for FBSS. North et al (2005) demonstrated that the mean per-patient cost was $48,457 for SCS versus $105,928 for reoperation, establishing SCS as both more effective and less expensive.[25] A 5-year follow-up by Kumar et al showed that annual healthcare costs were $29,000 for patients with SCS compared with $38,000 for nonstimulator controls, with higher costs in the latter group attributed to greater medication use, follow-up visits, imaging, hospitalizations, and rehabilitation services.[27] Furthermore, if SCS fails, subsequent reoperation is unlikely to be successful and should generally be discouraged.[28]

Complex Regional Pain Syndrome: Level B Recommendation

SCS is associated with pain reduction, improved perceived effect, and enhanced quality of life in patients with CRPS. Some studies have proposed a Level A recommendation, although the overall quality of evidence remains limited.[29] Kemler et al compared SCS plus physical therapy with physical therapy alone in 42 patients with CRPS. After 6 months, those receiving SCS reported significant pain relief and were more likely to rate themselves as “much improved.” Functional outcomes did not differ; however, the 2-year follow-up confirmed the durability of the analgesic effects.[30]

Angina Pectoris: Level A Recommendation

SCS effectively reduces anginal attacks and nitrate use while improving exercise capacity, with outcomes comparable to coronary bypass surgery but with lower morbidity and mortality.[31] This mechanism is thought to involve sympathetic modulation, which enhances distal microcirculatory perfusion, as measured by transcutaneous partial pressure of oxygen (TcPO2).[32] Despite strong supporting evidence, SCS remains underused in cardiology practice.

Peripheral Ischemia: Level A Recommendation

In patients with critical limb ischemia, SCS can enhance perfusion and reduce the risk of amputation. Ubbink and Vermeulen reported an 83% limb-salvage rate with SCS, compared with 20% to 64% with conservative management, and improved quality of life and reduced analgesic use across 9 studies (444 patients). TcPO₂ increases of ≥10 mm Hg were commonly observed and correlated with favorable outcomes.[33] Results from subsequent studies failed to show a significant reduction in amputation risk, highlighting the need for further investigation.[34]

Emerging Technologies and Long-Term Outcomes

• CL-SCS

  • Closed-loop spinal cord stimulation systems automatically adjust stimulation based on evoked compound action potentials (ECAPs) to maintain consistent and stable analgesic effects.

    • In nonsurgical refractory back pain, ≥50% pain relief was achieved in 79% of patients and ≥80% relief in 48% at 12 months, accompanied by improvements in physical function, sleep, emotional health, quality of life, and opioid reduction.[35]
    • Preclinical rodent models validated ECAPs as objective biomarkers for dosing, showing significant reductions in mechanical and cold hypersensitivity.[36]
    • The EVOKE trial demonstrated superior outcomes at 36 months for closed-loop versus open-loop SCS, with 77.6% of patients achieving ≥50% pain relief and 49.3% achieving>80%, compared with 49.3% and 31.3%, respectively. Notably, precise neural activation was achieved, and no explants resulted from loss of efficacy.[37]
• Subperception SCS

  • Techniques such as fast-acting-SCS (FAST is a novel subperceptual spinal cord stimulation therapy that uses charge-balanced, symmetric 90 Hz pulses) can achieve rapid pain relief, providing paresthesia-free analgesia while maintaining long-term efficacy.

    • Long-term follow-up indicates ~85% of patients sustain ≥50% pain reduction and 64% report minimal pain (numeric rating scale [NRS] ≤2) over 2 years.[38]
    • Real-world applications show significant improvements in functional disability and quality of life for chronic back and leg pain patients.[39]

Spinal cord stimulation is a clinically effective and cost-efficient therapy for refractory neuropathic pain and ischemic conditions, with robust evidence supporting its use in conditions such as FBSS, peripheral ischemia, angina, and CRPS. Emerging technologies such as closed-loop ECAP-controlled and subperception SCS systems further enhance analgesic durability, patient comfort, and functional outcomes, solidifying SCS as a cornerstone of contemporary neuromodulation therapy.

Enhancing Healthcare Team Outcomes

Successful spinal cord stimulation (SCS) therapy requires coordinated efforts and well-defined strategies across a multidisciplinary team to optimize patient-centered care and safety. Physicians and advanced practitioners lead patient selection, procedural planning, and long-term follow-up, ensuring that appropriate candidates are identified and that diagnostic imaging, psychological assessment, and trial stimulation are carefully executed. Nurses and surgical technicians maintain strict sterile technique, monitor perioperative status, and provide comprehensive patient education on wound care, device management, and postoperative expectations. Pharmacists contribute by reviewing medications, managing perioperative antibiotic prophylaxis, and optimizing multimodal analgesia to minimize opioid dependence. Clear communication among these professionals is essential to anticipate complications, adjust therapy, and promptly address concerns related to infection risk or device issues.

Effective care coordination hinges on regular interdisciplinary communication, both in the perioperative environment and during long-term follow-up. Team members must share real-time updates on patient progress, device performance, and pain outcomes to guide individualized therapy adjustments. Device representatives collaborate with clinicians to ensure accurate programming and to troubleshoot technical issues, while primary care providers and rehabilitation specialists help reinforce lifestyle modifications and monitor comorbid conditions. By establishing structured protocols, leveraging shared electronic health records, and engaging patients as active partners in their care, the SCS team can enhance functional recovery, ensure patient safety, and maintain high team performance, ultimately improving quality of life and sustaining long-term therapeutic success.

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References

1.

Kumar K, Nath R, Wyant GM. Treatment of chronic pain by epidural spinal cord stimulation: a 10-year experience. J Neurosurg. 1991 Sep;75(3):402-7. [PubMed: 1869942]

2.

Shealy CN, Mortimer JT, Reswick JB. Electrical inhibition of pain by stimulation of the dorsal columns: preliminary clinical report. Anesth Analg. 1967 Jul-Aug;46(4):489-91. [PubMed: 4952225]

3.

Willis WD. The pain system. The neural basis of nociceptive transmission in the mammalian nervous system. Pain Headache. 1985;8:1-346. [PubMed: 2983301]

4.

Moayedi M, Davis KD. Theories of pain: from specificity to gate control. J Neurophysiol. 2013 Jan;109(1):5-12. [PubMed: 23034364]

5.

Linderoth B, Foreman RD. Physiology of spinal cord stimulation: review and update. Neuromodulation. 1999 Jul;2(3):150-64. [PubMed: 22151202]

6.

Devereaux MW. Anatomy and examination of the spine. Neurol Clin. 2007 May;25(2):331-51. [PubMed: 17445732]

7.

Mangano N, Torpey A, Devitt C, Wen GA, Doh C, Gupta A. Closed-Loop Spinal Cord Stimulation in Chronic Pain Management: Mechanisms, Clinical Evidence, and Emerging Perspectives. Biomedicines. 2025 Apr 30;13(5) [PMC free article: PMC12108722] [PubMed: 40426918]

8.

Hord ED, Cohen SP, Cosgrove GR, Ahmed SU, Vallejo R, Chang Y, Stojanovic MP. The predictive value of sympathetic block for the success of spinal cord stimulation. Neurosurgery. 2003 Sep;53(3):626-32; discussion 632-3. [PubMed: 12943579]

9.

Cheng J, Salmasi V, You J, Grille M, Yang D, Mascha EJ, Cheng OT, Zhao F, Rosenquist RW. Outcomes of Sympathetic Blocks in the Management of Complex Regional Pain Syndrome: A Retrospective Cohort Study. Anesthesiology. 2019 Oct;131(4):883-893. [PubMed: 31365367]

10.

Kumar K, Toth C, Nath RK, Laing P. Epidural spinal cord stimulation for treatment of chronic pain--some predictors of success. A 15-year experience. Surg Neurol. 1998 Aug;50(2):110-20; discussion 120-1. [PubMed: 9701116]

11.

Celestin J, Edwards RR, Jamison RN. Pretreatment psychosocial variables as predictors of outcomes following lumbar surgery and spinal cord stimulation: a systematic review and literature synthesis. Pain Med. 2009 May-Jun;10(4):639-53. [PubMed: 19638142]

12.

Huygen FJPM, Soulanis K, Rtveladze K, Kamra S, Schlueter M. Spinal Cord Stimulation vs Medical Management for Chronic Back and Leg Pain: A Systematic Review and Network Meta-Analysis. JAMA Netw Open. 2024 Nov 04;7(11):e2444608. [PMC free article: PMC11565267] [PubMed: 39541119]

13.

van Eijs F, Smits H, Geurts JW, Kessels AG, Kemler MA, van Kleef M, Joosten EA, Faber CG. Brush-evoked allodynia predicts outcome of spinal cord stimulation in complex regional pain syndrome type 1. Eur J Pain. 2010 Feb;14(2):164-9. [PubMed: 19942463]

14.

Lamé IE, Peters ML, Patijn J, Kessels AG, Geurts J, van Kleef M. Can the outcome of spinal cord stimulation in chronic complex regional pain syndrome type I patients be predicted by catastrophizing thoughts? Anesth Analg. 2009 Aug;109(2):592-9. [PubMed: 19608836]

15.

Lanza GA, Grimaldi R, Greco S, Ghio S, Sarullo F, Zuin G, De Luca A, Allegri M, Di Pede F, Castagno D, Turco A, Sapio M, Pinato G, Cioni B, Trevi G, Crea F. Spinal cord stimulation for the treatment of refractory angina pectoris: a multicenter randomized single-blind study (the SCS-ITA trial). Pain. 2011 Jan;152(1):45-52. [PubMed: 21084162]

16.

Vu PD, Slitzky M, Miller K, Yong RJ, Robinson CL, Chung M. Provision of up-to-date magnetic resonance imaging conditionality for current peripheral nerve stimulation and spinal cord stimulation systems in pain management. Pain Med. 2025 Dec 01;26(12):924-929. [PubMed: 40580942]

17.

Malige A, Sokunbi G. Spinal Cord Stimulators: A Comparison of the Trial Period Versus Permanent Outcomes. Spine (Phila Pa 1976). 2019 Jun 01;44(11):E687-E692. [PubMed: 30365415]

18.

Burchiel KJ, Anderson VC, Wilson BJ, Denison DB, Olson KA, Shatin D. Prognostic factors of spinal cord stimulation for chronic back and leg pain. Neurosurgery. 1995 Jun;36(6):1101-10; discussion 1110-1. [PubMed: 7643988]

19.

Simopoulos T, Sharma S, Aner M, Gill JS. A Temporary vs. Permanent Anchored Percutaneous Lead Trial of Spinal Cord Stimulation: A Comparison of Patient Outcomes and Adverse Events. Neuromodulation. 2018 Jul;21(5):508-512. [PubMed: 28901641]

20.

Pahapill PA. Surgical paddle-lead placement for screening trials of spinal cord stimulation. Neuromodulation. 2014 Jun;17(4):346-8; discussion 348. [PubMed: 23815416]

21.

North RB, Kidd DH, Zahurak M, James CS, Long DM. Spinal cord stimulation for chronic, intractable pain: experience over two decades. Neurosurgery. 1993 Mar;32(3):384-94; discussion 394-5. [PubMed: 8455763]

22.

Meglio M, Cioni B, Rossi GF. Spinal cord stimulation in management of chronic pain. A 9-year experience. J Neurosurg. 1989 Apr;70(4):519-24. [PubMed: 2538588]

23.

Rosenow JM, Stanton-Hicks M, Rezai AR, Henderson JM. Failure modes of spinal cord stimulation hardware. J Neurosurg Spine. 2006 Sep;5(3):183-90. [PubMed: 16961078]

24.

Van Buyten JP. Neurostimulation for chronic neuropathic back pain in failed back surgery syndrome. J Pain Symptom Manage. 2006 Apr;31(4 Suppl):S25-9. [PubMed: 16647592]

25.

North RB, Kidd DH, Farrokhi F, Piantadosi SA. Spinal cord stimulation versus repeated lumbosacral spine surgery for chronic pain: a randomized, controlled trial. Neurosurgery. 2005;56(1):98-106; discussion 106-7. [PubMed: 15617591]

26.

Kumar K, Taylor RS, Jacques L, Eldabe S, Meglio M, Molet J, Thomson S, O'Callaghan J, Eisenberg E, Milbouw G, Buchser E, Fortini G, Richardson J, North RB. Spinal cord stimulation versus conventional medical management for neuropathic pain: a multicentre randomised controlled trial in patients with failed back surgery syndrome. Pain. 2007 Nov;132(1-2):179-88. [PubMed: 17845835]

27.

Kumar K, Malik S, Demeria D. Treatment of chronic pain with spinal cord stimulation versus alternative therapies: cost-effectiveness analysis. Neurosurgery. 2002 Jul;51(1):106-15; discussion 115-6. [PubMed: 12182407]

28.

North RB, Kidd D, Shipley J, Taylor RS. Spinal cord stimulation versus reoperation for failed back surgery syndrome: a cost effectiveness and cost utility analysis based on a randomized, controlled trial. Neurosurgery. 2007 Aug;61(2):361-8; discussion 368-9. [PubMed: 17762749]

29.

Taylor RS. Spinal cord stimulation in complex regional pain syndrome and refractory neuropathic back and leg pain/failed back surgery syndrome: results of a systematic review and meta-analysis. J Pain Symptom Manage. 2006 Apr;31(4 Suppl):S13-9. [PubMed: 16647590]

30.

Kemler MA, De Vet HC, Barendse GA, Van Den Wildenberg FA, Van Kleef M. The effect of spinal cord stimulation in patients with chronic reflex sympathetic dystrophy: two years' follow-up of the randomized controlled trial. Ann Neurol. 2004 Jan;55(1):13-8. [PubMed: 14705107]

31.

Eliasson T, Augustinsson LE, Mannheimer C. Spinal cord stimulation in severe angina pectoris--presentation of current studies, indications and clinical experience. Pain. 1996 May-Jun;65(2-3):169-79. [PubMed: 8826504]

32.

Gersbach P, Hasdemir MG, Stevens RD, Nachbur B, Mahler F. Discriminative microcirculatory screening of patients with refractory limb ischaemia for dorsal column stimulation. Eur J Vasc Endovasc Surg. 1997 May;13(5):464-71. [PubMed: 9166269]

33.

Ubbink DT, Vermeulen H. Spinal cord stimulation for critical leg ischemia: a review of effectiveness and optimal patient selection. J Pain Symptom Manage. 2006 Apr;31(4 Suppl):S30-5. [PubMed: 16647594]

34.

Amann W, Berg P, Gersbach P, Gamain J, Raphael JH, Ubbink DT., European Peripheral Vascular Disease Outcome Study SCS-EPOS. Spinal cord stimulation in the treatment of non-reconstructable stable critical leg ischaemia: results of the European Peripheral Vascular Disease Outcome Study (SCS-EPOS). Eur J Vasc Endovasc Surg. 2003 Sep;26(3):280-6. [PubMed: 14509891]

35.

Hunter CW, Raskin JS, Mekhail NA, Petersen EA, Lad SP, Pope JE, Costandi SJ, Kapural L, Boeding RB, Antony A, Rosen SM, Heros RD, Sayed D, Li S, Raslan AM, Smith GL, Goree JH, Leitner A, Soliday N, Duarte RV, Deer TR. ECAP-Controlled Closed-Loop Spinal Cord Stimulation for Chronic Nonsurgical Refractory Back Pain: Subgroup Analysis From Two Prospective Multicenter Clinical Trials. Spine (Phila Pa 1976). 2025 Dec 01;50(23):1637-1647. [PMC free article: PMC12594148] [PubMed: 40590186]

36.

Versantvoort EM, Dietz BE, Mugan D, Vuong QC, Luli S, Obara I. Evoked compound action potential (ECAP)-controlled closed-loop spinal cord stimulation in an experimental model of neuropathic pain in rats. Bioelectron Med. 2024 Jan 10;10(1):2. [PMC free article: PMC10777641] [PubMed: 38195618]

37.

Mekhail NA, Levy RM, Deer TR, Kapural L, Li S, Amirdelfan K, Pope JE, Hunter CW, Rosen SM, Costandi SJ, Falowski SM, Burgher AH, Gilmore CA, Qureshi FA, Staats PS, Scowcroft J, McJunkin T, Carlson J, Kim CK, Yang MI, Stauss T, Petersen EA, Hagedorn JM, Rauck R, Kallewaard JW, Baranidharan G, Taylor RS, Poree L, Brounstein D, Duarte RV, Gmel GE, Gorman R, Gould I, Hanson E, Karantonis DM, Khurram A, Leitner A, Mugan D, Obradovic M, Ouyang Z, Parker J, Single P, Soliday N., EVOKE Study Group. ECAP-controlled closed-loop versus open-loop SCS for the treatment of chronic pain: 36-month results of the EVOKE blinded randomized clinical trial. Reg Anesth Pain Med. 2024 May 07;49(5):346-354. [PMC free article: PMC11103285] [PubMed: 37640452]

38.

Metzger C, Hammond B, Ferro R, North J, Pyles S, Kranenburg A, Washabaugh E, Goldberg E. Two-year outcomes using fast-acting sub-perception therapy for spinal cord stimulation: results of a real-world multicenter study in the United States. Expert Rev Med Devices. 2025 Jan-Feb;22(2):155-164. [PubMed: 39819320]

39.

Bayerl S, Paz-Solis J, Matis G, Rigoard P, Kallewaard JW, Canos-Verdecho MA, Vesper J, Llopis JE, Kyriakopoulos G, Gulve A, Raoul S, Papa A, Love-Jones S, Williams A. Two-Year Outcomes Using Fast-Acting, Sub-Perception Therapy for Spinal Cord Stimulation: A European, Real-World, Multicenter Experience. J Clin Med. 2024 Nov 20;13(22) [PMC free article: PMC11595255] [PubMed: 39598142]

Disclosure: Anterpreet Dua declares no relevant financial relationships with ineligible companies.

Disclosure: Sara Collier declares no relevant financial relationships with ineligible companies.

Disclosure: Karolain Garcia declares no relevant financial relationships with ineligible companies.

Disclosure: Sanjeev Kumar declares no relevant financial relationships with ineligible companies.