L5–S1 basivertebral nerve ablation for chronic vertebrogenic low back pain following lumbar fusion: a case report

Abstract

Background

Basivertebral nerve ablation (BVNA) is an established treatment for vertebrogenic low back pain associated with Modic endplate changes, but trials and current on-label use have excluded patients with prior lumbar fusion. The clinical efficacy of BVNA has been established in the SMART (Surgical Multi-Center Assessment of RF Therapy) and INTRACEPT trials. Patients with prior lumbar fusion with symptomatic vertebrogenic low back pain were excluded from these major trials, but remain a clinically significant subgroup of patients who may benefit from BVNA.

Case Description

A 55-year-old man presented with severe chronic axial low back pain persisting for more than 5 years after stand-alone L5–S1 interbody fusion performed in 1995. Pain was predominantly midline and mechanical, worsened by sitting, bending, lifting, and driving, and improved with standing or walking. He had failed extensive conservative and interventional therapies including nonsteroidal anti-inflammatory drugs, acetaminophen, epidural steroid injections, facet injections, medial branch blocks, sacroiliac joint injections, radiofrequency ablations, prolotherapy, acupuncture, and chiropractic care. Preoperative visual analog scale (VAS) score was 7/10 and Oswestry Disability Index (ODI) was 48%. Computed tomography showed a stable fusion construct without evidence of pseudoarthrosis or hardware complication. Magnetic resonance imaging demonstrated Modic type 2 endplate changes at L5–S1 adjacent to the fusion cages, supporting a vertebrogenic pain generator. The patient underwent fluoroscopically guided BVNA at L5 and S1 without complication. At 12 months, VAS was 3/10 and ODI 16%, exceeding the minimum clinically important difference (MCID) for spine surgery. The patient reported a 75% subjective improvement and return to unrestricted occupational activity.

Conclusions

This case suggests that off-label BVNA may provide meaningful and durable relief in carefully selected post-fusion patients with persistent vertebrogenic pain and persistent Modic changes.

Highlight box.

Key findings

• This report describes successful off-label L5–S1 basivertebral nerve ablation (BVNA) after prior lumbar fusion, with durable 12-month improvement in pain and disability and no observed procedural complication.

What is known and what is new?

• BVNA is supported for vertebrogenic pain in patients with Modic changes, but prior lumbar fusion has generally excluded patients from trials and routine on-label treatment.

• This case adds a detailed post-fusion example in which imaging, symptom pattern, and follow-up outcomes were all consistent with vertebrogenic pain that remained responsive to BVNA.

What is the implication, and what should change now?

• Prior fusion should not automatically exclude vertebrogenic pain from the differential diagnosis. When fusion is radiographically stable and persistent endplate-driven pain remains likely, BVNA may merit consideration as an off-label option in carefully selected patients. Larger studies are needed before broader adoption.

Introduction

Background

Chronic low back pain remains a major source of disability worldwide. Within this broad diagnosis, vertebrogenic pain has emerged as a distinct pain phenotype linked to nociception arising from the vertebral endplates and carried by the basivertebral nerve. Clinically, its presentation is similar to the common discogenic pain generator, a common source of low back pain in adults (1). Modic type 1 or type 2 endplate changes on magnetic resonance imaging can support this diagnosis in the appropriate clinical setting (2). Basivertebral nerve ablation (BVNA) has demonstrated clinically meaningful improvement in pain and function in selected patients with chronic vertebrogenic low back pain (3-7). The SMART trial was a prospective, randomized, double-blind, sham-controlled study of patients with axial low back pain for at least 6 months, Modic type 1 or 2 changes, and failure of at least 6 months of conservative treatment. Patients in the BVNA group improved their Oswestry Disability Index (ODI) scores by an average of 20.5 points at 3 months, compared with 15.2 points in the sham group. The INTRACEPT trial similarly demonstrated reductions in pain and disability, with more than 75% of patients reporting at least a 2-point reduction in visual analog scale (VAS) and approximately 60% achieving at least a 15-point improvement in ODI at 12 months.

Rationale and knowledge gap

Despite encouraging trial data, prior lumbar fusion has typically been an exclusion criterion in major BVNA studies and in standard on-label treatment pathways (3-7). That leaves uncertainty about whether vertebrogenic pain can remain active in fused segments and whether BVNA can still be technically feasible and clinically useful when anatomy has already been surgically modified. For patients with persistent axial pain after fusion, this question is clinically important because treatment options are often limited and symptoms may otherwise be grouped under broad post-surgical pain labels without identifying a specific endplate-mediated pain generator (8). The post-fusion subgroup was restricted from initial clinical trial inclusion but represents a substantial population of clinical patients who may benefit from this procedure. This gap in the evidence has been clearly documented in the literature (9).

Objective

The objective of this case report is to describe the presentation, imaging findings, procedural course, and 12-month outcome of off-label BVNA performed at a previously fused L5–S1 level in a patient with refractory vertebrogenic low back pain. We present this article in accordance with the CARE reporting checklist (available at https://jss.amegroups.com/article/view/10.21037/jss-2026-0097/rc).

Case presentation

Patient history and presentation

A 55-year-old man was evaluated for chronic low back pain persisting for more than 5 years following stand-alone L5–S1 interbody fusion performed in 1995. The patient had a 15–20-year pain free interval before the gradual recurrence of progressive vertebrogenic low back pain over the 5 years preceding his consultation. Pain was predominantly axial and midline, accounting for more than 90% of total pain, with less than 10% leg symptoms. The patient described worsening with sitting, driving, forward bending, and lifting, and relative relief with standing and walking, a pattern consistent with anterior column loading and vertebrogenic pain. He reported only minimal or temporary relief from nonsteroidal anti-inflammatory drugs, acetaminophen, epidural steroid injections, facet joint injections, medial branch blocks, sacroiliac joint injections, radiofrequency ablations, prolotherapy, acupuncture, and chiropractic treatment (Figure 1).

Figure 1.

Preoperative intake form showing vertebrogenic pain screening.

Baseline assessment

At presentation, the back pain VAS score was 7/10 and ODI was 48%, consistent with severe disability. Intake screening additionally suggested long-standing vertebrogenic symptom behavior, including pain provoked by bending, sitting, and lifting.

Diagnostic workup

Preoperative standing lumbar radiographs revealed interbody hardware at L5–S1 and no significant pelvic incidence (PI)-lumbar lordosis (LL) mismatch or sagittal imbalance (PI 53 deg, LL 47 deg). Lumbar magnetic resonance imaging showed Modic type 2 endplate changes at L5–S1 adjacent to the interbody fusion cages (Figure 2). Computed tomography and plain radiographs demonstrated a stable L5–S1 fusion construct without lucency, hardware complication, or clear radiographic evidence of pseudoarthrosis (Figures 3-6). In the context of the patient’s symptom pattern and the absence of an alternative dominant pain generator, these findings supported an endplate-mediated vertebrogenic source of pain (2,5,6).

Figure 2.

T1- and T2-weighted midsagittal magnetic resonance images of the lumbar spine demonstrating Modic type 2 endplate changes at L5–S1.

Figure 3.

Scout computed tomography sagittal view.

Figure 4.

Sagittal and axial computed tomography images showing solid L5–S1 arthrodesis.

Figure 5.

Three-dimensional reconstruction computed tomography image.

Figure 6.

Sagittal and coronal computed tomography images of the lumbar spine.

Decision-making and consent

Although the patient met the clinical and radiographic profile for vertebrogenic pain, prior lumbar fusion placed him outside standard on-label BVNA use. The off-label nature of treatment, as well as the expected benefits, limitations, and alternatives, was reviewed in detail. The patient elected to proceed with targeted BVNA at L5 and S1 in hopes of achieving pain relief without disturbing the prior hardware or requiring revision surgery.

Intervention

Preoperative telemedicine assessment found no major untreated psychiatric comorbidity, no alarm symptoms, and no medical contraindication to same-day outpatient treatment under general anesthesia. Fluoroscopically guided BVNA was performed at L5 and S1 under general endotracheal anesthesia. Probe placement across the vertebral body targets was confirmed intraoperatively (Figure 7). The patient’s interbody cage hardware was not in the anatomic zone of BVNA and no posterior pedicle screws were in place to alter, limit, or interfere with traditional posterior transpedicular access to the basivertebral nerve. The procedure was completed uneventfully.

Figure 7.

Intraoperative fluoroscopy composite demonstrating probe placement at S1 and L5 in lateral and anteroposterior projections.

Post-procedural course and follow-up

After the procedure, the patient recovered in the post-anesthesia care unit with stable neurologic examination and adequate pain control. No drains or urinary catheter were required. He was discharged the same day with weight-bearing as tolerated, early ambulation, and oral pain control. At 2 weeks, VAS improved to 5/10 and ODI to 34%, with subjective improvement in pain and morning stiffness. At 3 months, VAS was 4/10 and ODI 26%. At 12 months, VAS was 3/10 and ODI 16%, representing a 32-point ODI improvement from baseline and approximately 75% subjective overall improvement (Table 1). Functionally, he returned to multi-mile hikes, tolerated prolonged sitting more comfortably, and resumed unrestricted work activity. No adverse event was observed during the follow-up period. No adverse events were noted.

Table 1. Clinical timeline.

Time point	Clinical event/findings
1995: prior L5–S1 interbody fusion	Stand-alone L5–S1 interbody fusion performed
>5 years before presentation	Persistent chronic predominantly axial low back pain despite extensive nonoperative and interventional treatment
Preoperative evaluation	VAS 7/10; ODI 48%. CT showed stable fusion without hardware complication or clear pseudoarthrosis. MRI demonstrated Modic type 2 changes at L5–S1 adjacent to fusion cages
2025: procedure day	Fluoroscopically guided off-label BVNA performed at L5 and S1 under general anesthesia in an outpatient setting; no intraoperative complication
2 weeks	VAS 5/10; ODI 34%; subjective early improvement and less morning stiffness
3 months	VAS 4/10; ODI 26%; continued functional improvement
12 months	VAS 3/10; ODI 16%; approximately 75% subjective improvement; return to long-distance hiking and unrestricted occupational activity; no observed adverse event

BVNA, basivertebral nerve ablation; CT, computed tomography; MRI, magnetic resonance imaging; ODI, Oswestry Disability Index; VAS, visual analog scale.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Key findings

This case demonstrates technical feasibility and durable clinical improvement after off-label BVNA at a previously fused L5–S1 segment. Over 12 months, the patient showed consistent improvement in both pain and disability, with return of higher-level function and no observed complication. Outcomes in this individual case with decrease in ODI by 32% and VAS pain score by 4 points at 1 year post procedure exceed the minimum clinically important difference (MCID) for typical lumbar spine surgeries (10).

Strengths and limitations

A strength of this report is the convergence of symptom pattern, imaging findings, and longitudinal outcome data. The patient had longstanding predominantly axial pain, persistent Modic type 2 change at the fused level, stable fusion imaging, and serial VAS and ODI improvement after treatment. The main limitations are those inherent to a single-case experience. Causality cannot be proven, placebo effect cannot be excluded, and the findings cannot be generalized without prospective study. Postoperative imaging was not obtained, and longer-term durability beyond 12 months remains unknown.

Comparison with similar research

The degree of improvement in this patient is broadly consistent with the pattern reported in prior BVNA studies performed in non-fusion populations, where clinically meaningful reductions in VAS and ODI have been observed over time (3-6). What distinguishes the present case is the post-fusion setting, which has largely been absent from pivotal trials and routine indication language (3,6,7,9).

Explanations of findings

The improvement is biologically plausible. Vertebrogenic pain is characterized by anterior column pain and can be screened with 3 practical questions: whether pain is worsened by bending and lifting, worsened by prolonged sitting, and alleviated by walking (5,6). This patient fit that pattern. His pain worsened with bending, lifting, sitting, and driving, and improved with standing and walking. Bending, lifting, and prolonged sitting increase compressive stress on the anterior column and vertebral endplates and can mechanically activate nociceptive signaling from the basivertebral nerve when Modic degeneration is present (2,5,6). Relief with upright posture and walking further supports an endplate-driven mechanism. Together with the persistent Modic type 2 changes at L5–S1, stable fusion on CT, and absence of infection or acute inflammation, this supports chronic vertebral endplate degeneration as a reasonable source of vertebrogenic pain in this case (2). Fusion does not necessarily eliminate nociceptive signaling from vertebral endplates, especially when persistent Modic changes remain at the treated level (5,6). Stable hardware and absence of overt pseudoarthrosis and sagittal imbalance on computed tomography also strengthen the rationale for considering endplate-mediated pain rather than revision instability as the dominant explanation.

Implications and actions needed

This case suggests that prior fusion should not automatically exclude vertebrogenic pain from consideration. In carefully selected patients with stable fusion, persistent Modic changes, and refractory axial pain, BVNA may be a reasonable off-label option. Future work should focus on procedural feasibility in altered anatomy, patient selection criteria, durability of benefit, and comparative outcomes against other post-fusion pain strategies.

Conclusions

Off-label L5–S1 BVNA provided substantial and durable improvement in pain and disability for a patient with chronic vertebrogenic low back pain following lumbar fusion. This case supports the need for further prospective evaluation of BVNA in post-fusion patients with persistent endplate-mediated pain.

Supplementary

The article’s supplementary files as

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.