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Complications of Basivertebral Nerve Ablation

Ameer Ali DO¹, Melissa Lau MD¹, Michael DePalma MD¹, and Douglas Beall MD²

¹ Virginia iSpine Physicians, PC, Richmond, VA, USA
² Summit Medical Center, Oklahoma City, OK, USA

Introduction

Chronic low back pain remains a ubiquitous, heterogeneous problem that has many etiologies and has proven difficult to reliably diagnose and treat. There are a few imaging findings characteristically associated with back pain and can be used reliably to direct target-specific treatments [1]. The presence of degenerative end plate or Modic changes (MC) on Magnetic Resonance Imaging (MRI) reflect vertebral end-plate disruption and have been shown to correlate clinically with the presence of low back pain [2]. The cartilaginous end plates (CEPs) are densely innervated by the basivertebral nerve (BVN) and its branches, which have been found to contain substance P, a neurotransmitter of the tachykinin family associated with the transmission of pain [3]. As such, the BVN has been implicated in transmitting nociceptive stimuli from the CEPs and subchondral end plates. By targeting the BVN, intraosseous basivertebral nerve ablation (BVNA) can disrupt the neurotransmission of pain and thereby reduce pain originating from the vertebral CEPs also called vertebrogenic pain [4]. Numerous clinical studies evaluating its therapeutic effect have demonstrated BVNA to be a safe, effective and durable intervention [2–5].

Anatomy and Pathophysiology Overview

Axial low back pain has been shown to emanate from a number of different locations in the lumbar spine including facet joints and intervertebral discs [6]. As discussed, the vertebral cartilaginous end plates (CEPs) have also been implicated as a source of chronic low back pain [7]. The CEPs permit nutrient diffusion from blood vessels to the mostly avascular intervertebral discs [8]. During spinal loading, the vertebral end plates transfer compressive forces through the intervertebral discs and the vertebral bodies, and are therefore vulnerable to injury and damage due to repetitive stress [3, 7]. End-plate fractures are associated with inflammatory changes within adjacent discs, which can involve the discs, the end-plate defects and the vertebral bodies, and can ultimately result in nociceptive pain [9]. Vertebral end plates are highly innervated by the BVN, which transmits the nociceptive signals from the end-plate injury and is subsequently perceived as axial low back pain [2]. Because the CEPs are difficult to image in detail with standard imaging, the prevalence of CEP-mediated pain is not adequately known and has certainly not been well studied [6]. There has not yet been a widely accepted and validated diagnostic test for CEP-mediated low back pain but provocation and anesthetic lumbar discography may help.

Prior to arborization, the BVN bundle is a single or paired nerve that originates from the sinuvertebral nerve and enters the vertebral body posteriorly via the basivertebral foramen. It courses centrally within the vertebral body, generally following the basivertebral vessels sending multiple branches toward the vertebral end plates [10] (Figure 37.1). In addition to substance P, the BVN fibers have been found to express calcitonin gene-related peptide (CGRP), consistent with its role in transmitting pain [3, 11].

**Figure 37.1** Anatomy of the BVN (green) and its vascular supply (blue) [12].

The typical CEP thickness averages 0.6 mm, making it difficult to discern and evaluate on standard MRI evaluation [13]. The CEPs are responsible for supplying the avascular intervertebral disc with nutrients and, if damaged, the CEPs will demonstrate erosive changes and sclerosis that thereby diminish blood supply to the intervertebral disc (Figure 37.2).

**Figure 37.2** Histologic appearance of bone marrow lesions at sites of cartilaginous end plate damage [7].

In 1997, Brown et al. evaluated the immunohistochemistry of intervertebral discs, vertebral bodies and end plates in patients with and without low back pain. Patients with severe back pain were found to have more end-plate cartilage defects and erosions that were associated with an increased density of nociceptors in their CEPs and immediately adjacent vertebral bodies. Based on these findings, the authors concluded that both the end plates and vertebral bodies were likely pain generators in these patients with chronic low back pain [3].

Interrupting the nociceptive pathway through the BVN complex via BVNA has been extensively explored in multiple clinical trials as a treatment option for this type of back pain called vertebrogenic back pain. The Intraosseous Basivertebral Nerve Ablation for the Treatment of Chronic Low Back Pain (SMART) trial is level 1 evidence showing that patients treated with radiofrequency ablation (RFA) of the BVN for chronic low back pain demonstrated sustained clinical improvements in ODI and VAS scores for up to 2 years following treatment [14]. This study suggested BVNA is a safe, effective, durable, and minimally invasive treatment for the relief of chronic low back pain [14].

Clinical and Radiographic Evaluation

History

End-plate mediated back pain is characterized by low back pain that is either midline in the low back, paramedian near the posterior superior iliac spine (PSIS) or present in both places. It is typically exacerbated by movements that compress the spine and increase intradiscal pressure such as forward bending, sitting and lifting.

Physical Exam Findings

The presence of painful sustained hip flexion and centralization with a McKenzie evaluation is consistent with the diagnosis of internal disc derangement (IDD) or discogenic back pain [11]. The presence of these findings in patients with chronic low back emanating from painful vertebral CEPs is ostensibly the same; the clinical exam for patients with vertebrogenic low back pain seems almost identical to those patients with discogenic back pain but the spectrum of similarities and differences has not been fully established.

Radiologic Evaluation

Plain films are a suboptimal imaging modality for evaluating the pathology and morphologic changes seen in a hyaline cartilage structure such as the CEP. Defects typical of CEPs seen in patients with vertebrogenic back pain are usually not seen on radiographs but overt end-plate fracture defects (Schmorl’s nodes) or subchondral sclerosis adjacent to the CEPs may be apparent on plain film radiography [7].

Computed Tomography (CT) evaluation can better demonstrate calcifications adjacent to the CEPs, subchondral sclerosis or end-plate fractures compared to plain films but do not adequately visualize the CEPs and is not useful for identifying more subtle degenerative end-plate changes [8] (Figure 37.3). Discogenic sclerosis is readily identified on CT evaluation but this type of degenerative end-plate change has not been shown to be responsive to BVNA [14].

**Figure 37.3** Subchondral sclerotic changes at the inferior L4 and superior L5 CEPs on CT evaluation [8].

The optimal imaging modality for evaluation of patients with chronic low back pain and discogenic or vertebrogenic back pain is MR imaging. This modality can characterize the degenerative end-plate MC based on the signal intensity changes of the subchondral bone marrow edema adjacent to injured CEPs. Type 1 MC have increased signal intensity on the T2-weighted images (T2WI) and decreased signal intensity on the T1-weighted images (T1WI) and may represent the earliest stage of CEP injury (Figure 37.4a,b). Type 2 MC have increased intensity on both the T1 and the T2Ws (Figure 37.5a,b). Type 3 MC have low intensity signal on both the T1 and T2WIs [13, 15

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