All right, everybody, good afternoon. I know that it is the last day of the AAPMNR. I didn't see anybody raising their hands when the slide was up. It said, raise your hands if you're with PMNR. No one's raising their hands still, but that's OK. I appreciate everybody staying a little bit late. This is the last day of full lectures, and we're on kind of the tail end. So I appreciate you being here. I appreciate you being at least modestly awake for us. The hope that we have for this particular next hour or so is to give everybody an understanding, maybe an insider's look, an insider's view, as to what three people who have been practicing this field for quite a bit think about what's happened to our field, what's happening to our field, and what may end up happening because of those changes. The title of the talk is the future of pain and where are we headed. I'll start off, and I'll just answer that question. And I'll have my colleagues here in this set of slides that I have here hopefully fortify that. And that is that we're headed into a world of percutaneous surgeries. I think some of you or many of you were already in talks yesterday about billing and coding and epidurals and radio frequencies. And the challenge that many pain practitioners face nowadays is billing slash compensation. Billing has become more difficult. Mike can tell you that. Mike just walked in. He's been doing this for forever. Collections have become much more challenging. And because of those things, research and development have pivoted. Due to the challenges of repayment, or payment rather, the world of pain medicine has become more in this percutaneous surgical phase, where spinal cord stimulators, which I think many of us know about, still exist. There is more research that's been developed and continuing to be developed into defining what these are from a translational medicine point of view, and then bringing that into the clinical forefront with clinical studies. Those are the things that are needed. There are sacroiliac fusions. There are percutaneous intraspinous spacers. A lot of the energy and a lot of the money that industry is putting into the space is primarily because physicians have become dissatisfied. Patients have become dissatisfied with some of the treatments that we've offered in years past. Now, I would argue that a lot of those things work, as long as you know how to select your patients. I think even with the talk today, we still have to understand that art. And I think that everyone in this room is primed to be able to do that. And I don't think many can say that, but I think that the people in this room and the people in this community can say that. That's where it begins. I'll give you a short story. About six years ago, I was working with a company called Virtos, which some of you may know of. They're the group that developed minimally invasive lumbar decompression. And they asked me to partner with them to get them a cat one code, a level one code. And I believed in the product. I still believe in the product. I do not have any consultant disclosures with that group. But I said, you know what? I think that this is where this field is going to be in 10, 15, 20 years. And it has. And it's unwoven. And it's unraveled to be that. They were having struggles with getting their cat one codes. Medicare then went to the company and said, look, we want you to put together a study, which we will oversee. We will subsidize it. And based on the results, we will, CMS will, decide whether or not we give it a cat one. And at the end of the study results, these are the things that we want to meet. So we sat with CMS. We talked to them. We had two independent PIs create this study. I was one of the co-PIs. And we exceeded every marker and every measure that they wanted. They wanted one year results. We gave them two. They wanted a certain outcome as compared to the control arm, which was epidural steroid injections. And we exceeded that. We exceeded even relative risk ratios. And then at the end of the year, and when they looked back upon our results, they said, you know what? I think we need more. So the cat one did not end up happening. And the more information that we gave them, they kept demanding more. And I think that this is another trend. We're falling into the space where we're becoming more surgical. So the demands and the outcomes from research are going to need to match surgeries, and even open surgeries, if that's what we are going to be competing against. So research has to change. It has to flip over into translational sciences. We have to understand mechanism of action that Dr. Parikh will talk about. We're going to need to know how long the data points need to be made in order for private insurance groups to pay for this over some other things, which Dr. Kim is going to talk about. So I decided to make my slides a little bit different. So I'm not focusing on the spine-related stuff. In the last few years, I've been focusing more on paraxial-related stuff. Now, I do many of the things that Dr. Kim and Dr. Parikh are going to talk about. But I felt like there needs to be a change, and there needs to be a change specifically for PM&R. So I started working with a device. And I started to understand the device a little bit better. And so let me just slide through. These are my disclosures. I am a Boston Scientific consultant. And I also do research with them. I am the PI on a FAST, on an F-A-S-T trial, and a pro trial. One is retrospective. Another one is prospective. I have research funding with Abbott, looking at spinal cord stimulation as well. I have two studies with Virtos, where we looked at epidural steroid injections versus mild, and also conservative management versus mild. Most of those are ongoing. Some of those are close to enrollment, but we're still in data collection phase. And I receive educational grants from Medtronic, Abbott, and Boston Scientific for my fellowship. The interesting thing is that the device that I'm going to be talking about, I haven't received one penny for, and I do not expect to receive. And some of you may think that that's silly. But I also think that this is, because of what I mentioned, because of how passionate I am about where our field is going, I needed to do some of the things and investigate the device and procedures. So some of you may know what percutaneous tenotomy is. I think many of you understand percutaneous tenotomy as devices that decalcify tissue. My hope is that at the end of the next 15 or so minutes, you understand that there's more to these kinds of products than just that. And offline, we can talk about what I think that these things really, really do or really don't do. Some of the stuff, a lot of the stuff online, I will disclose what I've found, OK? We have, I'll speak about adhesive capsulitis and coracohumeral ligament release and why the coracohumeral ligament is important. And then trochanteric pain syndrome, something that I think every one of you see often in practice, but still something that is unrecognized or remains relatively unrecognized. And I think primarily because we don't really know what to do with it, right? And we don't really want to know what it is. And I'll show you what the kinds of stuff that we've done and in hopes that it will make us recognize it a little bit better, OK? So the devices that are in production right now for these percutaneous tenotomies is a 10X device and a 10JET device. So the tool that I used for the research that I'm going to show you is the 10X device, primarily because the tool actually works as a, I believe that it works as a hammer drill. And there's things that we're doing right now to demonstrate that that's the way that it works. There are two needles in this product. There's an inner chamber and an outer chamber. And the inner chamber moves on the outer chamber so that the inner chamber actually does a high-frequency poking of tissue. The thought is the company believes that what it does is it breaks apart tissue and actually sucks in some of the calcium that one has broken up. I will show you that it can be used for other purposes as well. 10JET is a tool that uses high-frequency water to flush an area. It actually creates a high-velocity stream that tears tissue. I use a similar device for another reason that actually tears tissue and it works at such a high rate that it creates a high-frequency and it creates a low pressure around the area where the fluid is being ejected and it's supposed to suck tissue in. So that's what both of them do. But the fundamental difference between the top one and the bottom one is the top one, again, follow me for a moment, behaves more like a hammer drill. And the second one behaves more like a cutting or a lesioning device. But the mouth is angled. So you actually have to put tissue in the mouth where the stream is. I don't know how many of you can actually see this. But in the mouth right there, it's about a two to three millimeter opening. You've got to put the tissue right in there and you've got to catch it under tension in order to tear it or cut it. The research that we have for percutaneous tenotomies is not very great. It's level three, level four, and a lot of level five evidence. It's been looked at in various tissues, okay? And a lot of providers, a lot of insurance companies don't pay for this or don't reimburse very highly for this simply because the research has not been created, right? The space has not expanded yet and has not been fortified as of yet. There are a lot of papers, but again, there's a lot of level four and level five evidence. In order to get Cat I codes, in order to get appropriate reimbursement, we need level one and possibly level two studies, okay, or high level two studies. What's the mechanism of action of these things? Well, is it a pseudo-prolo therapy where basically you're taken, and again, we're talking about the 10X device. Did you just poke a needle in the eye? 10X device. Did you just poke in holes with some fluid? Is it a pseudo-PRP because you're creating blood flow? Is it decalcification or fragmentation? Is it something called facal emulsification? For those of you who know anything about ophthalmology, facal emulsification is an ultrasound-related physical property where tissues can actually be destroyed by high-frequency ultrasound. There's some thought that maybe that's what it does. Or is it tissue modification? Well, that can mean a lot of things. One of the things that I've demonstrated in cadaveric tissue is that we can actually modify tissue, meaning we can cut it and we can even make the collagen tissue more lax, and you'll see some of that here, okay? There is a 10X bone that is powerful enough to actually create changes in a bone. So it's a modestly powerful device. This is one of their premium, more high-frequency tools, but just allowing everyone here to understand that you can actually go through bone. This is the femur of a baby cow, all right? Fairly dense. And we were able to make those three strips, one, two, and three, at about a minute and a half, minute and a half, and minute and a half, okay? And that's the video. I actually didn't think it was gonna work. Now it's only a few seconds, but essentially what that was supposed to show was you stay on the tissue, okay? And again, you can see how it works almost as a hammer drill. This is the Achilles of a turkey, okay? Full-grown turkey. This is what it looked like in the native state. This is what it looked like after about a minute and a half, okay? And this is what it looked like at about two and a half minutes, where we completely lysed, where we completely cut it. So the tissue can create change. It can impart change. Next slide. I think we're stuck. Let me do it one more time. I had one more slide in here that I wanted to show you. Okay. The other slide that I wanted to show you, slides aren't moving, was that when we took a gastroc tendon, which is not as dense as an Achilles, when we put this 10X next to it, essentially what we did was we were able to loosen the tension on it, and you could see that the collagen fibers had actually fractured, okay? One of the things that my group and I are working on now is that we're taking a patellar tendon, bovine patellar tendon, and we're putting it in an MTS machine. For those of you who don't know what an MTS is, essentially it's a bone crushing tool, but it can also assess tendon and ligament laxity as well. So we are assessing laxity of these tendons with and without treatment, okay? I'm stuck. Can you move it from back there? Thank you. All right. Okay. So essentially why this is important is because there are pathologies that we deal with that sometimes we don't have a great answer for, one of which is adhesive capsulitis. We inject steroids, we send our patients to physical therapy, and in case anyone here has any other great ideas other than those, maybe hydrodilation, we don't have another good option. So one thing that I did with this information is I went into our anatomy lab and I dissected cadavers' shoulders. And we looked at the caracal-cumeral ligament because it's easy to see, okay? In a cadaver, they're easily dissected without destroying the tissue. They're easily identified on ultrasound. And I want to see what this tool actually did with that caracal-cumeral ligament. I talked to orthopedic surgeons who would take that down during surgery, and adhesive capsulitis is one of the tissues that they would take down. And so I thought that this is something feasible that surgeons do, and I think that we have a tool that may be able to do the same. And as I was doing research, I saw that there was a Japanese physician, Yukata, who actually cut the caracal-cumeral ligaments and demonstrated that he could increase external range of motion and mildly improve abduction in these patients, in his patients, live patients. So then I went to my IRB and I said, look, we have this person who's using a scalpel and an ultrasound. Scalpels and ultrasounds are sometimes not a great idea, okay? And this person goes in and he cuts this tissue. Well, I've got this device, or I know how to use this device. We pass by it. Perfect. So this is the cadaver, some of the cadaver stuff, which we published down in the right-hand corner. And I have this device that I think I could do this and I could do this safely. And our IRB said, fine, let's just do a pilot study. So we took 11 patients and we cut their caracal-cumeral ligaments. Ultrasound guided, took us about 10 to 15 minutes or so. And every one of these patients at two months demonstrated at first, immediately afterwards, and then following them at two months, demonstrated improvement in their external rotation. How much improvement? Double. That means if these patients came into the office with 30 degrees, they ended up with about 60. When they had 40, if we started at 40, then they ended up having 80, okay? If it was under 30 degrees, we determined that these patients were probably not gonna do well. So then what we are doing right now is we actually put this against an RCT. And we actually did publish the small case series as well as a pilot to do our RCT. I'm stuck again, but that's okay. So we did, aha. So when we did our RCT, as we're doing our RCT, we realized that immediately after, at six months after, and now we're collecting one-year data. And remember what I said in the beginning, how important one-year data is. We're collecting one-year data on these patients and this information, and this data, these data points essentially are the same or similar. We looked at their range of motion on abduction, external rotation. External rotation improved by, again, double. 30 degrees being the limiting factor. If they were less than 30 degrees, we could not get them into a satisfactory external range of motion or satisfactory pain level. But if we were able to double them and they started off with 30 or plus, then these patients had improved OSS or orthopedic shoulder scores, okay? Their NRS decreased as well and their medication utility dropped also. So we are now looking at this, again, at one year. We have our six-month data so I can present that to you and I think we have an abstract in several meetings now so I can disclose that to you. And we're going too far forward, but the slide right before this, thank you. They don't project well. But basically what they're showing, what they're supposed to show is the coacocumal ligament, or rather, sorry, if I can see from here. The coracoid process, glenoid, subscapularis, and coacocumal ligament. For those of you who want to see this a little better, these slides will be available to you, all right? And essentially what I do with this is I define the coacocumal ligament a little bit better, which we're not showing to you here. I drop some local anesthetic on top of the ligament and underneath the ligament to define it. Once I've defined it, then I take the 10X machine and I essentially just go over it and I pepper it inferiorly and superiorly. So in the cranial direction and the caudal direction, until when I put my tool inside that there's complete laxity, all right? And then I do a measurement of their external rotation immediately afterwards. So I do a measurement in the office of their external rotation and abduction immediately before the procedure and immediately after the procedure. And then at follow-up at one month, at follow-up at three months, at six months, and then a year. And these numbers remain consistent. And this is essentially what we found. Basically what I've told this team. And all of this will be available. Thank you for going to the next slide. So this is essentially what the RCT looks like. So this was adhesive capsulitis, mind you, refractory to conservative medical management. So all those things that I mentioned to you before, these patients came to me from orthopedics. I reached out to them and I said, look, you have patients who aren't doing well with all of these kinds of things. If they can't be helped, can I see them? And they said yes, so they sent me all of their failed patients. So they failed either in my practice or they failed in another specialty, another department. And so we took these on. So these are some of the more difficult ones, okay? And then the control arm was just a local anesthetic injection over the CHL to see if we could mobilize their arms immediately afterwards. And then the treatment arm obviously was the CHL. Okay, second thing, trochanteric pain syndrome. Trochanteric pain syndrome. There is a new belief in the community. Notice how I didn't call it trochanteric bursitis. So I don't call it trochanteric bursitis. And my learners, both previous and future in the room, know that I don't call it trochanteric bursitis. Because for those of you who do ultrasound of the trochanter, please raise your hands if you've actually seen a bursa. I'm so glad that nobody raised their hands because it is difficult to see a bursa. So what we're finding out now, and there's a lot of orthopedic literature in this as well, is that this is either a gluteus medius tendinopathy or I believe that it's an ITB tendinopathy, okay? So it is an enthesopathy. Do we have a tool for enthesopathy? I would argue that we do. And we took this tool into the lab. So the picture right before, the picture right before shows you this gastroc, this gastroc soleus tendon. Before, one slide back, please. Gastroc soleus tendon, hold on a second. Let me see if I can move it. Nope. Two slides forward, please. So gastroc soleus tendon pre and post treatment. And post treatment, it is lax, okay? This is a publication by Champ Baker who is our last author on a trochanteric pain study that I'm gonna show you right now. But him and I were surreptitiously working on greater trochanteric pain syndrome. He was working on the gluteus medius using this tenotomy device, and I was looking on ITB. He is my last author on the publication that we've submitted, and hopefully we get results back with us soon. I was hoping to have already have him and present them here. But Champ passed away before we can get his disclosure so he was a giant in orthopedics. He was the chair of the Houston Clinic in Atlanta for those of you who know and who know him. She was an absolutely unbelievably great human being and towards the end of his life he devoted his work into doing less open surgical procedures especially for these kinds of enthesopathies. So we were in line and at peace with one another as we were creating this independently and then we became codependent with the next stuff. Next slide please. So we looked at 57 patients. We had 65 hips. These are patients again who had failed everything. This is a prospect. This is not a prospective. It's a retrospective study at large scale. We evaluated patients who we did iliotibial band percutaneous tenotomies on and I'll just share with you the results. Hit the next slide please. Okay. Essentially what we found was that... Next slide please. Okay. This is the study. These are the pictures that we have shown and I'll just share some information from this. In the end what we showed was that 80% of our patients had an 80% improvement of pain with improved standing, walking, and sideline tolerance. That's what we had demonstrated and those are the results that we're going to be publishing and again this has been presented at several cases but hopefully it will be in publication form very soon. Some of the interesting things that we found that I'm hoping that people here will also look at when they're doing your trochanteric pain syndrome analyses is that typically the tendon is very thick, more than 5.4 millimeters. What we also find is that the trochanter itself is also very rugged and sometimes has an apices on it and as physiatrists let's understand that if you have an apice, an apice, and you've got a tendon that glides on top of it, over time it's gonna shear, it's gonna tear, and it's gonna be inflamed. Okay. And you can have subclinical inflammation which means you may not necessarily be able to find it on an MRI unless you have special studies to identify that but with ultrasound it's actually pretty easy to see. So just take a look at these next time around when you're doing this your trochanteric injections and evaluations. Next slide please. Okay. Next slide please. Okay. This is essentially the study. We broke our cohort down into responders, partial responders, and non-responders. Next slide please. Responders were patients who had more than 50% improvement. What we, and this is what that demonstrates. Next slide please. Okay. Blue, blue is the number of patients out of total which is that entire bar which improved with side-lying, sit-to-stand, and walking tolerance. So these are, again, our responders. Pain responders. So these are now functional responders as well. Next slide please. As we, as we went into partial and non-responders, they also had non-responding in terms of function too. So again, the information, and we know this as physiatrists, but the information with pain actually translated over into their function as well and their satisfaction. Next slide please. You guys can debate on this. Okay. Any questions regarding the slides that I presented? Okay. Meditate on it. Yes. Were you seeing clinical weakness following tenonomy of the ITT? No. If we're done higher, would it be less tendent? Is that a greater risk? So when Champ, when Champ did his studies, he looked at 28 patients that he published on. He had 364 total. And of that 364, he did not see any weakness. So I actually haven't looked, I have another study open right now where I'm looking at ITB and gluteus medius. And let's see what that shows. But one or the other, we did not see. With both of these tendons, in practice, I have not seen it. But again, we have, I've been looking at that data now for about eight or so months. I haven't seen it. Okay. Who knows what will happen to them longer. But we'll see. This is why long-term data is needed. Maybe that's what the future is. Dr. Parra? Is this working? Okay. All right. So over the next few minutes, we're just going to be talking about conventional and novel spinal cord stimulation and waveforms, their utility, their efficacy, and maybe their potential efficacy or potential utility in the setting of chronic pain. And it's an exciting thing, the exciting thing about this is that, oh I'm sorry, I have no disclosures, stark contrast. The exciting thing about this is that with each coming... Sure, I do have those. But with exciting thing about this is that with each coming year, the field of pain medicine does seem to expand its reach and expertise in tackling some of these more challenging and elusive chronic pain conditions. Conditions like CRPS, in which delay of diagnosis, as we know, can lead to lifelong complications. Or even persistent spinal pain syndrome, which can affect up to 10 to 40 percent of patients post-surgery. Or even something like painful diabetic neuropathy, that affects close to 7 million people currently. And that diagnosis, which the IASP itself stated, that it can go unrelieved or inadequately relieved for about 40 to 60 percent of their patients. So the reality is that once spinal and supraspinal effects of chronic pain set in, conservative treatment for these conditions can be very, very challenging. And so sometimes this leaves an unmet need for more treatment. And this essentially is why, or in fact, the growth of neuromodulation in this population, I think, has been fueled by this unmet need. In part because the increase in prevalence of these conditions, the lack of sometimes good therapeutic options, and the fear around chronic medication therapy or chronic opioid therapy that it seems to be setting in. So that's how the advancements in neuromodulation for these specific diagnoses have really kind of come to pass. The true mechanism behind spinal cord stimulation is under constant investigation, and I think it always will be. However, it does stake its foundation to some degree in the selective activation of mostly large rapidly conducting axons, traditionally beta fibers, to inhibit pain transmission along the dorsal horn. SES involves the generation of electric fields between metal contacts residing in the epidural space, impacting the potential, the electric potential across membranes. And most commonly target sites are the dorsal columns, but also maybe the dorsal horn, as well as the DRG. The exact mechanisms are not clear, but what we do know, however, is that it's not just a factor of where the stimulation occurs, but also how it's done. Thus, we create electrical fields through various waveforms. In the last few years, we've witnessed an introduction of several novel waveform patterns and stimulation modalities. Conventional tonic bursts and high-frequency stimulation differ based on their waveform patterns. A waveform basically has a pulse, a brief flash of electrical current, a frequency of that pulse or a group of pulses, and an amplitude, as well as a charge balancing period so that to prevent the buildup of charge excessively on a stimulated nerve tissue. Conventional SES uses tonic fixed low stimulation frequencies, usually below 200 Hertz, but maybe below 150 Hertz, and amplitudes above perception threshold to activate the dorsal column axons and inhibit pain, but also in the process generating a paresthesia. Burst, in contrast, employs a variable frequencies with segments of higher frequency burst pulses that fire as a group and repeat at a lower frequency, and these patterns utilize sub-threshold amplitudes and remain paresthesia-free. Finally, there are high-frequency modalities of spinal cord stimulation that are also paresthesia-free, using higher stimulation frequencies, sometimes between 1 to 10,000 kilohertz or even beyond, achieving pain relief, but at sometimes at a slower pace in time scale compared to conventional SES. And sometimes modern stimulated programming can use sometimes a combination of these waveforms or even cycle between them. So why even put effort into novel waveforms? Well, customized care should always be our aim in the field, and what we are discovering is that these novel waveforms have, at times, higher levels of pain relief and efficacy and can also isolate, theoretically, and sometimes proven, different spinal and supraspinal nerve targets. There's also the challenges that conventional tonic stimulation has. For one reason or another, there is sometimes decreased efficacy over time with conventional tonic stim. Now that could be because of habituation, or that could also be because we're just not hitting the right target with the right waveform. Sometimes paresthesias can be poorly tolerated in some populations, and traditional tonic SES makes it hard at times for certain diagnoses, such as axial lower back pain. So when we talk about supraspinal modulation, these pain activation patterns have been demonstrated using EEG, fMRI, and PET scans, and pain signaling processes by two. The pain signaling is processed by sometimes these ascending and descending pathways, and so what's neat to hypothesize or even read about is that these different wave patterns can activate these different pathways in different ways, and that's why we get variation in results. The driving theory, for example, suggests that tonic stimulation primarily modulates the lateral pathways, whereas burst stimulation may modulate both lateral and medial pathways, perhaps explaining why it has a bit more efficacy. It's always great when you're talking and you see five people walk out. I'm just kidding. Traditional SES interventions utilize tonic waveforms, and overwhelmingly it was first utilized for failed back syndrome. The first couple of randomized controlled trials compared tonic conventional SES to either repeat lumbar surgery or even conventional medical management, and did show that in both cases conventional tonic stimulators showed a greater overall percentage of pain relief and even increased patient satisfaction and decreased overall opioid use. And yet another classic randomized controlled trials, patients in the peripheral diabetic neuropathy population also, when compared spinal cord stimulation to conventional medical or best practice medical therapy, show that overall pain scores decreased by a measure of almost 50% or more in the spinal cord stimulator group when there was sometimes no change in the conventional management group. Stimulating the dorsal columns produces an inhibitory effect on the dorsal horns, and tonic spinal cord stimulation has been shown to increase the release of inhibitory neurotransmitter GABA in the spinal cord and also induce a subsequent decrease in glutamate, which is excitatory. And also animal studies have shown that it has a profound effect on the y-dynamic neurons, so we can see why these these results do come to pass. With burst waveform, now we're talking about close clusters of high-frequency electrical impulses delivered in groups, followed by a quiescent or quiet period or recharge period. It's relatively novel, however it's been rapidly adopted as, in my opinion, the go-to waveform currently. At its inception, it was based on mimicking a natural burst firing in the central nervous system, usually by unmolynated fibers. And the SUNBURST trial, which is a large randomized control trial, showed not just non-inferiority but also superiority when comparing burst spinal cord stim to tonic stim. In fact, 68% of patients that wound up preferring the burst waveform over tonic stimulation, most likely due to the paresthesia-free property. There's also a high degree of variability that you can introduce into the waveform itself. A study looking at intermittent dosing burst patterns with an extended quiet period or extended off period or quiescent period or the recharge period of over 360 seconds showed still significant pain relief and increased quality of life scores and decreased disability. And this finding is quite important because not only are we trying to improve outcomes from the patient side, we're also thinking about improving stimulator cell battery life too, because there is also a burden of burning out a battery, and so we want those batteries to kind of have a little longevity to them. Many studies have followed thereafter. Recent meta-analysis pooled a total of 268 patients together across five studies that demonstrated that the analgesic benefit and superiority of burst over tonic, and this was not just in SCS naive patients, but also in established tonic SCS patients, and also this benefit was also realized in tonic non-responders, which kind of also leads some evidence to the notion that it's not just that maybe a waveform doesn't work or a therapy doesn't work, but we have to have the right target, we have to have the right waveform, and we have to get smarter on what we're targeting with this therapy. Currently two variations of burst SCS are used in treatment in patients with intractable chronic back pain. These two variations differ with respect to the recharge pattern, so the charge balancing pattern, that one being passive and one being active. It was found that the active recharge pattern has been shown to activate both medial and lateral pathways, engaging certain cortical sensory motor areas involved in the location and intensity of pain, as well as the cognitive emotional aspects of pain, while the passive recharge exacts a similar effect, but preferentially modulating thalamic neurons, indicating that the passive recharge is more of a natural waveform for that thalamic target. So once again, similar effects, but it's interesting to see that we can kind of mimic the natural firing of certain cell groups using different waveforms. Surround inhibition, now this is something a new concept for me, and so but essentially surround inhibition is a waveform that employs a low frequency sub-perception, so below paresthesia threshold stimulation for chronic neuropathic pain, which is strikingly provides rapid onset of pain relief, unlike other paresthesia-free waveforms that I think are sometimes a bit slower. Low frequency sub-perception spinal cord stim activates a small number of dorsal column axons, which then inhibits the dorsal horn neural activity, and essentially what this what this technology is supposed to be really be emphasizing is the importance of spatial targeting. So once again, we're at sub-paresthesia thresholds, but what we're trying to target is not necessarily the site of injury, but the adjacent site of injury, to utilize that same concept of key theory and focus and expanding your receptive field, but targeting adjacent adjacent columns. And what's found that using this low frequency sub-perception waveform, you're still able to get some good results that are of a different method. So ultra-high-frequency, ultra-high-frequency is a paresthesia-free sub-perception energy platform at 10 kilohertz and produces direct neural inhibition by selectively targeting dorsal horn inter-inhibitory neurons. Although I would say the mechanism is a bit unclear, typically what we think of with spinal cord stimulation is that we have dorsal column activation, you know, A-beta fiber activation. This seems unlikely to play a mechanistic role in this case, and so what's interesting in some of the animal studies, it does show a reduction in wind-up, a further reduction in hyperactivity of wind-dynamic range neurons, similar to previous waveforms, however with little to no stimulation of the dorsal column, which makes, I think, the therapy quite unique. The most prominent ultra-high-frequency studies are the HF10 therapy studies, the Senza randomized controlled trials for both chronic back pain and also for diabetic peripheral neuropathy, which do show that there is sustained superiority of HF10 to traditional spinal cord stim, and sometimes over 80 percent, double that of the tonic spinal cord stim patients were responders of back pain and leg pain relief in these studies for chronic low back pain and as well as for diabetic peripheral neuropathy. Basic science research also sheds light on glial cell activation as a possible alternative, by Dr. Wiese, basic science research also sheds light on a glial cell activation as a possible alternative target to neuromodulation. As we all know or may not know, glial cells are support cells, they're greater in number than neurons, they do not necessarily participate directly in the synaptic interactions or electrical signaling, although they do have many supportive functions and sort of define or modulate or maintain these synaptic contacts. So glial cell dysfunction has been implicated in many chronic disease processes. I find this actually very interesting, I've been deep diving into sort of the mental health literature and glial cell dysfunction is also purported to play a role in depression, in opioid addiction, in many conditions. So it's interesting to see us actually trying to target glial cells. DTM stands for differential target multiplex programming, it's basically multiple different charge balanced pulse signals with a wide variety of frequencies and clinical trials have demonstrated that superiority of DTM over tonic spinal cord stim and sometimes a reduction of low back pain and leg pain, sometimes to a profound effect over 80% pain relief in some cases. And then we have of course ECAP's closed loop. So in the end the waveform is not the primary important thing that matters, but really the dose of that waveform, the dose of the stimulation on the target neuron is what they're actually experiencing, that's truly kind of what matters. In previous decades there's been no way of really knowing the real dose of stimulation onto our target cells, rather than testing this in an office setting with an EEG or EMG or an fMRI, even then you can't really tell what dose. The available spinal cord stimulator systems that we've talked about that are out there are mostly open loop, they don't measure or adjust for any changes in electrical field strength with position or with anything really. And the advent of the evoked compound action potential recording allows this activity to be directly measured and then quantified and then modified. So modifying the signal so that you have an even stimulation across that neural tissue, adjusting that dose and stimulation accordingly all within a closed loop. And the evoked randomized control trial is probably the most, is the most prominent study for this. We're now at two years data and there are significantly more closed loop and open loop patients that were responders to overall 50% reduction in pain in in this in this lower back pain pain study. I'm going to skip over this because I think for the interest of time. So new waveform research is uncovering intricacies of natural and physiological neuronal fine patterns and I find that very interesting. I think if we can try to mimic the way that the actual nervous system works and use it and adapt it to the way that we want it to work and customize and tailor waveforms not only to decrease the subjective pain intensity but also if we can modulate some of these other dimensions of pain. The cognitive, the motivational, the effective components of pain. I think that we we would get to a point where we can actually do some amazing, amazing work for these chronic pain patients. Because as you all know chronic pain is not just their, you know, their pain score but it's all these other suffering components. All these other fear, anxiety, motivational components that kind of get tacked on and layered on. It would be great if some way we can actually have spinal cord stimulation play a bigger role in multidisciplinary care, which I'm a huge fan of, where we can have tailored waveforms, tailored patterns, stimulate certain unique target sites even super spinally, you know, or exacting the effects super spinally and work within a multidisciplinary pain team to help tackle all the dimensions of pain which I think is something that we always strive for. So that would be great if we can get to that moment. Do you want to hand it over to to Chong? Afternoon everybody. You know it's bad one of the speakers leave before your talk. So now he had a, he has to be somewhere by four to get out of town so and his kids have a game tomorrow so. Who does spinal cord stimulation here? Who read the article in JAMA this week? So other than Dr. Van Acker I saw one other hand. So you want to tell us about it? So for those that did not, there was a placebo sham study published that was funded by an insurance care in Europe that showed that sham was just as equal as sub-threshold stimulation in somebody with radicular pain, that's post-lumbar laminectomy syndrome in JAMA. So not a good thing. Just reason I mentioned that is we have to be mindful not just what our field does but what else is coming because that really impacts our future. So we start with that just to preface that although I'm supposed to talk about some treatments for spinal stenosis as well as sacroiliitis, we're going to go through the thought process of what we used to do, why we're here, and hopefully some of that knowledge would kind of show us on where the heck we're going. Because it may be beyond our control unless we actually take charge of it. So my name is Sean Kim. I work for Metro Health. They pay my salary. I do hold an academic appointment at Case Western. I also run the pain fellowship there. This was a topic I was supposed to talk about and we'll go through that more in detail. I have long disclosures of anything, you know, from research to advisory roles and funded research. The only thing that has anything relevant to this talk is VertiFlex and Boston Scientific, because that's who bought VertiFlex and Virtos. But I've made zero sense on it, and I have nothing that is going to kind of impact what I say about them. Objectives, it's a real quick review. Because if you guys don't know the treatment of osteostenosis, you're in the wrong talk. If you don't know how to treat sacroiliac, you're probably in the wrong talk. We will go over some evidence of what exists and where we're at, and hopefully show you why we're going somewhere. I like to use articles and look at where it was published, because it shows you how valuable or how much worth they may have, the impact factor. So here's a review from JAMA, which means the Medical Society cares about lumbar spinal stenosis to me, or what we do. So here's the symptoms, here's the exam. Here's what they categorize in this table. So if you're my age, you can't see that, so I'll blow it up for you guys. Everyone's done this, right? It's conserved therapy. Those that benefit from it, obviously we do it. Typically by the time we get to, or they get to us, we're not seeing this to work that well. What you'll notice is that conserved treatment, first thing they notice is that it's safe, and it's probably relatively cost efficient. Medications, if you look at it, they haven't been studied, or it's crappy studies, or suboptimal studies of small in size. Nevertheless, it's commonly done. Right on the bottom, who does epidural injections here? Do we have residents and fellows in here? Okay. So epidural's been the bread and butter for a lot of our conditions, whether it's for radiculopathy of whatever ideology. But I think we're all pretty mindful that the evidence is pretty weak, especially for long term evidence. And even if you disagree with it, mainstream medicine and the insurance carriers would disagree with you, so that's all that matters. Because unless somebody's paying you cash, you're not gonna be offering it to them. And then from there, the big leap has been lots of studies on surgical outcomes. The sports studies, everything else. The surgeons have been very good about doing research, publishing, justifying why they offer certain treatments. So this is what JAMA published. Nowhere in between does it mention any of this stuff that we may be able to offer. And there's multiple reasons to that. So the Pain Society, if you look, it's a journal of pain research. Nowhere close to JAMA. Not that it's not a good publication by any means, but it's not JAMA. They published this recently. It's the second version. For full disclosure, it was funded by one of the companies, which you should just keep in mind who publishes and why. But it's really good for just looking at the algorithm. If you blow it up, they basically look at where the symptoms are, if it's diagnosed or not, and then break down to if they had surgery or not and what the options are. Who here does any kind of milli-invasive treatments for spinal stenosis? Got one. Like spacers. I got another hand. Anyone does the percutaneous decompression? Okay. One. Okay. Well, if you did, this is probably now getting you used to seeing. So for 50 years, we've been doing neuromodulation. We're kind of tinkering this area right now and has been probably for about the past decade, probably five years commercially. And then for those that are not, they also keep going back to what we've done before because we have no other options. And recently, we've kind of branched out to this other area. So what these sections are, basically it's the percutaneous image-guided lumbar decompression, the inner spinal spacer, and then recently, it's the inner spinous fusions that the surgeons have been doing that we've kind of taken into interest. So real quick, indications. Somebody with symptom stenosis, confirm their imaging. For the percutaneous image-guided decompression, they have to have hypertrophied ligament inflatable. Contraindication, common sense. Infection, prior surgery, gratitude spondylolisthesis, although it's a relative contraindication. Since only one person's done it, I won't really go into the details of technique because if you're not doing it, you should get trained. If you're doing it, this doesn't really mean much. Recently, Jason Pope published a publication that basically said that the epidural gram probably isn't needed. The outcome's probably the same. So those that do it, in the past, we were trained to use the epidural gram. Recently, a lot of people have gone away from it to decrease the radiation, as well as the fact that there was a contrast shortage. I'm sure you all ran into that as well. So this is what we're gonna start our focus on more because this will show you why it exists and why it may continue to exist and why we may be able to build on it. So evidence, not too bad. Two level one RTCs, two prospective studies, four retrospective studies, three case series, and then a meta-analysis of two of them. Reason I don't really value that significantly is they're just a combination of the studies that look good, but it does get you a pretty good rating in terms of level of evidence. Reason I say this has been around for a decade or so is this was first published in, I think, 2012. Laura Brump published, I think, 30-some patients basically compared epidural treatment injections to the decompression and basically found that it was better, just to say. That same year, although I'm not showing that, they actually published a one-year data of a multi-site study and Medicare CMS basically told them that was not good enough. So pretty shocking that you did a multi-site prospective study with one-year data and they said it was not good enough. So in 2012, it never made the market. So I got trained and started doing it as an attending when I was like a year or two out and then it no longer was available. They actually went back, did the MIDUS-2 study where Ramzan and Peter Stets and the rest of the team basically did a bigger study. They looked at about 300 patients and they had to publish two-year outcomes, although this one just shows the one-year outcome. As expected, the treatment group did well compared to the control group, which was epidural injections or typical medical management and the safety was pretty much the same. As expected, the two-year data basically reaffirmed that. So Peter published that with some of the other groups, including Stan Golovac. And again, the improvement was sustained up to two years. So new benchmarks, three months isn't good, six months isn't good. After this, they published other data to continue to make sure it's available and has been available since from CMS. So last year, they basically did a single-site study out of Cleveland where Nagy McHale and his group basically looked at 75 patients, followed them out and basically found that of the 75 they followed, only nine needed surgery in a five-year interval. In addition, they started publishing data that showed not just pain relief, functional improvement, but started showing how it decreased opioids. And recently, they started doing more of a real-world registries, because again, that seems to be the only way you can show that you can continue to have coverage, that when you show a study that it works, it's safe, it has long-term outcome than real-world in that the clinical trials, as good as it is for those that have participated in it, you are so controlling every factor that's controllable, it's sometimes not applicable. So at this point, they basically said, hey, we can do it in the real world. As expected, minimal risk, outcome is pretty good. So for those that don't do percutaneous image-guided lumbar decompression, it's probably something worth doing, because it's gonna get harder and harder to do the epidurals. They've caught it down to you can do it four times a year, and I think it's three times a year. They have significant regulations on failing conservative treatment, what you can inject, and what the reimbursement will be. And at some point, if you don't have another skill set, you will probably not be the one that they refer to. Any questions about the decompression? So the next one we'll move to is this interspaces spacers. If you look at the picture on the right, there's tons of them. They've been on the market for decades and decades. Orthopedic surgery and the spine surgeons have been doing this for a long time. Only one that we've, or the pain field, or the interventional spine, or just PMR, have tinkered with is the one that I highlighted. And all it's doing is basically limiting extension, basically open up the canal and the femoral narrowing. In general, the indications, some kind of stenosis, some kind of symptomatic patients. Contraindications, again, common sense. For this procedure specifically, this is what they publish, which again, makes sense. Neurogenic clonication, they fail conservative treatments. You can do up to two levels, from one to five, because that's where the spinous processes are in the lumbar area. You can't do five to one with this device, although with the newer treatments that we'll briefly discuss, you can do five one. Again, technique, there's a bunch of devices. Your goal is to basically get the spacer between the spinous process, deploy it, and this is what it looks like when it's done. All it's doing is inhibiting extension when somebody stands to improve their neurogenic clonication symptoms. More importantly, what's the evidence? So because it's been around so long, there's a lot of publications, depending on the device itself. Interestingly though, although there's a lot of randomized controlled trials, there's none comparing to each other, and there's none comparing to the gold standard, which is still open decompression. There's prospective study, retrospective studies, specific to what we've done in the field commonly. In 2011, look at where it's published though. Again, it's not groundbreaking news, but it's still a publication. They basically mentioned that it's safe, maybe worth exploring. It took them four more years to do a two year outcome, but look at the journal it got to. Spine, not too bad. Basically compared patients with stenosis with symptoms that have failed in six months of non-surgical intervention, and compared to the standard care at that time, which is X-stop. For those that don't know X-stop, it's no longer commonly used because it kept popping backwards. So although it worked, it wasn't safe, and because a few instances did that, it's not commonly used. But what they looked at is almost 400 patients, two groups, and they basically found it was non-inferior, which means it was just as good. Not better, but just as good. But it made the market. Since then, they've kind of looked at five year outcome, continue to show that it's worth doing. And the only reason I mention that real briefly is again, it's still on the market, it's still covered by most insurances, it's definitely covered by Medicare. Anybody heard of interspinous fusion in here? Anybody go to any, those residents or fellows have not gone to any of the trainings yet? So if you go to any of the cadaver courses, you'll probably start seeing them if you already haven't. So what it is, it's basically stabilizing the spinous process from a lateral approach. Instead of putting something in between and only, you actually approach, it's more of an open dissection, and you clamp it onto the spinous process when they're in a flexed position. Without going too far, I'll just tell you up front, the studies haven't shown anything specifically without a fusion. But it may be the next area the pain medicine goes to because of the fact that some of the past treatments that we have made, bread and butter, may not be available. So these are some of the options that exist for those that haven't seen it. Evidence specifically, as we discussed, it wasn't very good because there's no prospective randomized control trials to date that have been published, although there's been large retrospective data. And wrapping up, we'll move to SI joint because it's another area that's been commonly looked at. So I'm guessing most people that do epidurals do SI fusion, or SI injections, correct? Anybody here not do SI injections but they do epidurals? Who does RFAs of the SI joint? Bunch of hands. Who actually RFAs the joint itself? Couple. Who actually does lateral branch blocks first and then RFAs? Okay. So who RFAs 4, 5, S1, 2, 3, and 4 all the way down? What do you guys like to RFA? 5, 1, 2. 5, 1, 2, okay. Anybody do more or less? 4, 5, okay. Because histologic studies basically say there's a lot of it. It's an innervation of possibly 3 all the way to S4. We just assume it's probably 5 to S2. It's common. Who does the simplicity? Anybody? There's a lot, okay. So that's why you probably do more. It's easier. So for those that haven't seen it, it's basically a harpoon that you just lay on top of the sacrum. It was in for a while. Kind of out of favor in most places because of the cost. For those that don't know, at this time Medicare is basically saying, I think there was a talk yesterday saying, SI RFA is probably not going to be covered at this point unless something changes. And the reason is if you actually look at why we do some of it, the literature really doesn't exist. So medial branch block is probably the textbook of what we should do. They've looked at it over and over. They have a volume. They have expected percent relief. They have expected approach, temperature, needle size, duration. That's pretty much guideline. SI RFA basically nobody tells you, hey you should do a joint injection with this volume, with this concentration, expect this improvement. Whatever the insurance covers is what we've been doing. And as a result, basically they said, it's investigational. Which means unless some changes in 2023, Medicare will no longer cover SI joint RFAs. So for those, for background sake, here's a review algorithm diagnosis. A lot of societies already know this was coming so they're being relatively proactive. We're not going to beat this any more than we already have. One thing I do like is the one that Steve and then the rest of the crew did was basically give you an outline for interventionalists. And Steve will ask you for those that don't know he's a surgeon that's very commonly involved in the pain world. And the reason it's kind of interesting is for those that get really good relief for three months or longer, obviously you can repeat the injection. But for those that are less, they're saying, hey, here's your two options. SI joint RFA and the medially invasive SI fusions. The problem next year may be one of the options may no longer be on the table. And at this time, the way it's looking, the other option may not be on the table because they do not have a diagnosis code, which means as of next year, the reimbursement may be so poor that you'll lose money if you do the SI fusions. So as interesting this is, there was a big surge in the pain world where people do a lot of SI fusions from posterior and make it safe and simple. And then the volume has significantly dropped and as of next year, unless something changes, I would be shocked if anyone's doing it. For those that haven't seen it, this is a posterior single fusion for a posterior approach. This is another device that's basically doing a perpendicular approach stating that it's more stable. And then the most recent one is a medially invasive approach posterior, kind of like the first one, except they've actually have an additive version where you can do similar approach to a different target and actually do a lateral fusion. So if you look at the evidence for what the surgeons do for a lateral fusion, the evidence is actually pretty robust that it works. Now you have to get the right patient, diagnostic blocks, exam findings, so forth. So what the insurances have done is they won't cover the posterior medially invasive fusion approach, but they will approve a lateral fusion still, which mostly eliminates the non-surgeons unless you start learning new tricks. So what is the evidence? And you can already guess that from what we're discussing, the fact that they're gonna take it off the market from coverage, it's probably not very good. Bunch of retrospective data, bunch of case series, and this is talking for the posterior medially invasive approach, not the open lateral surgeries, because that evidence had been around a lot longer. The best review was about last year, and here's what they said. Everyone seems to get better, but again, it's case series, retrospective studies. And unfortunately at this time, that is not something that's enough for us to basically bank on. So in summary, because of the limitations of the treatment option, the success of it, I think we're gonna, in the spine end at least, we're gonna have to become much more invasive in terms of percutaneous or minimally invasive approaches, but if we do not build a foundation of reasonably solid data, there'll just be a flash in the pan. Any questions? You should have left before I started talking, huh? Give him a new one. Yes, sir? On the device where you were doing the fusion, one of the first things you were showing, you said that they did six months of conservative treatment before they did it, and so they were successful compared to that. What kind of conservative treatment was considered in the first, and was it all the same thing, or was it injection, or was it medication? Yeah, so therapy, rest, ice, over-the-counter medication, that's standard. No injectable treatments? No. For spinal stenosis? So no injections for spinal stenosis for the ones that you were doing the implantable device? So it was just medication, local treatment? Correct. That's why I said the clinical studies are good in the sense that the results are probably gonna be positive. None of these companies will get into it unless they already know it's gonna be good because they frame it a certain way. That's why they really do enjoy the real world registries and data, because when you get to the masses, we're not gonna be as picky. We don't have this patient population. We treat everyone, and if it's replicated within reason, that's when we know that it's a pretty good treatment. So sub-threshold, super-threshold, DTM, what's your algorithm for picking what you're gonna do? So, I mean, for me currently, I'm not very adventurous. I would say, I mean, if I'm speaking honestly, I mainly have a burst waveform and it seems to work well for my patients. And so I, you know, I don't know if you can find, but I haven't really gone too adventurous with the waveforms just yet. But, I mean, burst seems to work really well for my patients. And so I kind of- Do you do the burst for axial pain, or do you do the super-threshold? Say that again, sorry. Do you do high frequency for axial and then burst, or do you do an MA algorithm like that? No, I mean- I often say axial, I mean, you use high frequency, other things, but you do it with burst. I don't know, on your page of the internet. I've personally had great responses with burst, honestly. And so that's, maybe I tend to keep it too simple, but that's, you know, kind of a change. So from a, like, that end, like, if you actually look at the evidence, so the high frequency is the only one they've actually looked at actually low back pain. So you have to give them credit for running that study. It's all based on what they consider axial. So about 10 years ago, so for those that love neuromodulation, so there's, Chris Kumar did a process study. That's the benchmark for 50%, got 50% relief for two years. Like, that set the bar. After that, they actually did a subsequent study that didn't get the same press, that PROMIS study. They actually looked at axial back pain, but they actually consider axial back pain the iliac crest. So it all depends what axial back pain is. That probably dictates what you're getting away with because they cover low back pain, but if you look at the actual literature, the high frequency HF10's the only one that's actually studied it. There's case reports, anecdotal data, or, you know, retrospective data looking at DRGDL2. Obviously, the various burst models, but there's only, so one company will say the burst DR, that the Ritter is the only true burst that's cumulative, and if you look at the data from JAMA's publication, they actually looked at a burst sub-threshold not of the original cumulative burst. But in terms of my algorithm, I tend not to be a big fan of using still spinal cord stimulation for axial back pain because I'm not sure it works that well. But I tend to use, I've used all the companies, I still use all the companies. I actually based it on reimbursement because we're a county hospital and a teaching institution. So two of the manufacturers give us a significantly lower deal and we actually use it for patients who even have Medicaid and that really drives it. Now, if we're purely evidence-based with the fellows, we obviously start with HF10. So that's my rationale. But it's not, there's no guidelines for it. I don't think there's right or wrong. I think plenty of people have experience that actually shows that whether it's tonic, burst, DTM, low threshold, any program, it seems to work in enough patients. But is it significant enough? Is it actually lasting? So that's the other question. You can get the trials to work. I don't think that's the problem. For those that do it all the time, to trial success rate is never the concern. Six months is actually not the concern. It's a two years, three years. Are they still truly better in using it or they're kind of using it and they're just living with it? And I think that's what we're gonna be looking at, right? So one of the criticisms with tonic is that now they're looking at it decades after use and seeing the decreased efficacy of it. And so I think with all of these new wave forms, it's worthwhile, like you said, to see in the years to come, does it sustain? And that's what, and I agree. I think in the short run, and I think six months, even a year is still, for me is still a short run. It worked, but then really I wanna know five years down the line, is it gonna work? Isn't that, then it's useful for me. So who uses STEM for axial back pain here then? What do you, I think we heard you. What do you guys think? Actually, now almost everybody's MRI-conditional. There's nothing that's MRI compatible, they're all conditional. But I would, I think every system is now conditional to 1.5. I think they all pretty much have the same restriction these days. That's why you may want to tell the surgeon if you prefer something, you don't want to piss off a surgeon, but you can basically say, hey, you know, just so you know, here's all these options that are all MRI-conditional. Who do you have the long-term data for for high-frequency? Yeah, so she asked who has the data published. If you actually look it up, the HF10 is the one that had been studying axial lobe back pain and published on it. Dr. Stewart, what do you use? High-frequency. High-frequency? Okay. Any other questions? It's late in the day, but we can stay as long as you like. Or, yeah, I have one. Yes, sir, go ahead. Yeah, Phil Chang, Cedars-Sinai. I practice cancer rehabilitation medicine. But a really cool presentation, really awesome stuff. But is there anything newer on the horizon for, like, vertebral compression fractures? Or, like, have any of these, like, techniques been, like, looked at for that patient population? Are we still, like, vertebroplasty, kycoplasty? So, good question. You want to take that? For me, it's still a vertebroplasty, kycoplasty. Yes. So, at this point, there's nothing coming up. Will the basal vertebral nerve ablation get expanded? Or will the U.S. kind of look into, like, what overseas has that target the great communicants? Maybe. But in terms of the mainstream, nothing that I have heard that I'm aware of, unless somebody else here. Yeah, so, I mean, the gold stand is still cement, but I mean, I think there's that osteocole where they try and go and put the same thing, freeze everything in there for the cancer patients. So, but again, we don't have anything that's different than going into the vertebral body still. Hey, I'm Eduardo, I'm a resident at Emory. In terms of percutaneous decompression and interspinal spacers, have you noticed better outcomes with one as opposed to the other, and when do you determine which one you would go for first? So I actually prefer, well, so if it's just ligament hypertrophy, it's easy. So it's a very niche, very specific patient that would be a candidate for the percutaneous decompression. Like it can't be just they have stenosis because degeneration or arthritis. For the spacer, it tends to be easier because it doesn't matter where the stenosis is, what the cause is, you put that in. So if somebody just has ligament hypertrophy, that's easy. I think you should just do that because you're not leaving anything. You're just digging out the posterior elements that ligaments that basically has no function. That's not a candidate then, and they're not surgical. I actually never do anything without a surgeon saying, you know what, do that first. But that's kind of the, and then it's also politics because some of the neurosurgeons that do endoscopic do not like milds because they're like, I can do similar with a scope, but they don't care about spacer where the ortho spine, they'll be like, you know what? I don't like spacers because while I do a decompression, I'll do a inner spinous fusion. So that's the balance you have to have. So if you're in your own practice, have your own surgery center, you can probably do whatever you want. But if you're in a system, the other things you have to navigate the other specialties. Thank you. You guys have a lovely afternoon.

future of pain medicine

percutaneous surgical procedures

10X device

neuromodulation advancements

burst stimulation

spinal cord stimulation techniques

low frequency sub-perception waveforms

ultra-high frequency

glial cell activation

tailored waveforms

evidence-based practice