Good morning, I think we'll get started and if a couple other folks trickle in then that's great. It's nice to see some familiar faces today and I appreciate you taking the time to join our session titled a paradigm shift understanding vertebrogenic low back pain. About a year ago I was attending a multidisciplinary spine conference And presented a patient Presented a patient with a 56 year old female probably a scenario that you've seen many times of chronic axial low back pain who had failed repeated courses of physical therapy also from undergone multiple pharmacologic trials and Undergone several procedures including lumbar ESI and lumbar medial branch blocks with incomplete or inadequate improvement Yeah How's that do you get feedback on that though or no, okay, that's why I moved it away Okay, how's that any better I'll keep going So our Surgical, you know colleagues decided there's no surgical intervention indicated Our neuroradiologist noted that there were motor changes on MRI and somebody else suggested that I wonder if this is that new type of you know Type of axial low back pain that we're starting to better understand which is called vertebrogenic back pain and as dr Nagpal yesterday alluded to we like to Could we do something about the feedback there a little bit? See that helps out We like to stick needles and things and burn stuff, right so there is a portion of that available for For us and don't worry. Um, we'll still be able to talk about it Sorry Can I see you can you guys hear me? Okay. I'm just getting a lot of feedback. Are you okay? How are we doing? All right And so You know time and time again, we kind of see this clinical scenario with refractory low back pain We might have some imaging findings and a procedure that we can pursue But ultimately, you know, there is a much more nuanced approach to how we're able to identify these patients We have a really terrific panel here with doctors mccormick and conger who've done some of the seminal work on really helping us understand how these patients present clinically and how the Outcomes and data is presented through the procedure itself We'll start off with a brief introduction And by the end of the session you'll be able to describe the pathophysiology of vertebrogenic pain Recognize the clinical presentation and summarize the published clinical outcomes for basic vertebral nerve radiofrequency ablation Also be able to understand vertebrogenic pain within the greater context of your Within the greater context of low back pain and how it fits into your clinical practice Unfortunately, dr. Smook was unable to join us due to family emergency. However, uh, dr. McCormick will Have that portion of the discussion Much of the basic science work that i'll present is credit to dr. Jeff floats and his group at ucsf there are histologic slides Coming up so I will warn you about that. It is as bad as it sounds there for medical students here Don't worry. It will get better. You won't have to stare at these much longer I have nothing to disclose or any conflict of interest Chronic low back pain is the leading cause of disability worldwide with a lifetime incidence between about 50 and 85 The one point prevalent One year point prevalence in the u.s. Population is about 15 to 20 percent with estimates of recurrence at one year between 25 and 80 percent And 60 to 80 percent within two years, of course the estimated prevalence can vary uh, depending on the surveillance period and the Specific type of low back pain presentation 80 percent of individuals experience at least one episode of disabling low back pain in their lifetime and in the u.s Low back pain is the most common non-cancer related reason for opiate prescription About 40 percent of individuals seek Help from their primary care physicians acute low back pain is the second most common symptomatic reason for pcp office visits 40 40 percent See a chiropractor for their initial evaluation and it's still the most common reason for orthopedic neurosurgical and occupational medicine clinic visits The personal social and financial costs of back pain are substantial in the u.s We could have direct annual costs of around 40 billion dollars Indirect costs through lost wages and productivity legal insurance overhead and impact on family can exceed 100 billion dollars important acute care costs Result from over utilization of diagnostic and treatment modalities and as well as inappropriate activity restrictions The small number of persons who become chronically disabled actually consume about 80 percent of that cost Diagnosis can certainly be challenging and an anatomic diagnosis May not always be made in cases of many cases of low back pain. It's important to distinguish leg dominant pain from back dominant pain leg dominant pain may involve the Uh nerve roots be radicular or neuropathic in nature While axial low back pain may involve the spine supporting structures classically, we understand and recognize muscle or ligamentous issues sacroiliac joint dysfunction facet orthopathy and uh dyskogenic pain We're going to take a look at a particular subset of these patients That we will define as vertebrogenic pain Although the anatomy of the lumbar spine is complex several key anatomical structures contribute commonly to clinical problems including the vertebral body the disc facet joints paraspinal musculature and the ligamentum flabum In broad strokes we can further generalize these into innervated versus non-innervated structures So There we go Innervated structures include the bony vertebral body the outer annulus of the disc facet joints ligaments muscle and nerve roots Non-innervated structures that tend to contribute indirectly can include ligamentum flabum thickening or protrusion with the disc inner annulus or the nucleus palposis We're going to particularly look at the anterior column Structures and much more focusing on the end plate and disc interface The intervertebral disc is an avascular fibrocartilaginous structure That allows movement between adjacent vertebral bodies, there's three major sub tissues There's the jolandus nucleus palposis the fibrous annulus fibrosis and the cartilaginous end plate. The nucleus is centrally located It's composed of hydrated proteoglycans and serves as an osmotic mechanism That generates pressure and volume support for the spinal forces The annulus is firmly attached to the vertebral edges surrounding the nucleus and serves both as a ligament to kind of help guide Intervertebral body movement as well as a barrier to contain nuclear swelling and facilitate disc pressurization The cartilage end plate is a thin hyaline cartilage layer That separates the nucleus and annulus from the adjacent vertebra it's supported by particularly Porous subchondral bone and serves as a semi-permeable membrane that allows communication between the disc nuclear cells in the vertebral vasculature through diffusion As well as to prevent large molecular weight proteoglycans from leaving that nuclear space The nucleus cells rely almost exclusively on nutrients that are supplied by the vertebral capillary bed It makes sense that these end plate That's much more porous centrally facilitating diffusion Highest in that region versus a little bit lower Peripherally and also lower when it's under a higher higher magnitude of the mechanical strain This is a contrast to the outer annulus, which which is attached more much more firmly Through an emphasis, which is a fibrocartilaginous composite Into into the calcified cartilage on the bony edges there historical data suggests that There is in fact structural weakness At the cartilage vertebral end plate junction And this shows that there's there's a potential weak link or in the disc vertebra interface Histologic sections also confirm this um The cartilage end plate is loosely adherent and not firmly anchored into the bony end plate and therefore can be easily separated When we look a little bit towards the periphery you see actually relatively well integrated annulus fibers within the cartilage end plate while Figure c as we look a little more centrally. There's clear demarcation of the bony and cartilage end plates with little integration D and e also show small gapping with little little Bridging collagen fibers in those areas again supporting the findings that this is an area of weakness in in that zone Biomechanically the end plates are subject to significant And complex loads through activities of daily living with tension compression and shear forces the end plates distribute these intradiscal pressures onto the adjacent vertebrae And prevents the pressurized disc from bulging into the subchondral or subtubricular bone Nutritionally the end plate is the primary pathway for transport between the vertebral capillaries and the cells within the disc nucleus Thereby creating a really delicate balance between strain dependency and nutritional permeability And because the inner annulus and the and the the inner annulus and the cartilage end plate are really well Integrated tension at that cartilage end plate bony interface can avulsa cartilage from the underlying bone And resulting in various types of end plate damage So here we see a kind of common avulsion from tension or tugging We can see tide mark avulsions towards the periphery at that that side that we had labeled as the emphasis on the outer end area of the outer annulus We can see small fractures at the level of the end plate and here we see a schmorls node Where the nucleus is pushed through the subchondral bone and into the end plate Changes of the structure and composition of the end plate alters nutrient Nutrient availability that contributes to further disc degeneration Focal damage then weakens the end plate and allows greater disc bulge or damage into the vertebral body So The disc in its healthy state is otherwise a vascular and a neural with few nerves and vessels In the annulus the adjacent vertebral body. However Is highly vascularized and innervated cell culture studies demonstrate that there's this crosstalk or communication between the nucleus and bone marrow The triggers in a response with expression of increased pro-inflammatory markers and an upregulation of neurotrophic factors in addition to an immunologic response for end plate damage another source could potentially be and has been identified as occultus gaitus in which It proliferates within the disc induces degeneration and causes fibrovascular changes within the end plates With end plate damage there is certainly increased Communication again between the disc and the Bone marrow resulting in release of increased pro-inflammatory markers and that creates neuroproliferative changes Where we can really see up to two times as many nerve fibers No, susceptive fibers at the end plate compared to a peripheral These end plate changes could probably best Visualized as modic changes on MRI Michael Modic Was a neuroradiologist at Cleveland Clinic in the 1980s who first described these changes? There are three different types of modic changes just As a reminder, you know when we typically see you'll take a step back t1 images tend to Demonstrate fat a little bit better than t2 weighted images would show fluid more appropriately a type 1 modic changes as we see here Show an active inflammatory stage in the presence of bone marrow edema and inflammation within the vertebral body We tend to see a hypo intense t1 signal and hyper intensity at t2 because there's that fluid and edema in the bone marrow type 2 modic changes Correlate with fatty marrow replacement within the bone marrow and the vertebral body. So again At this point we're starting to see a little more hyper intensity at the t1 signal is that fat mirror Fat infiltrates the marrow and we'll continue to see some hyper intensity at t2 type 3 changes are represented by decreased signal change with Within the t1 and t2 weighted images and this correlates with subchondral bone sclerosis and potentially be considered a burned out phase For that reason we tend to focus a little bit more on the type 1 and type 2 modic changes and You can think about this as a progression potentially going from you know inflammatory phase to fatty marrow replacement and the sclerotic stage Modic changes that on MRI can often accompany degenerative disc disease and the prevalence can behind the low back pain population In a meta-analysis, there was 43% median prevalence in symptomatic patients compared to only 6% median prevalence in the asymptomatic population In patients undergoing provocative discography, so we're injecting the discs To provoke recorded pain and symptoms those patients that had type 1 and type 2 Modic changes on MRI that were injected those levels versus control Had a reproduction that recorded pain with a relatively high specificity anywhere from 88 to 100% These end plate abnormalities that appear to be useful in the prediction of painful disc derangement in patients with symptomatic low back pain So where these end plate nerves come from anatomic studies by Bogduck described the sign of vertebral nerve coming off of the ventral root distal to the DRG with autonomic fiber supply through sympathetic chain by the gray remus those the sign of vertebral nerve passes courses past the posterior longitudinal ligament that further branches Into the basal vertebral nerve alongside blood vessels through the basal vertebral frame in which we can see posteriorly here The perineurovascular bundle courses about 50% of the vertebral body so halfway through it starts to arborize towards the end plate in patients with chronic low back pain and degenerative disc disease Retrieval end plate changes demonstrate high levels of neovascularization and proliferation of nociceptive fibers including substance PS 100 CGRP among others So the in summary the end plate plays a particularly critical role in in balancing and maintaining between mechanical load and nutritional support damage to the end plate At the disc vertebra interface can result in motor changes that can be seen on MRI at an up regulation of nociceptive fibers those nociceptive fibers Arise from the basal vertebral nerve via the sign of vertebral nerve So understanding this pathophysiology provides the basis for understanding the vertebrogenic pain and next dr. McCormick will help us better recognize the clinical presentation of these patients All Right good morning everyone so dr. Garib certainly Set the stage and you know we're gonna start to translate some of this You know the the pathophysiologic knowledge that's been Much of it's been developed at UCSF by Jeff loads as dr. And start to translate that to the you know our clinics And you know how do we integrate this into our practice and in whom so? I'm gonna talk. I am gonna talk a little bit about the clinical profile. How do we start to recognize these patients? Who are they? and Really quick so just quick disclosures I have received research support from relievant med systems And I'm gonna talk about some research that we did it was investigator initiated, but that is a relevant disclosure, so We're gonna talk about a series of studies Really in brief with the time that we have Where we started to try to define you know who these patients are? And ran some predictive models for who might respond well to basal vertebral nerve ablation Dr. Conger is going to talk in much more detail about some of the actual outcomes But I'll talk a little bit about just again You know patient selection who these patients are how to recognize them And who is the most likely to potentially respond to this this newer treatment that we have? And before we really dig into that Just to recapitulate a little bit or sort of reframe this I Were all very familiar, and we all use the term discogenic pain for ages, right it exists throughout the literature In our textbooks, and I think it probably just rolls right off our tongue every day in clinic right a discogenic pain How many folks before today? We're already familiar with this concept of vertebrogenic pain a good number? That's that's fantastic so and I think that and that's great. I think that even more so we need to start to re Rethink our nomenclature and talk about disco vertebral pain and some of this comes from What dr. Garib had alluded to this crosstalk that that happens between the nucleus pulposus cells migrating through damaged end plate, sensitizing nerves just underneath the cartilage end plate. And then, you know, in some folks, that presents as modic changes. Not all modic changes, type one or two, are painful. But certainly in a specific patient, these seem to matter. But remember, you know, from the neuroanatomy, the outer disc annulus is innervated by the center vertebral nerve. The cartilage end plate is innervated by the basal vertebral nerve. But I'm not sure it's so simple as pure nociception through the center vertebral nerve, or pure nociception through the basal vertebral nerve. And that's a major area that we need to work on. You know, the science is gonna, I think, help us define that better. But big picture here, a lot of these anterior column patients that we've always called discogenic, you know, they're pain is discogenic in etiology, we probably need to call it discovered vertebral. And there are some who have maybe closer to pure vertebrogenic, or end plate pain, and some with closer to annular pain, pure annular pain, with nociception kind of respectively more so through those two different afferent channels. And some of it's gonna be mixed. So, you know, the picture is still a little cloudy, but just something to start thinking about, I think, with your patients, and as you conceptualize the anterior column chronic axial back pain. So, just digging into this set of research that I'm gonna show you guys, you know, we obviously got interested in who are the right candidates for this new interesting procedure that everyone's talking about, basal vertebral nerve ablation, BBNA. And, you know, from that, so I'll show you guys some predictive models and how we can best select patients for the procedure. It helps us, it sort of helps us with defining a patient with true vertebrogenic pain. It's an imperfect proxy. We don't really have a better gold standard right now for saying that's a patient with pure vertebrogenic pain. So the best we can do is say, well, who gets a robust response clinically, reduction pain, improvement in disability, et cetera, from the BBNA ablation procedure. That's kind of the best we have. So when we talk about this clinical profile, I guess, healthy grain of salt that, you know, we're making the assumption that a patient who has a robust response to BBNA has true vertebrogenic pain. But people have placebo responses, right? Their, you know, back pain's complicated. So until we have a better gold standard, this is sort of the best we can do. But we still can learn something from this. So we look to define demographic and historical factors, factors related to patient-reported pain location and exacerbating activities, all patient-reported. And then more granular MRI characteristics than just type one or type two modic changes. And start to take a look at who does truly respond well to BBNA ablation based on a little more thorough analysis. So what we did is we took the two original randomized control trials, the SMART trial, which was sham versus BBNA. And then we took the intercept trial, which was BBNA versus all other non-operative care. And then a single-arm cohort study from Eric Trumese and Kevin McAdig and the two groups in Indiana and Texas. And all the patients who underwent BBNA. So not the sham patients and not those who were randomized to conventional medical management in intercept trial. All those that had BBNA, we pooled them into one single cohort. And that resulted in 291 patients. So that was our set. And importantly, you know, who are these patients? These are not all comers with back pain, obviously. So again, these are three prospective trials that had fairly similar inclusion exclusion criteria. So important to note, every single one of them to be enrolled in the trial had to have type one, all three of these trials had to have type one or type two MODIC changes. So we did not look at anybody who didn't have MODIC. These are all patients who had MODIC one or two. And they had to meet this very reasonable criteria of at least six months of axial back pain refractory to other conservative care. Including interventional care, but non-surgical. And then certain pain and then ODI thresholds. They had to have a reasonable amount of pain and a fair amount of dysfunction associated with that pain to be included in these studies. What did they not have? There's a laundry list of diagnoses they did not have. And it's a little long, so I just made a shorter slide. These were the big take homes. So in all three of these studies, patients could have had a radiographic stenosis, radiographic evidence of a nerve root abutment, for example, but they couldn't have been complaining of any kind of neuropathic or radicular pain at the time of enrollment. They also couldn't have any meaningful spinal instability. They couldn't have scoliosis. And there was a certain limitation to their depression scores. I think it was a BDI score of 24. So some amount of potential depression reporting, but certainly not someone who's clinically, significantly depressed. And these were not, nobody was obese. BMI cut off at 40, so morbidly obese. But so, just again, for frame of reference, this is not everyone who walks into your clinic with low back pain. This is a restricted set, a restricted cohort. But from that, we wanna take a look at, are there factors that will help us select from that inclusion criteria or that sort of subpopulation of low back pain, this unique phenotype who have true vertebrogenic pain and who would theoretically do well with the ablation procedure. So one of the things we did in these analyses as well is every patient had a pain diagram. So much like you might give on your intake form in your own clinic, patients all were asked to mark where their pain was. And then we created a grid system and overlaid that grid on each of these pain body diagrams. And basically coded it in a binary fashion, one or zero, or there is pain in this small cell or there's not. And then we can sum those together to create a heat map. So across all 291 patients, we start to see patterns in where patients mark their pain. And we can separate them into those that were responders and those that were non-responders. And I'll show you those, of course. So this is what these heat maps will look like. We also essentially coded these pain body diagrams into regions of clinical interest. So you can kind of imagine that midline region is where we would sort of expect a patient to mark pain if we're thinking they have, quote unquote, for tubergenic pain. It also would kind of fit with what we've always called discogenic pain, back pain. And then you've got the paraspinal regions off to the side where we might think about facet pathology or myofascial pain related to multifidi or the other paraspinal structures. And then, and so on and so on, maybe quadratus lumborum in four or five. But basically breaking these body diagrams also into regions of clinical interest, not just that grid system. And then finally, MRI factors. So I think, you know, as Dr. Grebe highlighted, there's clearly something important about type one and type two MODIC. And this is where we see these pathophysiologic changes occurring at the end plate, you know, that then correlate with increased innervation, nerve fiber density increases in specific nerve fibers that carry nociceptive signals and neurotransmitters that are involved in nociception. But what about the size of the MODIC change, right? I think we've all seen a patient who has a tiny little sliver of MODIC. And then the patient who has a giant, just, you know, voluminous MODIC change at a given level and thought to ourselves, huh, that, you know, tiny little sliver, does that matter at all? Versus the giant change that that patient's gotta have or tuberogenic pain. But is that actually true? Do the number of defects, the size of the defects, the shape of the defects and so on. And I'll show you these factors, but we wanna take a much more close look at all those things. So we created three different responder models because we need some definition of success to go with, right? One of them was based on pain alone. So at least 50% pain reduction. And I think if you treat back pain, I think you would agree that in folks that have failed a lot of other care, chronic refractory axial pain, 50% improvement in pain, pretty good, right? I think most of us in our patients would be pretty happy with that. Second one is an ODI improvement of 15. Also pretty darn good. So if you look at the literature on back pain, you can find a minimally clinically important change. Somewhere between 10 and 15 points is kind of the range of what you'll see, depending on the study you're looking at and the subpopulation. But 15 point change in ODI, pretty good, right? Like that's, most people would agree that's a good definition. And the final one was looking at either or. So with the thought process that if a patient comes back and they say, yeah, you know, my pain's a couple points better, but they fill out an ODI and they're functioning super well, that's, I think in our world of back pain, that's good, right? That's success through our lens. And then we can calculate the predictive, we enter these into stepwise logistic regression models and can calculate the predictive value or ability of these different models. And I'll show you those. So first of all, demographic and historical factors. These were all factors that were entered in the model. These four factors survived into the final model, you know, based on low P values on the stepwise regression. And actually, I'm gonna skip through that one, sorry. So these are the factors that entered, the demographic and historical factors, exacerbating factors entered into the final model. And the big take home from this is that patients who reported self-reported pain that was worse with physical activity, they had twice the likelihood of meeting our responder definition, one of these robust definitions of clinical success following BVNA. The other was pain that was worse with backwards, with essentially lumbar extension maneuvers, they were half as likely to respond. So pain that's worse with physical activity, you could say, well, that's pretty nonspecific. That's a lot of things and kind of fits with what we might think of as pain generation from numerous different axial back structures. But it's still valuable to understand this. You know, if you see a patient in your clinic who fits these sort of criteria, has type one or type two motic, and they're telling you that their pain is worse with physical activity, they're twice as likely to respond to this, to BVNA. So that is helpful for selection. This is also interesting. So pain that's worse with backbending. Technically, in all three of these studies, the enrolling investigators had to deem the pain clinically suspicious of anterior column or vertebrogenic. So they basically all were saying, these patients don't have facet pain, but they were not required to have media branch blocks to be entered into the study. So certainly there could have been patients with a heavy amount of facet pain, or maybe mixed pain, facet and anterior column vertebrogenic, and they could have made it into these three studies. So it's interesting here that when patients reported that their pain was worse with backbending, they had half the likelihood of responding to BVNA, meeting these responder definitions. So then these heat maps that I promised. So this is what shook out. This is all comers. This is what, when we do those grid overlays, this is what we see. So the darker like maroon or deep red color indicates that more patients marked pain in that area on their pain diagram. And as you get out towards yellow, you have far fewer. So in everyone in the cohort, this is what you see. When you begin to separate them out by responders and non-responders, there aren't huge differences because remember, I mean, this is still a very select population, not all comers with low back pain, but this you see substantially more midline density in the responders compared to the non-responders. So that deep maroon again is indicating that a larger proportion of patients marked that area. And you might say, well, this looks like discogenic back pain. And well, that's kind of the point. So again, like going back to our nomenclature, we really need to be thinking about discovered vertebral pain and we're going to, you know, over the coming years, we're going to start to understand more about what is annular, what is end plate, what is mixed. But this is what a patient is marking when they respond well to BVNA. So, and BVNA does not denervate the center vertebral nerve. And really we see the same pattern with when we separate by level. So I'll kind of scoot through these for the purposes of time, but same thing, if we look at just the L4-5 level, 5-1 alone. And if we look at essentially ribbons where we don't separate by each individual cell, but just the distance from midline. So midline pain, again, looking at responders versus non-responders, there is going to be greater density towards midline. MRI characteristics. So we had a lot of hypotheses about what might matter and what might actually predict treatment success. And I think, in my mind, I thought that the height or the volume of changes, the number or size of defects would definitely matter. And those were sort of hypotheses that we have going in. But as we, I'll just scroll through these quickly. There are a lot of them. If you're interested, the papers have much more detail. But BMIC is bone marrow intensity change. So, and if you look at the four columns, we entered all these into the models. None of these Ps are significant, right? They're all too high. So end plate defects, the shape, defect size, the essentially Furman score, or the degree of disc degeneration, the proxy, the Furman score, nuclear signal change, disc height, none of these things came out as predictive. Interestingly, high intensity zone, right? So this is thought to be annular fissure, perhaps a calcified annular fissure, but has classically been thought as a radiographic marker of quote unquote discogenic or annular pain. You know, one might say, well if they had an annular fissure, I would expect they wouldn't do well with BVNA, right? Because BVNA doesn't address that vertebral nerve mediated pain. It only addresses the BVN mediated pain. This didn't matter. Disc contour, so remember patients could not have anything more than a five millimeter protrusion. So, you know, an extrusion wasn't like a giant extrusion, but if they had one, it didn't seem to matter. As long as they had MODEC and fit the other criteria. I alluded to nerve root contact and remember they could not have been complaining of radicular pain or any kind of neuropathic like pain. So again, they could have radiographic features of some of these things, but without neuropathic pain and none of these were predictive. Listhesis without instability, grade one only and then elements of stenosis, same idea. So what came out of all of this and this was honestly totally shocking to me and to others involved in this study was the only thing that predicted success or failure was the presence of facet joint fluid. And if you look at this odds ratio, essentially that's saying that if a patient had facet joint fluid at a level that was treated with BVNA across these three cohorts, they had half the likelihood of reporting success. And that fits again with what I mentioned before where patients were reporting extension based pain. They had half the likelihood of responding to BVNA. My interpretation of this is that some of these patients had facet pain. Now, not that facet fluid is a perfect correlate. It's not, right? MRI is not a great way of diagnosing facet pain, but they didn't have medial branch blocks to rule out facet pain. And so I think this is one big takeaway is you gotta rule out facet pain in these patients before potentially offering BVNA. So these are the big take homes here. The predictors of success, I've got them right there. I kind of scooted by analgesic use because we were talking more about clinical profile. So opioid use has nothing to do with a clinical profile, a phenotype of low back pain. But we did see in our modeling that folks that were on daily chronic opioids had about half the chances of responding to BVNA. But these are the big ones here. So patients got pain that's worse with activity, and they tell you that. Pain that's not worse with lumbar extension and midline predominant pain with possible gluteal referral. These are the folks that do well, right, with this procedure. So we're starting to build out this subphenotype of back pain who have, let's call it, dominant vertebrogenic pain because they do well with the BVNA procedure. And then again, back to the MRI, I think it's baffling to me, but this is what we found, that nothing other than type one or type two MODIC actually predicted response when we pull out everyone that had symptomatic particular symptomatology, scoliosis, instability, more than grade one spondy. So in the interest of time, I'm kind of going to end there, but I'll talk about some of this on the last lecture as well. Just very briefly, I think important that we don't have a better gold standard right now, just to recapitulate that, we don't have a better gold standard of vertebrogenic pain other than response to BVNA. And that's something we're gonna have to learn more about. There are major challenges in creating an interventional diagnosis for this pain phenotype, call it vertebrogenic pain or discovered vertebral pain, particularly because discography both stretches the annulus and creates end plate deflection. And so discography is not a great way of distinguishing annular pain, pain mediated through the SVN compared to end plate pain with pain mediated through the basal vertebral nerve. It perhaps helps you understand anterior column pain as a whole, as opposed to other etiologies, but it's not gonna help us figure out end plate versus annulus. And I think the last thing is just that we are, over the coming years, gonna learn a lot more from novel imaging sequences and imaging biomarkers. And in my opinion, I think that's actually how we're gonna start to learn more about who has vertebrogenic versus annular versus other pain. So thank you guys very much. I'm gonna hand it over to Dr. Conger, who is gonna speak on more of the actual outcomes from the clinical trials and the clinical evidence for BVNA. Thank you. Good morning, everybody While we're pulling this up, I just wanted to gauge the room I think dr. McCormick had people raise their hands if they're familiar with this concept of vertebrogenic pain I'm just curious for myself and maybe everybody else would be curious how many people here have performed EVN ablation Okay, it was interesting just seeing people kind of raise their hands earlier But this has been talked about like more and more and more It seems like every year and every time somebody gives a talk on this everybody asks like how many people do this? How many people are aware of it? There's more and more hands that are popping up every time one of these talks are given about vertebrogenic pain I think in Just quickly scroll through this I wonder if mine will pop up next no, how do we select mine? This is dr. McCormick's Okay, I could just give I could just give his again Conger The first study was published the pilot study was published in 2017 I was training at that point and I remember seeing it being like oh, this is kind of interesting I think I even talked to Rich Kendall about it. He probably doesn't remember this but I Remember when the very first study came out on this stuff And so it's been very interesting to see it kind of progress over time and for everybody to become more familiar with it And now it's really kind of mainstream or becoming mainstream So these are my disclosures the relevant one being that I've had some funding from relieving as well. That's related to this work I'm so you should know about that So I want to start out with a case here and this is hopefully This kind of coalesces a lot of what dr. McCormick was just talking about. This is a real patient of mine One of my first patients that I've been treating for a number of years at this point, but you know, she's middle-aged very active Has chronic flexion based back pain after a back injury unable to You know Perform her job anymore, which was teaching Zumba classes just absolutely miserable and I watched her kind of go through this progression of you know from acute low back pain to subacute to chronic Low back pain trying everything conservatively under the Sun to help her with this Massive amount of you know therapy and rehab and all kinds of things You know her her clinical presentation matches a lot of what we were just talking about, right? So flexion based back pain pain in the midline Constant worse with activity Relieved with extension to some degree, you know, she didn't have obvious radiculopathy or anything like that I did MEBs at one point in time zero percent relief And so think about I want you to think about this type of prototype person as we're going through the literature and And I'll try to answer some of these questions You know about her and and your type of patients to see whether they'd be candidates or not for this procedure Whether you can generalize the results in these studies to somebody like this and this is not going to play but this is This is basically a video on here to show you kind of her whole imaging sequence But you can see at her l4 5 disc that far left Image pain is a stir sequence, which is a little bit easier to see on the screen here showing type 1 motor changes basically and the same thing Is present on on the other pains, you know dark on t1 and light on t2 And that CT you can't see it real clearly there But you can see sclerosis about the end plates and when we were able to pan in and out there You can see small end plate. You can call them nodes You can call them end plate fractures and plate defects But those are visible on CT as well and they correlate perfectly with the location of those type 1 motor changes And I think the other thing to keep in mind about this imaging, right? So we were talking just a moment ago about the size and the morphology of these defects You might look at this and just be like, okay. Well, those are pretty small. Maybe that doesn't matter so much But again harkening back to what dr. McCormick was just talking about sometimes small things are just as likely to be associated with for tuber genic pain and those not or at a minimum Can succeed just as frequently as large volume motor changes when BDN RFA is applied So everything I'm going to talk to you about today is contained within a systematic review that we recently published there's been a couple of these in the last couple years and you know, this is kind of the The criteria for the review, you know I only looked at intraosseous BDN RFA and it was type 1 or type 2 motor changes kind of the thing that has been indicated originally in all these studies And the main outcomes we're looking at were 50% pain reduction or a 15 point ODI improvement So the same types of things that have been in most of these studies And if you want to look more in-depth at this you can see this paper Which is published in the same supplement as the other studies. So just you know brass tacks here You're talking about two randomized control trials. One of them was the first, you know sham controlled trial That's that's smart. And then you're looking at another large trial, which was open label randomizing people to either BDN RFA or continued You know standard care which really could be anything as defined and then four single group cohort studies two of which are non industry-funded one of them Was done in Italy by a neuroradiologist the other one in Ukraine. You're about 400 patients or so I Won't go I don't want to put a giant table up there with every single inclusion and exclusion criteria But I kind of want to paint this with broad brushes so it sticks a little bit better But all these people it basically six months of pain all of them had to have type 1 or type 2 motor changes most of the studies excluded patients that had you know significant spondylolisthesis Dysprotrusions bad depression obesity And and what you know and what the authors thought was facet joint pain Although really only one study has required medial branch blocks to this point. I'll go through that in just a minute Anybody that had radicular pain or symptomatic spinal stenosis isn't in any of these studies Those are all you know expressly excluded and really none of these studies Have have they've either all excluded patients that have had a fusion or they haven't said one way or the other whether Any of the patients in the data set had a fusion at a different level So fused patients really have not been in these any of these data sets Some of the studies have included people that have had a prior laminectomy or decompression as long as they didn't have active radicular pain for six months Just as importantly as The inclusion exclusion criteria, I think are the patients that actually ended up in these studies the demographics, so this is kind of broken down From the trials which were probably Better at Really listing out all of the demographic factors and then the cohort studies also did you know kind of usual things? But most patients were Caucasian non obese college-educated employed Most the vast majority were in their 40s to 50s Many of them in most studies had pretty chronic low back pain I think about 70% of the populations basically had pain for greater than five years Some of the prior treatments that had been used in these patients that were reported by investigators opioids in about one in three spinal injections about three and four Minority had had prior RFA a lot of them had physical therapy Chiropractic sounds like a lot of patients that might show up to your clinic right with chronic low back pain continued symptoms When we look at kind of the technical details of how this procedure is done I think we're gonna have some time for dr. McCormick to talk more about this, but it's evolved a little bit So in the earlier studies the targeting was a little bit more anterior and then And then in some of the more subsequent studies The target was sort of brought backwards towards the posterior wall to target the BVN a little bit more proximally but in either case targeting success based off of post ablation MRIs and those You know blinded radiologists in some studies and in other studies They didn't really say it was probably the investigators that scored of this on target or not But in any case, you know 95% or higher Targeting success when this was done in the early studies or in the latter studies And then I already mentioned the comparator to in these two studies I should mention though so the sham study One more show of hands who who is kind of read through most of these papers Oh great, okay So I'm gonna be telling you guys some stuff that you don't know So the sham the the sham study they had a great I mean in my opinion a very good robust Sham procedure. They actually had patients go under, you know, either general or conscious is about 50-50 mix and they You know, they made a small incision and docked the introducer into the pedicle so Pretty pretty good Blinding I think in that regard and then for the standard care arm again They allowed just about anything and to be fair, you know Maybe a potential criticism would be these are all the things that I just showed you those patients were already doing, right? At least in this in this study. So to be fair So just starting out I'm gonna try to get into the outcomes here and I'd like to touch on every study if I have time here but But it'll be hard to get all of them. So Becker. This is that 2017 pilot study This is the first one where it was done. I think one of these patients was treated with Kind of an extra-pedicular approach, but all the other ones had trans-pedicular BV intubation. You can see this is the this is what the authors There we are so this is this is kind of their ODI chart this is what their primary outcome I mean you see a number of patients kind of a mean here and then a big drop in ODI scores that are basically maintained out to about 12 months This is looking at the other one of the other sort of real-world Population studies That's done the same thing again. Same population same inclusion exclusion criteria the whole deal and this is showing essentially a percentage pain reduction from baseline out at 12 months And so you've got the vast majority of people that are either 75 to 100 percent or a hundred percent improved with you know, really maybe 20-30% of people that did not get at least 50% pain reduction So This this DeVivo 2021, this is the this is the study from Italy done by a neuroradiologist there And so this was done under CT And you can if you just get used to looking at these things You'll notice that for those of you that are used to looking at this this looks different Than some of the other devices that create this ablation. It's a very large That particular device is used for tumor ablation a lot of times But it was adapted and used for BVN in this case. It was done under CT guidance The one interesting thing about that study that actually if you read the manuscript very carefully they required To you know the the same clinical criteria, but then all those patients underwent a CT spec study And then if the CT spec showed end plate changes Then all of those patients had medial branch blocks. It's kind of an interesting Selection paradigm that doesn't totally make sense to me, but it's it's buried in the manuscript so there is a study where everybody's had MVBs to be able to move on and The success rate in that study in that cohort study was extremely high. I mean 90% of people had 50% pain reduction 80% of people had a 15 point ODI improvement Shanko this is the study from Ukraine actually and You know they they reported similarly high Reductions in pain and they basically created their inclusion exclusion criteria almost identical to to smart and intercept. I think on purpose So they were basically just trying to reproduce the same results Which largely they did? So I'll kind of try to get into each of these studies the RCT is really deserve a lot of time More than I can really give to look at the nuances of kind of you know when patients were Allowed to cross over and those sorts of things so I'll try to show some of that here But I think one of the big things to understand is you know they kind of did an intention to treat analysis And they did a per protocol pop you know Analysis and the protocol analysis basically means for patients that had targeting failure or protocol deviators. They didn't include them So like many RCTs there's usually multiple analyses that are done To understand the differences between the two One of the big things that came out of this study was this huge sham response That people had which is not that dissimilar to like sham kyphoplasty or sham surgery things like I mean As Dr.. McGovern mentioned earlier The human mind will do a lot so there's this enduring sham response in those in those patients to the point that there wasn't a huge difference in certain outcomes at certain thresholds between the sham group and between the Between the BVN group in the intention to treat analysis But there were differences in the per protocol analysis and the vast majority of patients were in protocol violators I think there were 16 of them that were excluded based on targeting failure And you have to remember, and this is still a an early a early Type of procedure that was you know being developed and used by people and it's not perfect right and so there was some targeting failure And that's where most of those papers for patients were Excluded so if you think about excluding people where you know you missed the target. It's probably a smart thing. That's the way I think of it So looking at the outcomes for that study, this is showing kind of categorical Response rates so for different thresholds for 10 point ODI for 15 point ODI and for 50% pain relief And so you'll see some some fairly separated Responder proportions with separated confidence intervals, but when you start looking at bigger chunks You know you wouldn't say these things are statistically different At least at three months, but there were there were statistically significant differences especially mean mean changes So this is the same study, and they've you know there's been like three different publications on this so just following it forward You know originally 225 Fault goes for 12 months the crossover was offered to the sham patients at 12 months the vast majority Chose to cross over and so all of these patients this 57 patients or so are included in the 24 month Outcomes and the five-year outcomes from the same sort of population of people So I you know All of these numbers are going to kind of look the same right it's so I don't want to belabor it But I mean still at 12 months at 24 months the same things were true right for the most part The responder rates were basically the same small and as in all studies some people were lost follow-up, but fairly low You know still 70 plus percent of people maintaining that significant ODI reduction pain reduction I think more so than even the To me more so than even the reductions in pain and improvements in function very few patients were coming back for spinal injections for RF Many of them had stopped using opioids which I think speaks even more It's sort of like proof-in-the-pudding basically a lot of people were not having further healthcare utilization the five-year results were very similar again You know 60 to 80 percent of people depending on the the threshold of success that you choose We're still reporting significant improvement At five years in this group of people and 3% had had a lumbosacral RF Or spinal injection in the one year preceding the five-year data collection 73 percent Had reduced opioid use at five years fusion surgery was less than 10% So for this group of people I think it was pretty significant This is a great picture on the right side here Because this this you can use this to sort of counsel your patients if that makes sense if your patients match Sort of what my patient was at the beginning of this or what you know the type of people that have gone into these studies You know you can quote things like One in three people you know and these studies have reported 100% pain relief for five years But the failure rate is you know if you define failure by less than 50% pain relief or really maybe what you should do is less than 25% But you can say the failure rate is this And so we'll kind of go into that in just a minute, but this is what's been reported in five years Okay, so this is the other study So this is the other randomized trial, and this is what you know was compared to To standard care and so at three months Pretty massive differences in in significant pain relief And you know again to be fair 15% pain reduction Might be expected in a cohort of people that were basically doing what they were already doing But significant pain reduction in the BVN group 63% of those people This is just kind of a picture basically showing again that 20-point ODI reduction or two-point DAS reduction You know 60 versus 60 or 70 percent versus you know very small reductions in the standard care group And this is the intention to treat analysis so the study had a Had a data monitoring committee that basically because of the super large differences between the two groups Recommended that you know for ethical reasons to stop the comparative aspect of the trial and offer crossover to the other group So the kind of the comparative data ends at three months And then you can see here. These are sort of the standard care patients that chose to crossover and at that point So this is VAS Scores so those dropped significantly and then started to kind of match the other groups and same thing here You know basically at that same time point people cross over and they kind of go on And join the other happy group so to speak so this is the two-year results from that same study Showing again the same type of picture here right about 30% of people with 100% pain reduction And then you know if you kind of total these things up right here You've got roughly 70% of people with at least 50% pain reduction and very similar Results in terms of health care utilization very few people coming back for epidurals And those sorts of things low rates of fusion a lot of people stopping opioids So this is the review that we did And this is gonna you know these numbers are basically the same thing that I just showed you so I'll just take a second to explain this thing so this is not a lot of people are used to looking at forest plots And you're talking about a compare. This isn't technically a forest plot. It's a proportion plot So this proportion is basically saying like zero percent here and a hundred percent is one And we're talking about the outcome that we're talking about is 50% pain reduction So if you see something that's sitting down here at the 25 that means 25% of people in that study had 50% pain reduction If you see it over here, it means a hundred percent of people had pain reduction if you see it Right there. It's like 80% right so all of these individual dots and their little confidence interval whisker on each side Is kind of where these things fell at and they sum to right here, and that's the proportion 60 Yeah, so if you sum them all together at 12 months at 65% Responder rate for 50% pain reduction That's at six months and that 12 months It's about 64% so very similar, and that's kind of putting all of the studies together Not just the industry funded, but the non-industry funded studies, which ironically the non-industry funded studies if you look at them here They're actually better Whatever For ODI reduction, it's the same thing So again, you can see the success rates are here for each individual study sum them together about 75% That's at six months, and then at 12 months. It's about 75% so I probably sound like a broken record here One last ones I'll show you here, and so this is looking at basically all the patients over time So all the patients all the studies At six months 12 months 24 months and 60 months this of five years right there only one one data set one You know one group that's made it out to five years here It's been reported on And the main point here is it's a straight line right like the people that were responders in the beginning seem to be responders in the end There's lots of criticism from people though same thing for all Just a minute same thing for ODI reduction right relatively straight line here again about you know 75% responder rate So you know when you read if you go in-depth in these studies You'll see that like with all studies people over time. There's attrition right now everybody at five years was followed Actually, that's a multi-center studies. There's a lot of European sites They didn't continue to follow European patients out to five years So I think that was like 30 people or so all of those people were not followed for longer But even if you assume that every single patient that was either excluded for protocol deviation Which is not many or for? missing so like you know by the post MRI analysis Or if they were just lost to fall if you just assume that every single one of those patients must not have succeeded Just probably not true, but as a worst-case analysis It's still pretty good, so you're still sitting at 60% and then this is when you see it go down That's just because time is going on and not everybody's following up right? But even then you're still sitting at above 50% in both of these categories Which is unlikely to be the true case because some of those patients probably were successes Okay, so back to that patient back to my patient So what can you say about her CT MRI? She's got type one motor changes. She probably has end plate defects It's hard to you know fully It's hard to see those on conventional MRI and CT you kind of see the You see the after effects of it right you can see these small little Schmortles nodes and plate fractures if they're big enough on CT, but you need some of the other research Basically available in certain academic centers and research Type MRIs to actually see small end plate defects, but so those are some of the things that were Significant about her imaging is she a candidate yes What can you tell her about the success rate? I just went through that with you guys I mean basically you can tell her if she matches the clinical criteria that there's a 65 to 75 percent chance That she's going to achieve you know at least 50% pain relief if she is a success at six months one year It's likely that she'll continue to experience pain relief a third of people In report 100% pain relief at those same time periods, but up to 20% of people don't So those are kind of the odds and the chances based on the published literature So you know my take on this I think that it's effective. I think the literature supports that it's effective I think we're still trying as Dr.. McCormick mentioned to figure out who best to to select for this procedure I think there will be more non-industry funded studies that are going to pop up over time. There's a registry as well And I think what we're trying to do is again figure out who to use this for and what are the other things that those are the references. I encourage you, I mean, if you're super interested in this, like, that supplement has all these studies in it. If you go back and read some of the things Mahmoud was talking about, the Lopes studies, Aaron Field's Pathobiology of Motive Changes, that really blew my mind when I read that stuff originally, to understand that it's not necessarily two separate boxes, right? This is a single complex, and probably a continuum and a spectrum of a disease process that may begin as dysgenic pain that eventually evolves into sort of the end state of the process of motive changes and vertebrogenic pain. So it's a very interesting area. Thanks for listening to us talk. I think we still have some time, and Dr. McCormick is gonna talk a little bit more about clinical practice, PEARLS here, so I'll hand it back over to him. Thank you. Thank you so much. So as Dr. Green mentioned, Dr. Spook had to, was gonna give this talk, but had a family emergency he had to attend to, so I threw together some slides that I think you'll find helpful, and this is really kind of starting to conceptualize, you know, where does this really fit in your practice? And some of you already, it looked like from show of hands, you are performing the ablation procedure, and many of you are familiar with the phenomenon, again, of discovered vertebral pain or vertebrogenic pain, but just to highlight a few things here. So this is a procedure that is unlike anything else that we've had before, I would say, in the back pain world, non-surgical back pain world. From what Dr. Conger just showed us, these, you know, the data that we have, the outcome data that we have right now are incredibly encouraging. I mean, if you just think about all the treatments for quote-unquote discogenic pain that have come and gone, IDET, baculoplasty, all the intradiscal injectates, you know, there's some excitement initially, and then as time goes along, it peters out, and that treatment really kind of just goes by the wayside. Getting durable five-year outcomes from, you know, a treatment for discovered vertebral pain is pretty incredible, and just to, some of you might be wondering, well, how is that possible? You know, we do ablations for facets, and you have to repeat them every six to 12 months, or maybe two years if you're lucky, in a given patient. The basal vertebral nerve is not a myelinated nerve, so it doesn't have a scaffold for regrowth the way that all the other, pretty much all the other nerves that we classically, in interventional pain or spine, target for ablation, they do, they're myelinated, so there's a scaffold for regrowth, and that's why we see pain reoccurring. So that's a major difference, and, you know, sort of a wonderful coincidence for treating this subpopulation. But this really is, I mean, what you're hearing today is like, this is a unique phenotype, and it is definitely a small proportion of our patients with chronic axial back pain, but it's super encouraging that we have this subphenotype that really does respond well to a new treatment intervention. What I would definitely emphasize is that, you know, some of you already do this procedure, some of you might be considering it, implementing it into your practice, is that you remain stringent with your selection. So this figure really just kind of captures the big ones. I mean, you saw the long, the laundry list from the clinical trial, but, you know, at least six months of back pain, relatively, you know, high amount of disability. This shouldn't be a procedure that we're offering for patients who are really kind of getting by okay, but really higher levels of dysfunction. So, you know, all these studies require an ODI of at least 30, right? So like a fair level of functional disability related to back pain, and then, of course, the type one and type two motor changes, and then, again, you know, the key exclusion criteria. So these, you know, patients that have radicular pathology that have stenosis, the symptomatic instability, herniations, et cetera, these are not the right patients for the procedure, and I think that we all have to, you know, collectively be very judicious with this because, like many other treatments, as soon as there's over-utilization because of excitement, they go away, right? If anyone was here for the talk yesterday about, you know, coverage challenges and, you know, reimbursement challenges coming forward, it's, you know, this is what happens. So I think, you know, collectively as a community, we just have to be really careful that we're using this procedure that works really well, but for a subset of patients. And, you know, I talked about this, so I won't go back through the elements of anterior pain, but this is an interesting study that came from Vanderbilt and was just recently published, and they really tried to look at all comers, you know, with back pain. The patients that came through with axial back pain had an MRI in their clinic consecutively. How many of them would actually be eligible for, you know, based on clinical trial criteria, the ones that we've been talking about this morning, and they found that it's about 3% of patients. So kind of keep that number in mind. I mean, of all the patients that come through your clinic, there's probably, and they've got a confidence interval from one to 5%, but maybe one in every 20 to one in every 40 patients with low back pain, with chronic low back pain that's refractory to other treatment is, you know, would actually fit these criteria. So it's definitely, I think we have to be careful about who we're offering this to. If we're careful and we offer it to the right patients, we've got a great treatment. If we overdo it, we're going to lose that treatment. So I would just put out that word of, you know, of caution because this really does seem like a very, very promising treatment for the right patient, and that's based on my own anecdotal experiences with the procedure, but also all the trial data that Dr. Conger went through. So just to put this in perspective, you know, this is a figure that was created from one of those that Dr. Conger showed, the two-year data from the SMART trial, and so what you're seeing is, you know, the baseline ODI scores in patients that were initially randomized to conventional medical management, non-surgical care, really doesn't drop much. This is the group that received Intercept that we saw, you know, after 24 months, big ODI drop. It's maintained at two years in that study. In the SMART trial, the five-year cohort, it continues to be maintained. But just compare that to other typical treatments that we might use for chronic axial back pain and the type of ODI drop that we'd expect over time, and this comes from, you know, aggregating other studies, acupuncture, NSAIDs, Pilates, multidisciplinary rehab, that's the green line, and then surgery. So for fusion, for axial low back pain, I mean, there have been a number of studies, right, that have, this is not a, we know, I think most of us in this room know, you know, fusion for axial back pain, not a great idea, and responsible surgeons really don't offer it, but there's the ODI change you see after two years when you kind of sum up the results of the literature that's out there and exists, and just compare that to what's possible. But in this specific subpopulation, so that's the key, is the right patients for this procedure. So I will take a moment to just talk through a little bit of the procedure itself, because if you are thinking, hey, this is something I'm interested in, you know, maybe I have a, you know, if you do kyphoplasty or vertebral augmentation, there are some similarities and some differences. But, you know, we talk through a lot of this anatomy. Dr. Gharib, I think, showed a slide that was very similar, but, you know, here you're seeing the basal vertebral foramen. So at the lumbar segments, it's really kind of at the equatorial line of the vertebral body, and that is where the neurovascular bundle enters. And that's our treatment target. So obviously we're trying to catch the stem of the basal vertebral nerve here, or as you're seeing in this figure here, that stem before it begins to arborize and shoot out its termini to the respective end plates. So if we can place a lesion, you know, more posteriorly at the stem of the BVN, you know, that theoretically is the perfect targeting. Like Dr. Conger mentioned, earlier studies targeted a little bit more anteriorly, closer to 50% midline of the sagittal diameter of the vertebral body. But we now know that if we're probably closer to maybe one third of the sagittal diameter, closer to the posterior cortex of the vertebral body, that's probably the perfect place to be. And there have been pig model studies that show that even a lesion that's essentially touching the posterior cortex of vertebral body doesn't heat up the CSF. So that's a concern, right? We don't want to be burning nerve roots, clearly. But as long as we're safely inside the vertebral body and probably about one third diameter, that's a great place to be to target this nerve. So I'll walk you through the actual procedure itself just to get a flavor for it. But it is a pedicle access procedure. So essentially we're typically starting in an oblique view, identifying the pedicle, anesthetizing down to periosteum, and then advancing. This is an eight gauge trocar, so many people will use general anesthesia. I know that there are folks out there that use MAC, but I've changed to completely using general anesthesia just for patient comfort. And then you're looking at the lateral view. So this is definitely a procedure where you're very carefully triangulating where your trocar position is between APs, laterals, and you can of course add obliques. But making sure that you remain inside the pedicle until you enter the posterior vertebral body is really the most critical part of this procedure from a safety standpoint. Pedicle breach is the big issue. So you're seeing that the trocar really in the posterior aspect of the pedicle here beginning to advance and really correct a little more inferior, because our target is really this equatorial line probably about right here. And at mid-pedicle, this is a point where often we would check, we would go back and check an oblique or an AP to make sure that we're still safely lateral to that medial border of pedicle. So you can check an oblique, this is an oblique obviously, but good to also check an AP again, just for safety purposes. And you can't really check too much. I mean, as you get comfortable, fine, but encourage folks to just flip between your APs and your laterals frequently to make sure that you're in a safe position. So now that tip of that trocar is touching essentially just about to enter posterior wall. So at this point, if we were checking the AP, it would be acceptable for that tip also to appear at the medial border of the pedicle because we're gonna enter vertebral body, so you're not gonna breach pedicle and end up in the canal. And there we are where the tip of the tool, the sharp tip of it is in the posterior aspect of vertebral body. The cannula here is seated just at that posterior wall, and that's a good position to be in because the next thing we're gonna do is insert a cutting stylet. So this is a nitinol J-shaped stylet that's gonna help medialize the tool to create a channel over to midline. So unlike kyphoplasty or vertebral augmentation, where you're trying to advance your tool much more to the anterior aspect of vertebral body, we need to get our tool to get to stay posterior to catch that stem of the basal vertebral nerve like I was showing. So this tool gets advanced, and you're seeing that cutting tip here. Obviously in a lateral view, it's hard to appreciate that it's J-shaped and it's curving, but that's what's happening. So as we advance it along, it's starting to, there's an AP view of where we're at now. So medial border of pedicle here, we advance the tool. We're not quite at midline, but we're trying to make our way with this cutting tool to get to midline where the BVN is and back to lateral. This is starting to curve at us, and instead of that sort of long paddle look from a couple of slides ago, where you've got a sort of elongated paddle shape, it's starting to curve at us, and it's appearing a little bit more like a dot as it comes at us from that lateral view. And then we've advanced it past midline. So this has now created a channel where when we place an electrode here, we can, we're right on the stem of the basal vertebral nerve. And so this is a bipolar electrode, one of the electrodes appears very radio opaque. The other is fairly translucent, but you can see it there. And it's creating about a 1.2 centimeter diameter lesion, radio frequency lesion. With a 15 minute burn, there is a new way of doing this. Recently, the technology has been improved where you can do a seven minute lesion, and it still creates a nine millimeter diameter lesion. So if you're spot on on your target, you can actually just eliminate your burn time by eight minutes. But this is what you should see in a lateral view. So, you know, more or less at the equatorial line, that the lesion itself is actually being created at about here. Again, because this is coming at us, some of this is still curving. So we are, I know, I'll estimate maybe we're like 40% diameter, people may disagree with me, but 40% of the sagittal diameter. So that's a good place to be. We could be a little posterior to this. We could be a little anterior and probably be fine given the burn radius, but this is what we want to look at. This is what we want to see. And this is what these lesions look like on MRI. So MRI six weeks later, six months later, this is what these lesions look like. I will say that these aren't, this is actually not one of my patients. And I think this lesion is a little too anterior. I think we'd like to see it more like this one, but something to let your radiologists be aware of if you are starting this procedure, they will think that this is malignancy. So you may, a radiologist may kind of sound the alarm and say, this patient needs an MRI with contrast or to delve into a workup for cancer when they see this, if they're not aware of the procedure and what the sequelae of the burn look like. So essentially, we've highlighted this thoroughly now this morning that we really had this new phenotype of back pain, this sub-cohort, it's a small sub-cohort, but we have what seems like an incredibly promising treatment for it based on what we see in all the published literature, both sponsored and arm's length from industry as Dr. Conger highlighted. And this is quite powerful compared to all the other treatments that classically have been used for axial back pain across the spectrum of physical therapy, multidisciplinary rehab, acupuncture, and then fusion surgery, right, that has, in the surgical world, has classically been used for these patients when all else is failing. And then finally, like I mentioned, it's a pedicle access procedure, so the critical balance here is not breaching the pedicle, but also being able to advance your tool medial enough that you can catch the stem of the BVN. So this is what makes it harder than a kyphoplasty or vertebral augmentation is maintaining posterior final access point, but not damaging nerve and breaching pedicle. The other thing that makes this harder than kyphoplasty is that a lot of these patients, like we saw, I mean, from the trials, the average patient was 51 years old. This is a younger population. It's not an osteoporotic population, and the bone can be incredibly dense, and it requires potentially significantly more hammering. There's actually a tool, a drill that can be used to help get through hard pedicle or whatnot, and S1 in particular, there's often a very hardcore bone. It's not the same. It does not have the same feel as kyphoplasty where an osteoporotic patient makes it much more challenging. We didn't touch on this, but just one last point is that the S1 innervation to the S1 end plate is different from every other level. Every other level, we have that posterior equatorial VVN foramen. In S1, you have two infiltrating branches of basal vertebral nerve that, if I go back as an example, we don't have a great view from S1 here, but it is thought to be at about 40% of the diameter between essentially the end plates, but the body of S1. So instead of being at a 50% midline, we want to be at about 40% of the distance from the S1 end plate, superior end plate, and those two penetrating branches don't coalesce until about 50% of the midline of the material body, so we don't want to be way posterior with S1. We actually want to be probably around 50% to 60% of the sagittal diameter where we're actually favoring being a little bit anterior, and that's our best chance of capturing the VVN after those two penetrating branches have coalesced at the S1 level, so the anatomy is different there. And there are honestly way more procedural pearls that we could go into, but we did want to save some time for questions, and I think we may be over, unfortunately, but I hope that, you know, I think we all hope that that was interesting, that it maybe changes your practice, or how you think about this subcohort of patients, and discover vertebral pain. So thank you so much for your attention. I think we're glad to take questions afterwards. Thank you.

vertebrogenic low back pain

basal vertebral nerve ablation

treatment

physical activity

midline pain

gluteal referral

diagnosing

novel imaging sequences

biomarkers

clinical profile

selection criteria

BVNA