Welcome, everyone. Everybody, good evening. My name is Corey Hunter. I'm the current president of NANCE. I want to thank my very distinguished panelists for coming. I'm sure no one needs an introduction for Dr. Tim Deere. We have Alexa Mora, who is one of our fellows. Also, Jay Greider. And we have Kiran Patel, who's our current vice president of NANCE. So we've had a lot of these over the last year or two. This one is really exciting. We have some great panelists. And I think it's a very poignant topic with some good evidence. So I'm going to turn it over to Dr. Deere. Well, thanks, Corey. And welcome, everyone. I think this is a topic that really is of great interest to me, since I've done quite a bit of research on the topic. That's non-surgical back pain for neurostimulation. And we're going to take a deep dive. We have about 59 minutes to explore this issue. If you have any questions, certainly feel free to ask those in the question box. And we're going to try to get to really the really important points to help you understand this topic better. We're going to kick this off with a dear friend of mine, Alexa Moraria, MD, who is a physician who I met when she was a resident in Miami. Now she's moved to Rush University as a fellow, where I'm sure she's doing a fantastic job with the team there, which is one of the best in the world. And she's going to really kick us off on, what does it mean to have non-surgical back pain? How common is it? And really, what is the ramifications of the disease process itself? So Dr. Moraria, here you go. Thank you, Dr. Dear. I'm just going to go ahead and share my slides. All right, so just to get started, a little bit of background information here. So chronic low back pain is the leading cause of disability worldwide. It affects around 13% of adults in the US and greater than 500 million patients worldwide. The prevalence of chronic low back pain increases with age and is higher in women, smokers, and obese patients. So chronic low back pain acts as a significant societal burden stemming from direct costs associated with health care utilization and indirect costs related to lost productivity. So it can be challenging to treat chronic low back pain due to the multifactorial nature of different etiologies that can cause it. So you can see here in the figure to the right, many different causes of pain generators that can cause chronic low back pain, including spinal stenosis, spondylolisthesis, disc herniation, scoliosis, degenerative disc disease, and facet disease. So in a subset of patients, patients may have multiple disease on imaging with no definitive causation of their symptoms. Although etiology of pain remains elusive, these patients still experience substantial disabling pain. So when it comes to treatment, spine surgery becomes an option with patients with chronic low back pain when it presents with an identifiable etiology or a surgical target. However, many patients present with non-specific chronic low back pain, which is not amenable to surgical intervention. Conservative medical management includes physical therapy, chiropractor care, massage, acupuncture, oral analgesics, and image-guided injections. Even with an algorithmic approach, many of these injections do not provide long-term relief, leaving patients in a repeated ongoing cycle of increasing invasiveness, including repeat imaging and attempts at radiofrequency ablation. So the main topic of today is non-surgical low back pain. What really is this? This term is defined as chronic low back pain, refractory to conservative medical management in patients with no history of spine surgery and who are also not acceptable candidates for spine surgery. So the current treatments for non-surgical low back pain continuum, as it states right now, represents the practice of exposing patients to the least invasive and least expensive treatments for the improvement of their pain, leaving neuromodulation usually as a last resort option. Usually, this can lead to an escalation in opioids and their associated risks, causing detriment to their quality of life. Prolonging unrelieved back pain can lead to deterioration of patient physical condition over time with progressive impairments of function and psychological comorbidities, including anxiety and depression. Intervening with neuromodulation therapies earlier in patients with refractory chronic low back pain may improve patient outcomes with reductions in hospitalizations, clinic visits, and opioid usage. And those are my slides. Thank you. Melissa, that was a really great talk. When you think about non-surgical low back pain, in particular neuromodulation, what would you say would be the best indication and would be the worst indication? Gotcha. Let's start with the worst indication. For neuromodulation, I would say anything that has clear signs of there's a surgical target or instability. I think that requires a surgical opinion versus electroceuticals with neuromodulation. For patients that have multifactorial chronic low back pain, like facetogenic etiology or perhaps a spondylolisthesis of a lower grade, they might have benefit from neuromodulation for chronic low back pain, so more like axial. I want to ask one quick follow-up to that before we go into the next topic. And that is, I think I have a plan. My part two of this, we did many studies, which I'm sure we'll hear from Jay's recording on this, because we're talking about DRG. But one of the things I'm planning to look at next is big data on this issue over the next few years. Because a lot of people were done with non-surgical back pain before the IDE approval. So what's your guess? It's pretty much a yes or no question. You can expand on it, though. Is the big data going to show that we're successful with SCS for non-surgical back? Or are we going to see, because of the heterogeneity of it, it's going to be very difficult? What do you think? So I mean, data is our currency, right? So we can only get better with more studies and understand outcomes with testing this on multiple patients from not just randomized control trials, but also post-market, real-world data. So I believe that my guess is yes, we will see success with neuromodulation for chronical back pain. I hope you're right. I think so, too. I think, Corey, you're going to kick off the next topic. All right, so our next speaker is Jay Greider. He didn't think it was enough to get a medical degree, but he got a PhD and an MBA as well. He's a chief physician executive at University of Kentucky. He's a very well-published gentleman, over 50 publications, I think almost 100 publications to his name. A lot of those are guidelines papers. I've been fortunate enough to help him out with a couple of those. And when I say help, I mean just through the writing where he did a lot of the design. Jay's very well-known, very well-respected in the field of neuromodulation, particularly with intrathecal pump targeted drug delivery. So I think we're going to play a video for him. So we're going to him and I'll comment at the end. Well, thank you. I'm excited to present the data around current thinking around spinal cord stimulation for non-surgical back pain. My name is Jay Greider. I'm at the University of Kentucky and I have no conflicts of interest to disclose at this time. Diving right into the data, we want to begin with a discussion of what is non-surgical back pain. And it's already been gone over to some degree, but it's the etiology that pain has not been identified. It hits about 13% of our population. And I'm going to begin with a systematic review in neuromodulation in 2021. 10 studies, over 350 patients, largely observational and cohort studies. There was a general trend that spinal cord stimulation in surgically naive patients had a treatment effect that improved both quality of life and had an increase in efficacy around pain control. But since that time, there have been several key randomized control trials that have come out that we want to discuss with you today that make the genesis of the evidence that is more level one around what would be the current thinking around treatment for non-surgical back pain. The first one we'll go over is the DISTINCT study. And so this is a durable outcome with a passive recharged burst waveform. So not wanting to use any industry jargon terms, a passive recharged burst waveform. So this study utilizes conventional medical management, 107 patients in spinal cord stimulation, 162 patients. And it's a study that we've done in spinal cord stimulation, 162 patients. And they passed down through a 12 month process to get either medical management or spinal cord stimulation using the passive recharged burst waveform. And the results are compared, which we will go over here in just a moment. So this is a relatively large randomized control trial. Several of the members of this panel are on this, it's a very distinguished and well-designed trial. What we find with that is in the AQUA line for average numeric pain rating score, conventional medical management, the patients continued on at six months having pain of around eight. And then you see the dotted line, which is the allowing of the crossover from conventional medical management to the spinal cord stimulation waveform, where you see a dramatic change and shift in the patient outcome around numeric pain rating scale. Now, the solid black line are patients who received or randomized directly to spinal cord stimulation, and they had an abrupt several percentage point change in numeric pain rating score down to around three. And that was durable over the 12 months of the study, which mirrored the result of the conventional medical management patients once they crossed over. Same thing from a responder rate standpoint, 60 to 70% of patients initially responded with spinal cord stimulation, and that responder rate was durable throughout the 12 months. Very few patients responded in the conventional medical management, but crossover was almost identical to the original cohort of patients that received stimulation. Likewise, in disability ODI, lumbar ODI, you see the same pattern that conventional medical management was essentially non-responsive and then changed dramatically at crossover, whereas the spinal cord stimulation group had durable results from the initial baseline to the three-month period. And the crossover was, again, the same from a responder rate standpoint, suggesting that not only was the effect effective initially, it was durable for 12 months, and patients who were treated with conventional medical management could have a significant change in their overall pain, suggesting also the conventional medical management is not all that successful, which we all know. The second major study that we wanna focus on is using 10-Hertz stimulation, the capital group and extension of the SINSA trial. From 12 months out to 24 months, 159 patients randomized to conventional medical management, or 10-Hertz stimulation. You see that they passed down through the three-month endpoint, the six-month endpoint, at which point there is also crossover in this study. You see that 121 completed the 12-month study, 98 went to completion at the 24-month study. At six months, patients could cross over, and 67 conventional medical management patients did so. 56 of those went to implant. So a very similar sort of concept to the distinct study. Let's take a look at what occurred. You see, again, visual analog results from 7.4 as a numeric pain rating scale, down to, or as a visual analog scale, down to 2.2, which was durable throughout the 24 months of the trial. You also see the responder rate, again, at around 70 to 80%. That was consistent across the time. And here you see the number of profound responders. 58% were profound responders, 81% total as responders, with a very low non-responder rate. 159 patients randomized. And again, there was that crossover at six months that was allowed, which created a fairly significant number of responders and a very low number of non-responders. Same thing again with ODI, Lumbar Oswestern Disability Index. You see that the number of responders, 72%, whereas the number of non-responders were relatively low. And again, several patients had very profound ODI changes suggesting that they were highly debilitated and had effect. But a 10-point ODI change is significant. And you see the dropped horizontal line there suggesting the responder rate at 10-point change on the ODI. Even several of the non-responders had movement that would be improvement in many clinical settings, but strictly by the guidelines of the trial criteria, a 10-point change is what's statistically significant. Now, how do we exclude or include? So patients that were presenting with moderate to severe back pain, plus or minus leg pain, the clinical examinations were ruling out the exclusions. And the conventional medical management options were exercise, the typical things we do, physical therapy, steroid, nostril injections, activity lifestyle modifications, radiofrequency ablation. They were excluded if they had an infection, fracture, tumor instability. If there was a surgical candidate, they moved into spine surgery. And if they were not a surgical candidate, again, non-surgical back pain, high-frequency stimulation was trialed. A lack of clear surgical target was one of the main issues or a high risk for surgery or the patient just declined surgery. So this is a real world setting again, where we have patients that don't want surgery under any circumstance, and can they get durable relief? Are there high risk for surgery or there's just really not a clear target? Now, finally, in this series of three trials that we wanna go over, we have the EVOKE trial, which is closed loop or later on you'll hear it described as fixed output spinal cord stimulation for non-surgical clinical low back pain patients. 134 randomly assigned, 67 to closed loop. 67 were then also assigned to open loop or fixed output, as we'll see in the El Dhabi review in a few moments. You see 62 and 63 went on into primary therapy. 59 concluded the 12 months of spinal cord stimulator. 59 were included in the other arm of the study. And looking at the data around that, you see overall that back pain secondary to, back pain hierarchical secondary outcome in the closed loop group and the open loop group. Here, 72% back pain overall relief, 57% in the open loop group. VAS responders, 82%, 62%. Back pain reduction, 81, 57. Leg pain reduction, 81, 68. Overall, the back and leg pain reduction, 58%, 43% at three months. Going along into the 12 month group, you see continued widening of the treatment effect, durable on the fixed output group. In the open loop group, it was a little different at 37%. So here you're starting to see a description of some of the older waveforms with a fixed output versus the closed loop and the suggestions around how that may be perhaps more effective. And that was highlighted in this systematic review, which was just released by Aldabi. This is ahead of print. So this is information that is available. It's not yet in print form. And the findings of this systematic review suggest that closed loop spinal cord stimulation and fixed output spinal cord stimulation are both superior to conventional medical management. So you remember the distinct study and the SINSA study both compared to medical management and found that spinal cord stimulation, whether it was a passive recharge waveform or a 10,000 Hertz waveform was superior to conventional medical management in nonspecific clinical low back pain. But this trial looking at the evoked study suggests that there is clinical evidence that there are advantages of the closed loop over fixed output. As a matter of fact, within that evoked study, it used language, which was a little bit interesting. They said that evoked stimulation dominated the fixed output stimulation, which suggested they looked at several parameters and had the response rates and were able to compare the data statistically. And the conclusion of the Aldabi group, again, of which several of our members are on that study as well, suggested that the closed loop had clear advantages for clinical low back pain that was non-surgical in nature. Now, also in the NASS journal just recently published, looking at the waveform differential targeted multiplex stimulation, this was not included in the Aldabi systematic review because the data is just evolving quickly as we speak. This is a 12-month randomized controlled trial, 121 patients, non-surgical back pain, DTM versus conventional spinal cord stimulation with crossover. 14 patients were allowed to crossover. You see 121 randomized, 51 test subjects completed the DTM spinal cord stimulator, 54 subjects with conventional spinal cord stimulation. So the evoked trial was closed loop versus fixed output. This is DTM waveform versus conventional spinal cord stimulation taken out to 12 months. And again, you see that the DTM waveform has at three months, six months, nine months, and 12 months, a durable effect of response on clinical non-specific, non-surgical low back pain, however you want to describe that, versus conventional spinal cord stimulation. And you also see the VAS scores in red, the conventional spinal cord stimulation did have a treatment effect, and it was found to be less efficacious than DTM spinal cord stimulation. Again, all of these advanced waveforms for clinical non-specific, non-surgical low back pain, moving from around seven to eight, down to one to two to three and a half, somewhere in the VAS range, and the DTM study shows a very similar type of outcome, and that was durable over 12 months. Also want to describe, those were four new randomized control trials and a systematic review, looking at three of those randomized control trials. There's also a recent observational study that has come out, just want to make sure, so we not only are talking about randomized control trials, but observational studies still point us in directions and give us good information. So here's an observational study by Mons et al, using Burst-DR. 19 subjects were enrolled with discogenic back pain. They were found to be discogenic because they were negative for posterior column or for SI joint issues, so they're thinking it's anterior column pain, as we're learning more about anterior column with other treatment modalities. Focusing on discogenic back pain and becoming better at diagnosing that is key for us. And so within this study, the 19 patients were enrolled with not posterior column pain or no SI joint pain, and 13 made it through to the 12-month follow-up. And in that study, numeric rating scale, at the end of the trial, at three months, six and 12 months, there was a movement from around 75-ish on the numeric rating scale. Of course, at the trial, you have the trial effect. We often see that where the trial weren't great, it's not quite as good as the trial, Doc, but here we go. It's a significant treatment effect. And using the ODI here, we see, and I like this because it spells out very well, the 10-point change that you see with ODI. Well, at 100, this is bed-bound, cripple, severe disability, moderate disability. This lays it out very nicely so that you have some sort of a picture of what's going on. Moving from an ODI of 40 down to 20, again, a 10-point move is clinically and statistically significant. This is almost a 20-point move, moving from the borderline of severe to moderate disability down to minimal disability, which is what we would desire for many of our patients. So in this observational study by Mons for dyskogenics specifically, that's why this is important, non-surgical back pain can be a lot of things. Facet, it can be, you know, even SI is in there, but to focus in on a signal for dyskogenic back pain is, in my mind, important, and that's why I included it in this review. So in summary, there appears to be a treatment effect of advanced spinal cord stimulation waveforms on chronic non-surgical back pain. And of course, you know, the target, we've been talking about this for years, but T8, T9 seems to be confirmed in these randomized control trials as the target. So from a clinical standpoint, that's where you wanna be landing, and that's where you wanna be stimulating. Newer waveforms do appear to have greater treatment effect than conventional spinal cord stimulation and conventional management. So taken on the whole, the data that we just presented would suggest that conventional spinal cord stimulation and conventional medical management, there are advantages over any of these advanced waveforms for nonspecific back pain. So it's a treatment option for any patient that is not desiring or is high risk, or you just can't find the etiology, and since that etiology is unclear, a good surgeon won't operate. Now, the systematic review by El Dhabi suggesting that closed-loop may have a significantly greater treatment effect, the data presented in that systematic review is convincing, but I think in fairness and in balance, there probably needs to be a little bit more work done on that before the strength of the statements made in that systematic review can be fully validated. I agree that based off of that one comparison of the Evoke study to the other two studies in that review, there does appear to be a robust treatment effect, but I think we would wanna verify that with a little bit more time. So I think I would treat that as a good, strong signal and something to strongly consider in your patients if they, for some reason, did not have an outcome with fixed output, advanced waveform stimulation, you could consider retrialing. I think that you would be able to go to payers and say, I think that there's a good reason to continue on. And that is our presentation. Thank you very much. Jay Grad, you're doing a great job there for us. Corey, just a quick discussion point before you announce Dr. Patel. He mentioned dyskogenic pain. I'm not sure the methodology there was great as far as discovering it was a definitive dyskogenic pain, but that was pretty convincing. And as well as the other distinct Evoke and Senza all had dyskogenic patients in there. Do you think the future is biologics and autologous nucleus pulposa and BVN, or is the future for dyskogenic or vertebrogenic pain SCS? But what's your initial thought? So I was on four of the clinical trials right now for biologics. Ultimately, I think the patients will kind of veer towards the idea of like, they can fix it. Whereas, I mean, but it's gonna be hard to get that over the hurdle of like advocacy and getting it like approved by insurance companies, because it's under like a really, really high threshold. So I think for like long-term, I'd like to see it go towards biologics, but I think like for the short term, and I mean, probably the next 10, 15 years, we're still gonna lean on neuromodulation. Great, no, I tend to agree. I think both will be very important and more studies are needed in biologics for sure. And we're gonna do those. So that'll be important, I think, as you pointed out. Our next speaker is a really great speaker. Corey's gonna introduce her, and we're gonna hear a little bit about the other neurostimulation for low back pain. So I'm really pleased to introduce my very dear friend and colleague, Dr. Karen Patel. She's a vice president of NANDS, has served the society for as long as I have. She's the fellowship director for the fellowship at Lenox Hill Hospital, which is right down the street from me. And I think everybody knows her work and her passion for neuromodulation, particularly DRG. So with that, I'm gonna turn it over to my friend, Karen Patel. Thank you so much, Corey. And thank you so much for the NANDS webinar committee for having me here tonight with this wonderful group. I'm just going to get my slides up here. All right, so, you know, as Dr. Marrera just shared with us, there's a significant disease burden of non-surgical lower back pain in the United States. And for all of us who are tuned in, who are part of the pain treatment and spine care treatment pathway, we know this from our day-to-day work. And Dr. Greider just did an amazing presentation about big data for SES. And I'm gonna turn it over to Dr. Greider for SES, you know, a particularly highlight in the Aldabi systematic review that's recently published or about to be published and available. It suggests that, you know, for conventional waveforms of SES, there is evidence that, you know, SES helps significantly for non-surgical lower back pain. And whether, you know, how closed-loop functions into that, you know, remains something to consider as well. But what I'm gonna share with you is kind of, you know, we don't have a large data looking at the use of dorsal root ganglion stimulation in for non-surgical lower back pain. But what we do have are small cohorts of very significant data, which certainly suggests that we should look more closely at this technology as a way of alleviating non-surgical lower back pain. So I'm gonna start the story with our colleagues Europe, who first were using L2-DRG stimulation for the treatment of axial lower back pain. And Dr. Hegan in 2018 published the use of stimulation at the L2-L3 dorsal root ganglia for the relief of lower back pain. Oops. These were 12 patients who had non-rating lower back pain and some who had lumbar radiculopathy. They had leads placed at L2 and L3 and were followed for 12 months. And they found that, you know, on average there was a 45.5% decrease in VAS and similarly improvements in mood and quality of life. This then led to the work of CalWord, which looked at patients who had a diagnosis of failed back surgical syndrome following discectomy. I present this because it's kind of the, you know, the real genesis of how we've come to use dorsal root ganglion stimulation for some of us for the management of non-surgical lower back pain. So these were placed at L2 and these patients, these 12 patients, the average decrease in VAS was 72%, an improvement in ODI by 58%, 38% improvement in EQ 5D and a 94% increase improvement in POMS. So this then led to the work again of CalWord looking at a prospective study of dorsal root ganglion stimulation at L2 for non-operative discogenic lower back pain. So at this point, you're probably wondering why L2? And as was I, when I read many of these articles. And so the premise is two things. One, that the anterior elements of the spine, the vertebral bodies and the vertebral discs are innervated by the sympathetics and that the sympathetics converge at L2. And so this is the premise which led our colleagues in Europe to use L2 to try to alleviate back pain for those who had had failed back, but then also those who had non-operative discogenic back pain. So this was 15 patients and these are patients who had a negative response to medial branch blocks and concordant discograms. They were followed for 12 months. Their average pain relief was 68.3%, an improvement of ODI at 58%. Their EQ5D and their POMS improvement was pretty significant 141% and 101%. And again, these improvements are pretty substantial. Small number of patients, but substantial. So I include this here. You know, this is commenting on the Sir Alexander Fleming on the discovery of penicillin. So he actually had left some plates and went on vacation. And when he came back, he noticed that this particular compound had led to a significant decrease in bacteria and this would then become penicillin. And so what I would say here is that there's serendipity in science. And so similarly, a bunch of the physicians in the United States actually kind of had a very similar situation. We had patients who we were replacing dorsal root ganglion stimulation at T12 and L1 for post herniopathy, groin pain, CRPS type two symptoms. And we found that when we program these patients, they often also said, hey doc, my back pain is better. And so it wasn't quite the discovery of penicillin, but this is quite a unique opportunity to also provide stimulation and pain relief to the lower back. And we found this with placement of leads at both T12 and L1. And so a group of us in New York actually published a case series. This was some of the earliest publications led by Dr. Kenneth Chapman. 17 patients, a median follow-up of 8.3 years. And what we can see here is that of them, about a third of them, five of these patients had low back pain alone and had not had any type of spinal surgery before. And what we found in this group is that greater than 50% of these patients had more than 80% pain relief and their average decrease in VAS or improvement in VAS was 76%. Similarly, we had substantial improvements in EQ5D as well as SF36. And then this was also mimicked in the improvement in ODI. At baseline, the majority of patients were at either severe ODI, and then at their last follow-up, they had less than or equal to minimum scales on the ODI. And the average improvement was 78%. So other outcomes were looked at. The number of interventional spinal injections decreased as well as their opioid usage for some of the patients. And there are some of the adverse events that were associated with this group. So moving forward, another study published in Neuromush was looking at the use of T12 as a salvage therapy. And with this, I would highlight that 32% of these patients of the entire group of 60 patients, so more than half, had leads placed at T12. And of those, four of these patients were those with non-surgical lower back pain. Again, the primary diagnosis, CRPS, failed back syndrome, but some of them with no surgical lower back pain. And some of them with non-surgical lower back pain. And they had tried and failed other systems before, tonic stimulation, birth stimulation, high frequency. And what was found is that the NRS for this group decreased on average from 8.7 to 3.8. That's a 56% reduction. And the ODI improved as well. Patients moved from crippled to moderate. EQ5D increased, an overall 77% improvement. We saw that there was also an improvement in morphine milliequivalence. So moving along, another excellent work by Dr. Ken Chapman was the publication of looking at T12, dorsal root ganglion stimulation at very low frequencies. These were 20 patients, some which had lumbar transfusion, two which had laminectomy-discectomy, but 10 of which had non-surgical lower back pain. And what was found here is that there was an improvement in their VAS of 77%, an improvement in their ODI of 72%, and 145% improvement in their EQ5D, as well as a significant improvement in their morphine milliequivalence reduction from 87 on average to 43, as well as a significant improvement in the number of interventional spine procedures performed. The same group also published looking at 11 patients, six of which had failed back surgical syndrome, and then five of which had non-surgical lower back pain. And so similar improvement, a VAS improvement of 77%, ODI improvement of 62, EQ5D 80%, MCS 24, and pain catastrophizing of 104%. In addition, there was normalization of pain pressure, mechanical detection thresholds, and conditioned pain modulation. This suggests that possibly this particular type of treatment may have elements of capturing both nociceptive and neuropathic pain, which is something that hasn't quite been explored in traditional neuromodulation. So if we look at all of the data that was looked significantly, specifically only at non-operative back pain, non-surgical back pain, we should look at the CALWERT study and the MON study, but why is it worthwhile looking at both L2 and T12? And why do we think T12 has any efficacy? Well, we think that the lower back is innervated from the dermatomes of L1 to L5, and the anterior elements do send the sympathetic afferents to L2, and that the skin and subcutaneous tissues are innervated by T12. So at T12, what we find is that there's a convergence of the deep lower back pain fibers that enter the source track and ascend laterally, and then combine at their designated levels to the T12 afferents, including L2 and others. So not only are we able to potentially capture pain that may have some type of pathology in the anterior column, but potentially also in the posterior column. So as stated, non-surgical lower back pain is a significant disease burden worldwide. There is some compelling, small, but compelling data that T12 and L2 may provide reproducible and very effective treatments for non-surgical lower back pain that hasn't been responsive to other conservative therapies. And based on the small observational data, I think a high quality, adequately powered, randomized controlled trial is certainly relevant to look at the benefit of dorsal root ganglion stimulation compared to conventional medical management and possibly even dorsal column stimulation. Thank you. Fantastic job. I think the question I have for you, Karen, as you know, you present a great overview and you and I think a lot alike, as you know, and we have both an affinity for DRG. Why wouldn't we do a study at T12 and L2, so four leads? And I guess the question would be, if we do that, what would you think the comparator should be? Should it be medical management as we did with Distinct? Should it be, you know, another device like we did with Acrit for DRG? What would be the comparator in your opinion? I think at baseline, I think conventional medical management, I'd actually like to see it where we have three arms. I'd love to see that, you know, and even potentially in a way that we can do it with sham control, right? These are, there are many therapies that are, you know, sub-perception, sub-parasthesia, and should be run that way. And I think that there's a potential to have those three arms and then potentially even have them with a sham arm as well to really look at that effect. And I think that would be a really robust trial to answer a lot of questions that we have. I think Corey and I both are ready to sign up to join your study. Corey, you have a question for Karen? Yeah, so I was going to ask like just what your experience has been with T12, DRG for like discogenic pain and vertebrogenic pain, like with those patients, I know you do a lot of BV anteblation. Have you had any patients who have failed it and then you've tried T12 on? You know, it's interesting, patients who, so I love B, you know, basic vertebral nerve ablation. I find that it's quite efficacious for the patient who is symptomatic from that. But it is so common that we don't find patients who just have vertebrogenic pain, right? They have elements of so many other things, but it is not something that necessitates a surgical intervention, right? None of our surgical colleagues would say, yes, definitely, that's the target, I'm going to fix that. For those patients, I do think that there is a significant role for T12 because it captures not just one pathology, there's multiple patients who respond to this therapy because it really helps with, you know, elements of both posterior and anterior column paint. Great job. I think that was a wonderful summary. Thank you so much. It's a wonderful addition to the webinar. Corey Hunter will be our last speaker of the night. You heard about BVN, you heard about autologous injection of nucleus pulposus cells, you heard about other injectables, but there's an algorithm for discogenic pain and non-surgical low back pain. Corey's going to finish the night talking about the algorithm for neuromodulation for non-surgical back pain. How do we get there? Corey? Thanks, Tom. When I thought about non-surgical low back pain in the beginning, this was something that when being a part of a lot of clinical trials, I didn't know what the big deal was about why people were trying to gather data on it and parse it out in particular, because we all do it for it. We've been doing it. It's not just CRPS and failed back. We're always doing it for non-surgical low back. What was the big deal about getting data on it? Then I started getting more involved in the AMA and CPT, reimbursement and advocacy, and seeing where the space is going. Unfortunately, with payers now, they're asking for neurosurgeons or spine surgeons to sit there and look at a patient and say, are they not a surgical candidate? You have to jump through all these steps. I applaud the companies for putting together this data, because it's something I never really thought that we'd need, and we need it now more than ever, because they're not covering this therapy when we know it works. Even a lot of other things that we do that are specifically indicated, and we'll go through that. Data, as Tim mentioned, big data, it's really important. I think just even more so publications like the ones that Karen showed you that she did. Physician-driven, physician-initiated studies are even more important because of the whole concept of bias, and we're really just trying to ice skating uphill against payers. There are a lot of non-surgical indications. I'm just going to highlight these four in particular. Facetogenic, vertebrogenic, discogenic, and also multifiditis function. So the first one, facetogenic, no pain doctor really needs a lesson in what it is. This is our bread and butter. How do we define it? I'm sure there's a lot of different ways we can define facetogenic pain. I think most of us would agree on the fact that it's axonal non-radiating pain, worst withstanding an extension. If all else fails, you do your medial branch blocks, and you do your rhizotomy. I think we all believe it works a lot better than what it does. It does work. It works really, really well. I'm not saying it doesn't, but I think that we have a bias. What do we do when it doesn't work? Because there are other patients it doesn't work on. So when we think about data for RFA, I think we take it for granted that there's data to support because it's so widely approved. In reality, there's not a huge amount of data on it, but most of the data that's out there is either traditional RFA in isolation or comparing traditional RFA to pulsed RFA. Overall, if you parse together the publications that are out there, the five publications or the six publications that are there, it has about a 60% efficacy rate. That means 60% of patients will get 50% or more pain relief going from six to 18 months. This is an aggregate of five publications. I'm sorry. Then the average amount of patients is 145. This is what we hang our hat on with RFA. Again, it's 60% efficacious. The other 40%, what do we do? Now, next, vertebrogenic pain. This is something that's been, I think, before five or six years ago, before the concept of BV anablation, no one knew what to do with this. I don't think even most of us in our field never even knew that it had a name. This has now obviously been popularized by the fact that we can treat this. Now we're thinking about it. I'd ask Karen, I think it was a couple of months ago when I was starting to do this particular procedure, how do you identify it? I was asking Tim, how do you identify these patients? Because it was something admittedly we never covered in fellowship. Similar to facet pain, it's excellent on rating, but the differentiating factor is worse with flexion. One of the things that got tattooed in my brain is the concept of patients sitting down, bending forward to tie their shoes. Now we're looking at MRIs and we're looking at something called MODIC. MODIC changes, we look for type one or type two, and we go to the concept of basal vertebral nerve ablation. If that doesn't work, what then? These are some pictures of type one and type two. I'm not going to agonize over those, but this is what we look for in the MRI. A lot of times, radiologists won't comment on it, even if you mention it. If this is something that you're doing, I'd encourage people to read their own MRIs. Looking at the Correggie study of 2021, defining a responder as greater than 50% reduction in pain, which is something we do across the board in our specialty as something that's a success is defined as greater than 50%. It was almost three quarters of the patients were responders with almost a third of them pain-free at two years. That's pretty phenomenal just in general for something that if you were looking at the 1980s or 90s or early 2000s, these are people that would just be subjected to opioids. Now, not only is not that the case, but you can tell the patient you have a one in three chance of being pain-free. Again, a combined responder rate, defining that as an ODI improvement of greater than 15 or a vast reduction of greater than two as 73.7%. Three quarters of the patients will do very, very well with this, and then a quarter don't. What do we do then? We get the next one, discogenic pain. This is something I've been a part of for the last 10 years with the clinical trials that have been out there. There's only been four RCTs. I've been on all four of those. The idea is looking at the idea if you can regenerate the disc. Now, when I was in fellowship, the IDAT was starting to wind down, and that was really the last of the mechanical ideas of way to treat the discogenic pain. Discograms have been around a long time, but this has largely been the white whale for our field is how do we treat discogenic pain, and how do we define that a positive provocative discogram and a modified affirmative three to six on MRI. With this, we do our discogram. We look. That has to be a provocative discogram where you want to do a comparator, but you want to be careful with your comparators. If you look at the carriage study, patients are going to, if they have a normal disc, now you stick a needle in it, and it comes out normal, you can tell a patient more than likely now that's not going to be a normal disc. If it comes out to be that, we're looking at down the road. There is one product that's out, but the other ones are all coming probably a little ways behind intradiscal allograft. Biologics is something that I've done a lot of work on ever since I was out of college, and this has been something people have tried for a very long time to make it, to figure out how to get stem cells and allografts to work inside the disc. A disc is a very, it's like a toxic space when it gets to this point, and it's a void. It's like being in the middle of outer space. There's no nutrients. There's poor blood supply. If you stick cells there, how are you going to get them to survive? The difference between a lot of the companies is they're all using different forms of mesenchymal stem cells, and then using different, the special sauce is like the gene sequencing or the way they transfected the cells, how they express themselves, and then the scaffolding. One of the products that's out now doesn't have cells in it. It's just a micronized nucleus. You stick it in there, and the idea is you can just replace the product inside, and the body will know what to do with those pieces. Two of the other ones that are out there are using an organic scaffolding, which is kind of the trick, is you want to get the cells to know what to do. If you just stick stem cells in an area without giving them guidance, they're just going to become fibroblasts, and it's essentially a scar. How do you get them to become meaningful cells, and then arrange themselves in a meaningful fashion so cells just don't look like a blob on the floor? They have to line up like a honeycomb, or however it is in that product. This one study, Doug Beal was the primary author on. I was on it with him. This was studying the micronized disc nucleus, and it showed a clinically meaningful reduction of ODI greater than 15 points. In this study, the one that was differentiating this from the other two is that patients could have a positive disc at two levels, where the other studies, they could only have a single positive disc, and they can only be treated at one level. If we think about our patients out there, two discs is probably a lot more likely than just having a single degenerative disc, not to say that people don't have just one. I have just one in my L5S1, but if we look at this as about three out of four patients were responders in ODI, which is really, I can tell you as someone who suffers from degenerative disc disease, function is what gets you the most. I've seen that we have three quarters of the patients had greater than 15 point improvement in ODI at 12 months is very, very meaningful, but what do we do for those other one quarter patients? So, taking these three and parsing them out, we can do spinal cord stimulation. So, Jay highlighted a lot of the evidence. I'm not going to just, you know, redo it again, but I just want to highlight these three publications. It was the one with the distinct study, the Patel study, and then Eldabeh's study on high frequency. So, just one of the main points, and I'll start with distinct. I mean, this was just a very, very well-designed study, and I just want to make sure that's important to note that this was the burst waveform as defined by Dr. Ritter, which has like the recharge, and people, I think, at this point know the difference, and then the 10,000 hertz study was where really important was talking about cost-saving analysis. So, what people don't realize is that conservative medical management, while payers will sit there and say, like, that has the best evidence, it has more evidence over spinal cord stimulation, conservative medical management is expensive for these patients, and it's not just, you know, coming to get injections. They're on a lot of name brand medications, like pregabalin, duloxetine. They're getting their opioids. They're coming in. So, these patients are very, very expensive. So, this is where spinal cord stimulation, this really does, it's a preservation of healthcare dollars. We're helping save patients because conservative medical management doesn't work that well. It's something we all know, and then lastly, go over some data from the closed loop. So, not to completely rehash this, but again, this was a very, very well-designed study. So, looking at the intent to treat analysis, which is taking all the patients together, it was about three out of four patients had a greater than 50 percent reduction in six months compared to conservative medical management, which was in the single digits, and we also had statistically significant improvements over conservative medical management, NRS reduction, OBI, pain catastrophizing, and the PGIC score, and then highlighting PGIC at the end, in particular, it was three out of four patients reported feeling better or a great deal better versus two and a half percent. We'll look at the high frequency study, the Patel study. This one was really important in the fact that, like I said, it mentioned the cost savings. So, it's defined as an acronym called ICER, or I-C-E-R, which stands for incremental cost effectiveness ratio, and they show that the patients at three months, or I'm sorry, at six months had, I'm sorry, it was three months, it was almost $5,000, and then this was a crossover study. So, the patients that crossed over at six months, just at six months, it was saving them about $8,000. So, it was almost double that. So, it's something that we all know from the studies that were done back in the day that if you take the lifetime of the patient and you look at a spinal cord stimulation, it's cheaper than conservative medical management. That was a retrospective study from one doctor in their practice over like a decade or two decades, but this is a prospective study to formally analyze that, and again, so you see that there's almost three out of four patients on the PGIC score reporting to feel better or a great deal better. So, again, this also highlights now not just one waveform, but now a second waveform showing that conservative medical management just doesn't work for these patients, and not only does it not work, but there's something glaringly obviously there that we can do in the form of spinal cord stimulation. And then lastly, looking at closed-loop stimulation, I was on this clinical trial, the evoke one, and this is a sub-analysis pulling together two studies, the evoked double blind RCT and the Avalon prospective single arm study. People sometimes ask, like, how can a spinal cord stimulation study be a double blind RCT? So, when we were on it, the patients didn't know if they're going to be closed-loop, and the doctors who were the implanters didn't know if they were closed-loop. We didn't find out until after, so there was no, they eliminated as much bias as they could. It showed that 40 percent of the patients reduced their opioids. This is something that I always really enjoy seeing in publications. Prescription drug abuse is something that I saw firsthand in my own household. So, seeing patients be able to get off their opioids is really important. So, it doesn't really mean anything if you can get a patient, they're vast down to nothing. If they're still taking oxycodone, we really haven't won. Looking at things like the EQ5DL, 70 percent of patients got significant improvements, and then 83 percent of patients show statistically significant improvements in ODI, and 63 percent reported significant improvement in sleep. And then lastly, multifidus function. This is also something that's really been brought to the forefront over the last, like, four or five years, solely due to the fact that we have a therapy for it. You know, you ask any radiologist, you know, what do multifidus muscles look like? They all know what they look like, but you ask them the last time that they commented on them on an MRI, they'd probably say never. So, this is something that's really just taken our field, I think, and put it on its head because it's something we never considered before. Again, axial non-radiating pain, so that's really just a common thread through all four of these with non-surgical low back pain. And how do we test it? So, there's the PITT test, AMT test, and multifidus lift test, and that's how we identify in physical exams. So, if we're thinking about with facet pain as the MBBs and the discogenic pain as a discogram, those are your tests right there that you look at. And then ultimately, you're going to look at the MRI, you're going to see the degree of multifidus atrophy or fatty infiltration. So, what do we do for PNS? So, we do multifidus stimulation for it. The leads essentially go right where we would put our cannulas and our probes to do radiofrequency ablation. Some advocates of the therapy of multifidus stimulation believe that people getting repeated RFAs over the course of their life will end up rendering this sort of multifidus dysfunction. So, it's not to say that we don't do it or that we shouldn't do it, but maybe this is why over time the RFAs start to fade. Or maybe it's a reason why when we do medial branch blocks on patients, they do better, but the RFAs don't work. Or maybe this is those 40% of patients, so we said it was 60% of patients will be responders to RFNs, 40% doesn't work. Well, like I said, most of us were never looking at the MRIs to look at the multifidus. So, this was a phenomenal study, and the fact that it went out to five years. There are very, very, very few studies in spine and or pain that go out this far. So, the fact that it went out this far and anybody who's familiar with the study shows that this is not only an efficacious therapy, but it's a durable therapy and it lasts out to five years. And over the course of the first year, the second year, the third year, it continued to get better. The only other time we saw something like that was in the evokes trial when they followed up to three years, the patients continued to get better. And here we see 71.8% of the patients had a reduction of greater than 50% ODI, and this is out to five years. So, what happens if this fails? Well, then maybe we can try any one of the other things we mentioned before in high frequency burst or closed loop or any other therapy that's out there that can show to be durable with these patients with non-surgical low back pain. So, this is, I think the next big kind of field for us is like just looking at this non-surgical low back pain and kind of taking on these patients that if you, this were the 1980s or 1990s, these patients would end up on a lot of opioids and they would end up getting surgery anyway and they end up getting a pump. So, now we have something to offer them and we have evidence to support it. Thank you. Great, great job showing the evidence and all the new things and technology is pretty staggering. We have time for one question. The question is this, if somebody has multiple comorbidities, for example, Distinct had the average 60% of people had three diseases, you know, facetogenic, discogenic, stenosis, you know, a lot going on there. Do you have to treat everything first before you get to neuromodulation or do you ever go to neuromodulation first? I think what you said, I mean, going to neuromodulation first because that's what I was like was asking Karen. I have a patient right now that's, when she has a discogenic pain and vertebrogenic pain, I'm sitting there like as I'm talking to the patient and it's like, you know, maybe we'll do the discogenic pain first and the vertebrogenic. And then at the end of it, after I was trying to talk her into like the plan to support it, I ended up talking myself out of doing it and just recommended doing spinal cord stimulation for it for the exact reason. Cause that's, you know, throwing spaghetti at the wall to see what sticks. And then you have this therapy that we've all gotten so used to using it for everything. And then we see now that we have the evidence to support that. So rather than, you know, treating a patient with three or four different procedures, which, you know, they're minimally invasive by themselves, but you want to stick a needle in a disc and then stick a trocar on the pedicle and you do a couple of things, or you could try one thing and do a trial and see, and it's less invasive and you may just end up in the same place and much, much less steps. Yeah. And I think the other great thing is that, you know, you're going to have someone who has a device who's doing well and still treat some other things that evolve. So there's no reason you can't do them in a multimodal fashion with that. Thank you everyone for joining us. I think it's been a great discussion and we're right on time at 9.30. And Corey, a final word? Actually, now our panelists are back. A final word from you, Karen, before we close? Sure. I think, you know, I think it's important a takeaway is that, you know, the perfect patient who has one pathology really rarely exists in the real world. And I think it comes down to asking the patient and trying to look at their MRI and find out what's the loudest voice, right? What's the loudest voice in the room? What's the thing? If there's something that's screaming, you know, vertebrogenic pain, if there's something that's screaming discogenic pain, you know, take note of that and look at the evidence-based therapies for that. But for many of our patients, it's a combination of a lot of things. And I think in that case, neuromodulation, you know, whether it's SCS or DRG, I think it's great options. Wonderful thoughts. Alexa, any final thoughts? Yeah, I, you know, really excited to hear Dr. Patel's, you know, idea for a future study comparing even conventional SCS with conventional medical management versus DRG. And he described it so well with basically sandwiching effect of T12 to F1 for chronic low back pain. I'd love to see that study and looking forward to more studies to add and build upon our resources as pain doctors to treat patients with pain, so. Absolutely. I think, hopefully, as people watch this broadcast later on social media, we need more funding for all those studies. I think that's very important. Corey, last thought? I just want to thank you, Tim, for putting this together. This is a great presentation. You really, I think, hit the point home with the assignments you gave us and really kind of educated our audience. So thank you for that. I want to put in a plug for two meetings coming up. We have the Aspirin Collaborative Pain Summit that's going to be coming up October 11th through 12th. It's going to be at the Grand Hyatt in Nashville. And then the NANS annual meeting, which is going to be in Disney's next year at the end of January. So I hope to see everybody there at that. So with that, thank you so much, everybody, for making the time on a Tuesday evening to learn about this important topic. See y'all later. Thank you very much. Bye. Thank you.

neuromodulation

chronic low back pain

Corey Hunter

non-surgical treatments

neurostimulation

spinal cord stimulation

dorsal root ganglion stimulation

randomized control trials

pain management

medical innovation