Endoscopic Spine Surgery Treatment of Lower Back Pain: Pathophysiology and Radiofrequency Treatment of Sinuvertebral and Basivertebral Neuropathic Spine Pain
Article information
Abstract
Chronic low back pain (CLBP) is a common health problem and a major cause of patient disability worldwide. The number of people with low back pain (LBP) and their years lived with disability are increasing despite technological advances. There remains a definitive gap between the evidence for effective management of CLBP and current practices. Degenerative disc disease is a major contributor to chronic back pain and also leads to activity limitation and work absence. CLBP is a complex, multidimensional condition yet to be fully understood. In many patients with LBP, magnetic resonance imaging scans show no obvious neural compression. Sensitized nociceptors within the posterior annulus have long been identified as a source of discogenic pain. However, the recent literature also supports the nociceptive capacity of the basiverterbal nerve, which carries vertebrogenic pain from the endplates. In degenerative disc disease, there is pathological neurotization of the sinuvertebral and basivertebral nerves due to stimulation of inflammatory pathways resulting from endplate damage. Radiofrequency ablation of the sinuvertebral nerve and basivertebral nerve provides effective and well-sustained pain relief to patients with LBP. The popularity of endoscopic spine surgery is increasing because of its magnified and clear visualization due to constant water irrigation. The objective of this manuscript is to provide a comprehensive review of discogenic pain, vertebrogenic pain, pathoanatomy, pathophysiology, and the pain generation pathways involved in degenerative disc disease and the role of endoscopic radiofrequency ablation in sinuvertebral and basivertebral neuropathy.
INTRODUCTION
Chronic low back pain (CLBP) is the leading cause of musculoskeletal disability affecting individuals across the globe and is a public health problem that causes major economic, professional and social burden [1-3]. During its lifetime, 84% of the general population will experience an episode of low back pain (LBP) [4]. Nonspecific LBP is defined as axial/non-radiating pain occurring in the back with no obvious underlying condition like spinal stenosis, disc herniation, spondylolisthesis, infection, ankylosing spondylitis or cancer [5]. Persistence of LBP for more than 12 weeks is CLBP and degenerative disc disease is the leading cause for it in the aging population [6]. The term disc includes nucleus pulposus, annulus fibrosus (AF) and adjacent cartilaginous end plates [7]. The discogenic model for CLBP states that sensitized nociceptors in the AF of degenerating discs lead to discogenic pain [8-10]. However, the current literature suggests growing evidence of vertebral endplates being richly innervated through branches of the basivertebral nerve (BVN) and can transmit vertebrogenic pain.
The normal disc is an aneural and avascular structure; however, pathological discs undergo neurotization due to stimulation by inflammatory pathways and their secreted cytokines [11]. With ageing there is disc and endplate degeneration which leads to increased communication with vertebral bone marrow, resulting in marked release of inflammatory mediators and appearance of Modic changes (MC) on magnetic resonance imaging (MRI) [12-14]. The sinuvertebral nerve and basiverterbal nerve are associated with the pain pathway [7]. Some of the randomized control trials have already shown the efficacy of radiofrequency ablation of BVN for treating CLBP [15-18]. Most of the studies have used fluoroscopic guidance for BVN ablation. With recent technological advances in the form of 4k ultra-resolution endoscope, surgeons can get high-resolution magnified real-time images of the disc space and epidural space which helps to increase the accuracy and safety of radiofrequency ablation. Therefore, in this narrative we have discussed the current literature on pathophysiology and endoscopic management of sinuvertebral and basivertebral neuropathy.
TYPES OF LOWER BACK PAIN
There are 6 categories of back pain as described by Borenstein et al. [19]. The types are: (1) 'Superficial somatic pain' refers to sharp and burning pain caused by cellulitis and herpes zoster, mediated by cutaneous A fibers from the skin and subcutaneous tissue. (2) 'Deep somatic pain' includes pain originating from muscles, fascia, periosteum, joints, ligaments, vessels, and dura, which is transmitted through the sinuvertebral nerve and medial branch of the posterior primary ramus. Examples of deep somatic pain include the intense, sudden discomfort of a muscle strain and the persistent, dull ache of arthritis. (3) 'Radicular pain' category includes radiating or shooting pain caused by a herniated intervertebral disc or stenosis, which is mediated by spinal nerves. (4) The sensation of 'burning pain' is caused by neurogenic claudication, which is controlled by a combination of sensory and motor nerves. (5) Unmyelinated C fibers of the autonomic sensory system transmit 'viscerogenic pain,' which can present as profound heaviness, tearing, boring, or colicky pain. (6) Pain of psychological origin- 'psychogenic pain.' Amongst these 6 types, surgeon often treats patient with deep somatic and radicular pain. Deep somatic pain is mediated by medial branch, sinuvertebral nerves and BVNs and spinal nerves mediate radicular pain.
EPIDEMIOLOGY
The leading cause of back pain is degenerative disc disease. In recent study by Wu et al. [20], they analyzed the data extracted from the Global Burden of Disease, Injuries and Risk Factors Study (GBD Study 2017). They have shown that the number of LBP sufferers and years lived with disability (YLDs) have increased substantially from 1990 to 2017. LBP remains the leading cause of YLDs however, it still is inadequately recognized as a disease burden in the population [20]. Many countries still prioritize only communicable diseases over noncommunicable diseases such as LBP. In the recent Lancet series, they have mentioned that there is a definite gap between evidence for effective management of LBP and current practice and policy [1,21,22]. The prevalence of MCs on MRI in lower lumbar levels ranges from 5 to 62 % in literature and they positively correlate with age, obesity status, and people doing heavy labor [23,24].
ANATOMY OF INTERVERTEBRAL DISC AND PATHOANATOMY OF DEGENERATIVE DISC DISEASE
The intervertebral disc consists of nucleus pulposus (NP), AF, and cartilage of adjacent vertebral endplates [25]. It acts as a shock absorber and distributes the weight and impact occurring during the daily movements of the vertebral column [26]. The total height of all the discs makes up 20%–30% of the total height of spine in a standing human being. The supply of the nutrients to the disc is by passive diffusion from adjacent end plate vessels and predisc vessels reaching outwards in centrifugal pattern from the inner layer to the disc's outer layer [27]. Degeneration of the disc occurs due to multifactorial causes which can be nontraumatic or traumatic. In nontraumatic degeneration, there is a decrease in nutrient distribution along with changes in the extracellular matrix due to aging [28] and necrosis of chondrocytes in NP. This leads to cartilage-collagen interphase degradation leading to syndesmophytes formation and calcification at adjacent vertebra [29]. While the traumatic degeneration is in response to multiple macro and micro traumas occurring during lifetime which leads to microscopic changes and pain sensitization of the discs. These microscopic damages induce neutrophil proliferation through cytokine signaling and promote nerve ingrowth and hence sensitization occurs which leads to LBA. Also, genetics and smoking play a key role in decreasing nutrient availability and neovascularization of the diseased discs leading to back pain [30].
CLINICAL PRESENTATION OF LOWER BACK PAIN
The back pain may be described as aching or burning which may or may not be associated with electric shock like sensations. CLBP is a complex, multidimensional condition and determining the exact origin of nociceptive signals from spinal or paraspinal structures can be tricky. Since the beginning, the intervertebral discs have always been considered the most common structure involved in pain signaling [8]. However, recent evidence shows that pain signals can also be transmitted from the vertebral body endplate via the BVN. The sensitized nociceptors within the posterior annulus were identified as a source of discogenic pain, however the nociceptive capacity of BVN gives an additional hypothesis: that in some patients the pain is vertebrogenic. Antonacci et al. [31] in 1998 were first to illustrate the presence of nociceptors on endplates that trace back to BVN. The endplates after getting damaged allow communication between the NP and vertebral bone marrow resulting in inflammation which is visualized as MCs on MRI [13]. This inflammation ultimately leads to endplate nerve proliferation which on mechanical stimulation transmits pain signals to the BVN, finally perceived as LBP [32]. Patients with MCs on MRI usually report a greater duration and frequency of LBP with worse outcomes with conservative or surgical management [33-35]. The progressive damage to intervertebral disc leads to decrease in disc height which leads to microsubluxation of facet joints, followed by spinal instability and buckling of ligamentum flavum.
PATHOPHYSIOLOGY
The normal disc under physiological stress loading does not cause any pain. There is a hypothesis that neuronal sensitization of the diseased disc leads to hyperesthesia. The damage of annulus exposes NP as a foreign antigen to the immune system [36,37]. This leads to release of several growth factors such as basic fibroblast growth factor, transforming growth factor-beta1, tumor necrosis factor (TNF)-α, interleukin (IL)-1β and nerve growth factor which ultimately stimulates the production of macrophages and mast cells to repair the damaged AF [38]. The induced cytokines like IL-1, IL-6, and cyclooxygenase-2 are associated with pain in degenerated disc disease. Bjorland et al. [39] in their systematic review showed that 3 biomarkers; i.e., TNF-α, IL-6, and interferon alpha, were linkedwith persistent back pain. Kim et al. [7] in their prospective case series postulated that neovascularization and inflammation along with adhesion formation is associated with pathological neuronal sensitization of nerve fibers at the annular fissures. The inflammation leads to hypoxia and low pH which increases the bradykinin-stimulated calcium response leading to increased susceptibility of intervertebral disc and dorsal root ganglion to pain [40].
El-Badawy et al. [41] in their study demonstrated that in patients who had chronic back pain and failed back surgery syndrome, there was sympathetic dysfunction on in the electrophysiological studies. The sinuverterbal nerve and BVN have large contributions from sympathetic nervous system and as sympathetic responses are hard to detect clinically more studies are required to evaluate the significance. Yeater et al. [42] in their study showed that patients with CLBP have blunted sympathetic reactivity from measured skin conductance level. Chronic pain negatively impacts the typical autonomic responses needed for walking performance and also there is potential impact on brain.
ANATOMY OF SINUVERTEBRAL NERVE
The sinuvertebral nerve was described for the very first time in 1850 by Dr. Hubert von Luschka and is derived from spinal nerve. It has connection to sympathetic nervous system with intersegmental anastomoses and recently its distribution has been shown to extend as far as AF [43,44]. The somatic root from the ventral ramus of spinal nerve is joined by the autonomic root of gray ramus to form the sinuvertebral nerve. At each vertebral level the sinuverterbal nerve has bilateral innervation to posterior longitudinal ligament (PLL), vertebral body and pedicles. Its [45] innervation also extends to intervertebral foramen and anterior spinal canal through neural anastomosis. The sinuvertebral nerve after the union with gray ramus communicans takes a recurrent course to re-enter the spinal canal through the spinal foramen via the deep anterior intraforaminal ligament, lying medial to the pedicle and cephalad to corresponding intervertebral disc [43]. The sinuvertebral nerve lies ventral to dorsal root ganglion in the intervertebral foramen and travels next to spinal branch of lumbar artery. Just lateral to PLL the sinuvertebral nerve divides into main ascending branch and a lesser descending branch where they interconnect with adjacent sinuvertebral nerve of adjacent levels. There is controversy regarding the distribution of sinuvertebral nerve whether it is segmented at the spinal nerve of origin level or branching out rostrally and caudally in spinal canal [46]. The exact role of sinuvertebral nerve in generation of discogenic back pain is yet to be understood [45]. Sinuvertebral nerve lies in superior part of Kambin triangle and this anatomical knowledge helps in transforaminal endoscopic approach to treat the pain related to sinuvertebral nerve. There is a debate in literature if sinuvertebral nerves are only autonomic origin or dual somatic in upper lumbar and purely autonomic at lower lumbar levels. Breemer et al. [45] in their study found that at L2 vertebral level, 90% are derived from somatic and autonomic roots and at L5 level, 40% are somatic and autonomic roots, while the remaining are purely autonomic roots. Just adjacent to PLL the sinuvertebral nerve divides into superficial and deeper networks which are primarily sympathetic and somatic respectively. The sinuvertebral nerve not only supplies the annulus and PLL, but also several other anterior spinal structures such as ventral and lateral surface of the dura mater and sparing the dorsal surfaces of dura and somatic supply to the periosteum of the vertebrae and the ligaments of facet joints. But the sensation to the facet joint is supplied by medial branch of the posterior ramus rather than sinuvertebral nerve [47,48]. The anterior spinal vasculature in the vertebral marrow, vertebral bodies, end plates, and outer annulus also gets innervation from sympathetic fibers of sinuvertebral nerve. The neuronal message mediating substances like tyrosine vasoactive intestinal polypeptide, substance P and calcitonin gene related peptide are found in superficial and deep divisions of the sinuvertebral nerve.
According to literature 26% to 39% of patients who suffered from low back pain have increased sinuvertebral nerve activity [9,49]. The sinuvertebral nerves are more densely populated in the endplates of degenerated disc than normal disc [50]. The sinuvertebral nerves penetrate deeply upto NP in diseased disc as compared to normal disc [51,52]. The vascularized granulation formation triggered by degeneration of disc, brings in neurotropic factors to promote the pathologic deeper penetration of sinuvertebral nerves to inner part of disc. Kim et al. [7] in their study found that patients who had sinuvertebral and BVN pain may present with radicular pattern of pain despite no direct neural compression seen on MRI scan however, on endoscopic view there is inflammation around the region of sinuvertebral nerve distribution.
ANATOMY OF BVN
BVN is paired nerve branches derived from sinuvertebral nerve which supply the endplate as pain nociceptive transmission [12,13]. The sinuvertebral nerve gives rise to BVN upon entering though the central vascular foramen into the vertebral body which lies alongside basivertebral vessels [53]. BVN continues to branch out to supply different parts of the end plate [16]. Antonacci et al. [31] examined 69 vertebral bodies and found that nerves entered the vertebral body posteriorly via the basivertebral foramen and they had postulated for the first time that these nerves play a role in low back pain. Fagan et al.[50] in their study showed confirmatory evidence for BVN complex transmitting nociceptive signals by staining them for the presence of substance P. According to current evidence the pain mediating substances are found to be substance P, protein S-100, Protein Gene Product 9.5, and calcitonin gene-related peptide [54-56].
CENTRALIZATION OF PAIN
As the inflammation and subsequent neuronal sensitization progress, the normal mechanical movement of the back can generate pain to the patient. Centralization theory states that pain which originated in spine referred distally and subsequently retreats back to axial back pain in response to repeated movements. Albert et al. [57] proposed that the injury creates “irritable focus” at the spinal cord. This knowledge of centralization of pain helps as a guide for physiotherapy and psychotherapy in the management of patients with chronic back pain [57]. Over the time these patients develop avoidance behavior due to significant axial back pain leading to paraspinal muscle atrophy and contracture due to hypersthesia and centralization of pain [58].
ASSOCIATED MICROINSTABILITY
Advanced disc degeneration leads to collapse of the disc space and the stress patterns change in spinal ligamentous structures and facet joint. Ultimately this leads to capsular and ligamentous laxity and secondary segmental instability resulting in facet joint abnormal subluxation during physiological movements [59]. As a response to abnormal loading of the spinal segment, there is anomalous fiber realignment and collagen fiber disorientation [60]. Abnormal stretching of the facet joint leads to pain due to stress on the medial branch of posterior ramus which supplies the joint capsule. This nerve is enclosed in the fibro-osseous tunnel bounded by accessory process, the mamillary process and mamilloaccessory ligament and subsequently exits through the intermammillary fascicle and mamillostyloid fascicle of multifidus muscle [48].
DIAGNOSIS OF SINUVERTEBRAL NERVE AND BVN NEUROPATHY
Patients with discogenic pain of degenerative disc disease have worsening of pain in flexion movement as in this position there is more compressive stress on the intervertebral disc. Classically this mechanical pain radiates to bilateral buttock without radiation below the level of the knees as seen typically in radicular pain arising out of compressive pathologies like lumbar disc herniation. Kim et al. [7] in their study found that radicular pain in degenerative disc disease pain can occur without any significant compression on MRI scan and hence provocative discogram is gold standard test for diagnosing discogenic pain. This involves injecting the contrast into the concerned disc tissue and is considered positive if this reproduces the pain which is similar to patient’s initial complaints. According to literature a well performed discogram is more specific than MRI scan [61]. The other common causes of back pain such as facet arthropathy, lumbar disc herniation, spondylolisthesis and spinal instability should be ruled out before opting for provocative discogram (Figures 1,2).
Diagram of the lumbar spine showing anatomical relationships of the sinuvertebral nerve. A, sympathetic ganglion; B, pedicle; C, dorsal root ganglion; D, sinuvertebral nerve giving rise to branches; D1, ascending branch that courses intraosseously and gives rise to the basivertebral nerve near the pedicle; D4, D2, descending branch providing a supply adjacent to the posterior longitudinal ligament and disc; D3, direct branches to the intervertebral disc. LMBB, lumbar medial branch.
Pathological neovascularization and neurotization around the disc with hyperalgesia from signals transmitted by the sinuvertebral nerves and basivertebral nerves.
TREATMENT OPTIONS
Once the diagnosis of sinuvertebral and BVN neuropathy is made there are few strategies available in the literature with limited evidence. Some clinicians choose to give the therapeutic effect while performing provocative discogram by adding 4% xylocaine or 0.75% bupivacaine to the contrast [62]. Other treatment options available that are electrothermal based through catheters are intradiscal electrothermal annuloplasty, disc-FX [63], transpedicular intraosseous probe insertion( intracept or equivalent) or epiduroscopic laser ablation for BVN ablation [16,64]. While percutaneous technique of transpedicular intraosseous probe is a promising technique with preliminary good results, as most endoscope are of size 4–7 mm outer diameter, there is not sufficient space in pedicle to allow insertion of a rigid endoscope to perform direct visualized radiofrequency of BVN.
ENDOSCOPIC RADIOFREQUENCY ABLATION
Fischgrund et al. [15] and Kim et al. [7] in their studies have shown the efficacy of radiofrequency ablation for treatment of low back pain related to sinuvertebral nerve and BVN. With the current technological advances and to improve safety and accuracy of radiofrequency ablation can be done with the help of endoscope. Kim et al. [7] in their study included patients with low back pain and radicular pain with MRI showing degenerative disc changes Pfirrman type 3 with significant MCs of adjacent vertebral body (types 1 and 2). They performed provocative discogram to confirm the diagnosis and then offered conservative trial to the patients. Those patients who failed with conservative management, they went on to manage them with endoscopic radiofrequency ablation of sinuvertebral nerve and BVN with either transforaminal or interlaminar approach. In their series they achieved a excellent to good pain relief score according to MacNab criteria in 93.3% of the patients. They also introduced new system of grading neovascularization on endoscopic view, grade 1 (no vascular changes), grade 2 (presence of neovascularization), and grade 3 (presence of neovascularization and adhesions to neural elements). In their study they could find that patients with discogenic back pain have at least grade 2 or 3 neovascularization. Fischgrund et al. [15] in their randomized controlled double blind sham control study showed clinically significant improvement of patients after radiofrequency ablation of BVN through transpedicular probe however, they did the procedure under fluoroscopy. The advantage with endoscopy is doing under magnified clear vision under continuous irrigation which increases the accuracy rate of identifying the nerves.
TECHNIQUE OF ENDOSCOPIC RADIOFREQUENCY ABLATION
The principle of endoscopy surgery is of target-oriented approach and first step is to safely enter the spinal canal with or without removing the ligamentum flavum. The second step is thermal shrinkage of any bulging disc with the help of radiofrequency coagulator [65]. The last step is to expose the region of sinuvertebral and BVN in order to ablate them by applying radiofrequency under vision [16]. The endoscopic radiofrequency ablation technique can be performed by interlaminar or transforaminal approach based on surgeon experience and presence of concomitant pathologies (Figure 3).
Figure showing the site of application of radiofrequency (RF) for ablation of branches of the sinuvertebral nerve.
There are 2 approaches to target the BVN, the transpedicular and the parapedicular approach. The transpedicular approach needs preoperative mapping of the terminus BVN and is performed under fluoroscopy. In the parapedicular approach the radiofrequency is applied to the dorsal surface of the vertebral body and around the supero-medial aspect of pedicle where there is dense supply network of sinuvertebral nerves before they branch into BVN. For the parapedicular approach, the endoscope can be inserted either through interlaminar or transforaminal route.
There is a classical Kim and Wu’s triad of discogenic back pain with sinuvertebral neuropathy [66]. Neovascularization of nerve roots, fatty infiltration with adhesion and on application of radiofrequency probe on the region of sinuvertebral nerve adjacent to the pedicle away from the nerve root, there is evident twitching of the affected buttock of the patient (Kim’s twitching) (Figures 4–6).
Case 1: Full-endoscopic images of radiofrequency (RF) ablation in a 39-year-old woman with chronic low back pain due to sinuvertebral nerve and basivertebral nerve neuropathy. After dissection of the region of the space between left S1 pedicle and S1 nerve root, the area of inflammation and adhesion with sinuvertebral nerve neuropathic nerves among the inflamed tissue adjacent to venous structure is seen (blue star). After endoscopic RF ablation on the inflamed region marked by the blue star., the patient felt better in terms of chronic back pain.
Case 2: Full-endoscopic images of radiofrequency ablation in a 25-year-old man with chronic low back pain due to sinuvertebral and basivertebral nerve neuropathy. Upon dissection of the region at left L5–S1 disc, an area of inflammation is seen adjacent to S1 nerve root. Radiofrequency is applied with the nerve root protected on the area of inflamed tissue (blue star). Contralateral view showed a similar area of inflamed tissue adjacent to the contralateral S1 nerve root, which was treated with sinuvertebral and basivertebral nerve endoscopic radiofrequency ablation on the inflamed region marked by a blue star.
Left figure, intraoperative picture of the left L5–S1 disc space with the classical triad of discogenic back pain with sinuvertebral neuropathy. Neovascularization of nerve roots and fatty infiltration with adhesion are shown. Upon application of radiofrequency probe on the region of the sinuvertebral nerve adjacent to the pedicle away from the nerve root, there is evident twitching of the affected buttock of the patient (Kim’s twitching) as per the figure on the right.
INTERLAMINAR APPROACH TO THE SPINAL CANAL
Patient is positioned prone on Wilson frame over radiolucent table under general or epidural anesthesia. Skin marking is done to identify the correct levels and after the skin incision the obturator is introduced and the levels are rechecked. Interlaminar endoscope is then introduced after serial dilation and docked at the lamino-facet junction. The endoscope with a 30° viewing angle and working channel diameter 3.7 mm is used for the procedure. First the soft tissue is exposed to identify lamina and facet joint. Then according to surgeon comfort either the ligamentum flavum is split with the help of probe or it is detached from the bony margins with help of endoscopic burr or Kerrison rongeur. With the help of working cannula, the nerve root and dura are retracted towards midline and annulus is inspected for any bulging disc or annular tear. For any degenerated bulging disc thermal shrinkage is performed or for the annular tears where annuloplasty is done. If there is no concurrent thickening of ligamentum flavum then, there is no outcome difference between ligamentum flavum splitting or removal technique [66-69].
TRANSFORAMINAL APPROACH TO THE SPINAL CANAL
The advantage of the transforaminal approach is that it can be performed under local anesthesia with or without sedation. Patient is positioned prone on Wilson frame over the radiolucent table. Skin entry point is decided on preoperative MRI scans and is usually around 8–12 cm from midline. After administration of local anesthesia to the skin and fascia needle is introduced through predetermined entry point which is in line with disc space on anteroposterior view of intraoperative fluoroscopy and in slight cephalo-caudal direction (5°-10°) and with 25°–35° angle to horizontal in axial plane. The angle of trajectory varies by case-by-case basis and docking is usually targeted at the base of the Kambin triangle. The transforaminal scope usually has a 30° viewing angle and 3.7-mm working channel. The outside in approach is much safer and involves drilling some part of superior articular process to access the disc space and epidural space [70]. For any bulging of the disc thermal shrinkage is performed with radiofrequency and annuloplasty for the annular tears.
ACTUAL ABLATION OF NEUROPATHIC SINUVERTEBRAL NERVE AND BVN
In both the endoscopic approaches, this is the final step and most crucial step. The working cannula protects the neural elements. Knowing the anatomical location and identifying the neuropathic sinuvertebral nerve and BVN on endoscopic view determines the success of the procedure. For ablation of BVN the radiofrequency probe is placed around the suprapedicular area and for the sinuvertebral nerve around middisc region between posterior annulus and PLL. At the area of pathological neurotization of BVN and sinuvertebral nerves there would be neovascularization. After this we applied low temperature and ultra-high frequency of (1.7–4.0 Mhz) of bipolar radiofrequency applied to medial suprapedicular area, following which twitching of the buttock known as Kim and Wu’s twitching can be seen. Kim and Wu’s twitching suggests that the target area for ablation is correct. Once the ablation is complete the Kim and Wu’s twitching would stop. Similarly, the sinuvertebral nerve is ablated just caudal to mid disc region of the intervertebral disc in the space between the posterior annulus of the disc and the PLL. As seen in BVN ablation Kim and Wu’s twitching suggests correct target point for the sinuvertebral nerve and the twitching stops on completion of its ablation [71].
POSSIBLE COMPLICATIONS OF ENDOSCOPIC SINUVERTEBRAL AND BVN TREATMENT
It is possible to for patient to feel short term paresthesia and dysesthesia after operation which typically resolve with conservative treatment after 6 weeks. Other complications are related to spinal endoscopy such as dura tear, hematoma and injuries to nerve roots is of similar incidence to spinal endoscopy.
CONCLUSION
Researchers have made considerable progress in understanding the pathophysiology of CLBP. There is definitive role of sinuvertebral nerve and BVN in mediating low back pain. There is growing evidence that radiofrequency ablation of the sinuvertebral nerve and BVN is more beneficial than conservative treatment alone for CLBP. By combining endoscopy with radiofrequency ablation, we can add to the safety and accuracy of the procedure. The current evidence is limited so further high-quality prospective studies are needed to confirm these findings and determine the optimal treatment protocol. Endoscopic radiofrequency ablation of sinuvertebral and BVN for CLBP can be a valuable treatment option for selected subgroup patients, offering significant pain relief and improved quality of life.
Notes
Conflicts of interest
HSK, a member of the Editorial Board of Journal of Minimally Invasive Spine Surgery & Technique, is the corresponding author of this article. However, he played no role whatsoever in the editorial evaluation of this article or the decision to publish it. No other potential conflict of interest relevant to this article was reported.
Funding/Support
This study received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.