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J Neurosurg Case Lessons
J Neurosurg Case Lessons
J Neurosurg Case Lessons
Journal of Neurosurgery: Case Lessons
2694-1902
American Association of Neurological Surgeons

10.3171/CASE24275
CASE24275
Functional-NeurosurgeryFunctional NeurosurgeryPainPainSpineSpineThoracicThoracicTechniqueTechniqueCase Lesson
Intrathecal placement of percutaneous spinal cord stimulation leads: illustrative cases
Olmsted Zachary T MD, PhD 1
Wu Peter B MD 1
Katouzian Alireza MD 2
Dorsi Michael J MD 1
1 Department of Neurosurgery, Ronald Reagan UCLA Medical Center, University of California Los Angeles Health, Los Angeles, California
2 Spanish Hills Interventional Pain Specialists, Camarillo, California
Correspondence Michael J. Dorsi: University of California Los Angeles Health, Los Angeles, CA. mjdorsi@mednet.ucla.edu.
INCLUDE WHEN CITING Published September 23, 2024; DOI: 10.3171/CASE24275.

Disclosures Dr. Dorsi is a paid consultant for Abbott, Nevro, Globus, Camber Spine, Vertos, Painteq, and LifeSpine.

23 9 2024
23 9 2024
8 13 CASE2427526 4 2024
11 7 2024
© 2024 the authors
2024
the authors
https://creativecommons.org/licenses/by-nc-nd/4.0/ CC BY-NC-ND 4.0 (http://creativecommons.org/licenses/by-nc-nd/4.0/)

BACKGROUND

Spinal cord stimulation (SCS), including the percutaneous placement of epidural stimulation leads, has been increasingly utilized to treat chronic pain. Although lead migration is a well-characterized complication, few studies have reported on malpositioned leads in the intrathecal space. Here, the authors discuss two cases of intrathecal lead placement necessitating surgical revision.

OBSERVATIONS

This report is a two-case series on the inadvertent placement of percutaneous SCS leads in the intrathecal space. The authors describe the identification of malpositioned leads, describe the clinical presentation, characterize stimulation parameters, and report improvement following neurosurgical revision for each case. Two patients originally presenting with chronic low-back pain underwent percutaneous SCS lead implantation. Both patients presented with atypical pain symptoms in the acute to subacute postprocedural period, raising suspicion for malpositioned leads. Imaging was consistent with intrathecal malpositioning. Both patients underwent revision surgery resulting in symptomatic improvement.

LESSONS

Indicators of malpositioned thoracic SCS leads in the intrathecal space include thoracoabdominal or flank pain exacerbated by movement, insufficient pain relief versus that in the SCS trial, very low electrode impedances, direct visualization on imaging, and lack of epidural lead visualization following laminectomy. Revision options include removal of the intrathecal leads and the surgical placement of a paddle electrode in the epidural space.

https://thejns.org/doi/10.3171/CASE24275

spinal cord stimulation
lead malpositioning
lead migration
epidural
intrathecal
stimulation testing
ABBREVIATIONS

BMI = body mass index
CSF = cerebrospinal fluid
CT = computed tomography
LBP = low-back pain
LOR = loss of resistance
SCS = spinal cord stimulation.
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pmcChronic pain syndromes such as persistent spinal pain syndrome that emanate from neuropathic pain processes and result in chronic low-back pain (LBP) can be effectively managed with spinal cord stimulation (SCS).1, 2 Stimulation of the thoracic cord can be achieved surgically by laminectomy and placement of paddle electrodes or procedurally through implantation of percutaneous SCS leads into the epidural space.3 SCS surgery has been extensively evaluated for safety and effectiveness, with well-characterized hardware and biological complications such as lead migration and infection, respectively.1, 4–9 While paddle stimulator implantation must be performed by a surgeon, percutaneous leads can be implanted by a number of additional specialties including surgery, interventional pain medicine, physiatry, and neurology.10 The majority of SCS devices are implanted via the percutaneous approach. Benefits of percutaneous implantation include less invasive intervention and tissue dissection, reduced operative times, reduced anesthesia, and shorter hospital stays. Since percutaneous implantation does not depend on direct visualization, initial inadvertent placement into extra-epidural compartments such as the intrathecal space is more likely as compared to that with surgical paddle stimulator placement.11–14 This complication is distinct from proper positioning with subsequent lead migration.4, 15–17 Lead malpositioning can result in a lack of clinical benefit, stimulation of unintended spinal levels or nerve roots, or potential injury to adjacent structures. Lead migration can result in a loss of clinical benefit and/or new pain. The incidence rates of percutaneous SCS lead migration vary widely in the literature, ranging from 0.7% to 22.6%6, 18 with an overall incidence of any hardware or biological complications of SCS ranging from 17% to 43%,4, 5, 19 although these rates may be improving.20 In contrast to lead migration, the rate of initial malpositioning without intraprocedural detection remains largely unknown, and cases of improper placement during the procedure are likely underreported. Currently, very few studies in the literature report SCS percutaneous lead placement into and stimulation of the intrathecal space.15, 16 Here, we report the cases of two referred patients with percutaneous SCS leads malpositioned into the intrathecal space that were corrected by the removal and implantation of paddle electrodes. We discuss methods to mitigate procedural malpositioning, a complication that we classify as distinct from subsequent lead migration.

Illustrative Cases

Case 1

A 70-year-old man originally presented to interventional pain medicine with chronic LBP and bilateral sciatica (weight 109.3 kg, body mass index [BMI] 35.59 kg/m2). Additional medical history included nonmalignant prostate cancer, hypertension, hyperlipidemia, diabetes mellitus type 2, spinal stenosis, and lumbosacral radiculopathy. The patient underwent multiple interventional pain procedures, including bilateral L3–4, L4–5, L5–S1 facet injections, bilateral sacroiliac joint injections, lumbar dorsal medial branch radiofrequency ablation from L3 to L5, and bilateral selective nerve root block injections at L5 and S1. After multiple targeted injections, the patient underwent a percutaneous SCS trial at T9 (Nevro) with 75% pain relief reported. A permanent percutaneous lead was implanted. Immediately after the procedure, he reported severe pain radiating to the abdomen and bilateral lower extremities. This pain worsened over 1 week postoperatively, and the patient was referred for neurosurgical evaluation due to concern for lead malpositioning or migration. Radiographic imaging led us to suspect that the electrodes were in the ventral epidural space or potentially intrathecal (Fig. 1A). The patient was taken to the operating room for a T10–11 laminectomy. Intraoperatively, it was noted that the SCS leads were not in the dorsal epidural space and were intrathecal. The percutaneous leads were removed without evidence of cerebrospinal fluid (CSF) leakage, and a paddle electrode was placed directly onto the dura in the dorsal epidural space (Fig. 1B). Due to the urgent presentation, the original device was not interrogated for stimulation parameters. The patient recovered well from surgery and had resolution of the unintended postprocedural pain symptoms. The longest follow-up time point for this patient was 29 months from the time of explantation. FIG. 1. Case 1. Radiographic findings of intrathecal lead placement before and after surgical revision. A: Postprocedural radiographs, anteroposterior (AP; left) and lateral views (center), at 1 month showing percutaneous SCS lead placement. A magnified image of leads on a lateral radiograph (right) demonstrates one lead positioned in the ventral spinal canal (arrow). B: Intraoperative fluoroscopy of lead replacement during revision surgery. The lateral view depicts new Nevro leads (epidural) positioned after T10–11 laminectomy and extra-epidural percutaneous leads prior to removal (left). The AP view depicts the midline positioning of new Nevro leads once the malpositioned leads were removed (right).

Case 2

A 77-year-old female presented with more than 20 years of LBP and right lower-extremity sciatica (weight 103 kg, BMI 36.77 kg/m2). Additional medical history included chronic neck pain, diffuse spondylosis, L4–5 and L5–S1 grade 1 spondylolisthesis not recommended for surgery, chronic kidney disease, hypertension, gout, recurrent lower urinary tract infection, and hypothyroidism with multiple vitamin deficiencies. LBP and sciatica symptoms were initially relieved for 3–6 months after epidural steroid injections, but this relief period diminished to 2 weeks over time. The patient ultimately underwent percutaneous SCS device implantation (Abbott Proclaim 3670 SCS system with Octrode 3186 leads) at the T8 level. Immediately after the procedure, she reported burning pain in her left ribs and left flank. Her preoperative chronic lower-extremity sciatica pain was initially well controlled. At the 1-month follow-up, she had developed worsening bilateral leg pain without relief from SCS, and left flank pain continued as her most prominent pain symptom. Left flank pain was provoked by sitting in the car with jolting of the spine and improved by lying on her side or lying flat. Despite continued adjustment of the SCS system, the left flank pain could not be targeted with stimulation, and electrode impedances remained very low (62–87 ohms across all electrodes bilaterally). The pulse width was 1000 μsec with a stimulation frequency of 40 Hz. Over the next several weeks, she developed sporadic episodes of shock-like pain from her torso into her legs. The patient was referred for neurosurgical evaluation due to concern for lead malpositioning based on her clinical presentation. Computed tomography (CT) demonstrated dual leads within the spinal canal (Fig. 2A). A CT myelogram confirmed thecal sac entry of the leads at T11–12 with intrathecal termination at T6 (Fig. 2B and C). The percutaneous electrodes and pulse generator were removed without complication. Several weeks later, she underwent T8–10 laminectomy and implantation of an SCS paddle electrode and a pulse generator (Abbott Tripole electrode and Abbott Eterna pulse generator; Fig. 2D). LBP and sciatica pain were controlled after revision surgery with the replacement device. The postprocedural left rib and flank pain resolved. The longest follow-up time point for this patient was 9 months from the time of explantation. FIG. 2. Case 2. Radiological findings of intrathecal lead placement before and after surgical revision. A: Postprocedural axial (left) and sagittal (right) CT scans demonstrate dual leads in the central spinal canal (red arrow). B: Sagittal CT myelogram (upper) depicting the intrathecal entry of leads at T11–12 (yellow arrows). A magnified image is provided (lower). C: Axial CT myelogram of dual intrathecal leads (arrows). D: Intraoperative fluoroscopy of a paddle stimulator implanted after the removal of percutaneous leads during revision surgery.

Patient Informed Consent

The necessary patient informed consent was obtained in this study.

Discussion

In this report, we discuss the surgical management of two patients presenting with percutaneous SCS electrodes malpositioned within the intrathecal space (Table 1). While migration of percutaneous SCS electrodes has been well described, albeit with a broad range of incidence rates, the inadvertent index malpositioning of electrodes can be underrecognized or underreported, as indicated by sparse representation in the medical literature. One case report described the accidental placement of leads into the thoracic subdural space and identified indicators of subdural stimulation, such as intentional and reproducible subdural anesthesia.15 Conductive properties of the subdural and intrathecal spaces can also be reflected in stimulation data, such as by impedance value or the threshold current required to elicit a motor response. Pope and Stanton-Hicks speculated that malpositioned leads are more common than previously acknowledged. Importantly, migration can still occur subsequent to malpositioning, for example, in the cephalad direction into the intracranial space, posing a threat to the dense and eloquent intracranial neural elements.21–23 Identifying indicators of malpositioned leads is crucial to evaluating this complication, and physicians should monitor for unintended pain symptoms due to physical irritation and/or off-target stimulation. TABLE 1. Summary of patient demographics, presentation, devices, and revision

Case No.	Age (yrs)/Sex	BMI (kg/m2)	Chronic Pain Symptoms	Comorbidities	Original Device	Postprocedural Indicators	Imaging Workup	Laminectomy Level	Replacement Device	
1	70/M	35.59	LBP, bilat sciatica	Spinal stenosis, spondylosis, radiculopathy, prostate cancer, hypertension, hyperlipidemia, diabetes type 2	Percutaneous leads, not interrogated (urgent presentation)	Abdominal pain, lower extremity pain, loss of SCS relief vs trial	Radiograph, CT (lead migration to ventral canal)	T10–11 (no leads visualized)	Surgical leads (epidural)	
2	77/F	36.77	LBP, bilat sciatica rt>lt	Spondylosis, spondylolisthesis, spinal stenosis, hypertension, chronic kidney disease, hypothyroidism, gout	Spinal cord stimulator, bilat leads	Lt rib pain, lt flank pain reproduced by movement, low electrode impedances	Radiograph, MRI, CT myelogram (intrathecal entry T11–12)	T8–10 (no leads visualized)	Tripole paddle stimulator (epidural), pulse generator	

Observations

In the cases described here, findings concerning for malpositioned SCS leads in the intrathecal space included reproducible thoracoabdominal or flank pain exacerbated by movement, insufficient pain relief versus that with the trial, and very low initial electrode impedances. New painful or neurological symptoms should prompt further imaging workup, which may show ventral or intrathecal malpositioned leads on radiography or CT and can be subsequently confirmed by a CT myelogram. We characterized leads as malpositioned rather than migrated due to the acuity of symptom onset with respect to the index surgery as well as radiographic and verified intraoperative findings of thecal sac entry. While it is possible that epidural leads can migrate rostrally and puncture the intrathecal space near the craniocervical junction, migration into the thecal sac at low thoracic levels would be much less likely for epidural electrodes that had been properly positioned initially. For case 1, the first indicator of lead malpositioning occurred postoperatively wherein unanticipated severe pain radiating to the abdomen and lower extremities was reported without relief in the ensuing week. SCS pain relief was not commensurate with the approximately 75% relief achieved during the stimulation trial. Pre-revision radiographs indicated ventral positioning of one lead, while preoperative CT demonstrated leads within the center of the spinal canal, raising suspicion for intrathecal malpositioning. CSF was not encountered during percutaneous implantation. Intraoperatively, after the T10–T11 laminectomy and exposure of the dura, it was confirmed that the electrodes were not in the dorsal epidural space. For case 2, new pain symptoms on the postoperative examination and persistent thoracoabdominal pain in the weeks after implantation raised suspicion for malpositioned leads and prompted referral for consideration of surgical revision. Upon interrogation, low electrode impedance measurements (62–87 ohms) were also inconsistent with epidural placement. Intrathecal malpositioning was ultimately confirmed by CT myelogram. No CSF was encountered during the percutaneous electrode placement.

Intrathecal positioning of the leads can be further categorized as subdural or subarachnoid, which are distinguishable.15 Subdural but not subarachnoid placement is characterized by the lack of CSF return despite lavage, the absence of post–dural puncture headache, and the inherent conductivity of dural spinal elements reflected by recorded electrode impedances.15 Interestingly, CSF was not encountered during the percutaneous implantation in either patient. In addition, neither patient had signs or symptoms of CSF leakage after the procedure. The loss of resistance (LOR) technique is the standard approach to needle access of the epidural space. Continued needle advancement after LOR could result in durotomy and a “wet tap.” Although a wet tap was not reported for either patient, it is possible that the needle violated the dura above the arachnoid and that only the electrodes passed into the subarachnoid space without CSF egress through the needles. In case 2, MRI demonstrated a paucity of epidural fat at the level of needle entry. Epidural fat serves as a buffer in the epidural space between the ligamentum flavum and dura. The dura may have been immediately encountered once the needle passed through the ligamentum flavum. The potential for CSF leakage after the removal of intrathecal electrodes must also be considered when planning revision surgery. Significant loss of CSF after the removal of the electrodes may predispose to spinal cord injury during paddle placement since the cushioning provided by CSF can be lost if the dura loses tension. For the patient in case 1, the electrodes were left in place until after the paddle was applied to the dorsal epidural space, thus mitigating the risks of spinal cord injury due to the loss of protective CSF pressure. Revision surgery for the patient in case 2 was performed several weeks after the percutaneous stimulator was removed when it was confirmed that there was no CSF leakage. Neither patient developed signs or symptoms of CSF leakage after removing the percutaneous leads despite having two defects in the dura from the bilateral electrodes. The lack of persistent CSF leakage is likely due to the lack of potential space and would be expected to occur at a similar rate to that seen after lumbar puncture or CT myelogram, approximately 1%–5%.24, 25 CSF leaks are often asymptomatic with age due to decreased sensation and altered pain perception.26 In addition to intraoperative and postoperative assessment, an appreciation of predisposing risk factors to percutaneous lead malpositioning and migration preoperatively can help to guide patient selection.7, 8

A high BMI, as in each of our cases (> 35 kg/m2), can predispose to malpositioning by imaging constraints, reducing visualization under fluoroscopy, as well as complicating the manipulation of leads. Patient-specific anatomy and comorbidities also guide patient candidacy for percutaneous placement of SCS leads. For the patient in case 2, canal stenosis, loss of epidural fat, diffuse spondylosis, and degeneration were complicating factors to percutaneous lead placement that were discussed with the patient preoperatively. These patient-specific factors predisposing to lead malpositioning overlap but are distinct from etiologies of lead migration. Migration is more likely to result from technical error, such as ineffective fixation or attachment to an implanted pulse generator, but canalso result from vigorous patient movement prior to soft tissue encapsulation of leads.22 In addition to patient selection, it is imperative that, prior to fixation, proper placement into the epidural compartment be confirmed by intraoperative imaging. Careful monitoring of pain symptoms and distribution in the immediate postoperative period and at follow-up visits is critical, with a low threshold for additional workup. In the two cases presented, routine imaging was not performed immediately after the index surgery because percutaneous lead implantation is guided by intraoperative fluoroscopy. However, if malpositioned leads are not identified during the procedure, it is important to identify this complication in the immediate perioperative or acute postoperative period. While imperfect, a lateral radiograph in the immediate postoperative period from the index surgery can help to screen for abnormally ventral electrodes. It is feasible that neuromonitoring could also play a role in detecting malpositioned intrathecal leads during the procedure. Lead malpositioning is distinct from lead migration that can worsen over time, possibly resulting in reduced SCS effectiveness. Undetected malpositioned leads can still undergo migration within the intrathecal space in the postoperative period, thereby increasing the potential for neurovascular injury and reducing effective pain management.

Lessons

Here, we identify indicators of migrated or malpositioned SCS leads into the intrathecal space, which are thoracoabdominal or flank pain exacerbated by movement, insufficient pain relief versus that with the SCS trial, very low initial electrode impedances, radiographic features, and lack of lead visualization in the epidural space following laminectomy. Patient-specific factors such as BMI and degenerative spine phenotypes may predispose to improper placement. Close observation in the immediate perioperative period and routine postoperative follow-up should be used to identify red flags, and improperly placed percutaneous SCS leads should be further evaluated with imaging and then addressed by revision surgery with transition to surgical leads or paddle stimulators. Proper patient selection, intraprocedural mitigation by validating epidural placement, subsequent lead anchoring, postoperative follow-up, and reporting on the frequency of malpositioning complications should be central in the practitioner’s mind.

Disclosures

Dr. Dorsi is a paid consultant for Abbott, Nevro, Globus, Camber Spine, Vertos, Painteq, and LifeSpine.

Author Contributions

Conception and design: Dorsi, Wu. Acquisition of data: Dorsi, Wu, Katouzian. Analysis and interpretation of data: Olmsted, Wu. Drafting the article: Dorsi, Olmsted, Katouzian. Critically revising the article: all authors. Reviewed submitted version of manuscript: all authors. Approved the final version of the manuscript on behalf of all authors: Dorsi. Administrative/technical/material support: Dorsi. Study supervision: Wu.

Correspondence

Michael J. Dorsi: University of California Los Angeles Health, Los Angeles, CA. mjdorsi@mednet.ucla.edu.
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