Basivertebral Nerve (BVN) Ablation

Basivertertebral nerve (BVN) ablation is a minimally invasive, intraosseous radiofrequency procedure that silences the nerve transmitting pain from damaged vertebral endplates. Candidates are typically diagnosed by their clinical presentation (history and physical examination) combined with their MRI appearance. The critical radiological finding is Modic type 1 (inflammatory) or type 2 (fatty marrow replacement) endplate changes on MRI. Discography is not required.

A targeted solution for vertebrogenic low back pain

The vertebral endplate is a thin layer of cartilage and bone that sits between each spinal disc and the vertebrae (the bones of your spine) above and below it. The endplate really is an extension of the disc. Think of it as the “cap” on the top and bottom of every disc. It has two main jobs. First, it acts as a mechanical buffer, helping to spread out the pressure that the spine experiences when you walk, jump, lift, or even just sit upright, so that no single spot on the disc or bone takes too much stress. Second, and just as important, the endplate works like a filter or gateway for nutrients. Spinal discs do not have their own blood supply, so the cells inside the disc rely on oxygen, water, sugar, and other nutrients diffusing in through the endplate from nearby blood vessels in the vertebra. Waste products also travel out the same way. In other words, the endplate is the disc’s lifeline.

Because the endplate plays this double role of shock absorber and nutrient highway, damage to it is now understood to be one of the most critical triggers of disc degeneration. When the endplate is damaged, two harmful things happen at once. Mechanically, forces are no longer distributed evenly, so certain areas of the disc get overloaded and begin to break down. Biologically, the flow of nutrients into the disc slows or stops, which starves the cells that make and maintain the disc’s healthy tissue. Without those cells, the disc loses water, shrinks, becomes stiff, and starts to tear, setting off disc degeneration. This is why many researchers now view endplate injury not just as a side effect of a worn-out disc, but as an early driver of the degeneration process itself, setting off a chain reaction that leads to chronic back pain and long-term spinal problems.

More recent research has shown that the vertebral endplate is not only essential for keeping the disc alive, it can also be a direct source of chronic back pain, a condition now called vertebrogenic pain. The key discovery is that the endplate and the bone just beneath it (called the subchondral bone of the vertebra) are richly supplied by a small nerve known as the basivertebral nerve. Under normal, healthy conditions this nerve is relatively quiet, but when the endplate becomes damaged, inflamed, or repeatedly overloaded, the basivertebral nerve and its branches grow in number, become more sensitive, and start firing pain signals. Doctors can actually see signs of this process on an MRI in the form of “Modic changes,” which are bright or dark patches in the bone right next to a damaged endplate that reflect swelling, inflammation, and fatty replacement of normal marrow.

These patients often present in similar fashion to those experiencing discogenic lower back pain – pain from degerated or painful intervertebral discs. Vertebrogenic patients often describe a deep, aching, midline low back pain that gets worse with sitting, bending forward, or activity. This new understanding has led to the recognition that patients with assumed disc related pain should have vertebrogenic pain added to their differential. In short, the endplate is now recognized as doing double duty in spine health: it is both the gateway that keeps the disc nourished and, when injured, a major generator of chronic low back pain itself. For decades, anterior column chronic low back pain was attributed primarily to disc degeneration. A growing body of histological, immunological, and radiological evidence has shifted that understanding: the vertebral endplates — the thin cartilage-and-bone structures separating each disc from its adjacent vertebral bodies — are now recognised as a significant, independent source of pain in a meaningful subset of patients with chronic low back pain. The best available interventional treatment (X-ray guided injection-type procedure) for this patient population is basivertebral nerve ablation, in which the nerve inside the vertebra is deliberately interrupted to quiet the pain signals coming from a damaged endplate.

Endplate damage triggers cross-talk between the disc nucleus pulposus and vertebral bone marrow, igniting a chronic inflammatory cascade. This process is visible on MRI as Modic changes and produces nociceptive signals transmitted via the basivertebral nerve (BVN) — a branch of the sinuvertebral nerve that arborizes through the posterior vertebral body to innervate the superior and inferior endplates. Radiofrequency ablation of the BVN at 85°C for 15 minutes interrupts this pain pathway at its anatomical source.

Understanding Modic endplate changes

Dr. Michael Modic first classified MRI-visible degenerative changes of the vertebral endplate in 1988. Both type 1 and type 2 are established indications for BVN ablation. No statistical difference in outcome was observed between patients presenting with type 1 versus type 2 Modic changes in the SMART trial.

The basivertebral nerve: anatomy and pain pathway

The basivertebral nerve branches from the sinuvertebral nerve and enters the posterior vertebral body through the basivertebral foramen, travelling anteriorly before bifurcating to innervate both the superior and inferior endplates. The RF probe is advanced via a unilateral transpedicular approach to a target approximately 30–50% across the sagittal depth of the vertebral body — the terminus of the BVN. A bipolar RF probe delivers thermal energy at 85°C for 15 minutes, creating an approximately 1 cm spherical ablation lesion. Because the intraosseous segment of the BVN is non- or thinly myelinated, organised nerve regrowth does not occur within the lesion zone, accounting for the durable long-term results observed across trials.

How BVN ablation is performed

BVN ablation uses the FDA-cleared Intracept® System (Boston Scientific). The procedure is performed in an outpatient setting under fluoroscopic guidance with either moderate conscious sedation or general anaesthesia. Up to four vertebral levels from L3 to S1 may be treated in a single session.

Step 1 — Pre-operative planning

MRI is reviewed to confirm Modic type 1 or 2 changes at L3–S1 and to plan the pedicle entry angle. The BVN terminus is mapped to 30–50% of the posterior-to-anterior vertebral body depth on sagittal imaging.

Step 2 — Transpedicular access

With the patient prone, an 8-gauge introducer cannula is advanced under biplanar fluoroscopic guidance through the pedicle to the posterior wall of the target vertebral body.

Step 3 — Intraosseous navigation to the BVN terminus

A curved nitinol stylet assembly is advanced to the BVN terminus — midline at 30–50% depth in the lateral view and across the midline of the spinous process in the AP view.

Step 4 — Radiofrequency ablation

A bipolar RF probe is activated at 85°C for 15 minutes at each treated level, creating an approximately 1 cm spherical ablation lesion.

Step 5 — MRI verification at 6 weeks

A T1/T2/STIR MRI confirms overlap between the ablation lesion and the BVN terminus at each treated level. Targeting success in published trials: 93–96% of patients, 97–98% of vertebral bodies.

Step 6 — Recovery

Outpatient procedure. Transient radiculitis is the most common post-procedure event (2–6% of patients), resolving with oral medication within a median of 42–92 days. No serious device-related adverse events have been reported across any published trial.

The evidence base: a decade of prospective trials

BVN ablation has been evaluated in two Level I randomised controlled trials, multiple prospective single-arm and community-practice studies, and a pooled 5-year analysis — comprising over 500 treated patients.

Fischgrund et al. 2018 — SMART Trial

Eur Spine J · Randomized, double-blind, sham-controlled RCT (N=225)

• 20.5pt ODI improvement vs 15.2 pts (sham), p=0.019 per-protocol
• 75.6% achieved ≥10-pt ODI improvement vs 55.3% sham
• 73% of sham patients elected to cross over to active treatment at 1 year
• No device-related serious adverse events. No evidence of avascular necrosis, accelerated disc degeneration, or spinal cord abnormality on MRI follow-up.

Khalil et al. 2019 — INTRACEPT Trial

The Spine Journal · Randomized, open-label vs standard care RCT (N=140)

• 25.3pt ODI improvement vs 4.4 pts (standard care); adjusted difference 20.9 pts, p<0.001
• 74.5% achieved ≥10-pt ODI improvement vs 32.7% standard care, p<0.001
• 3.46pt VAS reduction vs 1.02 pts standard care; 78% rated condition improved; 88% would recommend
• Independent data management committee halted enrolment early — results were so superior it was deemed unethical to continue the standard care arm.

Fischgrund et al. 2020 — SMART 5-year follow-up

Eur Spine J · Prospective single-arm (N=100, mean follow-up 6.4 years)

• 25.95pt ODI reduction at mean 6.4 years (baseline 42.81 → 16.86), p<0.001
• 66% reported >50% pain reduction; 34% complete pain resolution at 5+ years
• 73% reduction in opioid use; injection use fell from 59% to 4% at 5 years
• Outcomes improved incrementally from 24 months to 5 years — no regression to baseline.

Macadaeg et al. 2020 — Single-arm 12-month study

N Am Spine Soc J · Prospective open-label community practice (N=47)

• 32.31pt ODI reduction at 12 months; more than twice the MCID threshold
• 88.9% achieved ≥15-pt ODI improvement; 38% complete pain resolution at 12 months
• 70% reduction in opioid use; epidural injections dropped from 49% pre-procedure to 2% post-procedure
• Broader inclusion criteria than the RCTs — results support generalisability to less homogeneous clinical populations.

Schnapp, Martiatu & Delcroix 2023 — Independent community practice study

N Am Spine Soc J · First independently-funded US study (N=16, mean age 73.3)

• 21.1pt ODI decline at 6 months (p<0.05); exceeds MCID threshold
• 3.44cm VAS reduction at 6 months; all improvements statistically significant
• No industry involvement. Average age 73.3 years — outcomes comparable to the SMART trial at 6 months. No adverse events.

Khalil et al. 2024 — 5-year pooled analysis

Intervent Pain Med · N=249 with 5-year follow-up; mean follow-up 5.6 years

• 28.0pt ODI improvement at 5.6 years (twice the published MCID), p<0.0001
• 32.1% completely pain-free (NPS=0) at 5 years; 68.7% resumed pre-pain activity levels
• 65.2% of opioid users at baseline were opioid-free at 5 years; spinal injections reduced 58.1%
• 69% of participants were free of any additional lumbosacral treatment through mean 5.6 years
• Lumbar fusion rate for same pain source: 6.0% — less than half the published rate for isolated axial degenerative disc disease
• No serious device-related adverse events in long-term follow-up

ASPN Best Practice Guidelines (Sayed et al. 2022, J Pain Res): The American Society of Pain and Neuroscience assigned BVN ablation a Level A evidence grade using USPSTF-modified criteria — defined as high certainty that the net benefit is substantial in appropriately selected individuals. This is the highest evidence grade available.

Who is a candidate?

Patient selection is the single most important determinant of outcome. The published literature is consistent: most therapy failures are attributable to poor patient selection, not the therapy itself (Sayed et al. 2022). The following criteria are drawn directly from the published clinical trials.

Inclusion criteria

• Chronic isolated lumbar back pain ≥6 months, predominantly axial
• Failure of ≥6 months of conservative management
• Modic type 1 or 2 changes at one or more levels L3–S1 on MRI
• Minimum ODI ≥30 points (100-point scale)
• Minimum VAS ≥4 cm (10-cm scale)
• Pain worsened with sitting, forward flexion, and transitioning from sitting to standing
• Skeletally mature patient

Exclusion criteria

• Radicular pain following a dermatomal distribution correlating with imaging
• Symptomatic spinal stenosis with neurogenic claudication confirmed on imaging
• Disc extrusion or protrusion >5 mm
• Spondylolisthesis >2 mm at any level
• Facet arthrosis/effusion correlating with facet-mediated pain
• Beck Depression Inventory >24 or ≥3 Waddell’s signs
• Active systemic infection, metabolic bone disease, spinal malignancy
• Compensated injury, active litigation, or addiction behaviour
• BMI >40; spondylolysis at any level
• Modic changes only outside L3–S1

Discography is not required for diagnosis or patient selection and was not used in any of the published clinical trials on BVN ablation.

Recognising vertebrogenic pain

Vertebrogenic pain has a distinct clinical phenotype that distinguishes it from facetogenic, sacroiliac, or radicular pain. Diagnosis requires concordance of clinical presentation with radiographic findings.

Deep, aching, midline low back pain

Often described as burning or boring in quality, located at or near the spinous processes of the affected levels. Generally not associated with radiation below the knee.

Worsened by sitting and flexion-based activities

Driving, bending forward, lifting, tying shoes, and transitioning from sitting to standing all load the anterior column and characteristically aggravate symptoms.

Episodic flares interspersed with baseline pain

Weeks of low-level but persistent pain punctuated by 4–5 day flares of severe, debilitating pain. Activity levels substantially reduced during flares.

Physical examination

Midline tenderness on vertebral percussion at the affected level. Reproduction of familiar pain with flexion-based loading of the anterior column.

Published references

1. Fischgrund JS, Rhyne A, Franke J, et al. Intraosseous basivertebral nerve ablation for the treatment of chronic low back pain: a prospective randomized double-blind sham-controlled multi-center study. Eur Spine J. 2018;27(5):1146–1156.
2. Khalil JG, Smuck M, Koreckij T, et al. A prospective, randomized, multicenter study of intraosseous basivertebral nerve ablation for the treatment of chronic low back pain. Spine J. 2019;19(10):1620–1632.
3. Fischgrund JS, Rhyne A, Macadaeg K, et al. Long-term outcomes following intraosseous basivertebral nerve ablation: 5-year treatment arm results. Eur Spine J. 2020;29(8):1925–1934.
4. Macadaeg K, Truumees E, Boody B, et al. A prospective, single arm study of intraosseous basivertebral nerve ablation: 12-month results. N Am Spine Soc J. 2020;3:100030.
5. Schnapp W, Martiatu K, Delcroix GJR. Basivertebral nerve ablation in a community practice setting: 6 months follow-up. N Am Spine Soc J. 2023;14:100201.
6. Sayed D, Naidu RK, Patel KV, et al. Best practice guidelines on the diagnosis and treatment of vertebrogenic pain with basivertebral nerve ablation. J Pain Res. 2022;15:2801–2819.
7. Khalil JG, Truumees E, Macadaeg K, et al. Intraosseous basivertebral nerve ablation: a 5-year pooled analysis from three prospective clinical trials. Intervent Pain Med. 2024;3:100529.