Hello, good evening. Welcome to the second in a series of educational webinars put on by the Advanced Practice Provider Community of NANS. The APP community is a relatively new one and the support by NANS leadership has been incredibly strong the past two years, allowing us to develop and live up to our mission. As a committee with NANS, we are dedicated to promoting education and collaboration within our professional space. Specific members who have been instrumental to our success include some that are here supporting us today. Kim Stampp, our education coordinator, and Antoinette Guider, our membership and operations manager. Thank you so much to you both. Certainly, we would not be able to get these webinars off the ground without you. And we really appreciate your ongoing support and our efforts to bring our community together nationally. And speaking of nationally, thank you to everybody who has joined tonight. Logging in at seven or eight o'clock at night, dinnertime, bath time, commute time, whatever it might be after work. To join us to talk about research and technology really is a testament to the strong dedication to your careers and to your patients. So without further ado, I'm going to hand it over to our co-moderator Patrick, who will review tonight's agenda and lead introductions of our esteemed panelists who we are also so grateful to have leading our educational event tonight. Thank you, Amy. And thank you, NANS and APP subcommittee for hosting and putting on this webinar. So yeah, so kind of the pearls and highlights of what our agenda is going to include is talking about the overview of DRG, when to use this therapy, specifically for those with CRPS and causalgia. And we'll go into sort of the differentiating characteristics between these two. Identifying the appropriate patients who may benefit from this therapy, the mechanism of action, which is always sort of important, right? We have to know how any therapy works and any of the advanced procedures that we offer our patients. So hoping to kind of delve into the deep science of DRG, the evidence-based data to support the therapy. We'll highlight some of the key studies that are out there that have kind of really sort of highlighted the importance of DRG, kind of why we use this therapy and why it's important as compared to sort of maybe differences than conventional SCS. And then for everybody, how we educate our patients, what our talk track may be when we discuss with patients and their families this therapy, and then how we manage them from the trial to PERM process. And then we'll finish with kind of Q&A. But what we're going to do is have throughout the webinar, if anyone has any questions, you can use the chat function and then Amy and myself will sort of kind of interject those questions throughout the webinar. Okay. So as moderators myself, I'll introduce myself first. My name is Patrick McGinn. I'm a physician assistant in Central New Jersey. I work for National Spine and Pain Centers. I've worked in the interventional space since 2015. Our practice does use DRG. So I'm extremely honored and excited to be on this webinar with such an esteemed faculty to learn more and be able to sort of better educate our patients on this therapy. And then co-moderator, Amy, if you want to introduce yourself. Oh, thank you. So I should have done that in the beginning. I'm Amy Yates and I hail from Rochester, New York, Rochester Regional Health. I work in an interventional pain and spine clinic and we do a lot of neuromodulation and have been doing DRG for many years. So this is a topic near and dear to my heart and that have found it really works for a lot of patients. So happy to be here. Thank you. Dr. Dickerson, would you introduce yourself? I'm Dave Dickerson. I'm an anesthesiologist and pain physician in Chicago at the Endeavor Health System. And really honored to be here. I've been doing DRG stimulation since 2017 and look forward to presenting some of our experience and the data that guides us. And Casey up next. Hi everyone. Thank you, Amy and Patrick for the introduction. My name is Casey Grillo. I am a nurse practitioner in Manhattan, New York. I work alongside Dr. Kenneth Chapman at the Spine and Pain Institute of New York. I'm honored to be here to chat with you guys about DRG. It has been therapy that has been transformative to my practice. I've been in pain management now with Dr. Chapman for about 10 years and have lots of experience with neuromodulation, specifically DRG. So excited to be here. I'm also the chair of the NANS APP committee. So truly an honor and look forward to chatting with you all. And then we can segue into Dr. Chapman. Hi everybody. My name is Kenneth Chapman. I'm a pain management physician in New York City. My passion is dorsal ganglion stimulation. I believe the target of the dorsal ganglion is the future of neuromodulation. And we're going to talk about some of those reasons why later as this evening goes on. And last but not least, Brandon. Hi, my name is Brandon Johnson. I work at Endeavor Health with Dr. Dickerson. I'm a PA working in pain management. I've been doing this for a few years now. I had a short stint in neurology before this. And I'm really excited about where pain medicine is going. And we use DRG a lot in our practice. So this is really apropos. All right, wonderful. So I think we can go ahead and start our slideshow. And I believe Casey's going to kick it off for us. Okay, let's get started. So before we dive into why DRG and the science behind it, it's important to bring it back to the basics because choosing the right therapy for the right patient is paramount to the success of the therapy. And the only way to do that properly and effectively is to really understand the basics. So determining your treatment approach for a patient means that it is essential to establish the appropriate and correct diagnosis for your patient. Treatment options vastly differ between nociceptive and neuropathic pain. So it's really important to understand the differences there. Nociceptive pain is the most common pain that you'll see in your practice. These are patients that present with an injury, an injury that, for example, a bruise, a bone fracture, a burn, or anything, or cut, or anything that damages tissue. This is a physiological response of the pain receptors. And this is pain that typically resolves with healing. Our neuropathic pain is complex. Our neuropathic pain is complex pain that involves damage to the nervous system, including the peripheral nerves. This is pain that is more challenging to treat. This is pain that typically is described as you're shooting, you're radiating, you're burning type of pain. These are patients that present with significant impact to the quality of their life. And because this type of pain, this neuropathic pain, is really challenging to treat, it is essential and crucial that you obtain a detailed history, especially for our new providers, establish a correct diagnosis, perform a very thorough physical exam, and collaborate with your physicians to determine not only the correct diagnosis, but the appropriate treatment option and a neuromodulation device moving forward. Next slide. We often see in practice that our chronic pain patients are suffering not only with physical pain, but they're in this cycle of pain. This pain can affect every domain and every aspect of their life. It affects them physically, emotionally, right? There's this global aspect of pain that affects the patients, and it can affect their personal life, their professional life. They can be catastrophizing, depressed, suicidal. And our goal as providers is to become equipped and effective at what we do by learning what's out there and learning what the treatment options are for patients. And DRG is one of those neuromodulation treatment options that are available to patients that can change the patient's quality of life and break their cycle of pain. I've been doing this now for 10 years. Not only are we able to break their cycle of pain with a therapy like DRG, but we're able to do it much earlier in their treatment algorithm, especially using a collaborative multidisciplinary approach. Next slide. DRG, dorsal root ganglion stimulation, is an effective treatment option for our CRP patients treatment option for our CRPS1 and CRPS2 patients, our causalgia patients. If you are a new provider, it is really important that you understand what CRPS and CRPS2 is and what it means so that you're able to identify patients that can benefit from this therapy. CRPS1 is pain that chronic, it's a chronic pain disease that is characterized by extreme pain that's out of proportion to the original injury. These patients often present with allodynear, hypoalgesia, and their quality of life is significantly impacted. Our CRPS2 patients, causalgia patients, are patients that have severe pain due to a traumatic or surgical nerve injury. The Budapest criteria, which we'll get to in two slides from now, is not a requirement for causalgia. It is a requirement for CRPS type 1. The differences between CRPS1 and 2 reside with the type of inciting event, not the clinical presentation. Next slide. Peripheral causalgia, it's really important that you understand peripheral causalgia because when this became an established diagnosis, what it did for us was opened up the doors and this opportunity for us to treat a largely underserved community of patients. When I started 10 years ago, patients that had peripheral causalgia didn't have great options. We did not have great treatment options for them and they were suffering and often ended up with opioids or additional surgery that wasn't necessary. So now that we have this diagnosis, it's really important for you to understand it to be able to select the patients that meet the criteria for it. So these are some of the named peripheral nerves from the ACCRIATE study. The ACCRIATE study Dr. Dickerson is going to dive into in a little bit, but these are some examples of the nerves that were listed in the ACCRIATE study. The idea is that if you can name the injured peripheral nerve, you can diagnose them with peripheral causalgia. This is determined by a history, looking at their surgical history, their medical history, looking at op reports to see if there were any injured peripheral nerves, learning from the patient what surgeries they had and what their pain presentation is when they come to your practice. Some examples of peripheral causalgia that you'll see common in your practice are patients that may have had knee surgery that end up with chronic knee pain after some nerve damage to their knee, or patients that have had hernia surgeries and repairs and often have chronic pain from the hernia repair, traumatic fractures or injuries to the foot or ankle, patients that have screws and rods in their ankles or foot oftentimes present with some chronic pain. So again, if you can name that nerve, you can diagnose them with peripheral causalgia. Next slide. This slide is the Budapest Criteria. The Budapest Criteria is a framework that was designed to help clarify the complex diagnosis of CRPS. So not only is it a tool for you to help determine your diagnosis, but it is also a requirement of the insurance companies. So if you are diagnosing your patient with CRPS1, it is required that they meet the criteria, this Budapest Criteria. So I always recommend for when I started as a new advanced practice provider, I had this over my computer there for a while so that to make sure when I had a patient present with CRPS1, I was meeting all the criteria. Make sure that you're documenting it in either your physical exam or your plan or somewhere, but it has to be there as an insurance requirement. So become familiar with the Budapest Criteria. And again, it is not required for your causalgia patients, only for your CRPS1 patients. Next slide. What is dorsal root ganglion stimulation? Why is it unique and what makes it different? Next slide. So dorsal root ganglion stimulation is a type of neurostimulator that was designed to treat focal isolated pain of the lower extremities. And this is an illustration that was created by Dr. Chapman. So he's going to dive into this a little bit later, but it shows you here the anatomy, the DRG, right? So the DRG is a cluster of nerves there. And when you simulate the DRG, it's in the, you know, the dorsal, right next to the dorsal root spinal, there's the spinal nerve, the dorsal root, and then the DRG. When you stimulate the DRG, you are essentially putting up a traffic light, right? So that the painful signals and sensations are not able to get through to the nerve fibers and travel up the spinal cord to the brain. So you're eventually, you're essentially stopping those pain messages from getting through. And what's really, you know, we can go to the next slide. What is really unique about this is that compared to traditional SES, we are targeting a focal isolated area of pain, which we were not able to do with traditional SES. So this stimulation was designed to address the limitations and the limits of traditional SES. It's important to keep in mind that this is stable stimulation. So because there is limited CSF around the DRG, that allows the leads to be placed very close to the target. So you'll have less postural effects. It is well mapped and organized. So you'll have very specific simulation to the area that the patient complains of, and it has low energy. So again, those leads are placed very close to the anatomical target. So there's less energy needed to stimulate the sensory fibers. And what does that mean? It's power seizure free. And also, you know, we're seeing very long, we're seeing longevity of the battery life because of the low, low energy use. Next slide. The AP location of the DRG is always predictable, which, you know, is nice for physicians to know it's always going to lie underneath the pedicle in the epidural space. Next slide. Why target the DRG? So, you know, with this slide, I'd like to, you know, mention that 10 years ago when I started and I had a patient present to me with CRPS, I always, you know, felt uncomfortable seeing those patients because I didn't have anything for them, right? These were patients that were suffering in every aspect of their life. We only had sympathetic blocks for these patients, opioids, physical therapy. They were in this cycle of pain that we weren't able to break. And okay, maybe we offered them traditional SES. For example, if I had a patient present to my practice with CRPS of the foot, I may not be able to capture the foot with SES, but maybe then we sent, you know, some simulation down the leg, which didn't bother the patient. So, you know, now you have a patient that didn't get coverage of the painful area and now has some power seizure down an area that didn't bother them before. And it was truly a mess. So, you know, having now a treatment option for these patients that have focal pain of the lower extremities has been transformative for these patients suffering with CRPS1 and clausalgia. Next slide. As an APP and a provider, but I know this is an APP-focused webinar, it is really important to learn how to and get comfortable with explaining DRG to a patient because what we see now is that patients come into our practice, they've heard about simulation, right? But most of the time they've heard about traditional simulation and they have a lot of stories between friends and family members and colleagues and they're often misled, right? And they often have the wrong information. So it's really important for you as a provider to educate yourself and become, you know, learn the knowledge that's there so that you can be effective at what you do and give your patients the correct information and be confident about the therapy that you're recommending. It's important to explain to the patient that this is designed to treat the source of the focal pain. Have a talking track, you know, listen to the collaborating physician that you work with, you know, attending these webinars and utilizing the educational resources that are out there to formulate your own talking track is really helpful because the patients can sense your confidence and it goes a long way. Showing the models, the leads, the IPG. At this point in time, DRG is only offered from one company so that company can be very helpful in offering resources for you and support. Always review the trial procedure and review the implant process so that there's transparency and communication between the patient and their family members and caregivers. Next slide. Is your patient a candidate for DRG? Do they have isolated or focal pain? Has chronic pain been established, right? Has that pain been present for, and has it been persistent for months or maybe even years? And have you made a diagnosis as CRPS1 or causalgia? If you have made one of two of those diagnoses, then DRG can be a treatment option for your patients. Next slide. Some advanced practice provider considerations when you are considering utilizing DRG as a therapy. Have your patients failed conservative therapy, right? We always go from a more conservative approach to then advanced. So have they done physical therapy, had some interventional procedures? Have they had imaging updated within a year? Make sure that you're speaking to your collaborating physician. Know where this fits within practice. Some physicians require thoracic imaging, some do not, right? Knowing what you need to move this patient along their treatment algorithm. Have they been evaluated for other pain generators? And have you ruled out the need for surgery? And of course, the psychological evaluation, it's an important step not to overlook, and it is an insurance requirement in order to proceed with DRG as a therapy. I think the next slide is Dr. Dickerson going into the accurate study. Thanks so much, Casey. I mean, it's incredible to sit and listen to your presentation. I just think it tees up such a wonderful practical framework for how and why. And I wanna reinforce that with a review of the accurate study, which was published in 2017 in Pain. This is a level one comparative trial, RCT, and was actually the IDE that was required by the FDA because of the novel nature of dorsal root ganglion stimulation as an invasive therapy. The FDA did not wanna allow for this to be approved as being another spinal cord stimulation therapy under what's called a 510K, but instead required an IDE study. With an IDE study, you effectively have significant oversight from the FDA at every step of methodology development, assignment and enrollment of study sites and investigators, as well as the vetting of them, and then continuously, effectively measuring the, making sure that the study is compliant and following the highest level of ethical rigor due to the experimental nature of the new therapy. So this study effectively was going to compare DRG stimulation to spinal cord stimulation, dorsal column stimulation with tonic stem and this was gonna be a study that was looking at patients at three, six, nine, and 12 months. And we'll go to the next slide and we'll start to go over how this broke down. Patients being studied were receiving those two therapies being randomized into that for chronic intractable pain of the lower limbs, specifically CRPS type one or causalgia. When we look at the breakdown here, 152 subjects were randomized in this consort trial. If we were to expand this out from the study, 168 subjects were also excluded after being screened. Effectively, they were deemed not to meet the inclusion and exclusion criteria, which I will go over, but effectively 152 subjects were randomized into even groups of DRG and control therapy of spinal cord stimulation. Those patients received a trial and if they met the criteria, 50% relief, they were able to then move on. In the DRG group, there was 61 patients that met the criteria of greater than 50% relief on a VAS to move forward. Their baseline VAS in that group was 80 millimeters. So this was a group that had severe pain. And then in the spinal cord stimulation group, there was a similar VAS at baseline. And the number that moved on, I believe, was in the 50s, 56 versus, 54 versus 61. Moving on to that next phase, to receive an implant of the therapy that they had had a positive trial with. Those patients were then seen at three months for primary endpoints, which were safety and efficacy. And we'll talk about what those are specifically and how we're defining that, as well as the continued tracking out to 12 months with three month visits for these patients. Let's go on to the next slide. We'll talk a little bit about who the patients were, or excuse me, the endpoints. Then we'll talk about who the patients were and who they weren't. The exclusion criteria will be our slide after that. The primary endpoint was really looking at efficacy, looking at the subjects that effectively achieved 50% pain relief in the primary area of pain at the end of the trial and at three months to demonstrate efficacy. And then safety being the ability to have stimulation really focused in the area of stimulation, or excuse me, from stimulation induced neurologic deficit through three months, so that there was no impairment occurring from the therapeutic stimulation. Additionally, secondary endpoints would be positional effects of paresthesia, looking at three months, whether or not the groups were able to see a difference between how positions affect the paresthesia and whether or not that paresthesia was outside of their area of pain. Additionally, they would be looking at the percent pain relief in subjects with and without paresthesia at that three month mark. Tertiary endpoints, and this is really important, this is where we understand the holistic response of these patients to these therapies, comparing quality of life on SF-36, psychological disposition on a POMS, and then physical functioning on BPI, patient satisfaction through PGIC and stimulation specificity at three months. So also adverse events, of course, were tracked as this was an IDE, and those were looking at both minor and major events that were either device related or non-device related. Let's go to the next slide. Inclusion criteria, a nice broad cohort of ages 22 to 75 with chronic intractable pain of the lower limbs for at least six months, with a diagnosis of CRPS type one or CRPS type two peripheral cause alga. Pain had to be moderate or greater, so effectively, but really specifically a VAS of 60 millimeters in the area of greatest pain in the lower limbs, and they had to be psychologically appropriate for the implant. They also had to effectively be treatment refractory. They had to have tried some of the evidence-based pharmacologic treatments from at least two different drug classes, and they need to have had stable neurologic function effectively in the past 30 days. Also, they needed to be able to provide informed consent and able to comply with the follow-up schedule and protocol. Go to the next slide. So our exclusion criteria for the accurate study, back pain, if it was greatest region, you weren't gonna be in this study. So you could have bad leg pain, but back and leg was not what we were looking at, especially specifically in patients who the back was worse than the leg pain. Patients who had had a failed SCS therapy were also not included here. They were excluded. Any recent corticosteroid injection at 30 days or previous RFA of the DRG within the last 90 days would exclude them. A member of a vulnerable population involved in perhaps a population that could have an undetected secondary gain like litigation or worker's comp, unstable pain medication use within 30 days or a cancer diagnosis within two years. Additionally, any sort of cognitive, sensory, physical impairment that would limit the ability to operate the device led to exclusion as well as infection, medical comorbid coagulation disorders or other indwelling or active implant devices. So if the pain condition was changing within 30 days, effectively, they also would not be included. And imaging showing that there's contraindication for lead placement effectively on that preparation is the patient candidate based on the neuroanatomy at the target sites. This is where you go from that 350 plus patients with 168 not meeting these criteria on screening either inclusion or exclusion down to the patients that were randomized into the study, next slide, please. When we look at the two groups as they were randomized, they were comparable. Pain duration was greater than seven years in both DRG and control SCS. And the diagnosis of CRPS type one was around 56 to 58% in the two groups. So very closely matched as well, the peripheral causality or CRPS type two making up 40%. And this is why it's important when people discuss with you the need for Budapest criteria, which you do not need to meet to have peripheral causalgia, need effectively a history and a nerve that you could name where you see nerve dysfunction and unremitting pain. So 40% of the patients in this study have that did not meet the Budapest criteria, but were enrolled and effectively trial. Next slide, next slide. When we look at the really exciting data of the accurate study, which there's a lot of things to highlight in this study, but one is this high responder rate. The patients in the DRG group at three months, at least 80% pain relief being that definition of high response, 70% of the DRG patients achieved this. And interestingly, half of the patients with spinal cord stimulation also did. So this is one of the best studies demonstrating the efficacy in a large population over 60 patients of spinal cord stimulation in a randomized trial, Dorsal Comstim to have that 52% of patients getting 80% relief. And what this tells us is that effectively, if you look at the comparator group, they were effectively not given a lesser opportunity to respond. And in that study were demonstrated perhaps some of the highest efficacy for spinal cord stimulation as well with that 50 or 2% high responder rate. And this is really looking at our implant responders at three months. Let's go to the next slide. Interestingly enough, the other outcomes was looking at parasitology outside the painful area. The DRG stimulation group, 95% really had stimulation only within the area of where their pain target was. So the ability to dial in DRG stimulation to the painful region is something that was seen in this study versus 61% of the SCS control group. And this is something that was tested with position changes to see whether or not there was a consistency of the DRG stimulation as well in that area. So this wasn't just static, but this was also with going from multiple positions to see that that parasitism remained within the painful region. Next slide. This was one of those primary outcomes. When we look at the holistic metrics that were compared here, we can see that there was improvement in both groups, but the degree of improvement in general health, social health, and that POMS was looking at the blue bar, which is DRG and the orange is SCS, but significantly more in the DRG group by several magnitude in some instances like general health. Let's go to the next slide. When we look at safety, we can see that effectively the adverse events where there's no statistically significant difference between these two groups and severe adverse events, device-related adverse events or unanticipated device-related adverse events. And I really draw attention to this because at this time spinal cord stimulation is about a 50-year-old therapy in this study. And DRG stimulation has been around for less than 10 years, not quite an adolescent yet even, and still has this safety metrics. And this is when you drill down and you look at the performance of these, the average case time for these DRG implants was almost two hours, which is really significant when you think about that. It was longer than the SCS groups. And this just really reflects a lot of the fact that this was the dawn of DRG stimulation. We had people in the study that had really been doing their first cases as a part of the first cases and patients in this study. That learning curve is a steep one as we know. And effectively, we still see this safety and efficacy really in this early adoption phase of DRG. Many of the cases were done with early phase equipment. The ball tip lead, which is no longer used, was replaced with a slim tip lead. We also see that every patient in this study was receiving a paresthesia for the most part. 90% of the patients were receiving paresthesia-based DRG stimulation. So even the way that it was being dosed is perhaps a different paradigm. But it, again, reflects even in that early phase that the therapy itself was incredibly efficacious and safe compared to spinal cord stimulation, which was equally safe, but with perhaps a DRG of that superior efficacy here. Next slide, please. We look at that tornado plot of the patients receiving DRG implantation. Almost all DRG patients achieved greater than 50%. Each of these horizontal lines represents a patient. And there's really only three patients that received DRG implant that were not receiving greater than 50% relief. We can also see that high responder rate is really significant as well, and something we don't see with a lot of neurostimulation. And this is really where Dr. Chapman and Casey and our clinics are really excited and driven to offer this to patients with CRPS type one and type two, because this is the type of data we see in our clinical practice. Let's go to the next slide. So just to summarize, the 70% chance of being a high responder at three months and one year is really profound. And again, this is for type one and type two CRPS, with leads being placed for lower extremity pain in the T10 to ST regions. The VAS improvements are replicable in the real world. And I'll show a slide after this one that shows the breadth of studies that have been performed in over a thousand patients and study protocols with a significant replicatable impact, similar and comparable to the accurate study. And that DRG is also a safe treatment option. We see that from the accurate study. The improved quality of life through the SF36, POMS and BPI data that is included in the accurate study is really profound, and as well as that proven superiority for DRG over traditional tonic spinal cord stimulation in all of the analyses in the accurate study. Let's go to the next slide. That real world data really is reflected. If you look on the left here, the accurate baseline with that VAS of 80 millimeters being dropped down to at three months was 13 and at six months was 15. So pretty profound. That's represented by the green bar there. Then when you look at the other studies from 2013 to 2021, if that threshold of 25 millimeters on the VAS is that dotted blue line, we can see that across the board, these studies are all within similar response rates. And this is all over 10 years of studying over a thousand patients in 24 plus studies. And if we look at the Morgalla 2017 paper, these patients still were ending up with a pain score around 40 millimeters or just slightly higher than that. So getting down to that mild to moderate range. So we'll go to the next slide. So when I think about the accurate study, it's interesting. We didn't know what we didn't know. We published this last year under Dr. Chapman's leadership as first author, really the Aspen Best Practice Guidelines. And this compendium summarizes really our state-of-the-art understanding of the science and both practically as well as from a mechanistic bench basis for why these therapies we believe are working and why we believe they're valuable and how when we deploy them in a certain way or certain techniques that Dr. Chapman's gonna talk about that evolution leads to even more realized gains for our patients. This is an open source article that I encourage everyone to pick up a copy of if you're working in a clinic that's using DRG stimulation or in a clinic that is thinking about treating patients with Causalgia. And you notice I say it that way because if you're treating patients with Causalgia or CRPS type one, you really should be an expert in dorsal root ganglion stimulation based on this data. So I would encourage everyone to at least pull this paper up. I think it's a good understanding and recognize when you read it, so much there evolves from the NAC guidelines that have been published around DRG stimulation a couple of years prior. And then also you have to ask yourself that accurate data came before these clinicians and investigators had access to a lot of this knowledge from the real world use of the therapy. So I think it's really exciting to recognize that while one of the shortcomings of the accurate study may be the fact that people say, well, it's industry funded. Well, industry funded, but an IDE study. And the IDE really does help offset that bias due to the very close management of the methodology and the conducting of that research. So thanks so much. Go to the next slide. We hand it off to Dr. Chapman. Thank you, Dr. Dickerson. I just want to pause here a moment and remind our attendees, if you have any questions, to go ahead and type them into the Q&A panel. We did have somebody who asked if the accurate study was compared to one SCS or multiple, and Dr. Chapman did offer that it was against one company, Boston Scientific. Dr. Dickerson, could you let us know, was that with paresthesia-based or sub-paresthesia what it was compared to? And at the time of the accurate study, was the DRG stimulation paresthesia or sub-paresthesia? Right, so both were paresthesia-based tonic. And it was actually Medtronic, which is listed in the paper. So it wasn't left a mystery. And both devices were programmed by the representatives from those companies, which was really important to show that all of the nuance of that programming was available to those patients. And again, both were paresthesia-based. And both, of course, DRG's tonic, but we've evolved that to be a sub-perception therapy, which Dr. Chapman's gonna talk about. But it is interesting. It kind of shows the evolution of the therapy, as I mentioned, the way we studied it and how it's evolved into the current practice. That's a great question. Thank you so much. Okay, Dr. Chapman. All right, thank you. Okay, so I think when we look at these therapies and we try to choose the correct therapy for our patients, we have to look at DRG and say, well, why should I use this therapy? Why are you gonna go to your attending and say, hey, I think you should, this patient has CRPS of the foot. I think you should use dorsal ganglion stimulation, although you traditionally would try a dorsal column system. We already discussed that it's gonna provide better distal dermatomal coverage. And there's, we'll go over that in a little bit. It's also an ultra low energy device, right? And we're gonna get into all of these things in a little bit. And with this therapy, we're able to have equal efficacy at four Hertz, which is four cycles, four essential electrical pulses per second, which is far lower than the others at lower amplitudes, as well as being able to be delivered intermittently, which means you can have an on-off cycle, one minute on, one minute off, or even one minute on, two minutes off with the same efficacy. It's also, it, patient satisfaction measures, which are very important. It's a paresthesia-free system. It doesn't require any recharging. And the IPG longevity is gonna be most likely far longer than most of the other systems out there with the information that we have thus far. It's also incredible, it's sympathetic modulation, primarily because I think we're dealing with a system that's right at the dorsal ganglion. And when we activate these action potentials with our pulse, they go in both directions, and it's gonna shoot volleys into the sympathetic nervous system, which is in the sympathetic chain, which is directly adjacent to where we are. And so, in addition, what is of interest now to us primarily is the nociceptive pain component. And that's talking about pains like bone pain, chronic knee pain, chronic hip pain, things that traditionally SCS just does not help. And finally, we're gonna go over habituation, which is the loss of efficacy over time. Next slide, please. And all of this information that I'm going to review with you today is gonna be based on publications that are in literature, while, again, as Dr. Dickerson mentioned, this is a relatively novel therapy at less than 10 years. Spinal cord stimulation's been around since the 1960s, so there's a lot more evidence on SCS-related matters than DRG, but this is what's out there for DRG, and hopefully this stuff will help you understand why I think this therapy should be the first thing you think about when you have a person with CRPS of the lower extremity, type one or two. Next slide. Okay, this has been well-reviewed. You're not gonna have the same type of coverage in your distal extremity with SCS as opposed to DRG. And so this study, which was an accurate sub-study, essentially they showed, as it was mentioned earlier, you're gonna get better dermatomal coverage or coverage of the painful area with your paresthesia. Interestingly, you don't need to have paresthesia-based coverage as you do with SCS with this therapy. So not only do we get better distal dermatomal coverage, you don't actually have to program it to where you want to get it as close as you can, but it doesn't have to actually cover the foot because you're still gonna have the effects there. And that's been proven. And in the old days, when we had SCS and we had a person with a toe injury or like a distal foot injury, we would have to try all these different methods to get that covered, retrograde, you name it. And whatever we would do, it just may not cover it. Next slide, please. And when we talk about the energy, let's say, how much does it really matter? I think that's the first question. Does it matter how much we're zapping our nerve tissue with electricity? That is yet to be determined. However, I know that I would like the least possible effective dose of electricity in my body if I had that option. And so how do we know how much electricity we're delivering? There's a formula which is essentially amplitude times pulse width times frequency. And these, just so you know, these are the three parameters that we can program a stimulator with. The amplitude is how strong, obviously, our pulse is gonna be. The pulse width is how long we're gonna apply that stimulus for. So that's gonna be how long, how wide, essentially, that pulse is. And the frequency is, if you think of physics, cycles per second. So how many of these pulses per second are we gonna deliver? And it's been shown, it was initially shown several years ago with a small randomized study comparing the blinded study, comparing 20 Hertz versus four Hertz. And essentially, there was no difference. And so what that meant is that this device is gonna use the lowest possible amount of electrical pulses per second that this device allows, doesn't go lower than four Hertz. And then if you compare that to traditional stimulation, which is about 50 Hertz per second or 50 cycles per second, or high-frequency stimulation, which is 10,000 cycles per second. So you're getting 10,000 little electrical zaps a second. And okay, we said it doesn't matter. We don't know if it matters for our neural tissue, although there have been some studies which we don't, but we don't know. And basically, what it does make a difference with is gonna be our battery life and the need to recharge, the size of the battery, et cetera, et cetera. In addition, there's something called duty cycle, like how long is your device on for or do you have on-off cycles? And so because of the work we were doing on the opioid receptors and this device in particular, we kind of knew that this device, when we turned it off, we would still be able to have, it would still have effect. How long for, that varies, but in a randomized, small randomized study, one minute on, one minute off, compared to one minute on, two minutes off, they were the same. So basically, you have a device that's gonna be working at incredibly lower levels than any type of SCS is. And on the right there, this are, our group had done two smaller studies demonstrating this, and it was actually repeated by two other groups in Europe. One is where, and essentially, both of them tested patients at different frequencies. They tested them at four Hertz and 20 Hertz. And my friend here in Sweden, Pedram, he did it on a T12 for back pain. And at the very least, it's the same. Both of their studies showed that perhaps it could have been slightly better being at four Hertz actually, but ultimately, clinically, from what we see, it just feels the same, whether it's better or not, you can't tell clinically. Next slide, please. So, all right, so what does this matter electricity we are delivering? All right, there's a lot of numbers here. Basically, what you can really look at or think about passive recharge burst, that's essentially burst DR. And that gives us the total charge about 100 microcoulombs per second. And you wanna compare that to say tonic. And if you cycle that, right, we talked about cycling earlier on off paradigms. And it's been shown that burst DR can have as much as one minute or 30 seconds on 360 seconds off. So a one to six on to off ratio that drops their total charge per second down to 17 microcoulombs from 100, which is a very substantial change and which is definitely gonna extend their battery life. But then you look at tonic SCS, you're about 70 microcoulombs per second. And then high frequency stimulation, which is gonna be 10 times that amount or so. And then we really get into the DRG stuff and really at standard doses, which is that top line, you're talking 1.6 microcoulombs per second. You drop it down to four hertz. We're basically just dividing these numbers is down to 66 microcoulombs per second. One minute on one minute off 33 or 0.33 and 0.22. And I mean, very easily, you can see that these numbers are gonna be astronomically smaller per second delivered to neural tissue. Next slide, please. This was a study that we did evaluating our bat patients IPGs down the road after implant. And so, how are these changes gonna affect our battery? Like how much, what is this actually clinically gonna show? So just so you know, when you get a new bat IPG right out of the box, brand new, it's gonna say greater than three volts. That's what it starts with. A little greater sign and three volts. At 2.73 volts, the battery is gonna start beeping and you're gonna get the elective replacement indicator. And that means that, hey, you gotta replace this thing soon. And that usually will last a year or perhaps more. So again, we had these patients, we checked them, we split them up, and you can see that basically for the first three years, about one third of these patients were at 3.0 or greater, which is basically almost the same as it coming out of the box. It's used very little to none of the energy. And then after three years, it's at 2.974. We gotta go down to 2.73 to get that alarm to ring. And if you were to extrapolate this, now there's a curve when the lithium ion, vanadium ion in the battery is gonna die on its own, but there's a curve. And so at 2.73, they say that. And so if it wasn't for that, and we could just, if our battery was just like money in the bank and we could just take out what we need, at these numbers, a battery would last probably over 50 years. So this is gonna show, the battery life is gonna be incredibly extended. And we haven't replaced a battery yet for, or even come close to for this. And if you look at how much difference in electricity delivered to your body, the numbers are astronomical. It's almost feels like you're toxically overdosing someone with electricity if you're gonna give them, if you multiply that 300 times greater number per second, times 60 second, times 60 minutes, times 24 hours, we're getting astronomical changes as compared to SCS. Next slide, please. Okay, and so, Ari, why else would you wanna give this to the patient? Look, paresthesia-free modalities, when compared to paresthesia utilizing modalities, paresthesia-free wins. Nevro won, Burst DR won. This, although they, in the beginning they were using Tonic, this is really a paresthesia-free modality. You don't need, you don't wanna have your patients have. So that's patients want that, they appreciate it. If I had horrible burning in the ball of my foot and I had to walk around and feel a tingling in my whole leg, just to decrease that pain in my foot 50%, I mean, that's great, but it's kind of, I'd rather feel no pain and no tingling. And that's what DRG allows you to do. As I said, there's no recharging and this is going to extend our battery lives. Okay, and this, that little thing in the middle just says it's paresthesia-independent. That's another study done by Paul Verrels. Can we have the next slide, please? This is something that, the application for dorsal ganglion stimulation in sympathetic nervous systems is really something that I'm really passionate about. And this is a project that we're gonna be tackling next is applying the dorsal ganglion stimulation for sympathetic related issues. In particular, peripheral vascular disease, neuropathies, distal neuropathies, as well as, as well as abdominal pain related issues. We just had a publication, my colleague, Dr. Ajax Yang on Crohn's. It's really interesting. Next slide, please. Next slide. Okay, so using dorsal ganglion stimulation for mixed or nociceptive conditions. Where I'm getting into with this is knee pain. SCS, as we mentioned earlier, 60 some odd years or so years it's been around. If you do a literature search on total knee replacement pain or any type of knee pain, we'll say total knee replacement, you're gonna not find much. You're gonna find two case reports and a couple cases speckled into other studies. Whereas DRG in less than 10 years, we already have 70, 80 patients mixed in with multiple studies. Next slide, please. So there's something going on there. There's something, this is working for some reason when the other systems really didn't. And this gets into the mechanism of action for dorsal ganglion stimulation here for nociceptive conditions. And essentially, if you look at the slide on the left side of your screen, what we're doing with this electricity in kind of layman's terms is we're tapping into the body system. We're applying this stimulus at a frequency that we want these nerve fibers that we're targeting to send out their messages, right? So if we apply that on a DRG, we're gonna activate the A-delta fibers and the C-fibers and those for pain and light touch, as well as our A-beta fibers, which are proprioception and other touch modalities. But we're also gonna activate these things called low-threshold mechanoreceptors. And low-threshold mechanoreceptors for A-delta, C, and A-beta fibers are really meant to modulate or to modify the touch or pain process. And so we're turning on the nerve fibers that are gonna be used by our own body to modify touch and pain. And they work through the endorphin system, which is part of the endogenous opioid system, which are gonna be the same receptors that Percocet and opioids work on, except really focally, locally, right where you need them and really there only. Next slide, please. Dr. Chapman, it's a one-minute warning. Okay, so we have a study that we are currently undergoing for osteoarthritis of the knee. We applied this data, and now we said we're gonna do this for osteoarthritis. The outcomes, we're going to be presenting them in July in Miami. And what I want to just kind of preview for you guys now is the one of interest here is called the WOMAC. And you see it there on the right. And I didn't know what these numbers meant. I said, hey, can you, to our researchers, can you show me what knee replacement numbers are like. And our numbers are very similar to the numbers that you get in a knee replacement. And it's going to be, this is going to offer a treatment option for when patients didn't have a treatment option before some of them. Next slide, please. So this, we're going to wrap this up really quickly. This is a, and the reason there's an elephant on that slide right there is because when we talk about SCS, there's something that's not talked about, and that's habituation. And that's the elephant in the room that no one speaks about. And we know that this is a problem with SCS. We know that it stops working over time in a group of patients, not in all of them, obviously. And that's been proven over and over again. Next slide, please. So a dorsal root ganglion stimulation is first shown by Robert Levy in an accurate sub-study analysis and showed that DRG had less loss of efficacy as SCS. Then in our, you know, we did a study about anchoring leads, and we had about 250 patients, a bunch of doctors pulled together, and it showed, we took, we additionally looked at it and we saw that there was, you know, that there was less loss of efficacy there as well. Next slide. Next slide. Of complications, we're seeing much less with anchoring the leads. And here, my real thing is, in my opinion, DRG should be the gold standard for CRPS. If I had a family member with CRPS, I would really want them to have a dorsal root ganglion stimulator over a spinal cord stimulator. Consider it for salvage, at least. The patients that have failed your SCS, that lost efficacy to SCS, that have already tried salvaging with another SCS system, try DRG and, you know, learn more about it. And we're, you know, I'd be happy if any of you in the future would like to reach out. And thank you for your time. Thank you, Dr. Chapman. Definitely can tell of your passion for this subject. And Dr. Chapman is extensively published. So any new APPs or experienced who are out there looking for more to read, we have just a great birth of knowledge and studies to look at preliminary research for all kinds of different pain syndromes on the horizon. I'd like to hand it over to Brandon, who's going to talk a bit about the trial to perm process. Thanks so much, Dr. Chapman. And I'll try to zip through this to see if I can leave a minute or two for questions at the end. One of the biggest things for when you're talking to patients about what this entails in the trial, so there's a period of time where they're going to get to find out if the therapy really works for them before we go forward into the permanent placement. A lot of there's a lot of technical jargon that swirls around this therapy. And a lot of patients can sometimes come to this with anxiety and frustration and ongoing pain. Oh, am I not visible? Hold on. There we go. That's better. Thank you. So when they when that happens, you know, you need to create a space so that patients can really come to understand what it is that you're hoping to offer them. And speaking in terms that make sense, you know, using analogies, taking the terms like DRG and CRPS, you know, and stimulation therapies and neuromodulation and breaking them down and making them understandable, including family members and caregivers. We have models all over the place. They're ubiquitous in our clinic. I always say, give me a second. Let me run out and grab a spine and I can show you all of this. We have pamphlets from the company, educational resources, and then relying on on your team, you know, leaning on the attendings, leaning on the other APPs, leaning on the device reps to say, hey, if you have any questions, we have so many touch points that we can use to help you to understand this and to know how this is really going to benefit you. Next slide, please. So there's a few things that go into the trial itself. There's a lead, there's an IPG, and then there's a controller. So it's a dynamic therapy that the patient is going to get to participate in as well. I'm trying to explain to them, you know, Casey touched on this a little earlier, so it's kind of like a traffic signal or a traffic warden who's dealing with kind of modulating pain signals before they get back to the brain, letting them know that they're going to have something on the outside of their body and they may have a strange sensation with kind of wearing something around where they're figuring out how it works and then letting them know that they get to participate in the therapy, too. We're going to set the fence posts, but they can turn it up and down. They can sort of participate and it gives them a measure of control over their pain, which is a huge and meaningful thing to give back to someone who's in this chronic intractable pain that they haven't been able to address. Next slide, please. So this is the really important one that I want to touch on. And there's a couple of different things for both insurance reasons and for how meaningful this is to the patient. So pain is only one dimension of what we're really focusing on here. But the things that a lot of times even patients will lose sight of when you're focusing on percentages and how much and give me a number and how much should this improve, I can't tell you the number of times that I've had a patient say, you know what, I'm not sure what percentage it is, but I was able to take my dog for a walk to the beach for the first time in six months. And that was a huge, meaningful thing for me. I could get up and I could go out with my partner or my spouse or my kids. I'm sleeping better. My fatigue is less. My brain fog is less. And then as a fourth dimension, how much did it allow you, if at all, to reduce your medication burden? This is another thing that's really meaningful to both insurance companies and to patients. So maybe I have to take less medicine and that's really important. Next slide, please. So this is just once we get to the point where we've done the trial, the trial seems to be successful and now we're looking at a permanent implant. These are patients with CRPS or causalgia. So their body can react kind of strangely to the idea that they just had surgery, right? They have a surgical wound. There's something there that they're recovering from that's another pain generator. So you want to remind them that the reason we went forward with this was because you had a really successful trial. You want to look at their goals and their sleeping habits and all those different metrics that we just talked about that made this a really meaningful therapy for them. I like to schedule post-visit implants at one week, four weeks, and then two or three months out. And then we sort of let them go out into the wild. And after that, we'll kind of touch base with them on, you know, as we need to, anywhere from like every three months, at least once a year when you have somebody with a neurostimulator that's in. But some patients are more anxious. Some patients want more adjustments, things like that. And don't assume that no news is good news, right? Some of these patients are elderly. They struggle with technology. You want to make sure that you have all these touch points and a really robust net of contact so that you can follow up and make sure that the therapy is doing what we want it to do. Next slide, please. So I think we touched on all this, so we'll kind of leave it for questions at the end. But this just kind of goes over everything that I just talked about, really maintaining that you have a nice, close network of contact for your patients and making sure that if they need to get in to see you to make sure that therapy is still working for them, that they can do that. Next slide, please. Okay. So I'll turn it over for questions, and thank you so much. Thank you, Brandon, for bringing it home. So I guess it's kind of nice to kind of conclude the presentation as sort of, you know, any maybe pearls from you guys as the faculty, quick pearls that sort of hit home when you think about DRG therapy. Casey, we'll start with you. I think it's just really getting comfortable with identifying patients, right, get comfortable with identifying CRPS1, CRPS2, your peripheral cartilage patients, because there are so many of them in your practice that can benefit from the therapy. And be careful with your documentation. Make sure that you document everything, be really specific to your patients. Keep the documentation individualized so that you can give them the best chance of getting approval. Absolutely. We know that, you know, no insurance buy-in, no product. Dr. Dickerson, could you share a pearl for us? Yeah. As soon as you can move a patient to definitive therapy for CRPS, a disease that we used to struggle to treat with DRG stimulation, treat those candidates appropriately, get them to therapy and recognize it's a community. And in regards to that community, you know, join the club and support each other because it's a novel therapy. And we were so lucky to have trailblazers like Dr. Chapman bringing us science and to see the evolution of our understanding of this therapy, to be an end-user and to have that science at the bedside with us. It's incredible. I can't say thank you enough to the work that you and your clinic does for us and our patients. So I just want to take a moment to honor Dr. Chapman because he, no, no, for real, and you don't get to hear enough, but as someone who has changed the lives of hundreds of people with this therapy, you have opened up so many doors for us to do that. So my pearl is if you are reading Dr. Chapman's patient papers, you're missing out. And if your patients aren't getting DRG, you're missing out. So maybe read those papers and get your patients some DRG. Wonderful. Wonderful. Dr. Chapman, I'm going to hand it over to you to give us something to bring home. I'd like to say, Dave, thank you for that. You didn't have to say this as I go over the top and unnecessary, but thank you. I appreciate it. And I appreciate you. You motivate me. All I can say is just give it a try, you know, take your worst patient, your worst patient and not just with, well, I don't want necessarily the worst CRPS patients, but if you want to try for back pain, if you want to try for peripheral vascular disease, if you want to try it for, you know, cause alga type two, take, take the ones that have already failed the other ones and give those a chance because you're not giving your patients the best opportunity if you don't let them, them try this. And it may be a little bit different for the, your attendings, but you know, we all have to change. The game is changing and it's changing quickly. And you know, we need the results that this therapy can provide if we want neuromodulation to continue the way it is. How about you, Brandon? Thanks, Dr. Chapman. Just one quick one more for the APPs in the audience than anything. There will be a lot of paperwork and legwork and touch points and connections that you have to do to work this therapy through for your patients and to talk to insurance about, you know, why is this important? Why is this so important? Why are we at a point where this patient really needs to try this? Please, please, please, please do the extra work, go the extra mile, bring the patient back in, talk to them about how to clarify what they're, what they're feeling and experiencing because it really works. This therapy is amazing. And if you're willing to do those extra steps and you're willing to really kind of bring it home and take the extra time to talk to the people who need to be convinced this can be life-changing for so many people. So it's, it's really important. Our jobs as APPs, we get to do that each and every day. So that's really important. And I hope we can all do that for them. Thank you so much. I just have actually one question for the group, for my own. So in our practice, we get a lot of patients from general surgeons who have like, you know, post hernia pain, you know, from like ilioinguinal neuralgia. So for me, you know, when, where do you think in the algorithm, you know, think PNS versus DRG for those types of patients? Follow the evidence. So I think that that's, you've got the accurate data. That's, that's some gold standard data that goes along with, I really think you measure everything else up against when you're talking about a focal, focal nerve injury, CRPS type two. And again, that high responder rate, it's, it's hard to think about something else, but that said on the flip side, some patients are candidates because of their neuroanatomy. And then, then you're thinking about, well, what can I offer them from a neurostimulation paradigm? And so I will say that you have to work it in terms of here's my first choice. Here's my second choice. And really ask who's the patient. Could you briefly let us know just a few things that we might see on an MRI for some of the newer APPs that would take it off the table for DRG? You can go ahead, Dr. Dickerson, that's fine, we got you loud and clear. Yeah, sure. So, so what, what takes DRG off the table effectively? Like who's got it? Yeah. Like spinal anatomy for some of our newer APPs. Absolutely. Great question. So we're going to review all the imaging and effectively if the neural foramina, look at the NAC guidelines, understand which targets could be utilized because just because one foramina is mod is severely stenosed. Make sure you've looked at those images with your physicians and as a team, and then recognize that if you can't stimulate above, below, or at that ideal target, you can sandwich, you can do a couple other ideas, but sometimes fusions and again, like I said, spinal anatomy will limit you from being able to, to utilize DRG therapy. Those are the things that I'm really, really thinking about, but with all the different techniques we have, you can sometimes utilize it to lateral approaches and other things to get in. But I would also say, talk to your radiologist, ask, is it really severe stenosis? Is it moderate? What is it? But surgery at that site is to me a hard stop right now. And that's the biggest one. If someone's had a prior surgery at the area where I'm going to be working on that said, that's where a retrograde approach can sometimes get you in from above. And so our colleagues in New York are masters of where there's a will, there's a way I know that we try to mimic that. Thank you so much. So definitely in the spirit of collaboration, you know, if it looks tight or if there's another surgery, stop collaborate with your physician. Don't just order the procedure. Okay. I think that was everything, right? And then there was one question about MRI compatibility, which was approved, I think was answered right in the chat. I think this year it came through, it was approved, FDA approved, right? And that the older implants, right, are grandfathered in, is that correct, accurate? Yeah. So, and the question also asked about fractured leads. So yes, it's the devices now, the old devices are grandfathered in and the new devices obviously are. And, you know, if a lead is fractured, it's the same as with SCS. It's not going to allow you to go into MRI mode. So if you have a fractured lead, which unfortunately, you know, I briefly went over the migration problem that occurs. It doesn't occur, excuse me, it used to occur. But if you anchor your leads, it doesn't occur. And you know, that problem's gone, but fractures still can happen. And you know, that's something that I think Abbott needs to figure out or other people get together and find some different techniques. But yeah, so you can't, it does work, except if the leads are fractured. Dr. Chapman, somebody asked on which levels you can place a DRG lead, but on label, of course. On label is T10 to sacrum. Off label, email, everybody. In the literature, it looks like you can place them in many other locations based on what people outside of the US are doing commonly. And as well, there's a case series in the US discussing the safety and efficacy of off label placement. Yeah, absolutely. So there's, I think, right on Casey and Dr. Chapman's website for their practice, there's a wonderful library of research articles, preliminary research out there. So I would encourage everybody who is joined to go ahead and take a look at that and get reading because you can really, it's sparking a lot of creative interest about the future of DRG. And if the research shows, perhaps they will become on label. Okay. And we're getting messages, last question is to Dr. Dickerson, your hat, what does it mean? Well, it's the Greek letters, delta, rho, gamma. So it's not actually a fraternity because nothing would be worse than combining toxicology of Greek life with the toxicology of a medical device. But when you put two things that are so toxic together, they might just be perfect only when you do camo with a silver stick. And leave the sticker on too. I love that. I love that. Patrick. Yeah, I think that's it, right? I think the last, I don't know if there's one more slide, Kim, but I just want to thank you, everyone who attended, especially in the faculty for taking the time on a Tuesday night to present such a wealth of knowledge. So I know I'm better for it and everybody else is for listening to you, such an all star cast. And then my last kind of plug, right, is for those APPs out there who are interested in learning more about Neuromod or want to kind of get involved, Casey and Nicole, who's on the call, are co-chairs of the APP subcommittee. So please get in touch with any of us. We'd love to sort of continue to evolve and expand our group. We were kind of newer, but we're slowly growing in sort of force and we have a whole host of educational events throughout the year between these webinars, Ask the Experts, Journal Clubs, there's an annual conference. So if you're willing to kind of join in and help us and lean on one another and meet a great group of people and colleagues, and now that I call friends, we'd love to have you a part of our group. So. Thank you again, everybody. We really appreciate your participation tonight. Bye now.

dorsal root ganglion stimulation therapy

chronic pain conditions

spinal cord stimulation

patient selection

education

responder rates

quality of life

lower limb pain

targeted pain relief

efficacy

safety