So, it's 3.30, I think we'll get started. So welcome, everyone, to our panel on peripheral nerve stimulation and establishing an appropriateness consensus. So, I'm Jay Carey, and me, along with Nasser Hussain, are going to be co-moderating this panel, and it's a privilege to have everyone here. So, this is going to be in a pro-con format, where we discuss peripheral nerve stimulation compared to different neuroaxial interventions, including spinal cord stimulation and dorsal root ganglion stimulation for varying painful indications. So, with that, I'm going to hand it off to Dr. Hussain to introduce our first speaker. Okay, fine. So, our first speaker is Dr. Saba Javed, who is an assistant professor from MD Anderson Cancer Center, and she's going to be presenting on CRPS and favoring PNS as a stimulation modality. Thank you, Jay. All right. Good afternoon, everyone. Happy to be here to discuss the Establishing Appropriateness Paradigms for Use of Peripheral Nerve Stimulation. My talk will largely focus on presenting evidence favoring the use of peripheral nerve stimulation in treating complex regional pain syndrome. So, complex regional pain syndrome is a chronic pain condition that causes prolonged pain and inflammation in an extremity. The prevalence of CRPS is estimated to be between 5 and 26 per 100,000 people, and affects up to 7 to 10 percent in trauma or post-surgical patients. I think we all know CRPS 1 occurs after illness or injury, but is not associated with any specific nerve damage, while CRPS 2 is associated with damage to a specific nerve. CRPS is a diagnosis of exclusion, but the Budapest criteria is certainly a helpful tool. It is based on symptoms and signs of abnormal pain sensation, temperature or skin color changes, changes in sweating, and decrease in mobility of the limb. The treatment is most effective when started early. Main treatment options include medications, including pharmacotherapy and physical therapy rehabilitations, psychotherapy, guided imagery, and neuromodulation, including spinal cord stimulation, dorsal ganglion stimulation, as well as peripheral nerve stimulation. Again, the PNS is an advanced therapy that provides focal stimulation to a specific nerve that has presented problematically with regards to pain. It involves placement of an electrode next to or close proximity to the targeted nerve. There are multiple varieties of PNS system, including a temporary or percutaneous device or implanted permanent device. So looking closely at the literature to assess the peripheral nerve stimulation data for CRPS, there were no high-quality studies such as RCTs or NMIS controlled trials published on this, but there are a number of case reports, case theories, or retrospective studies. This is a comprehensive 30-year review by Camilla and co-authors published in Neuromodulation looking at the use of peripheral nerve stimulation for complex regional pain syndrome. Table 1 on the left shows the baseline characteristics. Total number of patients included in the study were 165. The mean age and implant was 42. 76% of the patients were diagnosed with type 1. 25% of the patients were diagnosed with type 2 CRPS. So table 2 shows targeted nerve sites. The most common target nerve site reported was sciatic nerve at 42%, followed by ulnar nerve at 23%. Lastly, the mean and median nerves were reported at 14 and 13% respectively. Table 6 shows a summary of pain scores and opioid use. Baseline mean scores was reported at 7.4, with pain decreasing down to a mean score of 5 at one month and 5.3 at six months, with a score of 5.5 at 12 months after stimulation. There was a significant drop in pain score at one month, but interestingly, the relief carried over to 12 months with pain score remaining below baseline. There's also sustained reduction in opioid use, both in the total number of patients as well as the total opioid use at one month, six months, and 12 months follow-up compared to baseline. So from the same study, table 7 here shows summary of revisions performed. So out of the 165 patients, a total of 64.39% of the patients underwent at least one revision of their PNS. And when excluding revisions related to routine replacement of end-of-life batteries, a total of 56 or 34% of the patients had revisions secondary to complications related to the PNS system. The most common reason for revisions was lead migration reported in 24, or 15% of the patients followed by revisions for coverage failure or worsening symptoms occurring in 22 or 13% of the patients. 19% of the PNS cases were explanted during the review period as seen in table 8. And of these, the most common reason for explant was lack of efficacy in 50% of these cases followed by infection, I think, 20, 28%. So another study, this is a case series of 10 patients on use of brachial plexus peripheral nerve stimulation for upper extremity CRPS. This figure shows 10 patients who had pain reduction of 50% for the tibial, from the trial and received permanent implants. So a 12-month follow-up, the VA's pain score was improved by 57.4% in the study. This figure shows pain and quality of life improvements following the brachial plexus stimulation for upper extremity CRPS. Figure A shows that even after 12 months of brachial plexus stimulation, patients reported significant reduction via scores compared to the preoperative baseline. And similarly, figures B and C show the physical and mental components of the SF12 assay were significantly reduced following the treatment. This is a study by Kari and other co-authors published recently from the 19-Question Survey exploring PNS-relevant clinical parameters amongst pain physician in practice. The findings reveal that in treating CRPS, a notable majority of the patients or physicians would apply PNS before intrathecal drug delivery system at 71.3%, whereas only a slight majority would apply PNS before other neuromodulation techniques, including DRG at 56% or SCS at 52%. So in treating CRPS, most practitioners would apply PNS before all other forms of neuroaxial neuromodulation. Lastly, in treating diffused CRPS of the hands, more than half of the respondents, or 57.4%, use PNS as a treatment option. Typical targets include terminal nerve branches in the proximal or distal upper extremity, less typical included cerebroclavicular region or infraclav region at 22%, or cervical roots in the interscaling region. In treating diffused CRPS of the ankle foot, 67% of the respondents use PNS in treating CRPS, with the most common targets being sciatic or tibial nerves, as well as common peroneal. So there are certainly other treatment modalities available to treat CRPS, and patient selection is key to choosing a personalized therapy for each patient. For PNS, particularly, the surgical incision is very small compared to dorsal column stimulation. So if wound healing or infection is a concern, it is certainly a good option available for patients. Secondly, PNS has a far lower power requirement when compared to SCS or DRG therapy, which means patients can stretch out the therapy life for longer. And lastly, PNS provides for a targeted peripheral nerve stimulation compared to other modalities of nerve modulation, which may be superior in some pain etiologies. So really in conclusion, for purposes of this talk, we demonstrate the viable use of PNS in patients with CRPS. It can provide long-term substantial relief by a reduction in VS pain scores, opioid consumption, and it can improve functional outcomes. The complication rates are similar to those reported in dorsal column stimulation. Again, the most important key take-home point really is patient selection. Is it really the right therapy for the right patient? I think that's all I have for you. Thank you for your time. So it's nice to see the room fill up. And obviously, as we see this weekend, there's been such a great interest and emphasis for PNS therapies. But really, it's unclear exactly how and when apply these therapies, especially in the context of dorsal root ganglion stimulation and dorsal column stimulation. And so with that, I'm going to introduce my next speaker, Dr. David Dickerson, who is the Division Chief of Pain Medicine at Endeavor Health. Dr. Dickerson completed his pain fellowship training at UCSF and has been well-established in the space and extensively published. And Dr. Dickerson will be presenting on favoring dorsal root ganglion stimulation for treatment modality. Thank you, Dr. Kharia, for the great introduction. Pleasure to join my colleagues here for this afternoon PROCON session. So I'm going to talk about DRG as being a superior therapy over peripheral nerve stimulation. And so it says con. I'm not going to con you out of anything. But I am going to favor DRGS as a treatment modality for the sake of this talk. And at the end, I hope to have a very balanced representation of not just the debate, but where I really think things are. I'm going to spend a little more time actually talking about peripheral nerve stimulation than DRG stimulation, because as lawyers say, I could just go with racive soloquitur, which means the matter speaks for itself. As I present the accurate study data, right, I mean, 86% of patients had at least 50% relief at a year when in this comparative IDE study of DRG stimulation versus SCS. Oh, wait, that's SCS, not PNS. So I don't have a comparative study of DRGS versus PNS. But I have a pretty good study from 2017 that the FDA had their hand in supervising and making sure that was done to a high standard. And effectively, we see this really profound response for people presenting with CRPS type 1 and type 2 with dorsal root ganglion stimulation. The patients were treated with leads between T10 and the first sacral segments. So pivoting away from that data and saying, what do we have to put up against that? And yes, I could say, well, what are the challenges with the accurate data? It's an industry-sponsored study. It was an IDE. But it had an IDE. It was an IDE. So the FDA was involved in it. We want to believe that there's some additional oversight from that, even though it's an industry-sponsored study. So other parts to that, too. Well, that data was procured while that therapy, DRG stimulation, was really just a toddler at that point in the United States and was with equipment and techniques that we were still developing. So maybe it under-represents the outcomes that we could potentially obtain with 50-plus years of experience like we have with peripheral nerve stimulation. So let's talk about what 50 years of experience gets us with peripheral nerve stimulation. So a recent study from Dr. Hathaway and colleagues, 131 subjects were consented. 89 got randomized. And this is a peripheral nerve stimulation study, COMFORT. If you haven't seen this, it's an RCT. The breakdown of patients, 50% had back pain. And then the other 29% of patients in there were broken in the foot, ankle, and shoulder pain. So that's where we get our extremity. I'm assuming that those back pain patients did not have CRPS. And then we could say, well, some of those may be met criteria for CRPS type 1 or type 2. And the responder rate was 84% at three months in the 58 patients that received active stimulation. When we look at the degree of improvement, 60% improvement in responders at three months, 70% at six months. So I think this is pretty compelling data, but maybe not CRPS specifically. So up there, I'm going to say generously less than 15 patients with possible CRPS. So it doesn't really give me a signal there as to did we treat patients with CRPS. OK. Another study, going back a little bit further, really the first randomized control trial performed for is an inferiority study, or non-inferiority study, really looking at a placebo control approach to peripheral nerve stimulation. This is the STEM router device. Dr. Deer was the first author. And effectively, wireless PNS, 94 patients. They were implanted with neuropathic pain of the left upper extremity, upper extremity and trunk. 45 were in the treatment, 49 in control. Three months of therapy. Details, details, details. Let's get to the main event. 27% reduction in pain. Not very impressive. Kind of under the threshold for many people getting placebo level effects here, right? OK. But 2.3% in the control group. So significantly better than control. There's 7x plants, but 27% reduction in pain. Very different from the Hathaway data with 67% and then even more, 70% at six months. So very interesting that we, again, have some level of, well, it's not 86% of patients getting 50% relief, which we had with the ERG stimulation, the accurate study. OK. There were no adverse events. That's important. Regional cesium pain medicine publication looking at phantom limb pain and residual limb pain. Dr. Gilmour looking at a percutaneous 60-day treatment. So this is an interesting one, right? Because these patients aren't getting a permanent implant. They're getting 60 days of treatment. They get four weeks of sham and then they cross over. That's the control mechanism. Patients are effectively able to then get stimulation. 14% of the sham patients improved versus 67% of the treatment patients. And then four out of five patients at the time of reporting at the one-year mark still had 50% relief. So this is an interesting model. And I would say that these patients, by definition, meet CRPS type 2. They have a known surgical nerve injury. So look, a CRPS study for peripheral nerve stimulation. But it doesn't say CRPS anywhere in the body of this text. I'm making that inference for the sake of our argument today because I wanted to have a CRPS-specific study, and we've got one. OK. There we go. Indirectly. So back to this, the matter that speaks for itself as I started here. Really interesting to look at the rate of attrition, too, at the three-month honeymoon mark post-implant. 93% of patients had 50% relief. Drops down to 86%. Pretty low attrition. And by God, if anyone wanted to know, does SCS work for CRPS? This study shows you it does, right? Look, we didn't kill the controls. 72% with only that tiny, tiny reduction of responder rate at 12 months. So the ACRIB study might be some of our best evidence in a randomized trial for dorsal colon for CRPS. Pretty cool. All right. Now we're talking about three options for patients. And that's what it's really all about. There is some additional studies beyond ACRIB, but it is the largest, really only non-pilot sized randomized control trial. But I do think it's fascinating to look at where are the effects of DRG stem taking place. It's also happening in the brain. That last Morgana paper is really looking at the cortical level changes when you're stimulating the DRG. So why do we think it's helping? We know it's restoring T-junction filter function, inhibiting noxious and autonomic afferent signals. We know that effectively we're decreasing windup at the wide dynamic range neurons. And we're really reducing the neuroinflammatory cascade by modulating glial cell activity in the DRG and most likely throughout the CNS. And it stabilizes the neuron membrane. So it's never that simple because DRG stimulation is only approved for T10 to S1. So upper extremity, I'm going with some peripheral nerve stem for those patients. T10 to S2, you got to talk me out of it. Maybe I look at all these other factors and make a patient specific response. But it's good to have options for our patients that are founded in really good evidence. So I look forward to giving this talk maybe in two or three years and seeing where we are then. Thank you. What a great debate. Okay, so now I have the pleasure of introducing myself. I'm Nasser Hussain. I'm one of the pain docs out of Utah State University. I am one of the associate program directors of the residency, and I have the honor of talking with Dr. Gurtej Singh, who's one of the pain docs out of Baltimore, Maryland. He works with an orthopedic practice, and we're going to discuss the pros and cons of spinal cord stimulation versus peripheral nerve stimulation for non-surgical low back pain. So, you know, to get things going, I want to take a little broader view because I got a weird one to debate. PNS is great. Yeah, we all agree you can do PNS for any nerve in the body, sprint, reactivate included, but the issue is, and this is a trial that was actually conducted, the RESTORE trial, the reactivate trial, they state it can only be restricted to patients with non-radicular, non-neuropathic pain with clear evidence of multifidus dysfunction. Now, I'll raise my hand. Is there an objective way to really assess the multifidus muscle, maybe like a neuromuscular ultrasound, but it's really through physical exam findings. So there's no clear objective measure of multifidus muscle dysfunction. So from that standpoint, the therapy can't, you should be very restrictive in who you're choosing. The initial trials, this is from the FDA approval notes, excluded patients with a BMI of greater than 35. In my practice, I would say that's going to exclude a lot of patients. So from that standpoint, I think the therapy is a bit limited. It's also not indicated for patients with pain due to inflammation or damage of the spinal cord or adjacent structures, so things like adjacent segment disease or arachnoiditis, things that spinal cord stimulation anecdotally and through case report evidence has provided evidence of relief for. In an unpopular opinion, patients with spinal canal stenosis, can you use something like Reactivate for that? For chronic, those patients that have chronic low back pain, from that? Not really, right? And spinal cord stimulation may or may not work for that either. But there is evidence, at least, for spinal cord stimulation in that realm. So broadly speaking, the reasons why I would suggest or I would be pro spinal cord stimulation for non-surgical low back pain, is that Wonders reproduce positive results. We've had trial after trial after trial, which is level one evidence, evaluating spinal cord stimulation for chronic low back pain. Here's a systematic review that was conducted, for instance, that looked at 10 randomized trials on the topic, or randomized and prospective trials, that looked at chronic low back pain patients that were non-surgical. You can see here on the left, there's pain reduction, and on the right is opioid reduction, or opioid, ceasing opioid use. Spinal cord stimulation has a variation of effectiveness. We know that. There's a paper published in JAMA that just said that, you know, may not work as what we want. But here you can see that for non-surgical low back pain, there's a reduction in pain scores and an improvement in patients stopping opioid use with spinal cord stimulation using non-surgical low back pain. The second reason why I would vote for spinal cord stimulation for non-surgical low back pain is a variety of indications, aside from just multifidus muscle dysfunction, for its use. Things like spinal canal stenosis, there's a randomized trial for that. There has been randomized trial for non-operative discogenic low back pain, which now we have other therapies for, but spinal cord stimulation can be beneficial for that as well. Radiculopathy, so low back pain with radiculopathy-type symptoms. The Hyland study, again, displayed benefit of spinal cord stimulation, traditional dorsal column for this condition. And then finally, the study that most of us refer to, the 10k spinal cord, 10 kilohertz study, high frequency stim, for chronic non-surgical low back pain. There are two studies for this, again, demonstrating benefit from a pain standpoint, function standpoint, and through ODI, and an opioid use standpoint with spinal cord stimulation. The third reason I would favor spinal cord stimulation over Reactivate is the durability of lead placement. So again, per the FDA guidelines, you can only place the Reactivate device at L2, the L2 medial branches, technically the FDA indication. So we're on label right now. In contrast, spinal cord stimulation leads can span a wide variety of dermatomes and regions. Typically, T8 to T10 to cover the low back, but you can do different areas as well because of that. And this here is just a flow diagram of what we have developed for spinal cord stimulation from a device standpoint and the durability in the research. Now, ECAPS is the big thing. So again, there's growing evidence regarding its use. Finally, for me, one of the biggest things is evidence. The hierarchy of evidence, as we all know, level one evidence is considered to be the best, right? Randomized trials, meta-analyses of randomized trials. In my opinion, for Reactivate, you know, it's a newer therapy. Obviously, there's not going to be a lot of evidence just yet, but spinal cord stimulation has had repeated randomized trial evidence for non-surgical opioid. Reactivate, that evidence is just growing, so it's not its fault, but there's retrospective data coming out and prospective data coming out, but it's still not randomized. If you look at the initial FDA trials of Reactivate, there is a sham responder rate, and it's about 30 to 40 percent. Now, you can argue with me, and I'm sure people will, that yeah, it takes about six months for the device to start working, but still you can't argue with that fact that there is a possible sham effect with the device. So in my opinion, spinal cord stimulation for non-surgical lobotomy has data from a wide array of evidence with primary evidence from randomized trials, which is what we should use as pain physicians. So, in conclusion, my con take, so in an academic way, you want to consider using spinal cord stimulation for non-surgical low back pain, but PNS may have a role, especially if multifidus function is determined to be the primary cause, primarily through subjective physical exam maneuvers. On my real take, neuromodulation can be used for non-surgical low back pain, however, the durability of the therapy needs to be investigated further. So that's the Reactivate procedure, in my opinion, needs further evidence regarding its use for me. Good afternoon, everybody. I just want to thank Dr. Carey and my colleagues for the kind invitation. I am stepping in for Dr. Chris Gilligan. Really, that's the correct way to spell my name, but Chris, unfortunately, had some family obligations, so if you'll indulge me in presenting for him. I think what's most important here today is to discuss what is actually standard of care. So that's point number one. Does the therapy actually work? Do we know how the therapy actually works? Can patients be reliably identified? Are the results durable? Are the results reproducible outside of randomized controlled trials? And is the therapy truly superior to what we have as current standard of care? I think when it comes to those who treat non-surgical refractory low back pain, and to be fair, I am actually faculty for Nevro and talk about the 10 case study all the time. The second point to make today is what are you actually treating? So for me, as a physiatrist, it has become absolutely routine for my team to perform a prone instability test and a multifidus lift test on every single patient that comes to clinic with chronic axial mechanical low back pain. If there is a radicular component, SCS works, we know that. That's really not part of today's pro and con. It's what about those that aren't radicular, that are more mechanical in nature? When it comes to discussion about multifidus atrophy, I think it's fairly clear how impressive the atrophy is on that on that slide. But yet I've certainly implanted folks whose multifidus atrophy is quite small. It's because we're not just simply treating an MRI, we're treating the clinical indication as well as the physical exam findings to help these patients literally change their entire life. Evidence. Well, I think this slide should win, and if this one doesn't, I've got a slide later that will, because the evidence for multifidus restoration and restorative care is becoming overwhelming. And for those who attended other lectures here at NANS today, the restore data was also published versus optimal non-surgical care. So first was a proof of concept. So this is a reactivate A. You can see greater than 50% reduction in NRS. You can see greater than 20 point reduction in ODI. So this sort of proof of concept helped us establish that yes, there is a valuable therapy in treating patients with mechanical low back pain. Proof of efficacy was determined by this level one randomized control trial. What I would love to debate further is two-year data enough or do you want five-year data? I'm sure my patients all prefer five-year data because we know the sustainability. And again, you can see not just at one year but at all time points after 60 months, you do continue to have reduction in ODI, reduction in VAS, and improvement in the quality of life measures. So reactivate PMCF was the compilation of five years of real-world data. So again, nice to have something that's not in an RCT because as prolific as Dr. Gilligan is in spearheading some of these studies, why don't we get it out into the real world for those of us who maybe don't have the hands of Dr. Gilligan or may not be say cherry-picking all our patients perfectly. That too you see here with reductions in NRS, ODI, as well as improvement in EQ5D. So the compilation of not just RCT data, the compilation of real-world data is again not just something that's at one to two years worth of efficacy and proof that actually stands out well past 60 months. This is a form of a tornado graph showing utilization of the neurostimulation in patients who perform that one-hour restorative therapy session per day. That must have been duplicate. And so here's another way we can actually look at it. And so you can see for individuals in that first year, I mean ideal would be 365. So 241 out of 365 for those in the first year. By the time you get to five years and patients continue to have this benefit, what you see is that they don't rely on the therapy as much, but they do still continue to use it about half the year. Reactivate C further shows changes in another way. This is a tornado plot because each of those dots are patients and you can see how they have improved the x-axis showing the NRS and the y the ODI. The restore data that just came out here clearly demonstrates when you talk about actual proof of superiority, the optimal medical management track actually got worse by 2.9, whereas actually got better by 2.9, whereas the reactivate patients improved by 20 points. You can see the tornado plots on the right for reactivate at the top right and control on the bottom right. Yes, there are going to be some folks who if you optimally manage them medically will get better. That's fantastic. You don't need to have something implanted. But the amount of patients who actually did worse is what we all see day-to-day when not using a restorative therapy. Proof again, basic science. Here's some stained slides of showing decreased fibrosis and increased vascularization in the multifidus tissues. More of these studies do need to be performed and presented so that this portion of the data can become far more robust. But if anyone questions, you know, does this work at a cellular level, it absolutely does. So it's not just something that, you know, you see a contraction of a muscle and it works. Again, accumulation of data. Here's the evidence portfolio. So if the earlier slide wasn't enough, here's more data all about reactivate for this specific disease condition. So what do we know? This is exactly what we know. We know that over a five-year period of time with multiple different studies performed in multiple different ways, patients with REACTIV-8 restorative neurostimulation succeed. Succeed on the pain scale. Succeed in the quality of life measurements. Succeed in function and ODI. So while restore will continue out over the next few years, I think we can all predict where that yellow graph is going. Finally, did we check all the boxes that we intended to today for the PROCON debate? Does restorative neurostimulation for the treatment of mechanical chronic axial low-back pain fall into the standard of care? And I think the slides today would help establish that it does. Thanks so much. Thank you, Dr. Tsang. And then for our last pain presentation, we'll be discussing PROCON use of peripheral nerve stimulation or dorsal column stimulation to treat peripheral focal neuropathic pain. So I'm Jay Carey. I'm faculty at University of Maryland, and I'll be presenting PRO, favoring PNS as a treatment modality. So I want to start off with a simple case presentation. I know we have a robust amount of data discussed so far, but going back to our patients, you know, this was a 35-year-old male I had with a surgical history of a right Achilles tendon tear with a repair and continued burning pain and numbness along the posterior aspect of the lower leg and lateral foot, aching pain with some plantar flexion as well. And some of the main questions I always ask is, you know, is there a focal distribution or neuropathic features? Is there a clear peripheral nerve dermatome implicated and or nerve injury? And sometimes I have electrodiagnostic evidence of a nerve injury as well and or response to a nerve block. And these are features that really help me understand if peripheral nerve stimulation is an appropriate treatment modality. And certainly this patient had fit most of those features, but they had already tried dorsal column stimulation by the time they'd come to me, and unfortunately, they weren't able to get great capture of the sural distribution or they got the entire leg without perfect, you know, analgesia over their painful dermatome. And so we opted to proceed with the peripheral nerve block first, and I was able to establish to myself and to the patient that the sural nerve was implicated and could be a potential target for neuromodulation therapy. So taking a step back, you know, what are some of the barriers to adoption for PNS therapy? And even though I'm favoring PNS, I really want to be balanced and evidence-based in my talk here. Really, we don't have any well-designed RCTs comparing PNS to other neuroaxial neuromodulation interventions, whether that be dorsal column or dorsal ganglion stimulation. The evidence is still very nascent and lacking. And therefore, a lot of insurance companies and, you know, commercial pairs consider PNS to be an experimental therapy. And as such, you know, we have significant variances in our outcomes when we're currently utilized, and this is reflective, presumably, due to variances in practice patterns and utilized devices. So to better understand that, we recently conducted a survey study with 100 physicians that utilize PNS as a therapy, and we found that the most indicated indication for physician preference was a peripheral neuralgia to favor PNS usage, 95%. And going back to the data, we have a, you know, a plenty and a robust amount of data favoring dorsal column stimulation, intrathecal drug delivery for conditions including CRPS, but really, you know, we have the evidence, but really, is that something that we want to incorporate to our practice? When looking at just CRPS or focal neuropathic conditions, you know, when we queried these patients, most physicians said, well, you know, 52 to 56 said, you know, we favor PNS over spinal cord stimulation and over dorsal ganglion stimulation, regardless of the evidence basis currently. And even though intrathecal drug delivery also has a historic track record and evidence, 71% of patients said they'd still prefer PNS for utilizing intrathecal drug delivery. It's also important to recognize patient preferences. So Peter Statz and Amit Gulati used a blinded fashion to provide patients information on various neuromodulation interventions and ask patients, you know, which system would you like to use? And we found very overwhelmingly that permanent implant with spinal cord or dorsal ganglion stimulation was a third or fourth choice for patients in about 90% of them. And in fact, 85% and more recommend, really preferred a temporary PNS system. Well, that's not really apples to apples, as one is temporary and one's a permanent implant. But even when they looked at permanent PNS, still 90% of patients said they would prefer a permanent implant peripherally versus something neuroxially. And these are patients that were blinded and given all the evidence bases and information, including pros and cons for all the varying therapies. So precision targeting, I think this is something else that PNS does extremely well and I alluded to in my case. So when we look at the entire upper extremity and all of our peripheral nerve targets, we really can provide very focal targeting with PNS compared to dorsal ganglion stimulation. For example, my ultrasound pictures are never this good to capture a coil, but shown here is a target of a temporary PNS lead over the musculocutaneous nerve. And we can show that it is targeting just those fascicular fibers of the musculocutaneous nerve that are implicated in this patient's pain. And certainly, you can target anywhere all the way from the endoscaling triangle to the supra and infraclavicular regions, all the way to your terminal nerve branches, either above or below the elbow. And so really, you can start to utilize precision care and targeting for what's appropriate for your patient and their pain presentation. And that's similar in the lower extremity. We have seven targets in the lower extremity. And so rather than stimulate everything at the dorsal column, which might be overkill and require the high charge burden, and still may not get the appropriate capture you need for that painful distribution, something as simple as placing a lead over the tibial nerve that is the only implicated nerve may seem, as proof of concept, to be more favorable. And then let's talk about system variances. PNS offers a lot of variances in systems. And obviously, that can lead to some detriment, because we have varying practice patterns. But there is a silver lining here. I can really tailor my therapy within PNS for my patient that's sitting in front of me. I can choose a system that utilizes one of four stimulating electrodes. Pulse generators, most of them are externally powered, but there are some internally powered as well. I can choose the duration of therapy from all the way from a temporary system to a more permanent implant. I can even choose a more secured implant with tines and anchors, should that be implicated. And when looking at charge delivery, PNS is actually quite robust. It can go all the way from pulse frequencies and amplitudes that are negligible to very high energy systems to the gigahertz or milliamps with amplitude to really get the appropriate capture that you require for analgesia. In future directions, I'll harp on this again. We need data. We have some data for PNS, but we need comparative data looking at the same painful indications and seeing how PNS fares in comparison to dorsal column and dorsal root stimulation. We also need standardization of practice patterns to establish better patient selection, appropriate nerve targets, as well as prognostic measures to better utilize and understand the therapy. So in summary, I want to, you know, close by saying PNS is a highly safe neuromodulation intervention. That's something that we recognize, that's something that the data shows us, and that's something that our patients are also starting to favor. Additionally, PNS provides maybe more reliable coverage of a discreet and focal dermatome over a noraxial intervention. Thank you. And now I'd like to introduce the Kahn debate favoring dorsal column stimulation. And this is Dr. Matt Chung, assistant professor at MD Anderson Cancer Center. Thanks, Jay. So, yes, I'm Matt Chung, so I'm going to be talking to you guys about treating focal neuropathic pain here, Kahn in favor of SCS-DRG as a favorable modality, treatment modality here. So before we start, really, just that this is quite a large topic or area of pain, right? So there's, the etiologies are vast, there's, it ranges from idio-infectious all the way to iatrogenic causes. Now, with all these different types of etiologies, there's many different proposed mechanisms for all these, you know, etiologies similarly. So, you know, with that in mind, we have many mechanisms of actions for, that we're actively considering for SCS and DRG, all of which may have some role continuously. However, with peripheral nerve stem, you know, we see some mechanisms out in the periphery, but also some proposed mechanisms central with inclusion of this therapy, and a lot of these land from SCS and our understanding of SCS and dorsal colon stimulation. So it becomes a little confusing, but certainly, the real question becomes, what does the evidence suggest here? And so if we really needed to narrow it down just for, just to really determine one topic of interest, I think painful diabetic neuropathy is one area that we can really look into. And it's quite obvious, right? So highlighted in dark blue and light blue, we have SCS and DRG data that is quite robust, and we see long-term data using high-frequency stimulation, even including tonic stimulation, where we've seen significant pain improvement and quality of life measures, and with Dr. Peterson's most recent RCT to date. Now, in comparison, unfortunately, in peripheral nerve stem, as Jay eloquently discussed, we're quite limited. And beyond focal neuropathic pain, we see a lot of that elsewhere for other indications, and we're quite limited to K-series and retrospective studies and small prospective cohorts. And even with that, we're seeing a lot of heterogeneity among those etiologies, as I described. So not one with, not necessarily dedicated to painful diabetic neuropathy in that sense. So we have to be understanding of, you know, the coverage and durability of PNS really addresses a focal and discrete nerve, as Jay discussed. You know, it's important for us to consider as clinicians that the chronic pain, much like chronic focal pain, can certainly be dynamic and has a risk of being progressive. So is a peripheral nerve stem enough to measure or counter, you know, counter a lot of these things in mind? And certainly, the question then becomes is, if not responsive to peripheral nerve stem, what's the next step? Is SES or spinal cord stimulation or central stimulation a reasonable next step? Should we be basing this on a tiered basis on level invasiveness or even level of acuity or chronicity or, you know, vaguely on basis of severity, depending on, again, your etiology? You know, I could make a case against SES, obviously, with long-term results with habituation and tolerance. However, we've not really looked into that too much in the space of peripheral nerve stem. So something for us to continuously investigate. I bring up this piece here of predictive value of diagnostic blocks. I think, you know, we've seen some suggestion that sympathetic blocks have a good role of teeing up of how we can see the long-term effects of what dorsal column stimulation may help us do. You know, there has been an investigation for peripheral nerve blocks and in practice to identify whether these are good candidates, as Jay eloquently described, really for long-term outcomes of predictable relief. We're not quite seeing that. It's, I think, in practice, everyone can agree that it's mainly to ascertain and confirm an anatomical coverage. And so I think there's a lot to consider. I mean, obviously, I've demonstrated, I've showed you the vast differences of evidence that's available for SES and DRG. However, compared to peripheral nerve stem, you know, it warrants further study and certainly with the question further becomes more so, how do we integrate all these therapies? It's not perhaps, and I'm being a little contrary to kind of the pro and con, you know, purpose of this dialogue and discussion here, but certainly it becomes more, how do we integrate all these into a more predictable manner in a real-life, real-world scenario? Do we integrate these based on chronicity again or severity or etiology? And I think another point to certainly throw out there is, you know, with all these various waveforms and programs, how do we integrate this into the idea of peripheral nerve stimulation therapy? So a lot for us to, as kind of one of the last ones here, I think it's really for, you know, something for us to continue to look into. And there's a lot of promising work that's in the pipeline and a very exciting time for our field here. Thank you, Dr. Chung. We have a few abstract presenters as well, and then I'm gonna open up the podium for a conversation and Q&A. So it's my pleasure to introduce Dr. John Hathaway, owner of Northwest Pain Care from Spokane, Washington, and he's gonna be speaking to us on two abstracts. First, pain outcomes from the COMFORT-2 trial, and then real-world data showing pain relief from peripheral nerve stimulation delivered by micro-IPG. Thank you. Thank you. Good afternoon, everybody. Pleasure to be here. And as you've heard with some of the previous presentations, we have a lack of evidence in the peripheral nerve stimulation world. So what I'll be talking to you today about is the COMFORT-2 study. Yesterday, Dr. Mitch Engel presented 12-month results from the COMFORT-1 study, which has been published both at six months and 12 months. The COMFORT-2 is a second randomized controlled study looking at outcomes for peripheral nerve stimulation. So COMFORT-2 is a post-market RCT. Inclusion criteria are post-surgical, post-traumatic, peripheral neuralgia, mononeuropathy. Other neurology are neuropathic pain or osteoarthritic pain. Exclusion criteria, anyone who has a presence of another implantable device. Intolerance to an external wearable device. Previously failed spinal cord stimulation or peripheral nerve stimulation. And any patients who are on greater than or equal to 90 milligrams of oral morphine equivalents per day. Primary endpoint was three months. The responder rate was defined as those patients that had greater than or equal to 50% pain relief. Secondary endpoints included percent change in pain, change in patient reported outcomes, including ODI, BDI, BPI, PGIC. And we also looked at the usability of an external device for peripheral nerve stimulation. On the left of the screen, you can see the study design, which is exactly the same as the COMFORT-1 study. Patients were screened. If they were not successful, they exited the study. If the screening was successful, they were randomized in a two-to-one fashion, two-to-one active to control. The active group was peripheral nerve stimulation with conventional medical management. And the control group was conventional medical management alone. The control group could cross over at three months. Most patients did cross over. If the patients had a successful trial, they went on to implant. If the trial was unsuccessful, they were exited from the study. They then went on to the three-month endpoint, and then the patients are being followed for at six, 12, 24, and 36 months. So 18 pain management centers were included across the United States, two-to-one active control as active to control randomization. As I said, 185 patients were randomized, 121 in the active group, and 64 in the control group. Enrollment is now complete for the study. It's ongoing for follow-up, and we are following these patients for 36 months. The other important aspect on this slide is the distribution of pain targets. The most common was low back, 82 patients, shoulder, 26 patients, knee, 43 patients, and foot and ankle, 34 patients. So looking at the outcomes in the active arm, PNS and conventional medical management was statistically superior to conventional medical management alone. You can see in orange the control group who had very little change in their pain scores. If you look at the solid blue line, that is the comfort two results out to six months. Remember, these are early results. These have not been published yet. And then the dashed green line will be the comfort one. And what you can see from that graph is the shape of the graph is almost identical between the comfort one and comfort two studies. We have 80 patients that have made it to one month, 64 patients to three months, and 38 patients to six months in the comfort two study. And in the control arm, 58 have reached one month, and a total of 46 have reached the three-month endpoint. Looking at the responder rates for those three timeframes, 70%, 78%, and 82%, and the percent pain relief, 55%, 66%, and 64%, respectively, very little change in the control group. 30% of the patients were high responders, defined as 80% or more pain relief. And what's important is that we had consistent outcomes across all of the pain targets. There was also consistent outcomes between comfort one and comfort two. Looking at functional outcomes, first, the Oswestry Disability Index. We're gonna talk a little bit about MCID, minimal clinically important difference or holistic outcomes. A greater than or equal to 10-point change on the Oswestry is considered significant. As you can see here, 75% met MCID for Oswestry at three months, and 71% met MCID for Oswestry at six months. Looking at other functional outcomes, BDI, BPI, and quality of life, you can see that all of those improved in the active group. The Beck Depression Inventory, 72% met MCID. With the brief pain inventory severity, 83% met MCID. For the brief pain inventory interference, 86% met MCID. And for the EQ5D5L quality of life, 77% met MCID. Looking at PGIC and satisfaction, at three months and six months, the PGIC met MCID, 97% and 92%, respectively. The majority of the patients were very satisfied with the PNS system. They reported comfort with the system, and they also demonstrated ease of use. So in summary, there was an 82% responder rate at six months with statistically significant reduction in pain and functional outcomes. There were no reports of serious adverse events, and also important, no reports of pocket pain at any anatomic location treated in the study. Subjects reported the external wearable at all anatomical locations to be comfortable. A micro-IPG can be used at various pain targets with positive outcomes and safety. And the results of the Comfort 2 study so far are echoing the results of the Comfort 1 study. Thank you. The next one. All right, changing gears a little bit. This is gonna be a presentation on real-world data showing long-term pain relief with a peripheral nerve stimulation system delivered with a micro-IPG. So what we are finding today is that insurance companies are no longer happy with randomized controlled studies, even two randomized controlled studies with level one evidence. They're also looking for health economic data and real-world data. Patient registries are a valid source of real-world data. A registry was initiated for patients implanted with a micro-IPG to provide real-world data as part of an ongoing effort to protect and enhance appropriate patient access to the peripheral nerve stimulation therapy. The real-world registry was open to all patients who met inclusion and exclusion criteria. Patients obviously had to be prescribed a micro-IPG implant. Patients had to provide informed consent. The patient had to be able to operate the system, and the patient did not have any evidence of substance abuse. Patients provided consent prior to the trial, and outcome data was collected at regular intervals every six to nine months post-permanent implant. The patients who did not go to implant were exited from the registry. The patients followed the standard of care for PNS implants. The registry is ongoing, has IRB approval, and follows the standards of good clinical practice. So what we looked at in the registry is patient global impression of change. This is a validated, easy-to-use, patient-centric instrument that provides the patient's evaluation of their overall condition, and its use is recommended by the impact group. PGIC allows patients to report on multiple factors that affect their life, including functionality, mood, pain, interference, and other items. So it's really looking at things beyond pain relief, and better reflects a patient's assessment of successful therapy, and may better reflect real-world practice. Multiple authors have documented the association between changes in pain and improvements in PGIC. A limitation of PGIC is that it does not individually score the impact of the individual factors that go into the patient's consideration. Minimal Clinically Important Difference, MCID, for PGIC is the report of improvement. So we have data for 2,273 peripheral nerve stimulation patients that have been followed up to 31 months post-permanent implant. Patients had permanent implants performed at over 150 pain physician practices, both private and institutional-based. Anatomic locations included greater than 40 nerves or nerve combinations. Patients in this analysis provided informed consents and completed at least one implant survey, regardless of anatomic location of the implant. And this registry includes both on-label and off-label indications. Patients with missing data were excluded from the analysis. So again, looking at the distribution of pain, again, there was over 40 different nerve targets, 11% shoulder, 43% low back, 19% knee, 10% ankle and foot, and 17% in other areas. The percentage of the major areas in this real-world data closely followed what we saw in both Comfort 1 and Comfort 2. Looking at the PGIC from this, there was 94% of the patients reaching MCID for PGIC. 19% were very much improved, 46% were much improved, and 29% were minimally improved. 4% with no change and less than 1% worsened. So this table shows the various anatomical locations and what you can see is that the percent of patients achieving MCID varied from 86.4% to 100%. We tracked all of these locations. And looking at the data very closely shows that the response rate was consistent through all of these targets, and there really wasn't a greater or lesser improvement for a particular anatomic target and or nerve. Again, the consistency with the Comfort data, those reaching MCID in the Comfort study was 95%, and with the real-world data, 94%. So again, it very closely echoed the RCT results. So in conclusion, payers are asking for more published data to support coverage of the appropriate use of PNS. We now have two ongoing RCTs, the first one with published six-month and 12-month data, the second one in progress. We have real-world data, which will be published soon, and we have published health economic data. This real-world data provides confirmatory evidence of the data published in the Comfort RCT, providing further support for patient access to appropriate PNS therapy. Data from this registry aligns very well with published data from the Comfort 1 study. As I mentioned, there's a second Comfort 2 study, and we have a published health economic data study as well. Thank you very much. And now I'd like to present our last. And our last presenter is Dr. K.G. Wang from the University of Michigan, who will be presenting on the anti-inflammatory mechanisms and central pathways of auricular vagal nerve stimulation on visceral hyperalgesia in rats. Hello, everyone. I think I'm the last speaker of today's next annual meeting. So it's my great honor here to be here to present at the 2025 next annual meeting. Today, I will share our lab's latest research findings about anti-inflammatory mechanisms and the central pathways of AVNS on visceral pain in rats. So, irritable bowel syndrome, IBS, affects approximately 4% to 15% of the whole global population, and with visceral pain being its primary symptoms. There is a currently lack of the effective treatment options in treating visceral pain. Visceral hypersensitivity is a primary cause of visceral pain which is largely attributed to low-grade inflammation. Vagal nerve stimulation, VMS, has been shown exert anti-inflammatory effects via the chronological anti-inflammatory pathway, which is called the AIP. So our hypothesis is when we do AVNS, the stimulation signal was transmitted to the NTS. And then there will be two pathways. One is the sacral efferent pathway, the green pathway. The signal from the NTS was transmitted to the Balanchine's nuclear, and then travels through the sacral efferent to dominate the distal colon and the rectum. And the other pathway is the vagal efferent pathway. The signals from the NTS will be transmitted to the dorsal motor nucleus of vagus, and then will travel through the vagal efferent pathway to dominate the proximal colon. And both of these two pathways, they will release the acetylcholine, and which will take an effect on the alpha-7 electronic acetylcholine receptor, and have an effect of pain and inflammation reduced. So the aim of this study, so the aim of the study is to, we want to study the effect of AVNS on visceral pain in a well-established low-dose model of IBS. Central pathway involving DMV and the Balanchine's nuclear, and the CAIP pathways involving the alpha-7 electronic acetylcholine receptor. So the experiment method is as follows. We use a 10 days old pups, which will receive the intrachronic acid. At the age of six weeks, we inject AVNS into the DMV, Balanchine's nuclear, and both DMV and Balanchine's nuclear. At the age of eight weeks, we implanted the unilateral alluclear contract for AVNS and the EMG electrodes to response it to colorectal distension. So let's move to the results. We measured the EMG values during colorectal distension in rats under different pressures to assess pain. So the white cell is the value of the EMG, which represents the pair of the reds. The first bar represents the EMG values of shim or no-stimulation reds. The second bar is the EMG values of AVS group. We can see AVS decrease the EMG values under all distension pressures. The third bar is the EMG values under different pressures with AVS plus DMV blocked reds group. We can see when we block the DMV, EMG at 20 and 40 were blocked, so it indicates that mild pain is mediated by the vagus nerve pathway. The fourth bar represents the AVS plus BN blocked group. We can see when we block the BN, EMG at 40, 60 and 80 were blocked. It indicates that severe pain is mostly mediated by the sacral effluent. And the fifth group represents the group of AVS plus both DMV and BN blocked reds. We can see EMG values at all pressures were completely blocked. For the preflow mechanisms, we used an alpha-7 electronic acetylcholine receptor antagonist, MAOA. Compared to the AVS group, we can see it partially blocked the AVS effect at 40 and 60. So we can get some conclusions. First one, AVS improves the colorectal hyperplasia in a rodent model of AVS, and the central pathways of AVS include the vagal effluent pathway and the sacral effluent pathway. The preflow mechanisms of AVS involving CAIP, but its effects are not entirely dependent on CAIP, as the central pathways are also involved. Okay, thank you. So now I want to open up the floor for questions and discussion. But before I start that, I want to just really, you know, credit Nance for helping us organize this panel. Everyone here utilizes multiple neuromodulation therapies, not just the ones we spoke about. So really when balancing these different therapies, when considering patient care, it's really helpful to understand some of the nuances. So you really have a wealth of information on this panel here. So if anyone has any questions or concerns, please feel free to ask them now. I'll also ask a question to Gortej. So in regards to reactivate and the data, you know, I guess I've seen it in acute pain with certain medications that have come out that have been studied by industry. But then non-industry sponsored studies have possibly shown a lesser effect. Do you think the same thing is happening with some of these chronic pain therapies, especially with something like reactivate where it's primarily driven by the company? There's clearly always going to be some form of bias when our industry sponsors, you know, put together these large RCTs. It kind of does become our responsibility as individual clinicians to try to put together our own real-world data so that, you know, we can help to either fully substantiate or partially substantiate the findings with industry studies. I think what makes reactivate so different is its restorative power. This is not a palliative therapy, and every single other colleague who's presented today has presented you on palliative therapies. And so from that perspective, in my cohort of implanted patients, we're seeing very similar metrics when compared to the RCT and actually am currently enrolling a real-world study right now. So it's too early to tell. You know, we're just only eight patients in, hopefully get to 50. But when you see these patients' lives literally change in front of you over a 9- to 12-month period, it's just something you cannot unsee. But the fact that it's not a palliative treatment, it's actually a restorative treatment, it's a completely different mechanism, and you're not really worried about some of the other column pathways. I think that's where you may not see that discrepancy long-term. Thank you. And Penn State's better than Ohio State. All right, for that, he gets another question. So I agree with that. I think that's a really interesting point that he makes. The one question I have, and this is for the panel overall. It doesn't just have to be Cortege. So it's a restorative therapy, and PNS is a restorative therapy, I was told, too. Do you think that we should be seeing MRI changes with something like Reactivate? I mean, maybe we haven't studied it just yet, but I know I haven't seen too much evidence of that. No, I don't know why, you know, we're all curious as to what the multifidus looks like five years later. Just look at the patient. Like, you know, nobody goes back after somebody has a successful spinal cord stimulator and starts imaging the brain. Nobody images the spinal cord after you put in a dorsal column or a DRG. So I don't know why everyone's so fixated on, well, what does the multifidus look like? If, you know, my 87-year-old patient was supposed to go to a nursing home, and now two years later she's still living at home independently, I don't need any MRI to tell me did this thing work or not. So, you know, yes, there is, I mean, there are bench data, right, shows decreased fibrosis, shows increased vascularization. So we know we are making tissue impact. But if we're going to get, you know, hyperfocused on, you know, did a muscle grow or not, as opposed to what the actual data shows, losing our focus. I think that's a great point. I think you treat the patient in this situation and not the image, which is what we should be doing as pain medicine physicians. And I think it would be certainly challenging to associate any muscle change and just attribute it to the PNS, right? Because in certain situations or most situations, the hope is that the patient has sufficient relief so that they're now engaging more in physical therapy, rehabilitation and conditioning the muscles. So that, in fact, the regrowth and regeneration of the muscle isn't necessarily directly from PNS, but more so the physical therapy, which is what we tell our patients essentially. Hey, we're doing these therapies for you to still continue the physical therapy, right? A lot of our interventions is so they can tolerate the PT ultimately better and continue the conditioning of that. Another question for the panel, and I'd really like to hear everyone's insight on this, but what are some gaps in care in PNS as a treatment modality? And when we do this again in three years, where do you see the field evolving or where do you see things taking shape? So I think we're going to, if we continue on the path that we're on, we're one in five patients who need these therapies get access because of insurance limitations. It's going to be abysmal to think we haven't made any changes there. But hearing Dr. Hathaway present, seeing the data that comes out of these meetings that is pre-publication, I think suggests that the future is going to hopefully have more access. I think it's going to be disease-specific, and I think that that's probably important because mission creep or labeling creep happens, and it's not going to help us when we're looking at real-world outcomes. Because coupled with more access would probably also be more scrutiny around our outcomes. So I commend everyone who's here and continues to be a part of the field and work with all of us. We work with you to really commit ourselves to outcomes. The first step is laying this groundwork to have access for patients, and we're all responsible for that by delivering good outcomes as we select patients wisely and then follow best practices to reduce complications and really stay on our industry partners to keep evolving technology to have less human factors in programming. Some of the things that Dr. Chung was mentioning that really get in the way and take us away from the effectiveness because we're inefficient in the way we deliver these. I'm curious to hopefully see improvement in both the way we deliver the systems, how the systems help us deliver them, and then hopefully we also see more patients getting to benefit, but also teach us along the way because there is an empiricism here and iteration that I think we're yet to really understand because these things are all in their, I say, toddler state. Come back in two years, what, they're like almost about to be not even a teenager? Okay. One thing, one limitation that I see currently for PNS specifically is how the therapy currently is only in our hands, and when I say ours, predominantly pain physicians. I'd love to have our surgical colleagues, including mostly ortho colleagues, and see how we can use this therapy acutely for acute pain, post-operative pain, for our ERAS protocols. For instance, I know that there is one study currently where they're using PNS post-op immediately after the surgery, again, to minimize the usage of opioid post-op after the surgery, but again, it'd be nice to engage more surgical colleagues in that respect and educate how PNS is not just for chronic pain syndrome, but in fact also for acute pain syndrome. I would just say selfishly, and also just to echo what Dr. Dickerson was alluding to, I think certain indications really need to be carved out here. I think, for example, the headache migraine population, right? Historically, we've been doing occipital nerve stimulation, supraorbital nerve stimulation with our SES products, historically off-label, and it's obviously a very large population that suffers immensely. I think since we've been using those SES platforms, we've obviously learned a little bit about what it does for our patients, but we really need to understand if there are programs, as I alluded to earlier, or waveforms that we can really take advantage of, that would really be helpful for, and I would love to see that grow, and hopefully, again, as, you know, partnering with our industry to really grow that space would be helpful. We just want to make sure, are there any questions for the APIRAC speakers as well? Those are some great presentations on three great topics. So one question I had, again, this is for the panel as a whole, and it's a quick one. There's temporary PNS and there's permanent, right? Do you guys think that, is there a role of essentially doing temporary PNS as a trial and then going to permanent, or are you just going direct to permanent? Is there a role? Yeah, go down the line. So I think we don't know what we don't know, and I think the reactivate therapy suggests a strong signal of value in skipping the trial because it's been studied as such. I think across a lot of the other therapies we're using for full nerve stimulation, we get to learn a lot about our patients, about their pathology with that trial. And because the systems can have a honeymoon period and then maybe fail, that's placebo effect lanes in three to six months, where we've placed these leads percutaneously may be a little bit challenging to remove. So I really think the medical necessity at this point for a therapy that we're just developing the efficacy data and where we have, I think with a trial then per model, good safety, I would say, and also with the revision rates we see. It probably makes sense to continue with that process. I think it would be really great for us to enter into the same sort of cost, you know, close claim study that we did with percutaneous image-guided lumbar decompression for Medicare patients for peripheral nerve stimulation and be able to look at what happens around the years before and after patients in that population receive peripheral nerve stimulation. While there'd probably be a really nice Hawthorne effect of having that observership, there probably would also be some learning at a population level that helps us really, maybe with machine learning, understand, you know, what dictates responders and gives us some of that real-world evidence that Dr. Hathaway was talking about. So I'm a proponent of cost reduction for things like radiofrequency ablation, going straight to ablation. I'm a proponent of going straight to implant with pumps also and for cancer patients. You know, there's value in trial, but I think we have to make sure we're not creating zero-sum games as we say things with authority like that because we should always still be able to do what we think is best to give us the right information to make sure that next step is the right next step for patients. I'll take an interesting stance. I'll say properly done diagnostic injection for a peripheral nerve target could equate to a well-done trial. And so why not consider for palliative PNS a well-done small volume anesthetic block and with success go straight to implant. So would you exclude people though if they had a negative block from a trial? Exactly. Or what would you promote in that model? So if they had a negative block, this will be filled? Yeah, why not? Right. Exactly. That's a good question. That's the question we asked in one of our surveys, right? I mean, the block doesn't prognosticate anything. So what use is it? I mean, there are some uses, establishing your anatomical targets, approaches, maybe patient comfort or ease. But as a prognostic or diagnostic tool, if we have evidence, we actually suggest that there's a lack of prognostication. Negative blocks have shown to yield positive results with a permanent PNS system. Doesn't really show you much. So that's your positive predictive value versus negative predictive value of a block. I think that most of us are getting blocks for these patients. We probably have that data set. It's just including another column or row on our collection sheet when we publish this stuff and tying it back. But I love the idea that there's like a psychosocial phenomenon to blocks that helps us also. Yeah. I'm like, I didn't go straight to STEM. Okay. I think the one thing that I was just going to add is certainly understand your patient population. So certainly where Dr. Chung and I practice, it's very unique in that it's predominantly cancer focused. So the limitations of that is having MRI compatibility and patients coming in for recurrent procedures and such. So for those reasons, you know, it's not one size fits all. But that being said, we do tend to prefer temporary PNS systems just in the event that the patient is going to need to have an MRI essentially. So we can remove the temporary system and for them to get the imaging that they need. Certainly since it's temporary, it can easily be reinserted back in. But it gives the patient more flexibility. Yeah. Nomenclature is important. I just want to specify. So the temporary PNS system is therapy in itself. It's not a trial. There are peripheral nerve stimulation trials that are shorter in duration, and that can be followed by subsequent permanent implantation. But, you know, we have data showing that just temporary placement of a peripheral nerve system has yielded chronic long-term benefits even after system removal. So it's not fair to say that that is a trial. Not that any of you did, but I just wanted to specify that. So I think this is a good point to close. Thank you, everyone, for staying. This was the last talk at NANS. I really appreciate everyone sticking around, and I hope everyone learned something.

Peripheral Nerve Stimulation

Complex Regional Pain Syndrome

Dorsal Column Stimulation

Dorsal Root Ganglion Stimulation

Spinal Cord Stimulation

Chronic Low Back Pain

Pain Management

Opioid Reduction

Patient Preferences

Non-Invasive Therapies

NANS Annual Meeting

Jay Carey