Hello, everybody. Hope everyone can hear me. My name is Dr. Gurtej Singh, joined with a couple of my esteemed colleagues, and just so thankful to see everybody else joining in tonight for this Member May interventional pain community session. So, first one we've run, so absolutely appreciate any feedback that you guys have. I've gone ahead and opened up the chat room. You're welcome to place questions in the chat throughout the entire presentation, and our goal will certainly be to answer all of them before the end of our session. So, I'll go ahead and share my screen. There we go. So again, welcome everybody to AAPM&R's Member May interventional pain member community session. I think this is the first one we've done in a little bit of time, so hopefully everyone appreciates the content and always welcome for suggestions on how to make this more interesting or more in depth, whether it's at the Academy meeting in November or for the next Member May session. Outlined here are the faculty members that are going to join us. Unfortunately, we've had a couple that have some children issues that have come up tonight, so we're going to do our best to ad-lib for a couple who can't make it, but we'll go ahead and get started. Dr. Tate, unfortunately, won't be joining us, but I'll pretend to be Jordan. I probably won't give this as well as she would, so I apologize for that, but here we go. So the first topic is spinal cord stimulation, sort of an update on what's transpired over the last few years and what's to come in the coming years. So what we decided to do today was just sort of outline the various stimulation waveforms that are FDA approved and are typically used in practices across the country and around the world. So we have one form that's known as what I call sub-threshold stim. So this is a tonic-based spinal cord stimulator, where we use a proprietary waveform known as the burst DR waveform, and patients get implanted with the device. The painful area is mapped, and so it is what we call based on paresthesia mapping, and then the stimulation is turned down so that it is below the perception or sub-threshold for the patient. There is level one randomized controlled validated evidence behind this waveform. It has certainly been demonstrated to be superior to the traditional tonic or what is now called open loop stimulation. One unique part of burst DR is that there have been findings of affecting the medial lateral lamniscus pathway, so where there is depression and other factors in how patients perceive pain can also be modulated, not just simply the paresthesia of their actual painful area. One unique aspect to the offering is what's known as DRG or dorsal root ganglion stim, something that does take a little more technical expertise for those who are very familiar with spinal cord stimulation, but one of the unique features when it comes to DRG is that it has wonderful evidence for complex regional pain syndrome. For our patients with lower extremity or upper extremity CRPS who have run through the traditional treatment algorithms, medications, injections, bio-social feedback, cord stimulation specifically targeted at the DRG has been very well established and has excellent real-world clinical data for patients specifically with CRPS. It doesn't mean that DRG is only used for CRPS, but for those wanting to find the type of stimulation that might benefit their patient in a very specific way, this would be certainly one option. Closed-loop stimulation is something that's relatively new. For those who've done spinal cord stim for many years, especially those who have been in practice for 10 years or more, we're very familiar with open-loop stimulation. The pulse generator delivered a particular energy level into the cord. The patient felt that paresthesia in their painful area, but then if they moved positions, went from sitting to standing or they went from standing to laying down, patients would have to make frequent dose adjustments to either increase the stimulation or decrease based on what they were feeling. What closed-loop has done is been able to record what's called an ECAP. This is a data point that can be electrically gathered from the patient's spinal cord. We all know that the percutaneous leads move in the epidural space and with positional changes, the cord itself moves within the dura. Those changes alter what the lead is recording as that electrical input from the spinal cord. That input then gets processed by the pulse generator and then can deliver the appropriate stimulation so that patients do not have to make as many adjustments as they used to in the past. Again, this is a paresthesia-based mapping form of stimulation. Closed-loop has three years of published level one RCT data, something that some of the other waveforms don't have and has shown superiority as many of the others have over the traditional open-loop. Another form of stimulation is what can be considered super threshold. Again, a patient on the table during trialing or after implant has their pain mapped under paresthesia and then the frequency is turned higher so that the patient doesn't feel it. It's still technically part of paresthesia mapping. One company uses what's called differential targeted multiplex. You have a multiplex form of waves that are continuously stimulating the dorsal columns. You get high dose and low dose. Part of it is proprietary to that company. Again, it has been shown to have success in patients with post-LAMI failback syndrome or what is now called persistent spinal pain syndrome, lumbar radiculopathy, arachnoiditis, complex regional pain syndrome, all of the typical diagnoses that we use on a day-to-day basis. WaveWriter, again, another proprietary waveform of dorsal column stimulation. Again, providing both paresthesia and paresthesia-free waveforms. One of their waveforms they call FAST. They've been able to show that patients respond quicker to the therapy and are therefore able to move faster. They're able to have a trial that might not last as long because they're able to get benefit from the spinal stimulation therapy quicker. One of the newer companies to the market is known as Biotronic. They also use a super threshold form of stimulation. These three are very similar in their overall thought process of how to deliver neuromodulation. This is more of a cascading delivery of micropulses. Again, finding ways in which to stimulate the cord to try to demonstrate that greater than 80% of patients are responders. What is a responder? Responder is considered to be having 50% or more pain relief. Nowadays, when you're looking at data and when you're trying to decide what stimulation therapy should I be using for my patient, you definitely want to consider research that has demonstrated an 80% responder rate. Many of these companies and many of these RCTs are showing about a 50% remitter rate. A remitter would be considered somebody that's getting more than 75% to 80% of their pain improvement. That could also be mapped out with a pain score of two or less on a VAS. That would also be considered a pain remitter. What's very exciting over the last five to seven years is that companies have understood that the old days of open stimulation or what's called open loop stimulation, that's just not good enough. Payers, especially insurers, are looking for greater success given the cost. Over the years, we've obviously had considerations and concerns for explants. Companies have turned their attention to finding waveforms and finding diagnoses that are better suited for the long term. Last piece with Biotronic is that they do offer an enhanced patient data capture. That could be for those who participate in remote patient monitoring. This could be something that you could use for remote patient monitoring as well. I believe this could be the last slide. High frequency stimulation, something that's been out on the market for well over 10 years now, certainly helped to advance the field. Prior to high frequency, open loop tonic stimulation was what the other companies used. This definitely helped to propel the field of neuromodulation forward. The target is not the dorsal column, but instead the dorsal horn. That's why this type of stimulation is known as paresthesia independent. You might find a patient who is driving quite a bit, truck drivers, those who need to be on the road for their job, being paresthesia independent allows them to have greater safety in not feeling an overstimulation when driving or doing physical activity. Their initial data back in 2012-2013 also showed an 80% responder rate and a 50% remitter rate. The one thing that high frequency stimulation has done to advance the field is they've looked at painful diabetic neuropathy as well as non-surgical low back pain. We've expanded the indications to treat patients with palliative neuromodulation. Lastly, it is the largest variety of waveforms. If you have more interest in that, I'm sure the companies can dive deeper into what we've talked about this evening. Diagnostic indications, so things again that we're already looking at and we're already taking care of, so chronic pain syndrome of trunk and limbs, CRPS, persistent spinal pain syndrome, lumbar radic arachnoiditis, newer indications, things that hopefully will come to market at some point with FDA indication, chronic pelvic pain, occipital neuralgia, chronic pancreatitis, and post-traumatic neuralgia. Then a little teaser of what could be in the future, so different ways in which to stimulate the cord. There are some companies that are overseas now across the pond, as we on the East Coast say, with ultra-low frequency as well as those who are ultra-high frequency. I think that does it for me, or at least for Dr. Tate's presentation, so I'll stop sharing. Dr. Raspoli, it is your turn. Everyone can hear me okay and see my slides okay? I kept my talk pretty basic today because I think peripheral nerve stimulation is still pretty new to some people still in clinical practice, so I just wanted to do a basic overview first and then talk about a little data. Why are we considering PNS in our practice, or why do I consider PNS in my practice? There's a variety of targets. There's a variety of devices to consider when using PNS. It's definitely a lower risk and less invasive option compared to other interventional spine interventions, for instance. Ultrasound and fluoroscopy is an option depending on the target. The technology is evolving, and we get approval for most PPOs and for Medicare. Who are we considering when we think about who's a good candidate for PNS devices? A lot of post-surgical chronic pain, patients that have come to you in clinic for repetitive injections and either are responding less and less to injection therapies or haven't responded at all and you're running out of options of what else to offer them. Patients that have had positive results from diagnostic nerve blocks and were looking for more of a longer-term treatment option, and clearly mononeuropathies that are surgical patients or don't have a surgical option, and an interesting patient population that I've seen a lot of in my practice is patients that have had failed SES and are still experiencing significant chronic pain. And then, of course, the patients that have a lot of comorbidities or medically complex that we don't feel comfortable offering either surgery to or spinal cord stimulation to. Some targets. In reality, if you can block it, you can target it with a PNS device. Here are the common nerves in the upper extremity, lower extremity, and the trunk that we see studied and discussed in literature as being successful and a good treatment option for patients. I guess more commonly we see talked about in the literature, including the geniculars for post knee replacement patients, tibial for tarsal tunnel patients, medial nerve for patients with chronic carpal tunnel, and then an interesting bunch that I'll talk about a little bit more that I include in my practice a lot are the clunials or the medial branch patients for the axial low back pain or the axial neck pain. And these specific are fluoroscopy guided. I figured I'd highlight this because this is what some patients feel either more comfortable utilizing as their image modality versus ultrasound. So the criteria for selection, patients have to have documented chronic and severe pain for at least three months. Obviously, failure of less invasive treatment modalities and medications, lack of surgical contraindications, you know, disclosure of risks and benefits. I mean, these are obvious things, but this is what Nordian or Medicare requires to be documented in there in your clinical note to be approved. And just like SES, we need a formal psychological screening by a mental health professional. And then we'll talk about the different devices as options, but with the implantable, permanent implantable devices, we need a successful stimulation trial with greater or equal to 50% reduction in pain intensity before implanting. So I didn't get too specific here, but, you know, the companies that are out there that are being utilized for PNS are a company that offers a trial for seven to 10 days, similar to the spinal cord stimulation process that we see that Dr. Singh just talked about. And, you know, the difference here is that this company in particular has a micro IBG, so it's a much smaller battery burden. So for me, at least when I'm able to talk about this with patients, it's, you know, more appealing to have a smaller battery implanted into their system. And I like that there's a trial too, so patients get to experience what the potential pain relief is like and if they feel comfortable using the device. And there's another company, which even has a smaller IBG. The IBG is actually within the lead, so there isn't even this implantable battery associated with it. And some patients even like the idea of not having an even battery. And when it's just the lead with a small, even tiny receiver, it's even less burdensome for patients to experience when they are offered a device option. And then the final system that we discuss most about in clinical practice and literature is the temporary 60-day system without an implant. And for most of you that are familiar with it or trained in it, the idea is that the neuromodulation that exists for 60 days offers persistent neuropathic relief. So just to review basic targets, I didn't touch all of them, but probably the more common nerves that we target using PNS device. A lot of times for post-TK or partial knee-replace patients, the non-operative osteoarthritis patients, severe crush injuries or CRPS, an easy target. I mean, most pain, interventional pain, are trained in how to target the genicular nerves, but can be a little more complicated. It can be seen under ultrasound and more commonly probably fluoroscopy with the superior medial and lateral genicular nerves targeted. Axial low back pain. So these are the clunial nerves. I don't really do a lot of clunial blocks, but we've found that, you know, patients obviously that if you did a diagnostic clunial block for a patient with axial low back pain, might be a good candidate to consider a more longer term option like peripheral nerve stimulator, targeting clunial nerves for patients that have chronic SI joint pain, post-laminectomy patients. A lot of times this is what I utilize for the failed SES and axial low back patients. I've seen a lot of, in my practice, a lot of severe scoliosis patients that are either going to be very, very difficult to access to do a spinal cord stimulator trial. So we, you know, weighing risk and benefit offer, they really only have axial low back pain, you know, offering clunial nerve trial. And usually you have to document whether or not they have a positive Tenell's test across the clunial nerve on their physical exam. It's usually supportive of that, plus doing a diagnostic nerve block usually supports, you know, offering this technique for patients. Tibial nerve, that's another common one. Targeting posterior tibial nerve for patients with tarsal tunnel, either patients that have tarsal tunnel that aren't surgical candidates or have had surgery, like decompression and have surgical scarring. And this is a little bit outside the box, but, you know, patients with ganglion cysts, Morton's neuroma, even neuropathy patients and post-traumatic patients have been, you know, documented in clinical cases here as being successful. And occipitals and cervical medial branches. This is still kind of like a hot topic. Targeting the occipital nerves, greater and third occipital nerve or cervical medial branch nerves for patients with axial cervical pain, referred pain to the head, headaches, migraines, even, and occipital neuralgia. We'll talk a little bit more about where the studies and the data is going with these options. But finally, just talk briefly about shoulder and suprascapular nerve. Patients with, again, non-operative OA, rotator cuff pathology, post-surgical, post-trauma, even those with C5-6 radiculopathy, and then commonly post-stroke shoulder pain. So, just touch briefly on the data. There isn't a lot of legitimate randomized control studies for supporting PNS quite yet, but there's a lot that are ongoing. I guess the big study that at least the highlight, and I did mention a couple of companies here, so Sprint is the temporary PNS, the 60-day device that had the randomized control study done with patients that had post-amputation pain, and it was a randomized control multi-center study targeting the sciatic and femoral nerve, and it was probably the most robust study at least supporting that patient population, showing 50% relief in the first four weeks post-operatively, and even a 12-month follow-up with at least 50% relief. The ongoing big randomized control studies from the other companies like NALU's comfort trial presented at Aspen in 2023, with six-month data showing 100% responder, which would mean that 50% reduction in pain across various nerve targets, so this study includes a variety of the targets we just discussed—low back, shoulder, knee, and foot—and 78% pain relief from baseline, 65% improved ODI. The data looks promising. Obviously, once these are published and there's more randomized control studies, we're going to have a little bit more confidence behind offering this to patients, and which company that you feel comfortable offering, which company and which device you feel comfortable offering in your clinical practice. Sprint also has another randomized control study for post-operative pain following a knee replacement, which there's a lot of promising clinical data supporting patients' improved quality of life and walking ability at month three, and this, interesting to me, is a little bit median time since surgery is two and a half years, so I think a lot of these patients show up to our clinic without a lot of options, and if we have anything to offer that's minimally invasive and that you feel comfortable offering patients from a technical standpoint, I think it's become, at least for me, a very large tool to feel you can help patients with their function and their pain relief. So we mentioned the comfort study through NALU. There's a few more clinical trials ongoing with Sprint, and they seem to have a lot more large studies that are ongoing that will be likely presented at some of the large pain conferences with ongoing support and clinical data. So yeah, I just put the slide in to make sure that we are choosing the patient selection appropriately and delving into which device and why, and to highlight really the downfalls also of why we wouldn't offer, why we would consider any kind of stimulator device, especially PNS, risky for patients. So not all of these devices are MRI compatible, so it's good to know which devices are and which products are and for what body parts MRI compatibility is. Not all of them are explantable, so even though you have the option of using peripheral nerve stimulator leads that have these little tines on them for some of the smaller, more peripheral nerves, that makes it very difficult to explant. So if you are putting this device in somebody and offering it to them and knowing that it may not be MRI compatible, that it might be for a lifetime. You know, some of the external battery appeal for some of these patients is also a burden for others. So it's important to make sure the patients are well aware of some of the downfalls of having an external battery. And just like SCS, we have this potential for lead migration. And then another potential pitfall for peripheral nerve stimulators that when we implant these and they're pretty close to the skin and we're not deep enough in the tissue, we have seen leads erode. And that could be obviously a big problem. So where the interesting things are, the hot topics of peripheral nerve stimulator and interesting data is going to keep an eye out for the upcoming conferences are medial branch stimulation, multifidus stimulation, which Dr. Singh is going to touch on more of, intercostals and its use for post-hepatic neuralgia, post sarcotomy pain and pelvic pain is always a hot topic to whether or not patients that have pudendal neuralgia or something variation of pudendal neuralgia will respond to peripheral nerve stimulator or not, and then whether or not it's safe to offer patients. And I think that's it. That's my slides. I appreciate that as sort of one hopefully easy question for you. I think when you compare patients that you see for ENS versus your patients that you see for SCS, do you find any sort of trends in terms of your trial to implant ratio or your overall short-term long-term success with these two different patient populations? Yeah, because I would say that, you know, even though I presented all the extremity options, you know, I see a lot of axial low back pain more than anything, because I have pretty good working relationship with the spine surgeons here and the few that do believe in neuromodulation and support it, you know, it becomes my choice whether to offer spinal cord stimulation versus peripheral nerve stimulation. I have to say lately I've been seeing like 100% trial to implant with my clunial PNS. I never would have expected that a year ago, you know, like looking at the data and even my experience as a fellow, but it's become a great option for the patients with axial low back pain. It's very specific. Axial low back pain have either had, you know, poor success or only ridiculous success with their SCS. And granted, those patients may be also candidates for battery replacements or maybe revisions or, you know, further workup, but most of them, if they've gone through all of that, don't want more invasive, they want the least invasive thing. So it's been nice to at least have that as an option in my toolbox. Thank you very much. I'll go ahead and share my screen. We'll move on to restorative motor stimulation. So another form of, by technical definition, another form of peripheral nerve stimulation, restorative motor stimulation. These are my disclosures. And as it relates to this particular set of slides, I do speak for Mainstay Medical, which is currently the only company that does offer this technology. So, you know, I think one of the biggest things that we, as a clinician, what I struggle with, two different things. One is, am I identifying the patient correctly, right? So am I understanding a patient coming in with a radicular, a neuropathic type of pain complaint, or do I have a patient that's more mechanical and nociceptive? So I think this is a really important concept for all of us, whether we are internists, whether we're physiatrists, whether we're sports medicine trained, pain trained, spine surgeons, you know, we got to be able to know what, where exactly do we think this is coming from and what's our etiology. And once we can kind of tease that out, well, I think, you know, with today's presentation, you'll see that there are so many different options for patients. The multifidi muscles are, so the role of the multifidi muscle, you know, something that, I guess, as physiatrists, we probably should have been thinking about a long, long time ago, but really never had. But based on our training and what we're supposed to be doing with patients in terms of rehabilitation, you know, the role of motor stimulation actually helps to accomplish that goal. So the target here is not inside the spine. And it's not a, it is a peripheral nerve, but stimulated in a different way where we target the L2 dorsal ramus branch of the medial branch nerve that sort of sits on the L3 transverse process. Patients typically will have some form of a back injury in life, and then that will start this cascade of dysfunction and where they don't use their spine correctly. We see this in knee pain all the time. You get a knee injury, and then we have arthrogenic inhibition of how we use our quads and our hamstrings and, you know, do they fire correctly and at the right time. And so a very similar pathophysiology is happening to our multifidus muscles. So when that patient comes in, this is sort of our dilemma. This is what we kind of, these are our options to choose from. I think for the most part, we've become very responsible in not going opiate first. Certainly in our practice, you know, we definitely emphasize physical therapy and patients trying to rehabilitate themselves on their own. But many times this doesn't work. And we've all had those patients probably today and tomorrow in clinic. And then, of course, you know, do we, what of these, you know, treatment options do we offer? And if they work, how often do we keep re-offering it to them? So I apologize for how busy the slide is, but I was trying to be, you know, sensitive with time. But how often do each of us read our own imaging? And for me, I really do try to make it about 99% of the time. I can certainly tell you 10 years ago, I didn't really care much about what emotic change was. I definitely, until about three, four years ago, never even bothered to consider that multifidus atrophy had a clinical presentation. But prior to that, it was very much, you know, how much disc degeneration has occurred? You know, is the spondylolisthesis mobile or unmobile? I remember when I first joined a neurosurgical practice right out of fellowship and they said, why are you doing these RFAs? And I said, because facet arthropathy is real. They go, no, it's not. We just blow through the facet when we're fusing patients. And it's just fascinating where that was back in 2010 and now where we are in 2024. And hopefully, you know, spine fusion surgery for facet arthropathy is no longer a consideration amongst any of us. It is important to read your own imaging and, you know, you'll be able to appreciate, you know, these top three images showing what a normal multifidus looks like versus moderate atrophy. And then, of course, severe atrophy. And tomorrow when you're in clinic and looking at your next lumbar spine, you know, take a peek there and see what you see. The REACTIVATE implant is the device. REACTIVATE B was their level one randomized control trial. It certainly has the most robust data amongst all neuromodulation devices that are available. Their published five-year data was just released earlier this year. So you can see, you know, patients' pain scores from initiation to the end of the initiation of therapy. It is also one of the only studies that did a true sham crossover. So everybody that was enrolled got implanted. And, of course, you see an initial placebo effect with that dotted red line. And then once that red line turned to head back towards the original pain baseline, that's when they went ahead and turned the devices on in the control arm. And then you see the two arms sort of meet at about two years. And the longer you use the device, the more pain relief patients get with their mechanical LOVAC symptoms. It is the only restorative neurostimulation device that's currently FDA approved. I think as physiatrists, it's something we very much should consider as it is a way to restore multifidus function. It's a way to break the arthrogenic disinhibition, if you will, with how our chronic back pain They are planted outside of the spine, so from a safety perspective, much more safe than necessarily going into the spinal canal. And then patients give themselves, you could say, their own PT sessions twice a day for 30 minutes. And when doing so, find that success out past six months. And then the longer they keep using it, the better they keep getting. Dr. Desai, I believe you are our next contestant on The Price is Right. Sounds good. Can you guys see me? I feel like I'm coming out of the screen. You look great. Can you all see my screen? Dr. Singh, can you see my screen? Yes, sir. Looking great. All right. Well, thank you, everyone, for being here tonight. I know it's always a little bit challenging to sign on after a long day. So I think we have a lot of time for questions. I'm going to turn it over to Dr. Singh. It's always a little bit challenging to sign on after a long day. So I think we all appreciate your presence here. I think from what I understood, the intent of this session was to really talk about some of the cutting edge new and emerging technologies that all of us as physiatrists may encounter, both as physicians who may do these procedures, but also physicians who may see patients who have had these procedures done on them. So I have the opportunity to present on sacroiliac joint fusion. And the fun part about my presentation is I don't really have to talk about data because there is a blissful lack of very much data. So I'm just going to talk about technology, which is kind of fun in some ways. I'm going to talk a little bit about the SI joint just very briefly. So my disclosures are that I actually helped develop one of the products. I'm not going to necessarily talk about that product specifically, but I have, I had stock options in a royalty agreement for that product. So the sacroiliac joint is a very, very complicated joint for those people, for all of us. I mean, we probably as physiatrists see this, see patients with pain from this joint all the time. I see patients every single day that have pain from this joint. And it's a complicated joint because it's got, it's sort of a two-part joint. It's one of the only joints in our body that's both diarthroidal as well as synovial. So a typical diarthroidal joint would be your skull. A typical synovial joint would be sort of your knee. And somehow this joint combines both functions and both sort of morphologies. In addition to that, it doesn't move very much as a joint. So it's a very, it's a very important shock absorbing joint. It, the movement of it is called nutation, counter-nutation, which is on the far right of my screen, where you've got sort of nutation on the left with the sacrum moving sort of dorsally and the ileum moving in sort of two different directions and counter-nutation on the other side, just to sort of give you an idea of how much it moves. In general, the joint moves very little, but it's, it's interesting how much perhaps it can move. One of the conditions in which it moves a little bit more is pregnancy, especially in the third trimester of pregnancy, when the relaxin hormone is released, the ligaments, the picture right to the left, where you see all the very, very strong or typically very strong ligaments that hold the SI joint together are located softened to allow sort of the ability of the fetus to pass through the pelvis and through the vagina. Interestingly, we would sort of in our brains would think that, okay, the baby's out, these ligaments all go back to the way they were, but it's not actually the case. Increasingly, there's been the popularity of a term called the fourth trimester. I, for one, think that it's probably not a trimester, but more like two years. And oftentimes, depending on how difficult pregnancy is, it can be much, much longer and people can have, for example, sacroiliac joint pain for years and years after, after delivering a baby. And then the far left, you've got sort of the innervation, right? So the innervation of the SI joint is actually incredibly complex. This is just one representation of what we think is true, but what we do know is true is that from person to person, from side to side, there is variability in the innervation. And what we really know is about the innervation of the posterior portion of the joint. We have very little ability, while we know about the anterior innervation, we have very little ability to affect the anterior innervation of the joint. So radiofrequency ablation, which was talked about a little bit in some of the prior talks, is a very common procedure. And for years, we were doing SI radiofrequency ablation. Increasingly, this is a procedure that is no longer covered by most major insurance carriers, including Medicare, which has really put sort of a fairly interesting burden upon both patients and physicians, because now what we're stuck with is either doing an SI joint injection or an SI fusion. Really, there's nothing at all left in the middle. So the way in our practice that we look at SI joints, a little bit at least, we try to categorize folks. And so in our practice, we tend to think of folks who are either hypermobile, so they have SI joints due to the sort of relative incompetence of the ligaments in the posterior portion of the joint that are hypermobile, or the other side of the equation is people who are hypomobile, people with an arthritic sort of component, whether they have a rheumatologic condition or even just injury or some sort of surgery above, which has now changed the pressure dynamics and the force dynamics in the SI joint. So it's sort of one way to categorize the patients with SI joint pain to try to perhaps better understand, as time goes on, who are the best candidates for intervention, whether it's an SI joint injection, there's some data about intraarticular PRP, there's some data about prolotherapy, there's data for RFA, there's actually three randomized controlled trials on RFA, which is sad that it's not covered, but the last trial came out just as a negative decision came forward, which is a really unfortunate consequence for the patients who've had good relief from RFA in the past. And then also, who are the right patients for SI fusion? So there's a whole host of SI fusion technologies available, and I'm going to try to briefly touch on all of them to some extent. So you've got, for example, in this image here, dorsal interpositional implants. These are typically allograft implants. There are lateral transfixing implants that go either from one portion of the joint across to a different portion of the joint. And then there's different portions of the joint that can be transfixed or fused. And so we're going to talk about all of that in the next several slides. So these are just examples, and I try to remain as non-corporate in this delivery. What I mean by that is I try to avoid using technical terms that are proprietary terms or terms that are specific to certain companies. But these are just three examples of allograft products. These are products, they're basically wedges that are made of bone that are basically placed within the joint with the idea that that was, and it's more to it, you typically place a needle into the joint, then you dilate the incision and prep the joint itself by scraping the sides of it for all intents and purposes to create some bleeding. And then you usually place one of these grafts in and place some bone graft in with the idea that they may fuse across that spacer or wedge. So that's one example of what's commercially available out there. Another one is the use of screw fixation. So if we go back to this image, you can see this on the right here and also on the left, where a screw of a different size. On the right, the blue screw represents a fairly small screw. On the left, that's more of a triangular implant that we'll talk about momentarily. These are just ways that you place a device across the joint in order to transfix it. And some people use one screw, some people use multiple screws, up to three screws. The product on the left in the middle here is this triangular titanium implant. That's where all three are typically placed, much more invasive of a procedure, but also the procedure that probably has the most longitudinal data. So that those three triangular sort of titanium implants. So really what this comes down to is that there are a host of options available in terms of fusing these joints. I think I may have added, yeah. So I sort of misplaced my slide, so I'll have to go back in a moment, but this is sort of what the triangular implant looks like. This, again, is the company that has the greatest amount of data, the greatest amount of longitudinal data, and probably the most safety data, the most prospective data. But this is, again, a very invasive, very sort of large, relatively speaking, surgery that requires patients to be non-weight-bearing for up to 12 weeks after surgery. So it's not necessarily right for every patient. These are some of the newer products that have been developed that are actually intended to both transfix and perhaps potentially assist with fusion in a more sort of with something that is made out of metal, which has a little bit more sort of perhaps robustness to it. So on the left is a procedure where you place this sort of device across both sides of the joint. And on the right is a device that you place almost like a wedge into the joint itself, and then it deploys two wings that then sort of catch on to the joint itself. So these are just products that are available. And I think one of the questions that remains is, and this is really for us to continue to debate, to discuss, to sort of push the companies that develop all these products and push them out, right? So this isn't really a coding talk, but one of the big things that's changed is that the coding has changed. So in order to do certain procedures or to get paid for certain procedures, you have to place a screw or something across the joint currently. There's now a code for doing an in-office SI fusion, which is sort of a little bit of, I don't know how to best say it, but it seems a little bit ambitious to fuse someone's SI joint in the office. But ultimately the question is, we continue to use the word sacroiliac joint fusion, but really are we fusing these patients or are we fixating these patients? So, and because the amount of data we have longitudinally that actually shows bone growing across the joint and the joint becoming one bone is very limited. We definitely do not have great prospective data to that suggesting or proving that by any means. And also, I guess, ultimately the question is, does it matter? Does it matter if we're fusing or fixating or are we really worried about whether we're helping the patient's pain? So, that's what I've got. I'm happy to turn it back over to Dr. Singh. Dr. Desai, thank you very much. One question for Dr. Desai. Sure. Regarding the whole like female and pregnancy thing, what about for patients that haven't had children yet, like your young female patient population, would you be a lot more hesitant knowing that they will have to go through that trimester of relaxing state? Yeah, no, I think it's, I mean, this is, we could probably have an entire conversation about sort of peripregnancy related considerations. I don't, I typically don't offer this even to my very, very young patients, especially if they're thinking about children. I think that most of my very young patients who come in who are coming in with SI pain are probably actually hypermobile and they, I don't know if I should, that anyone should fuse them, because they don't heal, right? So if you look at the average hypermobile patient, that they invariably have SI joint pain and they have like an L4-5 or L5-S1 annular tear and a disc issue, right? And every time any of my surgical colleagues have fused these folks, they're forever in my office, right? Because they just, they don't heal. Their connective tissue is missing integrity. And as such, it just becomes the fastest domino effect you've ever seen, right? So if you fuse one side, you're going to end up fusing the other and then L5-S1 and then what's left? The pubic synthesis, I guess, right, so. Would you ever consider medioclonial trial and the potential explainable device just as another alternative as being- Yeah, I mean, I would consider that. I would also, I mean, we're currently doing a trial where we're looking at a prolotherapy protocol that we came up with, where we're enrolling like, I think we've enrolled already six or seven patients in that to see what the outcomes look like. I've done over a hundred patients with this protocol that we came up with, me and a physical therapist here, and it's worked exceptionally well, but of course that's anecdotally, right? So now we're going to collect the, after having done a hundred patients, we're going to collect actual formal data and try to publish it. So I think for patients who have this kind of pain and they're relatively young, they're often incredibly desperate, right? So you sort of want to be thoughtful both about the options you're presenting them, but also keeping in mind what their goals are, which might be very different from someone who's 75 and has SI joint pain. Well, Leah, thanks. I'm going to switch it over to Dr. Wahizy. We are kind of going to come up pretty close to the 8.15 Eastern time mark for our talk. If anybody has questions, please start throwing them into the chat. We'll start answering them. Obviously something that we could put on the member community email server. So if you have questions, throw it up onto the email server through AAPMNR, and that'll kind of keep this discussion going as well. Dr. Wahizy, wonderful to see you as always. Thanks for participating. The floor is yours. You can unmute yourself. You're right. I should have muted myself. All right. You probably say that in about three or four minutes now too. All right. Now, I was given the task of speaking about an eight hour presentation in about eight minutes. So we're going to get going. The talk, by the way, for those of you who don't know, it's going to be about direct and indirect decompression. And essentially the evidence-based information that we have behind these two types of lumbar stenotic treatments. All right. I do have some disclosures. I was a principal investigator in two of the studies that we'll be talking about, and an author on a few more that we'll discuss here as well. I've received research dollars for my investment into these research projects. Okay. This is the outline for what we will be discussing. All right. I want to put a couple of what I think are not myths, but some ideas that have to be re-idealized. And I think speaking to physiatrists hopefully makes sense of some of these ideas that I'm going to be speaking about now. We have heard from Gert. We've heard from Mahul, who both have said really smart things like, the SIJ can cause back pain and muscle deconditioning can cause low back pain as well. Now, the interesting thing about both of their clinical and academic tasks tonight was to discuss with you, axial pain, buttock pain, sometimes even stuff that refers into the leg. But things like this particular slide that are often shown in many settings, I want people to understand, it has to be taken with a grain of salt. The idea of the person who has butt pain and or back pain and or leg pain who is in the supermarket and hunched over a shopping cart does not necessarily mean that that person has lumbar spinal stenosis. Okay. I think there's a lot more that one has to consider. And we'll talk about some of those things in a couple of slides coming up. When someone's hunched over a shopping cart, it could mean that they have weak erector spinae and or weak paraspinals. They may have an SIJ dysfunction and or they may have beset arthropathy. You know, think about it just from an anatomical point of view. So when a patient comes into your office and says, yeah, you know what, I have trouble walking up and down the supermarket aisles. And you ask the question, does it feel better when you are hunched over your shopping cart? And they say, yes, does not mean that they have lumbar spinal stenosis. We are supposed to be more thoughtful about how we ask questions and how we examine patients. So just be mindful of that. Those things don't equal lumbar spinal stenosis. Those things may be lumbar spinal stenosis. And then understanding how to read our images ourselves also makes us better evaluators and diagnosticians of lumbar spinal stenosis. And these are some things we'll talk about in a little bit and certain things that we've published recently as well in terms of how to make ourselves better evaluators of imaging, especially in older patients who have all of the pathology or more that I just talked about earlier. Okay. Neuroforaminal stenosis. Well, what does that mean? It means usually, usually, that there's an SIP hypertrophy. When do people have SAP hypertrophy? Usually when they have facet arthropathy. So generally speaking, patients who have facet arthropathy will also have lumbar spinal stenosis, where typically, yes, in this neuroforaminal canal, but also within this lateral recess here as well. Okay. So just be mindful of that when you're reading your images and when you're evaluating your patients. This, by the way, becomes important because when I start to talk about what patients may get better with which treatments, direct or indirect decompression, having an understanding of this anatomy hopefully will make it more important for those who are listening tonight. All right. We talked about this moments ago. Here's some things that I want you guys and gals to think about. From the point of view of what other kinds of things can cause it, one thing that I didn't mention was HIPAA. There was a patient who came to my office who was sent as a VVIP, who told me that they have back pain, who told me that they also had leg pain, and they could not walk for more than 1 1⁄2 blocks. What does it sound like? Well, something that should be highlighted in the topic of this talk, right? It turns out that this person actually had severe OA of the hip. We did a log roll on him. Person couldn't cross their legs, okay? We sent him for a pelvic X-ray. This person had hip OA. He had a hip replacement, and his symptoms went away. Before he had a hip replacement, though, we did do an intraarticular injection just to make sure that we weren't missing anything. Just be mindful that the hip is one of the most common causes of non-spine back pain, and it can also cause leg pain, right? Just because of biomechanical limitations and biomechanical maladaptations as well. Knee OA. Well, knee OA, when you ask your patients if they have back pain and they say yes, and you ask them if they have leg pain and they say yes, some of your patients may not know, may not know that you're asking specifically about leg in a myotomal or dermatomal pattern, and not necessarily in a sclerotomal pattern, right? So please do your exams. Just because you want it to be a lumbar spinal stenosis doesn't necessarily mean it always is. It sounds trivial, and it sounds kind of silly when I say it, but I'm telling you that there's a lot of hip OA and a lot of knee OA that we miss when a patient tells us they have back and leg pain, especially in spine clinics where our spine colleagues are sending us patients because a patient has back pain and leg pain, right? So please make sure that we've ruled out this and or this before we start to have the next part of the discussion that we're gonna have. Hamstring tightness, look, causes back pain, causes leg pain. Let's be smart about this. Let's learn how to read images. Let's learn how to read pathology in patients, right? This is different from reading radiology from when we were in medical school. Our patients come with significant scoliosis, come with other pathologies that we have to know how to read and have to know also how to teach our radiologists to interpret as well. I think that is an art and a skill that we have to have too because we, me and some of my colleagues, are trying to make even some very elevated learners be even better learners, okay? Vascular, please don't miss things like DVTs in the world of COVID. These things exist. Yes, it's acute, but if a patient tells you they have back and leg pain, but then they come acutely with something else, don't miss it. It's happened in our clinic. We haven't missed it, but we have caught several of these, right? When initially these patients were sent to us because they were thought to have a lumbar spinal stenosis. Vascular claudication. There's about a 40% crossover for patients who have neurogenic and vascular, okay? And if a patient has this and you do an indirect or direct decompression on these patients, they may not get better. However, if you do an epidural just because of the sympathetic block that occurs within the vasonervosum when you inject into the spinal canal, this may get better transiently, right? So again, let's be thoughtful about this. Peripheral neuropathies, you know, I think that we have to have an ability to be able to parse these things apart from a lumbar spinal stenosis. Again, guys, as a community, let's just be smart about this, right? And then when we're smart about this, our outcomes improve. What do we know about the kinds of things that we can deliver our patients for true spinal stenosis? Meaning the history fits the exam, fits the imaging. What we know is that physical therapy sometimes works. What we know is that medication management sometimes works. Injection therapy, moderate, level two evidence. And there is some data behind adhesiolysis. I don't do a lot of this anymore. I do do it for some select patients. It's level two, moderate. What we know about ESIs is that there's actually fairly decent evidence, but the evidence does not go beyond six weeks with or without steroids, okay? That's a conversation in itself. We can have that offline, all right? This is direct decompression. This is minimally invasive lumbar decompression. This is a tool that is created and named by Virtos Medical. Medicare has renamed this as percutaneous image-guided lumbar decompression, which by the way, direct and indirect decompression fall into, all right? Although they're coded differently. There's about 35,000 cases that have been performed to date. A couple of these clinical trials I've been on. Complication rates are actually, in our clinical trials and in other trials that have been done outside of the ones that we've run, they've been better than ESI. Why? Because ESIs, because of the aging population, because of patients who have hypertension, who have diabetes, those patients actually have worse side effects from the steroid that is delivered rather than the procedure itself, okay? Quality, look, we have RCTs. We have some of the largest RCTs in the pain industry. And moments ago, a five-year data was mentioned in our motion trial, which we've done, which compares mild to conservative medical management. We are now collecting five-year data. That should hopefully be published within the next one to two years, okay? This is the procedure. Basically, we have got a bone rongeur and a tissue sculptor that we put into the interlaminar space, obviously using fluoroscopic guidance. And we essentially debulk the ligamentum flavam from the central, central canal, okay? These are the tools. Okay. These are the outcome measures when we did our mild on-course study. This is a Medicare, this was a Medicare subsidized study whereby Medicare wanted one year, we gave them two. They wanted 150 patients, we gave them 300, okay? Compared to ESI, safety was better, ODI was better, and pain relief was better at six months, 12 months, and two years. This is all published. VertiFlex is indirect decompression, indirect how, because basically what we do is we take a little screw, which is basically a butterfly anchor, and we put this tiny butterfly anchor in between the spinous processes, and we raise the spinous processes. We distract them from one another. When we distract them from one another like this, what ends up happening is the central canal widens, but you also get a little bit of neuroflaminal opening as well, all right? There is five-year data for VertiFlex as well. Now, I'm gonna let everyone look at this. The similar outcome measures that were used for the mild studies, both motion and on-core, were used here. This is VAS, claudication questionnaires, which was a claudication questionnaire that's gonna take me too much time to remember. ZCQ, Zurich Claudication Questionnaire, which all endpoints, there are five different sub-outcomes that were measured. Every one of those decreased. Pain decreased, and again, five-year data, all right? Opioid reduction and patient satisfaction. This I think is really important. We don't talk about this enough, all right? What are the things that we have learned? Well, we've learned that through evidence-based guidelines from people who do these treatments, we published a MIDUS-1, Minimally Invasive Spinal Treatment guidelines, and MIS-2 guidelines that basically create an attack plan for how and when one should choose between indirect or direct decompression. Here are the pearls here. The pearls that we learned from this is when we were going over and asking experts in the field what they believe is true. Well, what we believe is that MRI by itself doesn't mean as much, and exam by itself doesn't mean as much, but doing them yourselves and being able to read the MRIs is very, very important in making clinical decisions, okay? There's low clinical evidence for the things that we've mentioned before, NSAIDs, NSRIs, tricyclic antidepressants, okay? Consensus points. Bracing is not very helpful with lumbar spinal stenosis, okay? Level one evidence. This was basically deemed a level one study just because it was a true systematic review, the way that we did it, all right? Over here, I'm showing you in this box that in general, if a patient has central canal stenosis, as a consequence of ligamentum flabum hypertrophy, usually mild was selected. If, on the other hand, there was lateral recess or neuroforaminal stenosis, then indirect decompression is selected in general, okay? We got a little bit more complex here. Essentially, what this whole mishmash means is that you have to consider other factors, like Gerd had mentioned earlier. You got to assess for listhesis. Guys and gals, if your patient's vertebrae are moving, it's not gonna be able to support a spacer that's supposed to be living in between and then fibrose in between the spinous processes. Your hardware is going to fail, so you must do that. Here's something that I'm gonna share with the group that I think is really important. We just recently submitted a paper that demonstrates that if you take a patient and you do a flexion extension on them, and a flexion extension does not demonstrate listhesis, does not mean that they don't have listhesis. The best way to assess for listhesis is you get any supine image. That's a CT scan, that's an MRI, and compare it to a standing. So there's gotta be no gravity versus gravity, okay? The flexion extension is not enough, all right? And this was a review. Same things that we said before, lateral recess and neophraminal, indirect may be better, and then ligamentum flavum, central. Please do not discount the importance of a listhesis and a dynamic listhesis in these patients. If a patient has a non-dynamic listhesis, more than grade two, please do not do a indirect decompression. However, if a patient is not able to go through any, is not able to have surgery for a medical reason, or a patient says, look, I'm not having surgery, that's a personal reason, you can do a direct decompression, even on a patient who has a grade two, right? In general, those are the things that I will now leave you with. Rohit, thank you so much, Dr. Desai, Dr. Raspoli. Obviously, a big thanks to Devin, who helped to support us from the Academy side. And without each and every one of you being here tonight, again, a busy Wednesday evening. Happy Member May to everybody. Certainly look forward to seeing all of you this November in San Diego at our Academy meeting. Events like this kind of excite us. For those who are in the audience, you guys wanna participate, please don't ever hesitate to reach out to myself, to Devin, to the Academy, to any of the speakers. We're happy to get everybody involved and wanna hear from our entire member community moving forward. So we're right up against the time. I think there's another member community about to start in about two minutes. So we have to say goodbye. Thank you to everybody. If people have questions, please throw that out onto the AAPMNR question platform, the email platform, and then we can all email each other with our thoughts. So to that, enjoy the evening and look forward to seeing everybody in November.

interventional pain community session

lumbar spinal stenosis

back and leg pain

SIJ dysfunction

facet arthropathy

hip OA

knee OA

imaging studies

physical therapy

minimally invasive Lumbar decompression