Welcome, everybody. If everyone could take their seats. We have a two-for-one special today. We've got two neuromodulation talks. I want to certainly thank Dr. Mike Salino and his faculty members. They are going to be the great neuromodulation debate to follow. And then I'm going to have my esteemed panel introduce themselves. We're going to talk this morning on indications to technologies, kind of give sort of a foundation of what's new in the space of neuromodulation, get a little bit of debate, a little pro-con. Certainly a couple things. Cell phones, so if you could please silence your cell phones. This is being live-streamed, so we would appreciate if you could silence your cell phones and take any phone calls you have outside. There is an evaluation form, so please let us know how we did and how we can do better for next year. Finally, there is a way through the AAPMNR app for the conference to ask questions. We also have a couple live mics, so for those who are tuning in virtually, please download the app and ask some questions. And then for those of you who are here, you know, we'll use the mics at the very end. My name is Girtej Singh. I'm the Director of Interventional Physiatry and Paint Management for the Centers for Advanced Orthopedics here in the Baltimore, D.C., Northern Virginia Metroplex. With me, and I'll start with Dr. Lee, if you don't mind just introducing yourself. David Lee. I'm taking the mics off. David Lee. I'm a PMNR trained in SUNY Downstate. I did an Interventional Spine Fellowship in Arizona. I currently work in Southern California with a small orthopedic group. Jordan Tate. I'm from Atlanta, Georgia, and I was an Emory PMNR trained and then Interventional Pain Fellowship at Mayo in Jacksonville, and have been in private practice doing single specialty interventional pain since 2014. My name is Wakas Karashi. I remember sitting right in these seats. I'm from South Florida. I trained at Long Island Jewish Medical Center, did my Interventional Fellowship at Beth Israel Medical Center, and now I practice interventional pain in a spine surgery group on Huntington, Long Island, and I'm happy to be here. All right. Here's our agenda for today's presentations. We're going to discuss some of the new waveforms. We'll review some of the current indications and FDA indications. We'll talk about some new technologies that are coming, closed loop stimulation, have a little pro-con debate on that, go over kind of an overview of PNS, and then finally some implant tips and tricks. So we're going to go ahead and start. Dr. Tate, if you don't mind, we'll take the first lead here. What is multiplex waveform and stimulation? So differential target multiplex is a unique and novel formulation of delivery of various frequencies combining 300 hertz and 30 hertz in different pulses at various electrodes along your standard octrode. So you're not only targeting different areas of the dorsal column, you're also using different frequencies in a layered mechanism. The intention of this, or how it was brought about, really was born out of Dr. Ricardo Vallejo's laboratory and his animal studies. He was looking at glial cells as being a potential target for neurostimulation or neuromodulation. We've always thought that we were targeting dorsal columns, potentially targeting dorsal horns, but really focusing on the neuronal activation that's created with our neurostimulation products. And in this case, we know that glial cells are ubiquitous in our central nervous system. We've thought of them as sort of the cleanup crew or the supporting party. And in this model of activation, the thought is actually that they are the star player. And what he looked at, specifically in his rat model, was the genomic array of glial cells. And what he found is that it was a corollary to having a pain-free state or a normal pain propagation system in the rat model. And so when you apply tonic stimulation to the glial cells, you see some retroversion from a chronic pain state in the glial cell genomic array. But when you apply this DTM model, what he saw was almost a complete resolution back to a normal genomic array of the glial cells. And this was that aha moment that perhaps there is something more interesting happening and that in order to appropriately activate the glial cells, this new and novel approach with DTM, these layered frequencies, is what is required. I'm just getting a couple comments from the, I guess, people who are virtual. Make sure that the mic is close to you. I guess the virtual team is having a hard time hearing you guys. Okay. Thank you, Dr. Tate, for that. Dr. Qureshi, 10,000 hertz stimulation. So 10,000 hertz stimulation, without getting too scientific, basically the old way of stimulation was just to stimulate and feel it and hit these fibers with a low frequency. And for those of us that did stim, you know, in the earlier days, the patient would feel what's called a paresthesia that would essentially mask their pain. Some patients liked it. Some patients didn't. Over time, you know, the model shifted towards exploring what if we tried a higher frequency. Essentially, think of it as like a dog whistle. Just because you don't hear it doesn't mean there's nothing going on. So they found that by giving a high frequency, low pulse, low amplitude dose of stimulation, you're not exciting. You're not stimulating. You're actually inhibiting. And you're inhibiting this wide dynamic range neuron, which is essentially where it's the gatekeeper of the pain. So instead of stimulating the lower frequency, we can stimulate to inhibit. We're essentially turning the pain down. And that's kind of where the 10 kilohertz technology comes in and why it's so effective. You know, by placing it in the dorsal column, you're not stimulating the fibers. It's more of an inhibitory effect. And, you know, clinically, the data's been good. In the real world, patients do really well with it. And it's here to stay. You know, there's other modalities and, you know, pulses and waveforms that everybody talks about, but it's hard to dispute the effectiveness of the 10 kilohertz. Thanks, Dr. Qureshi. Dr. Lee, burst, but the burst DR form. Yeah, sure. I also want to make a mention that when we place leads now, it's done anatomically. Previously, we had been taught in neuromodulation. I know when I did fellowship and residency to do paresthesia mapping with the patient at the end of the table with these novel waveforms I just mentioned, particularly that was started by HF, you know, the high frequency waveforms, is that they do anatomical placement with the understanding that the outcomes are equivocal. So I want to kind of go into burst DR. I think the timing of this is serendipitous because if you have been looking on social media or paying attention to the journals, there was a recent JAMA article that was published just a couple days ago, and there was a bit of confusion there. The article was talking about burst, but they actually talked about one form of burst and then applied a different form of burst in the study. It was a huge, egregious mistake by the authors and the leaders of that study, but it is a common mistake and one that, of course, needs a little explanation. So there is an active recharge burst and a passive recharge burst, the latter of which is referred to burst DR, named after the person who actually came up with it, Dr. De Ritter. The active recharge burst essentially is a clustered tonic waveform. So it's basically taking your normal tonic, taking a bunch of them and clustering them together, four or five waveforms together, and there are equal amplitudes in that cluster. The passive recharge waveform is actually derived from our natural body. It's found in natural body, thalamocortical firing patterns that were thought to believe to increase synaptic connectivity. And also historically has been used in treatment of tinnitus. So there were patients with tinnitus previously getting stimulation, transcranial stimulation with tonic waveforms, but some of them did not respond appropriately. And so they started utilizing burst waveforms with increased efficacy and salvage. So it was Dr. De Ritter in 2010 that essentially came up with this idea, why not utilize this in the, keep it in the central nervous system, but utilize it in the dorsal column. The idea seems pretty like no brainer at that time, but again, this was a time period where we were kind of set in our ways utilizing tonic stimulation. So the main thing that differentiates the passive versus the active burst is that in terms of the burst ER, what you actually have is you have five monophasic waveforms with increasing amplitude that are sodium derived that sit on a calcium plateau, which is controlled by T-type channels. And Falowski kind of studied this waveform thinking, okay, well, what is this? This seems unique and seems like it has potential here, but what are we actually doing? So he did a lot of electrophysiological studies looking at what kind of post-synaptic responses you get when you apply burst ER versus traditional tonic stimulation. And interestingly, what he found was that instead of getting a kind of one-to-one response from stimulation of tonic to post-synaptic discharges, what you got was kind of a wind-up effect. And I often try to describe this to residents and fellows kind of like when you pull a spring on a pinball machine and then you hold it there for a while and then you let it go. And so what he found was he got, after applying burst ER to the dorsal column, what he found was there was a cumulative super action potential, so to speak. And the thought process there was it's going to be able to activate neurons more effectively, efficiently, and hopefully produce an improvement in pain management. The other thing that he had found, and they did this in the ways of actually looking at the spinal cord and doing PET scans and looking at the activity, was that it seemed that when utilizing burst ER, it actually penetrated the cord deeper, stimulating fibers that were deeper within the dorsal column instead of superficially and also with less energy. So, Dr. Lee, there are sort of two types of burst stimulation that we can utilize in our patients. There's the original, quote-unquote, burst, and then there's burst ER. Kind of simply put, what are your thoughts in terms of the activation of the dorsal horn and how that may help the sort of the cerebral pathways? There have been some studies to allude that depression management could be helped. Yeah, thanks. So, the other main difference in mechanism of action is that with normal tonic waveforms, we know that the lateral corticothalamic pathway is stimulated. What has been found, again, on both animal models as well as human models in looking at the brain when burst is applied is that the anterior cingulate cortex is actually lighting up. And this is controlled via the medial pathway, which is unique. What does the ACC actually do? It deals with the psycho aspect, the psychological aspect of pain perception. So, pain catastrophizing, processing depression. So, the idea was, you know, not only are we activating cells and neurons that control pain, but potentially here we're able to modulate the experience of pain perception itself. Great. So, then finally with the traditional burst, what we're attempting to do. So, both burst and burst ER differ clinically when we're trialing these with patients. They're typically set up where you're going to do some form of tonic mapping initially, and then based on the tonic mapping, you'll then stimulate either the posterior column or the dorsal horn. The goal with more traditional burst stimulation is that once you've identified on the posterior columns, you can then activate surrounding neurons. So, kind of think of it a little bit as like a desensitization, right? So, you stub your toe. When you rub your toe, you distract yourself from the actual pain. And so, the thought behind traditional burst is that you're actually stimulating the neurons around the painful neurons. So, you tonic stimulate, find the painful neurons, and then allow the internal programming of the device to map around it. With traditional burst, some are using sort of like a specific frequency and a specific pulse width, and using sub-threshold amplitudes to get a quicker or faster response for patients. And those who use that device tend to say that many patients, even on the day of the trial, are already beginning to notice improvement in their pain. Let's move forward. I'm going to pick on Dr. Tate. So, we have a bunch of different indications, FDA indications, for the use of SES. I know that you've had a little bit more experience than the rest of us in terms of chronic pelvic pain. Could you share an experience for that? Sure. So, we know that the on-label indication for spinal cord stimulation is non-retractable back pain, as well as extremity pain. So, the trunk and limbs, once you have pain in that area for more than six months, and they're not responding to conservative therapy, in theory, spinal cord stimulation could be on-label. Now, of course, you have to fight the battle with your insurance companies to actually get this covered. And as we know, most of our insurance companies have limited their policies to coverage of failed back surgery syndrome or post-laminectomy syndrome, and really specifically of the lumbar spine. And many are not covering that same diagnosis in the thoracic or cervical spine, or complex regional pain syndrome. In addition, some insurances will cover chronic angina and ischemic limb, but in the U.S., these are not common indications for spinal cord stimulation. But what I was noticing in my practice, by using high-frequency stimulation on some failed back surgery syndrome patients, that some of them would come back to me and say, you know, Dr. Tate, that testicular pain I never told you about? Yeah, it's gone now. Or, you know, I was really struggling with bladder frequency and urinating throughout the night, and, in fact, my sacral stimulator was never very effective, but this stimulator seems to have corrected that problem. And, you know, so this kind of created an aha moment where I said, well, you know, maybe there's something more going on here, and that high-frequency stimulation, specifically, could be indicated for use in chronic pelvic pain. So initially, I went through what's called a physician or investigator-directed study and talked to the makers of the high-frequency stimulator and said, you know, I think we could do a little feasibility pilot study, that sort of thing. And they were excited by the idea and actually decided, instead, to make a bigger deal out of it than I had intended, put together a multi-center prospective study with two other physicians, Sean Lee in New Jersey and Thomas Dallas out of Wisconsin. And so, together, the three of us designed a study protocol and were able to enroll 23 patients. 21 went through with the trial. We had 17 trial successes, which was deemed at a 40% benchmark, but most of them were... 90% of them were actually above the 50% mark. Out of those 17 past trials, we had 14 that went to implant. One had an infection and had to have their device removed within a week. And so we had 13 that we were able to carry out to a 12-month follow-up. And this study was published in Pain Physician in 2020. You can search under my name. I ended up being the primary author because I was, I guess, the one to initiate it and also enrolled more patients. But the overall results were actually quite mind-blowing. We had low expectations. To be honest, I think we all know and agree that chronic pelvic pain is difficult to treat. And specifically, the studies have shown us that neuromodulation in the treatment of chronic pelvic pain is typically met with the least successful outcomes and ultimately met with the highest explant rate when using tonic stimulation in some retrospective studies that were performed. And so our expectations were low, but we were very pleasantly surprised. And overall, we had a 74% responder rate, which our responder rate was actually meeting that benchmark of 50%. And we were able to achieve that at three months, and it was a carried out durable benefit over 12 months without anybody losing their response rate. And even more exciting was that we had really low VAS scores. Down below three was considered a remitter rate, and we reached that in 69% of those 13 patients. We also saw incredible improvements in their disability index, their pain interference scores, and then some secondary outcome measures that we looked at, including urinary frequency and painful sex and different pelvic floor measures as well, were also statistically significant. So it was an exciting study. And what I would love to see the next step is to really open that up into a randomized control trial and make it an acceptable therapy that insurance companies will adapt. Congratulations, Dr. Tate. Thank you. Dr. Qureshi, CRPS, right? You mentioned a few minutes ago all about the dog whistle of high frequency. When you treat patients with CRPS, what is your typical waveform of choice? So historically, we had to kind of deal with what we had available, right? So we did our blocks, ended up starting out with tonic stim, moving on. You know, high frequency has definitely shown some improvements in the CRPS. That being said, it's kind of hard to ignore the elephant in the room. You know, it's not one of the big points of this talk, but, I mean, DRG is huge for CRPS. Like anything else, it's about patient selection, indications, knowing your patients, knowing how they respond. You can have two people with the same exact pain, and one of them does really well, and one of them is a failure. So my main go-tos right now are usually the high frequency and the DRG dealing with these patients, but more than that, it's just knowing your patient because CRPS is so complex, pardon the pun. Dr. Ali, I have a feeling you're going to jump in with one of those leads. I just want to qualify what DRG... So we're talking about the dorsal root ganglion, and I know we've been talking about all these different waveforms that we're applying to the dorsal column, but the dorsal root ganglion is a different target, so it is a different type of therapy altogether, stimulating different types of nerves. But I think that's a point well made. The studies that have been published for DRG stimulation specifically have shown it to be superior to traditional tonic stimulation in the 80 percentile range. And so a lot of people are reaching for it, a lot of clinicians are reaching for that now when a patient has a particular CRIPS picture, which is affecting a specific part of the limb. I will piggyback Dr. Tate's comments, and I didn't know about that study, but that's amazing, and I will read it. But I use DRG also kind of off-label, I will state for pelvic pain, abdominal pain, chest pain, where the patient has failed other conservative managements, of course, first. And with dorsal column stimulation, traditionally we've only been able to capture a lot of the back and limb, right? And anything anterior to the mid-axillary line has kind of been far difficult for us to treat. Historically, a lot of the other panel members who will be coming up here and sitting up here with me right now, we used to gutter the leads, you know, that was the old way of doing it. We would literally take the lead on purpose, throw it into the gutter, the far lateral recess of the dorsal column area, and stimulate to try to capture some pain that wraps around. And that was not truly very effective. I mean, I've done it a few times, and I can tell you during trials and implants, the efficacy was hit or miss. So targeting a lead directly into the nerve root that you're looking to achieve pain relief from is a novel therapy. Thank you. I may be still of the old school mind. Traditionally, I will put patients on a tonic stimulation. It was something that right from the beginning of my career after fellowship, which was the day of tonic, those CRPS patients did better than anybody else, especially those that were more just back pain. So even still today, I will use more tonic as opposed to some of the other waveforms. Maybe today's panel changes my mind. But speaking of tonic stimulation, flip to the next slide, try that again. Nope. Sorry. Nope. Okay. That's my next slide, I guess, yeah. Remote monitoring. I'm actually gonna go right back to you, David. There's a few companies that are offering sort of remote monitoring. Just sort of in a minute or two, can you just kind of tell us where this sort of new technology might take us? Yeah, so I don't need that much time. It's pretty self-explanatory. A lot of the younger physicians in the room probably understand this already, but we're moving towards this idea of empowering the patient and giving them accessibility to the stimulation. I think that's one of the biggest hurdles that neurostimulation has is both financially as well as geographically, socially, that neurostimulation has not been accessible for patients across the board. In order to allow that to make it easier, particularly after an implant has been done and reprogrammings are absolutely necessary. I disclosed that to most of my patients in the beginning, trying to give them realistic expectations, tell them, hey, I'm gonna implant this thing. We're gonna turn it on when you come back in for your post-op follow-up, but we're gonna probably need to reprogram this a couple times, two, three, to just fine-tune the device and kind of find where your stimulation needs to be. And that could be taxing. I mean, I live in a metropolitan area, Orange County, but that could be taxing, particularly for people in rural areas, that maybe the patient's coming from two hours away or so. Even if they're close by, every time you reprogram them, essentially the patient needs to come in, the clinical specialist needs to be there, and then you're there as well. So what the remote programming allows is that you download their proprietary app. Essentially, they can tap into the patient's actual hardware and then they can modify the waveform accordingly and reprogram them when they are not in the office, and the benefits are obvious here. Thank you. When it comes to artificial intelligence, I think this is where our field's gonna move forward over the next coming years. The ability to access a patient remotely right now is all predicated on the fact that the generator itself has been pre-programmed, and so the patient can make changes that the device company can suggest to them or the physician can suggest to them over the phone without actually having to come in like we used to in the old days. As sort of HIPAA technology, as well as sort of data security technology continues to advance, we'll be able to do far more in terms of being able to access the device, make changes from that perspective. In terms of true artificial intelligence, so in that, and I'm just gonna read real quick here, the FDA actually defines artificial intelligence as a fixed set of instructions and makes adjustments based on the inputs given, and then the algorithm that is established can then vary those multiple outputs. So it's a rather broad, generic sort of statement. But what we're trying to do is trying to say, are we gonna make changes that just the IPG will interpret and monitor, or are we gonna be able to make changes where the patient can actually input their information actively into the IPG so that the IPG can actually make that adjustment, right? So the excitement in the field has been over the last few years, the different waveforms, the new indication. The new excitement that may be coming is gonna be how do you continue to customize this per each patient? I think all of us in here who do neuromodulation know that almost every patient is themselves a unique and of one. So while we're able to get these large cohort studies, these large randomized RCTs, the truth is they're all different even as a subset within. So going forward, please keep your eyes and ears out for the new AI that's coming. There is also something coming, Dr. Tate, you may be familiar, a device soon to come to market for enhanced data collection. If you could give us a comment on that or what we're excited about that for. So yeah, I think there's a couple of companies who are actively implementing this idea of AI. And by doing so, they are closing this loop of we are putting in neuromodulation signals to the spinal cord. And then we are waiting for subjective results from the patient that can take sometimes weeks to achieve because they have to drive two hours back home and then they don't answer the phone for two weeks or what have you, right? So I think this remote monitoring is one way of helping to close that loop and make that smaller. The other way is by using the big data that many of these companies have started to accumulate. And one company in particular has over 90,000 patients in a large cloud-based data and they are utilizing that information to help drive and direct and allow the IPG to customize that response. So that's another way of closing that loop. But there's a new technology that should be coming out in January that's really specifically focusing on closing that loop in real time. And the way that they are doing this is their leads are actually not only just inputting signals into the spinal cord, but also reading signals back. And so by reading these ECAPs or evoked compound action potentials, those ECAPs are then being sent in real time to the IPG and adjustments are being made to the neuromodulation that is being delivered. And so by doing so, you are able to keep that patient in a therapeutic window for longer. So if a input is too strong, for example, the ECAP will be read outside of that appropriate therapeutic window. This would be somebody who's getting supra-therapeutic stimulation. And the IPG in real time can then deregulate that next impulse to be lower so that the patient is not oscillating in and out of this therapeutic window. We know our patients, they say, well, it shocked me that one time, so I turned it off and I don't want to use this thing ever again. Because our chronic pain patients have a lot of fear avoidance. And so by keeping that adjustment tighter, you're able to maintain that tissue activation longer and in a more appropriate setting. And that loop and that feedback is actually happening millions of times a day. Great. David, any sort of, as you see, advantages or disadvantages to this tonic form of closed loop? Yeah, so that's the only, I would say that probably that's the only real limitation in my mind. I'm a huge advocate for closing the loop in multiple different ways because we have this issue within the neuromodulation field. The elephant in the room is that there tends to be a lack of efficacy over time. And we're not exactly sure why that occurs. Some have attributed it to noncompliance. Others, psychosocial issues. Others, tolerance to the actual stimulation itself. So it's about eliminating or trying to minimizing those shortcomings. I love the idea of closed loop. The company who's putting this out there has a tonic waveform, but I think that that's a step in the right direction. In the future, there's going to be other companies already looking into their own form of closing the loop, utilizing different, these waveforms that we've been talking about. So I don't think it's a detriment to anything. I think progress is progress in my mind. And I think that is a step in the right direction. The one thing I will say is that why this is an easy way to understand closed loop and why it's important is when a patient lies down, for instance, the lead is going to be kind of closer to the actual dorsal column. And that's usually when patients notice an increase in terms of discomfort or paresthesias or uneasy feeling in their back or their legs. With the ECAP detection that Dr. Tate is referring to, then that adjustment will be made automatically versus right now, a patient has to go get the remote control and turn the stimulation down or off. And the more that the patient has to manipulate the stimulation, most likely the less compliant they're going to want to be with it, right? The idea here is you set it and hopefully forget it. And the more automated we get with that, I think the more our compliance will improve. Thank you. Dr. Qureshi, there've got to be some kind of a disadvantage, right? I mean, this is tonic stimulation, right? Over the last five years, we've left tonic stimulation. Why are we going back? Because gotta keep it fresh and exciting, right? Tonic is kind of where it started. Some patients liked it. Some patients, they felt that, if I don't feel it, it's not doing anything. So that's a part of it, that bringing the tonic back. So one of the things to kind of finish up here with closed-loop, there's sort of a few different definitions, right? So when we speak specifically of a particular waveform or when we are utilizing a tonic frequency there is an e-cap that's derived, you know, sort of information and then an adjustment on that information in live time. And then the other part would be in the paresthesia-free or paresthesia-independent stimulations, there will be different types of closing the loop. And so again over the next couple years these will be things we should be looking forward to. So we'll switch gears a little bit, flip over to PNS. There we go. Awesome, PNS. So Dr. Lee, if you don't mind, any sort of have you used much PNS? And if so, what are sort of the targets and what has been your experience? Yeah, so I'll start off by saying when peripheral nerve stimulation really came about it was derived and introduced in my practice really as a form of treatment of, you know, peripheral joint issues like in the suprascapular nerve, genicular nerve, ankle. I think to our credit and to the credit of a lot of people who are involved in neuromodulation, now the targets are, you know, have kind of exploded. So we're doing all of that, of course, but now we're utilizing it for treatment of more recently low back pain. Dr. Desai is over here, has done a lot of work with that. So I do integrate it into my practice, absolutely, no question. And I think it's a huge part of neuromodulation that's just going to build over time. I do think that there are somewhat limitations at this point. The biggest ones are really the IPG, right? The further you get away from the spine, the harder it is to handle the implantable pulse generator, which has to power this thing. There are different companies out there that have both internal, external devices for that, you know, and answers for that. I think the critical part of this that will allow it to be utilized with, you know, more broadly would be microtizing the implantable pulse generator. I think once that happens and it is inevitable, then you're going to see really those kind of indications explode. You're going to be able to utilize this and kind of think outside the box, you know, everything from occipital neuralgia to suprascapular to, you know, even intercostal. So, you know, the skies will be the limit. So one of my experiences working in a large orthopedic practice is I see plenty of patients who have foot and ankle pain following foot and ankle surgery, knee pain for individuals who are post TKA or just non-surgical TKA candidates, as well as patients who have shoulder pain, kind of for similar reasons. And so, you know, the educational point is there are certain advantages for using PNS. And for those who aren't... I mean, this was not something when I was getting trained that PNS was used. So it's been something that I've had to learn about and I encourage everyone to learn there. I'm going to... We're going to go quick. Hang on, David. We're running short on time. I don't want to jeopardize these guys. Dr. Tate, I'm going to put you on the spot. Yes or no? Why bother with a 60-day if you're just going to treat somebody with something long-term? Well, because the data does lead us to say that that's an effective treatment. We're not trialing them for 60 days. We're actually looking for a treatment process. And what I'm seeing in my clinic, especially with my shoulder patients, I feel like have been the most successful. By utilizing the small 60-day implant, they are getting that long-term relief and several of them have not had return of their shoulder pain after a year, two years. And so the data is showing us that that is a way to kind of rewire the peripheral nervous system when it's gone haywire. Great. Dr. Koresh, you're going to kind of finish this up and then I've got one last question for the panel. It's a yes or no, but if you could sort of just in the next two or three minutes... Make it fast. You got to make it fast. You know, NAC infection guidelines, any kind of tips or tricks for implants? So what is NAC? Probably the hardest part of this is the Neuromodulation Appropriateness Consensus Committee. Say that fast five times. Basically, it's not the standard of care. It's a clinical best practice. It's important to make that distinction. I'm just looking around the room. I see a lot of younger people. Awesome. You're going to be the ones doing this, I hope. That's why you're here. You know, you're the ones doing the trial. You're the ones doing the implant. All this technology and all this science is awesome, but we're not just taping the leaves on. You're putting them in the skin. This is a surgical procedure. You're involved with a lot of sensitive structures, and you can mess up and the complications can be catastrophic. So the NAC guidelines essentially are saying that, you know, for the implant, definitely pre-procedure, you want to give an antibiotic. Usually we're giving Kefzol or Clinda or Ivanko when there's an allergy issue. Typically, they like to discontinue post-operative antibiotics within 24 hours. Personally, I don't do that. I give a week of an antibiotic, knock on wood. I don't really have infections. I'd like to keep it that way. Hopefully did not jinx myself. Regarding implantation, it's pretty straightforward. You have to look at the implant as a whole process. It's not just the patient shows up and you're putting it in. You have to plan this. You have to meet with the patient. You have to plan the anatomy. You have to understand the anatomy. A lot of these patients have hardware in place. They have post-op changes. They have scarring. Things don't always work how they should in Netter's book. So it's important to get the imaging of the lumbar thoracic spine to make sure you can put this where you want to go. And then you want to plan it. You want to get your labs. You want to get cleared. If they have medical comorbidities like diabetes, smoking, any other active infections anywhere, you need to kind of squash those before you go in and you start working on these patients' spines. In terms of where you put the battery, typically I'm putting it in the area between the inferior costal margin and above the iliac crest. That works really well for most people. It's a standard two incision technique. It's important that you know how to work with tissue. Like I tell my fellows and residents, when you're doing the case is when you don't want to deal with headaches. That's the time to minimize headaches. Minimize bleeders. Make sure that everything is tied down properly. I like to anchor my leads. I like to tunnel them. What else? We close in layered fashion. Cover with stale dressing. I leave it on for a week. I see them in one week later for a post-op and a bit of a suture tag removal. Patients do really well. And it's just important to really not cut any corners because then if you do get an infection, if it's a superficial infection, you can treat it with antibiotics. But if it's anything beyond that, deeper into the pocket or even into the epidural space, that's a whole different deal. The system has to come out. I have the antibiotics. They may need other surgery. So the whole thing is just planning the procedure from A to Z and you should have as little complications as possible. David, this is the last question. We'll get the other group up here. David, you got one choice, a rechargeable or a non-rechargeable battery. Which one? Yeah, for me, it's pretty easy because I've been just doing this in my own practice. So I've always been primary cell non-rechargeable. It goes back to what I said earlier. I think if you can have a patient that said it and forget it, then the patient's not going to have to be worrying about recharging it. There are certain instances where I've, so probably about 5% of my cases I do rechargeable and those are probably younger patients who are motivated and requested specifically. But otherwise, I'm primary cell all the way. Sure. Dr. Tate, rechargeable, non-rechargeable. You got one choice. That's the impossible decision. It's like picking your favorite child. Pick your favorite child. Yeah. I'm gonna go, I'm gonna just go with rechargeable. Okay. For the smaller IPG profile. Okay. Dr. Qureshi, non-rechargeable or rechargeable? I offer the patient both options. Personally, I prefer non-rechargeable, especially the older patients, like Dr. Lee said. They just want to, they don't want to deal with the hassle of recharging it. They forget to charge it. They come in with a dead, you know, IPG that can't even be charged. So I tend to lean towards non-rechargeable. Everybody gets a rechargeable for me. All right. Thank you, Dr. Salina. Don't leave. There's more. There you go. Welcome, everyone. My name is Mike Cellino. I'm the Chair of Physical Medicine and Rehabilitation at Cooper University Hospital. I want to thank my colleagues for really putting the ball up on the T force. The Academy decided to have the DC universe and the Marvel universe combined forces. It does represent the members' interest in neuromodulation. We're going to take from what our colleagues set up and kind of describing the new technologies that are out there and all the different subtleties of them and actually present them as cases. The debate format, if you will, will be that I'm going to present a clinical case. These are cases that don't really exist. My panel have not seen the cases. They have been blinded to it. And the idea is, how do you pick from all of the choices presented to them to pick what therapy is most appropriate? So we'll take just a moment and have each member of the panel introduce themselves, who they are, where they're from, and that sort of thing. All right, well, I guess I'll go first. May hold the side. I'm in private practice in Washington, DC. Started off in academic practice at George Washington University Hospital after fellowship training. And then I realized that I preferred the private practice setting and started my own practice in 2016. I'm Eric Shaw. I did my PM&R training in San Antonio and did my PING fellowship there as well. I'm at the Shepherd Center in Atlanta. I've been there for 16 and a half years. I'm Himanth Kalia. I like to say I'm from the Napa Valley of the East, Finger Lakes region. Rochester, New York, I did all my training at University of Rochester and stayed with the health system there for about nine years. Started their fellowship program, and now I saw the bigger light, so I just went private. Hi, Rich Wilson. I'm from the Mental Health Rehabilitation Institute in Cleveland, Ohio. I'm vice chair of the Department of Rehabilitation at that institution. My clinical niche is actually in neurological rehabilitation, but I primarily perform research on using peripheral nerve stimulation for the treatment of chronic pain. Thanks, Steve. So I also tried to pick cases that even the general physiatrist might be interested in. So even if you're not going to be executing neuromodulation techniques, these may be cases that you're thinking about. These are my disclosures. Potentially, we might discuss off-label indications for these particular devices. I would ask my panelists, if they don't have to, please don't use brand names. If you think brand names are necessary for educational purposes, go ahead. So here are the ground rules. I'm going to present to you a case that you guys have not seen. And question number one, is this individual, this patient, a neuromodulation candidate? And your potential answers are, no way. Maybe, but let's try something else first. Or definitely, and if so, if it is a definite, what do we choose? For the purposes of discussion, let us assume that all prior interventions were done correctly. That you wouldn't say, oh, you know, let's go back and repeat that. Let's assume everything was done correctly. Secondly, are there any risk factors or characteristics of an individual patient that can either enhance or reduce the possibility of success? Are those characteristics modifiable? If so, how would you modify them? If your first neuromodulation technique doesn't work, would you then look at a second technique? And then lastly, any pearls of wisdom from your mastery? Sound fair? And I would then, before we actually delve into it, quote Mitch Daniels, recently retired president of Purdue University. He said that the advancement of science requires the collision of ideas. So it's OK to disagree. It's OK to say, I would do it differently. That's what we want to hear. We don't want to hear, necessarily, the same answer from all of you. OK. So case one, 60-year-old female with a history of right knee pain. Long history of DJD and OA. Failed all the conservative therapies, including intraarticular injections and visco supplementation. One year ago, had an uneventful knee replacement by our orthopedic colleagues. Our orthopedics colleagues say everything's OK with the implant. There's no loosening. There's no infection. Everything looks good at that perspective. Really doesn't describe any exacerbating or relieving conditions with regard to her pain. She was treated with oxycodone for two months post-operatively, and then stopped because it was considered outside of the post-operative period. She does tell you that it took the edge off, but it wasn't a deal breaker by any stretch. She's currently on gabapentin and amitriptyline at maximally tolerated doses, limited by sedation with the amitriptyline and edema on the gabapentin side. Had two genicular blocks after the surgery, done by someone who you trust. She says it helps, but it only gave her 40% relief, rather than greater than 50% relief. She lives with a very supportive husband, has well-controlled hypertension, hyperlipidemia, and hyperglycemia. She looks fine. She lacks a little bit of range of motion of full extension. You do pick up a little bit of quadricep atrophy on the affected side. Her strength's intact. She does have some edema in that leg. She says that was only present since the gabapentin was present. She has hyperalgesia to pinprick from a little bit above the kneecap to the tibial tubercle, mostly in a circumferential manner, but mostly anterior. She does have decreased stance phase on the right. So not an uncommon scenario, right? We see these kind of folks all the time. So gentlemen, what do you think? What should we do with this young lady? How would we approach it? Neuromodulation candidate? Don't be shy. That's why I picked you. So I would say that this person is a candidate for neuromodulation. Unfortunately, most of the things that would be offered to her aren't well studied. So much of the treatment will be going on the experience of the providers who would be offering the treatments to this individual. But at that point, there are things that you could deduce from treatment of other pain syndromes that might actually work for this individual. So one that hasn't been brought up is neuromodulation. It's actually intrathecal zyconotide. Hasn't been discussed today, but that is a form of neuromodulation is affecting the nerves. And somebody like this person who has a well-localized pain syndrome, that may be an ideal situation where zyconotide could improve pain, improve quality of life. It's just whether or not somebody wants a pump that requires refilling periodically. So I'd say that is one thing that hasn't been brought up today that really might work in this case. So I would agree that the patient's a neuromodulation candidate. I would take a step back and ask us, as physiatrists, to make sure that we do our own workup. So if you, in our community, the number of total joint surgeons that send us knees that are like, it's perfectly healed, it's great, it's great, it's great, it's high, but the number of people who may still have aseptic loosening is not as low as one would think. So if they've only gotten an x-ray and an MRI and it's past a year, you should consider getting a bone scan, because a bone scan is more sensitive for aseptic loosening than those other tests are, beyond a year, because you'd expect the healing to have occurred. And we've found a bunch of those in our practice. So that's one thing. Two, I think you sort of have to decide if you're gonna have a top-down or a bottom-up approach to a patient like this. What I mean by that is, you could go to, I'm not suggesting that an intrathecal pump wouldn't be on the list of things I would consider, but I personally probably wouldn't start with that. I'd probably think of this patient as, first line, as someone I would consider for peripheral nerve stimulation around the knee, potentially the geniculate nerves, potentially, which aren't really nerves, but let's just call them that. Possibly looking at the distribution of the patient's pain, femoral nerve, sciatic nerve, or adductor canal with the saphenous nerve. The thing to keep in mind is the hyperalgesia that you described, that's the one caveat. Sometimes when you stimulate a nerve in the area where there's hyperalgesia, you can end up with a syndrome where the patient has hyperalgesia and stimulation on top of it, and they find that very irritating. Next step up, if I was gonna work up from there, if peripheral nerve stimulation was either not successful or the patient didn't wanna try that, I would actually think about dorsal root ganglion stimulation for this patient, along the L3 or L4 or both nerve roots, or the DRG of L3 and L4. So that would be my thought process, is PNS, DRG, then possibly SCS or intrathecal drug delivery in this particular patient. Yeah, so I think the concept of hyperalgesia, especially after this, there are some sympathetic phenomenon that can creep up after peripheral joint surgery, and I think it's not inappropriate to consider lumbar sympathetic block for her, probably at L3, maybe even IV ketamine to see if that helps. I mean, there's not that many, we do it, so that's a more conservative approach. But I definitely agree, I would probably do peripheral nerve stim with this patient with a plan on micro-IPG implantation, if successful. I definitely think that the medications are problematic for her, the TCA and the gabapentin lead to sedation, increased fall risk for her, she's probably got a low peripheral neuropathy from her diabetes, so those risks are not so those risk factors go up pretty substantially, because balance definitely fades as we age, right, and peripheral neuropathy makes it worse, so her risk for falling and having something more significant happen goes up. So I think I would maybe think about those conservative measures, I agree with Dr. Desai about triple phase bone scan or even a CT scan of the knee can be a little bit more sensitive too, compared to MRI, because the MRI gets scattering from the implant. I would agree, this is a definitive patient for neuromodulation strategies, but it's important to kind of have a strategic approach to neuromodulation. So when we teach neuromodulation to fellows and residents, we always talk about identifying the site of pain modulation along the path of transduction and translation of pain. So you start from the periphery, whether the pain is getting modulated at the receptor level, peripheral nerve level, DRG level, dorsal column or spinal cord level, what it has really started modulating itself supertentorially, because if that's the case, then no matter what you do below the brain, it's not gonna work. And then once you have identified where the pain is getting modulated along this path of transduction and translation, next step is to look at the evidence. What is the evidence around different therapies which can guide you choosing that specific therapy for optimum outcomes and success? So PNS, DRG stimulation, dorsal column stimulation, and intrathecal targeted drug delivery, all are options for neuromodulation in this specific case. Let's talk about the evidence which is out there for each and specific modality in this specific scenario. At best, we are ranging between level three to level five evidence in all these different modalities. Now you can't go wrong in picking any one of those, but you have to go in with confidence. The confidence is gonna come by reviewing the evidence. So I agree with all my panelists' decision, but I think the choice of the modality should be guided by the evidence out there. Does the genicular block relatively ineffectiveness make her more likely, less likely, or have no influence on your decisions? Despite the fact that we trust this interventionalist, I may want to look at the floral films and see, because it's possible that that practitioner was too anterior with the placement of the blockade, because those nerves tend to be more posterior. Actually, what I would suggest is we need to reframe the way we look at patients like this. There's no definitive prognostic or diagnostic value to an injection in this setting. We tend to pull forward from our radiofrequency ablation sort of backgrounds, so we do medial branch blocks as potential prognostic predictors of success with radiofrequency ablation. There's never been any evidence that suggests that doing a diagnostic or prognostic block gives any positive predictive value to peripheral nerve stimulation or spinal cord stimulation in this kind of setting. So I would be cautious about over-interpreting the results from the geniculate block, A, and B, I think I would implore people to not document in that way, the way we document for radiofrequency ablation, where we have this insurance-driven, hey, 80% or whatever it is, 50 to 80% two times. That's been sort of codified in the way we talk to patients and the way we document things, and it's sort of somewhat dangerous when you start applying it to these other therapies, because it's never been studied and never been proven to provide any value. In our practice, we almost always use diagnostic blocks if we're considering placing more than one electrode and wanna understand if there's some modulation of that pain via other nerves. For example, if someone comes in to see me with shoulder pain and I'm thinking about a peripheral nerve stimulation device, and I'm wondering if I have to stimulate both the suprascap and the axillary, I may do a block. But otherwise, I usually don't use blocks other than to give me another data point. And I'm not actually exactly sure what to do with that data point, except for if I have a patient who's less confident and wants to try some things that we can further discuss. Would you have not done the block? Say that element of the history wasn't there. Would you have gone to a block first before doing neuromodulation? I would have only done the block on this patient if I was planning on doing a geniculate RFA. Okay. Or if I thought that there was an element, one of the challenges with the knee is you could block like a half a dozen nerves, right? So you've got, now you've got the nerve to the VMO, you've got the like infrapatellar branch, you've got, there's probably like seven geniculates have been identified, the femoral, the sciatic, the adductor canalis affinis. So that may play a part in how you decide to approach this patient in terms of diagnostic or prognostic blocks. But I wouldn't have done geniculates unless I was planning on doing an RF. In this specific patient, I would actually move towards doing a purely diagnostic block of obturator and or femoral and sciatic and see the response. That may guide me in choosing my site for peripheral nerve stimulation. Gotcha. Any risk factors that we need to modify on this lady before proceeding onward? I think the diabetes may play a little bit of a part depending, there's not really great guidance right now on what A1C needs to be followed, but you could, you may want to select a device that's maybe less likely. Some of the smaller devices are less likely to get infected. I would probably reduce, I would probably eliminate the TCA and reduce the gabapentin. If it's not having an effect or only marginal, there's no reason for her to be on it. It may be leading to some weight gain. Sure. Awesome. Exactly what we were hoping for, a divergence of opinion, but lots of good information. Okay, our second case. 25 year old with spinal cord injury related pain. The challenge I have is the whole insurance issue. Yeah. Come to tomorrow's talk. Dr. Furman brings up a great point. I mean, the access, the care access, especially for peripheral nerve stem is quite challenging. And I think that we're in the quagmire of the peripheral and central nervous system and all the different patient presentations and the dearth of evidence that we truly have for these treatments. I think it's a little bit more, I mean, I hate, again, maybe this is what you want, a little bit of disagreement. I think that the bottom line is the standard that's been set for data is probably an unreasonable standard outside of certain disease states, right? So randomized control trial, double blind, that's not necessarily something that we can completely successfully do in pain medicine or interventional pain medicine. I think there's challenges to that. The other thing is insurances are constantly moving the goalposts. I've met with, at this point, enough medical directors that probably cover a third to half of the US population. And they admit that basically they'd rather pay for opioids than to pay for procedures because it's costing them pennies to the dollar. And second, that if you do two randomized control trials with 250 patients total, and then you present that, they're gonna ask you for two more, right? So it's never, you can never quite meet them where they want you to be. And we're currently in an environment where it's not just PNS. But if you look at the sort of, everyone thought we were gonna get a break during this sort of COVID timeframe. But the number of changes that have come through from draft LCDs and then final LCDs for epidural serotid injections, facet injections, peripheral nerve stimulation, SIJ stuff just came up just the last week, prior authorizations for facet interventions. Can you imagine having to do a prior auth for every single facet intervention for every Medicare patient? You'd have to hire one to two more employees to be able to do that. And that's all in the setting of a 4.4% drop in reimbursement for like the final rule for payment. So this is a time where we, you're not wrong. There's a lot of payment related issues, as you said about peripheral nerve stimulation amongst other things. We're just gonna have to get a lot more active and a lot more together on our responses because we're too fractured. We've got 50 societies all putting out letters that are not quite together, I guess so. Totally agree with what you said, Dr. Fuhrman. But I also wanted to kind of leave it on the clinical side and you get into regional variation. Okay, next patient. Oh, was there another question? Oh, go ahead. Yeah I mean I think to answer your question I think the knee represents probably one of the most complex targets that's out there right and there's a there's several barriers to what you're describing one is what Dr. Fuhrman talked about financial it's really hard to block every single nerve and get paid for it but not everyone I would wager most of us aren't good enough with ultrasound to be able to identify all those block all those nerves either so that's another challenge we're looking at this because the ultrasound education as it's sort of set up for physiatrists or any other specialty if there's a lot of inconsistency in that so that that's another issue but fundamentally that's a joint that we we do need to learn more about and do more with to really be able to be successful long term with good sure so just in terms of housekeeping technically the session ends at 1115 the plenary begins at 1130 so we don't want to step on the plenary too much so we'll maybe go a couple of minutes long we'll get through this case and then then call it a day okay young guy spinal cord injury gunshot wound at t6 does have the bullet transverse the canal but he does have retained fragments so you can't get an MRI t4 to t8 posterior fusions has two pain syndromes the biggest one he talks about is a band like vice like component of pain that is generally constant and then a paroxysm paroxysmal bolts of lightning that run into his lower extremities he's on no hope no opiates currently they didn't help much in acute care he's on gabapentin at maximally covered doses by insurance has some spasticity but baclofen and tizanidine orally seem to take care of it uses cannabis with positive benefit generally independent at a wheelchair level but doesn't have a whole heck of a lot of support lives in a wheelchair community is dependent on others for transportation to your clinic has a t6 Asia a exam with a zone of partial preservation between t7 and t9 his wheelchair looks fine his skin's okay so you saw this patient on Monday right Eric you know your ma's put this in today this is Sean P Shaw patient one right I'm gonna take lead on this since this is this is 50% of what I see so we see this a lot and we get these patients referred a lot to us so I would first probably start with lithium treatment and if Mike and I've talked about this over the years if you guys haven't don't know anything about that I encourage you to look at the published literature which is quite robust on oral lithium for three for 12 week treatment for chronic neuropathic pain and spinal cord injury it's technically off-label it's extremely safe as long as renal function is fine and can be extraordinarily effective at 300 milligrams twice a day labs of course need to be monitored for medical legal purposes okay so assuming that is a partial or no benefit or they can't tolerate it I would consider IV ketamine for this patient we've had some success I wouldn't say dramatic it can be palliative you know frequently they might have a couple weeks to a month of benefit between infusions but I'm not I don't really infuse up about anybody every month so let's say we tried those two things and they either weren't effective or not tolerated I would probably get a myelogram and as long as the thoracic spine is fine I would probably stem them even if I couldn't get to the level of injury I could get pretty close you know there's typically a lot of epidural scarring after a traumatic injury like this with bleeding I might be only be able to get up to t9 and that may be because of the fusion or maybe because of the epidural scarring or both so it's it's so I would do that first I just did a case actually two three weeks ago on a 79 year old gentleman that did have a gunshot wound t3 and was fine motor and sensory incomplete or complete excuse me for 40 years and then had a syrinx that was resected and had a t2 through t4 laminectomy and that since I had just severe abdominal pain and perineal and radicular type pain so I stemmed him I could only get up to about t6 because of his surgery but his abdominal pain essentially went away and that was his biggest problem and so so in summary you would try some other things first so I would I would definitely do yeah sorry so I would do lithium probably and then I would probably not try any opiates there's no reason to trial that I would try IV ketamine I would stem him and then if that didn't work I would put a pump in him was like on time gotcha I would respectfully differ from that algorithm that's what we're here for I think over the years we have been focusing on evidence-based medicine and I see a lot of young folks sitting in the audience and I would encourage them to base their decisions on evidence if you do that one you will get confidence you will have home runs and then you can foray into the anecdotal medicine which dr. shock in practice now because of his experience of so many years but initially when you write off the bat follow the evidence you will have home runs and that will give you evidence in this specific case as far as neuromodulation treatment options are concerned we have close to about level 2 evidence for targeted drug delivery in this specific patient population so I would definitely not start with neurostimulation be it dorsal column stimulation or dorsal root ganglion stimulation both of them are options but not as the first line neuromodulation therapy in this specific patient based on the presentation the neuropathic pain which is at the level of the lesion and below the lesion I think this patient would be an excellent candidate for targeted drug delivery either using a non-opioid based medications iconotide or a combination treatment with some baclofen as well I'm not going to step on the plenary session so I'm going to call it quits it at this point I had a couple other cases to to challenge the the minds of the masters there I want to thank both our colleagues who went before us and as well as my current panelists please give us some evaluations if you thought this was a good session we could certainly look to repeat it next year and enjoy the rest of the conference on physiatry day

neuromodulation

panel discussion

indications

technologies

future advancements

waveforms

remote monitoring

battery systems

case study

treatment options

risk factors