Very good afternoon to everyone who's here for our session. As much as we all want our gluteal pain to be lumbar radiculopathy, a lot of times they are not. So the goal for this session is to familiarize ourselves, learn a little bit more about some of the deep gluteal pain conditions that we can diagnose as physiatrists and so that we can get them on the diagnostic path earlier. So I'll start with introducing myself and our faculty here. I'm Malathi Srinivasan. I'm an interventional spine physiatrist at the Rothman Orthopaedics Institute in Philadelphia. The two other speakers I have here really don't need an introduction. They are quite famous for all the important work that they do in and out of the academy. Dr. Amit Nagpal is the division chief of PM&R at the Medical University of South Carolina. And Dr. Desai is the medical director of International Spine Pain and Performance Center and chief of pain medicine at the Virginia Hospital. So I'm very excited to have them here, and I think this session is going to be very informative for you all to take back to your clinics to help your patients. So we'll get started. I have nothing to disclose. So deep gluteal syndrome is a diagnostic and therapeutic challenge, even for the most experienced orthopedic physicians, the reason being this area is anatomically dense and often gets underdiagnosed. The literature on this topic is also not that great. The majority of the previously published studies have been on piriformis syndrome, and more recently the term deep gluteal pain syndrome or non-discogenic sciatic nerve disorder has been used in several published studies, and it encompasses all posterior neurogenic hip and pelvic pain conditions. And the pathogenesis for pain in this location could be inflammation, compression, injury, trauma, or central mechanisms. So if we need to diagnose pain in the deep gluteal region, I think it's important to familiarize ourselves with the anatomy of all the deep gluteal structures that are potential sources of nociception in this region. And we also need to know about the referral sources for pain to this region, the most common being the lumbar spine, but other structures around the pelvis, which includes the hip joint and the pubic symphysis and the pelvic region. So we know there are several bones that live here, which is the sacrum, the sacroiliac joints, the hip joints, the pubic symphysis, the coccygeal joints. There is plenty of structures here with muscles, ligaments, tendons, and fascia. And of course the nerves, the most common being the sciatic nerve and also the pelvic nerves that lives in close proximity to the sciatic nerve, which are the podendal nerve and branches of the posterior femoral cutaneous nerves, which are the clonial nerves. So deep gluteal space is really the space that is marked by this blue dotted line that is bounded superiorly by the greater sciatic notch, inferiorly by the proximal origin of the hamstring tendons and the ischiofemoral tunnel, medially by the sacrotuberous ligaments, and laterally by the linea aspera, the greater trochanter insertion of the gluteus medius and the iliotibial tract. So you can see majority of that space is occupied by this big bulky muscle called piriformis. And the other muscles that live right below the piriformis are the deeper pelvic floor muscles, which are the arterators, the superior and inferior gamma ray of the arterators. And the right in front of the deep gluteal muscles, the deep pelvic floor muscles, is where the podendal nerve lives along the alcox canal. Interesting. So this is the deep gluteal space that we are talking about where majority of the region is occupied by this muscle called piriformis, and the deeper pelvic floor muscles, which are the arterators, the superior and inferior gamma ray. And the sciatic nerve travels just in front of the piriformis and leaves the inferior part of the piriformis to travel right underneath the arterator gamma ray muscles and leaves the pelvic region at the proximal ischiofemoral tunnel, which is a potential source for impingement. And anterior to that deep gluteal space is the alcox canal where the podendal nerve is with its three branches, the dorsal nerve to clitoris, the perineal nerve and the inferior rectal branch, and the posterior femoral cutaneous nerves lives around here. That also results, the branches that come out of the clunian nerves that live very close to the ischial tuberosity that causes the pain with sitting usually. So, the goal for this hour is to present three clinical scenarios that are related to deep gluteal pain conditions. We'll go over the etiology, the clinical approach and evidences for management of this condition. And we'll have time for questions and discussion. So, our first patient is a 64-year-old male who's a CEO of a finance company. He had a history of Parkinson's, treated with deep brain stimulator. He presents with two-year history of pain in the mid-gluteal region, non-traumatic and onset. He was worse with sitting or leaning forward and was relieved with stretching, yoga and some exercises that was particularly neck press with physical therapy. His exam, he had an unremarkable lumbar spine exam with a normal strength, sensational reflexes. There were some positive provocative signs such as tenderness in the mid-gluteal region on deep palpation over the greater sciatic notch. Some of the hip range of motion and the impingement tests were positive, which were the favor and the favor when he was caused some discomfort in the periformis region as well as in the sciatic nerve distribution. He was unable to do functional tests such as a single or double leg gluteal bridges. All hip impingement signs were negative including the Stinchfield's test. His MRI showed moderate central canal stenosis at L2-3. As you can see, it's not a very impressive severe spinal stenosis, but there is some crowding of cardiaquina at the L2-3 level and multilevel spondylosis. Before he came to us, he had a lot of injections. As you can see, he had a bunch of L3 transpraminals, medial branch blocks, sacroiliac joint injections without any relief. He had three surgical consultations. Two of them recommended surgery for L2-3 spinal stenosis. The third surgeon who happened to be in our group recommended physical therapy and a physiatry consult. So he started physical therapy and he wanted to try another injection. So correlating with his clinical presentation and lack of response to previous lumbar injections, we decided to do the piriformis injection under fluoroscopy. He did get 100% relief that lasted for about two weeks. His pain returned. A month later, he wanted to repeat the injection as he had very good relief. So it was repeated and it provided him one week of relief. Sorry. So since he had persistent pain, we decided to do an MRI for the pelvis at this point because his pain was very much localized to the pelvis and he failed response to lumbar interventions. It had some significant findings, the most prominent being the asymmetry in the piriformis bulk. So the left piriformis was slightly larger than the right. There were a couple of other findings in his hip including the hip arthritis and some labral cyst and some proximal hamstring tendinopathy. So this is the MRI because this is the coronal view. It's not very well appreciated on this view but you can see the piriformis slightly bulkier on the left side compared to the right side. This is the T1 axial pre-contrast images. This is where the piriformis lives and the left piriformis was slightly bulkier than the right and right in front of the piriformis is where we have the neurovascular bundle that includes the sciatic nerve and the blood vessels. Another interesting finding that we saw on the MRI on the fat suppressed T1 axial views lower at the level of the ischium, this is where the pudendal nerve lives on both sides. There was some enhancement of the pudendal nerve here which was not really reported by the radiologist. So it was just a finding that we were able to appreciate when we looked at his MRI but was not really reported on his report. So it sounds like he may have had some kind of an impingement in the pelvic region. So he had several symptoms and signs and response to injection that suggests that he possibly had a deep gluteal pain condition. He had failed response to lumbar interventions. He had relief with yoga and some leg press and had some positive diagnostic tests for piriformis impingement of the sciatic nerve. So what does the literature say? Piriformis syndrome is solely a clinical diagnosis and often gets underdiagnosed. It does happen in at least 6% of the patients with low back pain. So there is a good 6 to 17% incidence of deep gluteal pain condition in our patients who present with buttock pain. That is about two and a half million new cases each year. It's more common in females and males can get piriformis syndrome as well but they are a little bit older when they get it. Most common causes include tumors and anatomical variations. So the most common risk factors that are described in the literature are anatomical variations. And so the normal anatomy for the sciatic nerve in 85% of the patients, sciatic nerve leaves the inferior part of the piriformis, beneath the piriformis. In 15% of the patients, there is an anatomical variation. The most common variation being the undivided sciatic nerve splits right above the piriformis and the common peroneal component leaves above and the tibial component leaves below the piriformis. The second common variant is the common peroneal component leaves through the piriformis and the tibial nerve leaves below the piriformis. One of the other things that I wanted to point out to our group is the risk factor which is the leg length discrepancy that we commonly encounter in our patient population. Majority of us work with orthopedic groups and we do see quite a few patients with scoliosis and pelvic tilt and leg length discrepancy. There's also quite a few patients who have orthopedic hip or knee replacements with significant leg discrepancy that I think we should actively look for. It's an important risk factor for deep gluteal pain syndrome that's also been validated in some of the literature. So there are several physical exam tests that has been described for piriformis syndrome. The test that has the highest sensitivity and specificity includes the active piriformis and the seated piriformis stretch test. So a prospective study that was done on about 250 patients, it was published in the Annals of PMNR in 2013, they actually proposed a scoring system for diagnosing piriformis syndrome based on the history and the presentation. And piriformis syndrome is probably present if the score was over eight, but not if it was less than six. The scoring system actually had a very high sensitivity and specificity and a good positive and negative predictive value. It's not in clinical use now, possibly because it wasn't validated by more controlled studies after that, but it seems to be a good scoring system that we can possibly look into studying if anybody was interested in doing more research about how to diagnose them more accurately. Imaging studies are not really very helpful in directly diagnosing piriformis syndrome, but for patients who you have a very strong suspicion of piriformis syndrome and you're not getting good response to lumbar interventions, an MRI of the pelvis can be very useful to rule out tumors as well as anatomical variations, the most common being the atrophy or the hypertrophy of the piriformis muscle. So this particular study also showed that the piriformis bulk was larger on the symptomatic side in a significant proportion of patients compared to the asymptomatic side. And so something to look into to give the patient a diagnosis and directing them to the right treatment path. So management of piriformis syndrome is essentially conservative. Rest, activity modification, mobilization, working on the restricted range of motion around the hip. Physical therapy has been shown to be very effective if the diagnosis is made early. Increased muscle strength was noted in particular physical therapy exercises that the hips were flexed 220 degrees, externally rotated 250 degrees, and adduction to about 30 degrees. Repetitive exercises with physical therapy has shown to increase piriformis muscle bulk. This prospective study also showed that patient had complete resolution of pain, 51% of the patients had complete resolution of pain at seven weeks of physical therapy. So patients who failed physical therapy, there is a role for steroid injections. It has been studied in a couple of small-scale studies and has been shown to be effective to cause some significant pain reduction, lasting for about five to six weeks. And there was no significant difference whether ultrasound or fluoroscopy was used for the image guidance for these injections. There was also no significant difference whether lidocaine or steroid was used. And there has been a study published on hydro dissection on a small 38 patients who found significant relief when saline was injected prior to the steroid injections. There has been also some evidence to say acupuncture and the alternative treatment option acupuncture and dry needling has some good response to treatment and decrease in disability. Botulinum toxin has been studied. Unfortunately, we don't have a lot of studies on Botox and piriformis syndrome. There's a meta-analysis that was published recently from 23 articles with three randomized trials, two case control studies and two cohorts. The studies have been very heterogeneous using varied concentration of Botox between 100 to 300 units. So it is difficult to quantify the pain relief as well as enable to assess the functional outcomes. So right now, there is fair quality evidence that Botox may be safe to produce pain reduction. And it has to be used carefully because of the deeper location of the muscle and close proximity to the neurovascular structures. Image guidance should be used for piriformis injections and also to keep in mind the injection site pain, muscle atrophy, side effects. So these are some of the piriformis injections that we did under fluoroscopy. The goal is to identify the inferior sacroiliac joint. And the piriformis muscle lives just one centimeter inferior lateral and deeper to the inferior sacroiliac joint. And once the resistance for the muscle is felt, we inject the contrast. That's also confirmed on the lateral view. These are a couple of other pictures where there is some spillover to the arteries and a little bit. So, surgery, does surgery have a role in periformis syndrome? There has been some studies published on surgical outcomes for patients who have refractory to all conservative approaches in persistent pain. Endoscopic decompression of the periformis muscle has shown to reduce pain and improve functional outcomes. Currently, the level of evidence is grade four. So, to conclude, we want to keep periformis syndrome or deep gluteal pain syndrome earlier in our diagnostic pathway so we can diagnose them early and direct them to the right treatment path before wasting a lot of time doing lumbar spine injections, diagnostic blocks. I think a careful physical examination with provocative tests is very important to diagnose this and having all those risk factors in mind, including leg length discrepancy, which is very common in our population, helps us to make a little bit of an earlier diagnosis for these patients. And it's also good to involve a musculoskeletal radiologist earlier in the pathway as well and when you have an MRI of the pelvis, if you have a strong clinical suspicion, have them look over the images again, see if they see any signs of impingement or potential of enhancement or periformis asymmetry. That even gives a patient a valid diagnosis, which a lot of times, patients desperately need a diagnosis for their pain and I think giving them the diagnosis changes the treatment path and improve their care. And it also helps to reduce development of a chronic pain condition. And lastly, I want to, if people haven't read this, I want to introduce this book that was edited by Dr. McPaul. It has a chapter on trigger point injections that we wrote, has a lot of evidences about injections for periformis and also other interventional procedures in general. And thank you. I'll pass it on to Dr. McPaul. Thank you. Good afternoon everybody. It is my intention to hopefully keep everybody awake after our post-lunch lull. There are...and no pressure for anybody. There's a ton of seats up here if people don't like standing, but if standing is keeping you awake, then please by all means. This is Dr. Desai's slides. Can we switch over to mine? Thank you. So while we're doing that, how many people in the room are actively treating chronic pelvic pain at this time? Okay. Wow. That's a lot of people. That's great. You know, the first talk I gave on pelvic pain at AAPMNR was five years ago, I think, and I asked that question and it was a small group of people who raised their hand. So it's really great that this has become something that PMNR owns a piece of, and I'm glad that we have enough people in here and people who are becoming competent at treating this. Yeah, so I'm Amit Nagpal. I'm the division chief of PM&R in Medical University of South Carolina. Here's a case presentation, but I won't speak much of the case after this. But this is a classic case that you might see for somebody with this condition that I'm about to speak about. This is a 71-year-old female with a history of chronic constipation, frequent UTIs, six-month history of pain. And usually, it's more than that when they come to us, unfortunately. You see that the patient has her legs crossed and has to elevate her buttock while she's sitting, which is, by the way, oftentimes how patients with radicular pain also sit. So this is difficult to identify which is the cause, and people with SI joint pain. And the MRI of the lumbar spine is negative. They've tried extensive physical therapy without success. You suspect pudendal neuralgia. And what would be your next step in diagnosis and management? So this is what I'm here for to teach about today, is to talk about pudendal neuralgia, how we manage it, how we diagnose it. As a reminder of the anatomy, the pudendal nerve innervates the penis, clitoris, bulbospongiosis, ischiocavernosis, perineum, and anus. So it is a sensory motor nerve. It has both. So this isn't a nerve. How many people here are pain physicians? Would you call yourself a chronic pain physician, too? Not just pelvic. OK. So we love burning things, everybody who just raised their hand. We burn things all the time. Don't burn this, because there are important structures that then will consequently not be functional anymore, and you can have incontinence subsequently. The neuralgia of the pudendal nerve includes intractable pelvic and perineal pain in the distribution of the pudendal nerve. But then it also does spread out almost in a CRPS-type fashion in many people. They have hyperalgesia, genital numbness in some cases, sexual dysfunction, and abnormal urinary frequency. It tends to be unilateral, though bilateral certainly can occur as well. And then the locations I have listed here, I won't read it to you, but generally speaking, where you would see the patients complaining of their pain. Now, the reason that the pudendal nerve is so apt to get a neuralgia associated with it, as opposed to maybe some other nerves, is because it has three potential sites of entrapment. Those three sites include the greater sciatic foramen, where it emerges after the second, third, and fourth sacral nerves emanate out, create the pudendal nerve. It comes out the greater sciatic foramen. It can be entrapped there. Then it goes back through the pelvis over the ischiosacral ligament. And then it comes back out through the Alcox canal. So there are three locations where it can become entrapped. And Alcox canal, also called the pudendal canal, is an involution of a portion of the obturator internus muscle. So the obturator internus, in and of itself, if it's dysfunctional, can subsequently cause pudendal neuralgia, too. So there are so many different ways that the pudendal nerve can get entrapped. And that's why it's a more common neuralgia than some other nerves. The typical presentation of these patients are neuropathic pain, and of course, in that distribution, pain with sitting, significant reduction or disappearance of the pain when a patient is standing or in decubitus. That's a clear indication to me when a patient tells me that it's probably pudendal neuralgia. Because that does not happen with radicula. It gets better when they stand up and they lay down. But it doesn't go away. Aledinia and hyperalgesia can certainly occur. And a lot of these patients have chronic constipation or urinary frequency. And they've been diagnosed with UTIs. But it's not necessarily a UTI and sexual dysfunction. These are secondary phenomena. It's because people change the way they use their pelvic floor due to the pudendal neuralgia and then develop these things as well that we still have to treat. So exam can be totally normal for these patients. You can have complete normal sensory motor testing on your physical exam. And the best that we think, the best way to diagnose this is if a patient has greater than 50% relief of their pain with sitting after a diagnostic block. That's a little bit confirmatory though. Boy, I'm not sure. Someone told me, hey, I have 60% relief now. I don't love giving them that diagnosis. But the reason that they probably only had 60% is because they've developed all these secondary phenomena due to the pudendal neuralgia that sat around for months before they came to my clinic at least. Maybe some of you have clinics where they get to you sooner. But in my case, it's been a year, two years, three years, and they've had all kinds of injections as Dr. Srinivasan was mentioning with piriformis syndrome. They've had all kinds of stuff ahead of time that may have actually caused some problems. There's nonce criteria. This is a diagnostic criteria that everybody's familiar with, right? So the essential nonce diagnostic criteria are pain in the anatomic territory of the pudendal nerve, worsened by sitting, not woken at night by the pain, no objective sensory loss on clinical exam, and then they'll have a positive anesthetic block. But when we have diagnostic criteria, there's supposed to be a sensitivity and specificity associated with it. You're not supposed to pull it out of thin air to, I was gonna say something else, but pull it out of thin air. And that's not, nonce criteria is absolutely pulled out of thin air. You didn't wanna pull it out of the deep gluteal? Yeah, it was pulled out of the deep gluteal pain syndrome location, yes. But there's no sensitivity and specificity for this. So nonce criteria, a lot of people hang their hat on it. But if you look at, this is the diagnostic criteria for nonce criteria. Yes, there's the essential criteria, but then there's these complementary criteria and exclusion criteria. It's a beast and a burden, and it's not really proven to be valuable. But as you treat pudendal neuralgia, if those of you who do treat this have certainly heard of nonce criteria, those of you who are starting to treat it will become accustomed to hearing about it because people will bring it up, and it's just, it's not a useful technique. It's not a useful criteria, excuse me. So imaging can be used for this. There is something called MR neurography, which is available in, I think, most academic institutions at this point, but not everywhere. And in MR neurography, you're actually able to see the nerves of the brachial plexus if you're doing the upper extremity, or of the lumbar and or sacral plexus if you're doing lower extremity. You do have to tell your radiologist which nerves you're most interested in looking at because that's how they protocol the MRI, but they actually can get high-resolution images of these nerves along the tract of the nerve, and then you can find entrapment sites. I will say, honestly, the most common use for me in my practice is sciatic neuropathy from a piriformis syndrome, or obturator internus, or quadratus femoris, or one of those muscles, and that's the most common reason I'm prescribing it, this MRI. But I do use MR neurography for pudendal nerve, absolutely. And the original paper on this, original papers on this sort of talked about pudendal nerve more than some of the other nerves. And you can find all kinds of things. In this figure on your, I guess, your right, the anatomic left, is an evidence of a coronal view where you can see that there is a cyst, a perineural cyst, a pretty big one kind of sitting around the pudendal nerve and it caused a pudendal neuropathy for that patient. So there's another form of MR called MR tractography, and this excellent paper from last year actually compared MR tractography to MR neurography for diagnosing lower extremity neuropathy. It's like sciatic, most of these were sciatic. There's only 13 patients in this case series, but what they found, the tractography was much better than the neurography, is the ultimate resolution of their study. Now, you know, it's not an RCT. I don't know how you would do that. I'm not a radiologist. But certainly the MR tractography was better. The difference between these two, though, neurography is a high resolution MRI optimizing the field of view of a particular nerve. And like I said, I think it's available in most places. Tractography is a 3D modeling technique that uses diffusion tensor MRI to recreate the tract of the nerve, so it's almost recreating something. And it's really, at this point, only available in research. So there's no clinical utility at this time yet for MR tractography, but when I first talked about MR neurography at one of these sessions, either here or SIS, I talked about how MR neurography is not available in most places, and now it's widespread. So we may see tractography in the future. This is what a tractography looks like when they recreate it, and this is from that same paper that I showed earlier. So, you know, and it shows you where the entrapment site might be. So it's kind of cool. I'll never be able to read or interpret one of these things, but that's why we have radiologists, right? So treatment options, that's about everything we know about diagnosis of pudendal neuralgia. Now, for treatment options, pelvic floor physical therapy is necessary, but what it's really treating are the secondary problems that have arisen due to the pudendal neuralgia, the constipation, the tight pelvic floor, the inability to defecate due to tight musculature, and desensitization for the aledinia and hyperalgesia is important in those patients who develop it, too, and that can be done with pelvic floor physical therapy. Psychological therapy is very helpful for these patients. This is an incapacitating condition, and so many people do benefit from biofeedback, directly and indirectly, biofeedback, cognitive behavioral therapy, et cetera. Pharmacotherapy can be used, typically TCAs and anticonvulsants. I hope none of us are giving anything stronger than that to these patients for this condition, and then blocks, which I'll talk about in a second. Now, I'll say this is probably the order of importance of treatment, and I'm one of these people who loves burning things and putting needles in stuff, and I would put blocks at the bottom of the list in terms of importance for these patients, but there's a role for it, and we'll talk about that. So this is, on the left, a fluoroscopic image of a pudendal nerve block. You drop the needle on the ischial spine, inject contrast, and then block it. This could not be an easier procedure to do under fluoro. With ultrasound, it's incredibly challenging, because anybody who's BMI, I'll say like 27, 28, once you get that level and start going up, it's very difficult to find this nerve under ultrasound. It's very deep, it's directly in relation to the ischial spine, and it's right near the sciatic nerve, so I've done a lot of this, and I still sometimes don't know which is which. The pudendal nerve should be medial to the sciatic nerve, and it's right next to the internal pudendal artery. This is actually my pudendal nerve. This is from a paper that we published about 10 years ago, and I needed someone to scan a pudendal nerve and find a good model for it, if somebody was willing to do it, and I did it, but this is hard, it's hard to see, and it's pretty deep, so that's, but you can certainly block it that way, too. No needle was used in the ultrasound for that. So what does the evidence show us about block? So after a block at the three-month and 12-month success rates in a systematic review, so the three-month success rates was 62%, and 12 months ranged between 6.8 and 12.2% after a block. So, you know, 6%, up to 12% at 12 months. First of all, we don't anticipate any block to last for 12 months, right, that's number one, but 62% at three months is pretty good. I would take that, you know, that's better than a lot of the blocks that we do, and also the outcomes have been shown in a randomized trial to be the same for local versus local plus steroids. So you really don't have to inject steroids in this area at all. Local anesthetic will still give prolonged benefit, and that's a whole different conversation that we could, that'll take a long time to figure out, and none of us really know why, but local anesthetics blocks absolutely a prolonged benefit past the duration of the sodium channel blockade. So pulsed radiofrequency neuromodulation is something that I use in my practice for this quite often. It is not covered by insurance, so you do have to charge the patient cash for this, and so, but in studies on it, the only randomized controlled trial that there is from 2018 is Fang's group, and they showed a VAS reduction of about 5.7 to 3.9, and their success rate in the PRF group at three months was 92%, and only 36% in the peripheral nerve block group. So that's pretty good, that's pretty good. There are similar studies that have similar outcomes, but those are not RCTs. They're case series and case reports and things of that nature, retrospective case reports. So retrospective case series, excuse me. So the best data we have is an RCT, and that's pretty good data, but I was talking to Kelly Scott, who's one of the best pelvic health physical medicine and rehabilitation physicians in the world earlier, and she said, I don't think Pulse DRF really works for pudendal neuralgia. I was like, man, I'm gonna go up there and tell them it's a 92%, but I don't know if she's here. I'm sorry if I called you out if you're here, Kelly. Okay, what about surgery? So we heard about surgery for piriformis. This year, a systematic review was published on surgery for pudendal nerve, and I'll just get to the, I mean, the studies that exist for this have pretty good outcomes, actually, surprisingly, but you're not gonna publish your outcomes on pudendal nerve release unless you've been doing a lot of it, and so it's a little biased because you have to find somebody who knows how to do it, and then all of these have like 10 patients, something like that, so there's no RCTs in this area, but it's something that you could do. It is a great systematic review because they talked about the advantages and disadvantages of each of the types of surgery, so the method by which you get to the pudendal nerve, and so the last thing I'll talk about is stimulation, both dorsal reganglion stimulation and spinal cord stimulation in the treatment of chronic pelvic pain. All the data on stimulation, neuromodulation through stimulation for chronic pelvic pain is just that. It's for chronic pelvic pain, this waste vapor basket diagnosis. It's not for pudendal neuralgia. It's not for piriformis syndrome. It's all mixed together, so I'll say that before I tell you about the data. So Caporal, and this is a good group, Caporal and Nowruz and Nagy-McHale. These are legit people, and in 2006, they published on this, so it's been that long that we've been talking about this, and this was for visceral pelvic pain, though, so pudendal neuralgia would not fall in that category, but nonetheless, VAS got better in this small group in six patients, six patients. That's not many. There's the 10K, I'm trying desperately not to say the name of the company, but the 10 kilohertz stim for the treatment of chronic pelvic pain that was published in Pain Practice in 2021, and they had a fair number of subjects and did show pretty significant benefit, but again, it's chronic pelvic pain of all comers. This is a crazy study. I'm not gonna talk about it much. Some of these people got SES and DRG at the same time. They turned these people into robots, but there were only 11 subjects, and so, but this is it. This is the data we have for this. Now, my group published a systematic review on the effectiveness of dorsal ganglion stimulation for chronic pelvic pain and chronic neuropathic pain of the lower extremity in 2021, and we used the GRADE criteria, which is probably the best criteria for evaluating evidence, and what we said was the use of DRGS, dorsal ganglion stimulation, right, for the treatment of pain related to chronic pelvic pain and a bunch of other stuff is very low, whereas, and we said it was low for complex regional pain syndrome, but if one more RCT came out for CRPS, then it would be moderate, which is actually great, and people got really upset when we published this because they, oh, it sounds so bad, very low, but what the GRADE criteria means, all very low means is the true effect is probably markedly different from what the estimated effect is, and the estimated effect is stuff, is based on stuff like this, you know, so we don't have good enough studies to have the evidence to say it's better, but I can tell you that in my practice, I find DRG stimulation to be very successful at treating chronic pelvic pain. I also find it to be a pain in the ass to do, so I much prefer spinal cord stimulation because it's so much easier to accomplish, and I have less radiation time and so on and so forth, but from what I've seen in my practice, it doesn't seem to work as well for chronic pelvic pain as DRG stim does, and that's it. That's all I've got, and I will now, we're gonna do questions at the end, I think, sir, but I appreciate your enthusiasm, so thank you very much. On to Mahul. Thank you. All right, so hopefully my slides will make their way up there. So I didn't realize that there was so much knowledge of deep gluteal pain in the South Asian community here, so we're really going for the diversity of one group of people, but I practice in Washington, DC, which basically means I have a lot of opinions, and I'm gonna share some of them with you guys. Most of those opinions are grounded in nothing but my own fantasy life, but one of the things I wanted to share, it's sort of in follow-up to the prior two speakers. One thing is, and what's particularly unique about this patient population is that it's an N of one population. So we, Dr. Nagpal talked a lot about evidence, and clearly evidence is king, and it's very, very important for us to continue to generate high-quality evidence. At the same time, 30% of my practice is refractory pelvic pain. I get referrals from all over, sometimes all over the country. It is very much a customized treatment plan. If you're sort of thinking you can cookie cutter these patients, it's a failure, because they don't get better. It's really hard to aggregate data, because I would challenge anyone in the audience to tell me that they've had two pelvic pain patients that presented exactly the same way. Whether it's neuropathic pain primarily, whether it's sort of a musculoskeletal, nociceptive type of pain, they're all very unique, and the intersection of nociception and neuropathic pain is very high in these patients, because as we talked about previously, there's a density of structures in the pelvis. There's a tremendous amount of crosstalk between various structures. Nerves that we historically think of as motor or sensory also have a significant sympathetic component to them, and that autonomic sort of conversation is also going on. I joke with my patients that if you're from LA or from this area, it looks like the highway system if you're flying over the top, because everything's talking to everything else. The other thing I was gonna point out is it's really important. I mean, I would say incredibly critical to create, whether you have it within your own organization or externally, a virtual network with really great pelvic floor therapists. These folks will spend way more time with the patient than you'll ever get the chance to. The patients will be Facebook friends if they're old, Instagram friends if they're young, TikTok friends if they're really, really young, with their physical therapists. We have patients that come in for various procedures for pelvic pain. They'll be live streaming TikToks while we're doing the procedure, right? So it's how these folks communicate. So I think it's really important, all joking aside, to create that network and to have those folks, have them on your speed dial, because they'll call you. While I was sitting up here, I got an email from a pelvic floor therapist about one of our mutual patients. They know those patients. They've done really thorough exams on those patients, and they continue to do thorough exams on those patients throughout the duration of their treatment. So that's another really important thing in my estimation. We could probably spend an entire day easily talking about pelvic pain, and the nuances of treating pelvic pain, but understanding that balance between muscular pelvic pain and neuropathic pelvic pain is really important, especially in a lot of our post-pregnancy patients. Some of these folks come to us, they've had a grade two to grade four tear. If anyone remembers their OB rotation and remembers repairing a lack, it is not great surgery. These people are sort of squinting and they hopefully see what they're suturing. It is not good surgery. And I'm not criticizing our obstetrics colleagues. They're tasked with a very difficult situation, can't see very much, folks are in pain, and the structures sort of all blend together. So we get a lot of these folks that come to see us post-pregnancy. I had a patient just last week who had a grade four tear and a coccygeal dislocation during pregnancy. She can't sit. She hasn't been able to sit for five months. Now she's got plantar fasciitis because she can't sit. And she's got, from her babies, she's got bilateral carpal tunnel syndrome. So, I mean, she can't do anything. And she's got this coccyx that's like three millimeters displaced. Every time she sits down, she gets this awful neuropathic pain in her backside, basically. So, and the last thing before I really get into my talk, if I can suggest one tool that people use in their practice, I talked about this yesterday, the central sensitization inventory. It's a validated tool that you can use to measure sensitization for patients. And it can help you really understand if you should even do an intervention with a needle, right? So a lot of these folks need a lot of care. They need a lot of help. They need behavioral health folks, physical therapists. But there are times when we shouldn't put a needle in someone because they've got something that requires other things until we can get them to that point. So I think, I just wanna make sure I emphasize those things. My full disclosures are available on the app, but no relevant disclosures for today's talk. My case, like Dr. Nagpal's case, I probably won't talk about after this one slide, but this is probably a patient that every single one of us has seen in some iteration. 64-year-old female with a history of chronic low back pain of three-year duration. We tend to confuse or use the word low back when we mean buttock all the time. And we use the word buttock when we mean leg all the time. So we have to, it's really incumbent on us to sort of redefine how we describe these things because these definitions or labels follow people forward. So how many people get a referral from an orthopedic surgeon or a neurosurgical colleague and it says low back pain? And we sort of put our blinders on and this person has low back pain forever until maybe one day we wake up and realize maybe it wasn't low back pain at all. This patient had a prior spinal fusion for multilevel degenerative disc disease and spondylolisthesis from L1 to S1. Just arbitrarily made that up. And persistent unremitting right buttock pain. So what would be your differential diagnosis in this patient population? Now this is by no means exhaustive but Lombard, we always like to throw our orthopedic colleagues under the bus. Most of us wouldn't be employed if it wasn't for spine surgeons. So Lombard Post-Laminectomy Syndrome is very common. The data suggests 10 to 40%. That's probably a little bit of an underestimation of the true data. But I've never, maybe someone else has had a different experience but hardly ever do patients come back to me to be like, I feel great. That was the best fusion I've ever had. Can I have more fusions, right? So once in a while though, but they shouldn't. Looking for things like pseudoarthrosis, things of that nature is important in these patients. Adjacent level disease, it's really important. It happens, it happens all the time. Figuring out whether it's the cause of the pain or not is sort of incumbent on us to sort of sort through. And then sort of the one that we always talk about, sacroiliac joint dysfunction. Again, a topic that we could talk about all day. I'm gonna touch on that briefly as a cause of buttock pain. And then one that I've historically been very skeptical of but is gaining a lot of traction and we should talk more about is clonal neuralgia. So sacroiliac joint dysfunction, a wide variety of incidents ranging from 25 to 43% following spinal fusion. More common in women than men who have spinal fusions. These days, you should be documenting the Laslet Cluster. Many insurance and many payers require that you document the Laslet Cluster in order to get approval to do sacroiliac joint-based interventions, whether that's interarticular joint injections or radiofrequency ablation. The Laslet Cluster, historically at least, had a sensitivity of 88% and a specificity of 78% with two plus positive tests. And this includes ganglons, distraction, thigh thrust, compression, and sacral thrust. Typically, most people do the last four at least but ganglons, some people throw in as well. And we typically diagnose this with lateral branch blocks or interarticular injections, which is kind of interesting and funny because neither really, lateral branch blocks do not diagnose SI joint dysfunction. They diagnose ligamentous pain for SI joints. So it's basically extrinsic SI joint pain that lateral branch blocks diagnose, whereas interarticular injections are not diagnostic. They're therapeutic and probably 10 to 15, if not higher percentage of people have an incompetent anterior sacroiliac joint capsule where the medication spills out along the lumbosacral plexus, giving you a false positive oftentimes. So we have to be thoughtful about this. We can't get to the anterior innervation of the SI joint with any kind of diagnostic blocks, at least as yet. So we have to take these things with a grain of salt. In our practice, we look at all SI joint dysfunction as either extrinsic or intrinsic, right? So if it's intrinsic, it's arthritic, it follows that sort of pattern, whereas extrinsic is hypermobile or generally more mobile. I say that word with caution because I see a lot of, in addition to seeing a lot of pelvic pain, I see a lot of hypermobility in my practice. Probably another 15 to 30% of my practice is EDS, joint hypermobility, these days. And interestingly enough, the number of those patients who also have chronic pelvic pain is astronomical. It's probably nearly a one-to-one correlation between having joint hypermobility syndrome and pelvic pain. And we're gonna probably publish this pretty soon, but we did the central sensitization index in like 85 consecutive patients, and 79 out of 85 were sensitized, that were folks who were hypermobile. And in the pelvic pain population, about 75% were also sensitized. So these are things we need to be aware of as we try to successfully treat these patients. So, cloneal neuralgia. I mean, I asked this question, I still ask this question, does it even really exist, right? Is this something that's real or is this something that just provides us a convenient target to burn or stimulate or inject, right? So I think it's important to understand the anatomy a little bit, and then talk through that a little bit more. So we've got the superior, middle, and inferior cloneal nerves. We'll talk a little bit more about these. This is the distribution of these nerves. And sort of on the left, you've got the distribution of the nerves, including the posterior femoral cutaneous nerve. And on the right, you've got sort of where they would sort of emerge in the gluteal region. So the superior cloneal nerve is possibly responsible for about 1.6 to 11.7% of buttock pain. There was these papers by Maine and others that said the incidence was much higher, and they said it was responsible for 1.6 to about 14% of all low back pain. I would be incredibly skeptical of that data to suggest that it would be responsible for that much back pain, but I do think that it can be a source of buttock pain. We looked at this data, and we actually looked at the source data. They included about 894 patients, but 200 of those patients actually had thoracolumbar compression fractures. So we threw all those patients out, because thoracolumbar compression fractures can refer pain to the buttock. So that's not cloneal neuralgia, that's referred pain from like a somatic referral pattern. So we have to be a little bit cautious when we interpret this data. The superior cloneal nerve is formed by the lateral branches of the dorsal rami from T11 to L3, but it can be as far down as L4. And the superior cloneal nerve typically can branch into three branches of its own, the medial, middle, and lateral branches. And it's most commonly compressed at the osteofibrous tunnel at the posterior iliac crest. Most commonly, the medial branch of the superior cloneal nerve goes through that osteofibrous tunnel, and it's what's compressed when folks have superior cloneal neuralgia, but not always. Sometimes more than one branch can go through there, and sometimes the middle branch can also be in there. So there's a lot of data that looked at that, and a lot of anatomical dissections. And when I say a lot, I mean, this is pain medicine a lot, which means like 10, five, right, not like 500 or anything like that. So just to give everyone a frame of reference, all cervical RF is based on three cadavers, all lumbar RF is based on three cadavers, and I think thoracic is like three or four cadavers. So that's really where a lot of the science has come from. We don't have a lot of numbers, but we have a lot of clinical information. The middle cloneal nerve, this is the one that I'm most suspicious of, because it's essentially the identical innervation to the ligaments of the sacroiliac joint. So most sources report that it arises from the dorsal rami of S1 through S3, which is basically the same thing as what innervates the ligaments of the sacroiliac joint. There's really no reliable incidence data, although some people have claimed numbers that are nearly identical to SI joint dysfunction data, which again causes pause for me. The one exception may be where the middle cloneal nerve or the branches from the dorsal rami of S1 through S3 are compressed below the long posterior sacroiliac ligament. So that can happen. That usually results in sort of a point, a very specific area of pain. And oftentimes these are the patients that have what seems like classic SI joint pain. You do an SI joint injection and they just don't get better, but they still have pain in that location. The challenge is finding that nerve and finding that ligament under ultrasound. But if you can find that ligament, then it might be a good target for potential injections. And then finally, the inferior cloneal nerve. This is a sensory branch stemming from the medial and some lateral branches of the posterior femoral cutaneous nerve, or from the S1 through S3 sacral plexus itself, the anterior plexus. Again, very little information regarding the incidence of this. A lot of folks who have inferior cloneal neuralgia have concomitant posterior cutaneous femoral neuralgia too. And they tend to have pain sort of between the coccyx and the ischial tuberosity, for example. And it can often be confused with prudendal neuralgia. But these folks sometimes actually have inferior cloneal neuralgia or posterior femoral cutaneous neuralgia. Which is interesting, because in our practice we do a lot for pelvic pain, we do a lot of injections into the transverse peroneus and into the obturator internus. It's interesting to be in that anatomical location where also the inferior cloneal nerve would be traversing. And then we've got the posterior femoral cutaneous nerve. This arises from the dorsal divisions of S1 and S2, and from the ventral divisions of S2 and S3. It leaves the pelvis through the greater sciatic foramina, below the piriformis muscle. And typically this nerve is injured by direct trauma, blunt, or penetrating. So like stab wounds, for example, are a common source of pain from this nerve. So how do you diagnose this? Well, you could throw a dart blindly at something and hope for the best. But there is no specific radiographic imaging for these. I think that's an area, we talked a little bit about MR neurography. I agree that it's much more readily available now. The one challenge with MR neurography is that like many other things that we all do, it's based on the ability of the person to read it. So we're making an assumption that the person reading it is really good at reading it, when in fact that may not be always true. Unlike an MRI of the lumbar spine, cervical spine, brain, where I tend to sort of believe and trust that it's being read correctly, sometimes in neurograms I'm a little suspicious. In our area, we're fortunate, sometimes we send folks all the way up to Hopkins, because they really kind of pioneered MR neurography. So we're able to have that resource close enough and we trust that resource. Generally speaking, you could as a part of your diagnosis consider image guided low volume diagnostic injections. This brings up an entire area that I like, it's sort of become a pet area of mine, which is taking our paradigm from facet interventions and applying it to these kinds of areas is fraught with challenges, because we don't really know if these injections are diagnostic, and certainly we don't know if they're prognostic. So we had a patient recently where we did a superior clunial nerve block, she got 30% relief of her pain, but we targeted a bunch of other structures where she got 10%, 20%, 25%. She ultimately chose to move forward with a peripheral nerve stimulation of the superior clunial nerve, and during the trial she had 95% relief. I don't know how to reconcile 30% relief with a block and 90% relief with stimulation in a five day period, but I think that brings to light the idea that we really have to be cautious about the positive predictive value we achieve from any of these blocks. It's not, there's not necessarily a correlation between the outcomes people have from blocks and the outcomes they may have from other procedures, such as stimulation. I do think it's really important in these patients to rule out thoracolumbar disease. The first three months after March 2020, the number one diagnosis I saw in my office was neck pain from people who transitioned to working from home. So I work in an area with a lot of white collar government type consultant employees. Everyone's now using their mini little laptop on their bed, on their sofa, at the dining room table. None of it designed for people to actually do any real work on. And a lot of the boundaries that we historically had about working during work hours and not working in evening hours, which obviously don't apply to anyone in this room, suddenly stopped applying to other people too. Similarly, if you spend any time around people who are like in their teens, I've never, you know, my mom would freak out because she would always like come up behind me and poke me in the back if she saw me slumping. Everybody now has terrible posture, right? So everyone straightens up in their seats. And so, and the thoracolumbar junction is an area of significant transition. The facet orientation goes from primarily sagittal to primarily coronal pretty quickly. So you can get facetogenic syndromes in that thoracolumbar region that can refer pain to the buttock. You can also get discogenic changes at that thoracolumbar junction that can give you buttock pain. So really be careful about ruling that out. And finally, ruling out any kind of fracture that may be there that was occult. We also see all the time fractures being read as chronic when there's still edema on stir view. And I don't really understand how it gets called chronic then. And then finally, how do you treat all these things? Again, we could probably spend a long time exhaustively talking about treatment of SI joint dysfunction. But thankfully, if you come to the next session, you'll learn that you won't have RF as an option anymore. But the key is going to be that taking a systematic approach to this, right? So making sure if you're gonna use therapeutic injections that you've considered diagnostic injections first, despite what I said about the utility of diagnostic injections. Particularly for cloneal neuralgia, there is some data. Again, when I say data, there's few patients, small studies, almost none done in the US with both alcohol neurolysis and other radiofrequency ablation. You can see on the bottom here on the right, this is, sometimes it's hard to know exactly where the cloneal nerve is. So in this case, whoever did this procedure, it wasn't me, we did four different injections to try to get that nerve. Sometimes it takes that. I typically, when I do a diagnostic injection, start at the PSIS, I curve my needle and I land kind of at the, if I was doing the right side, I'd land at like the 10 o'clock of the iliac crest and then I ride that needle all the way across to at least the 12 o'clock and I leave a little bit of anesthetic along the iliac crest sprem. But you can certainly do it by doing multiple spots as well. If you're going to ablate this nerve, it is a sensory nerve, so theoretically you could thermally ablate it. I would consider sensory testing if you're gonna do a singular location. Otherwise you could do this sort of palisade type technique that's on the bottom here. And then neuromodulation, everyone loves, there's a group of us, subgroup I guess, that loves to put leads in everything that moves, right? So we can stimulate anything. As long as you can catch the person, you can put a lead in them. And most of our patients can't run very fast, so it works out really well. But there really is a paucity of data. There's work being done. There's currently a randomized controlled trial that's ongoing which will have a subgroup of patients with clonal neuralgia which they should have at least 25 patients out of 100 that will have clonal neuralgia. So we need more data. We need more, just at least to give us a better signal of what we should be doing. And then finally there's pretty good data. Again, most of this data is Japanese that looked at surgical release and had good success for these patients long term as well. So I think that's all I've got. And with that, I think we can take questions as a group. I think there's mics around if people want to ask questions. Hi there. I have a question about, for Dr. Desai, the central sensitization inventory, identifying patients who have more mental barriers that maybe need to get addressed first before interventional. Assuming that there is a need that you identify, you refer them out appropriately. At what point do you feel then more confident circling back and then talking about the interventional? What are we looking for? What kind of feedback with psychology or otherwise? What are the things that we're looking for? And then lastly, what are the things that we're looking for what kind of feedback with psychology or otherwise? What are we looking for? Yeah, I don't see behavioral health as an obstacle. I see it as a partner, right? So I think that there are patients who have depression, who have adjustment disorder. I don't necessarily think of patients who have psychological comorbidities as people that we shouldn't treat by any means. I think that we tend to follow our patients really closely. We have, you know, I'm in DC where everyone's smarter than me. They have like, everyone has a PhD or some other terminal degree and they have done their own research. But tongue-in-cheek, kidding aside, we follow all these patients very quickly, closely. We try to keep in touch with their other providers all the time so that we can intervene. And we don't, we actually think of things, when someone comes in to see me that has a very high central sensitization score, I actually don't think of it as I'm not gonna do something. I just change what I might do. So for example, in our practice, we do a lot of intravenous lidocaine infusions. And the idea there is that if I can turn the volume down, if I can temporarily even turn down the sensitization, it provides a window of opportunity to do something else. But if I stick a needle in someone who's got a central sensitization inventory score of 82, it's like going up to a wasp's nest and poking it and being surprised when something stings you. The difference is they get stung, not me. The only sting I get is when they call my office over and over again. But we don't want our patients to get worse, if at all possible, even transiently. So we tend to think of it sort of, when we have high scores like that, we tend to think of what can we do, 30,000 foot level, to really decrease those scores, get you to the right other folks, so that if you need an intervention, we can help you with that. And my philosophy on most intervention is that it's not, most injections are not gonna cure anyone. What they're going to do is facilitate the recovery process so that some other person, like Dr. Nakpal talked about on that list, is going to be able to help you a lot more. If you can't, if you're going to a pelvic floor therapist and they can't do a vaginal exam or a rectal exam on you, I've gotta do something to make that now a possibility for you, so. Yeah, so typically if, you know, I joke that in our office we just have an endless supply of Kleenex, right, so like there's a lot of crying, mostly me when I leave the room. But it sort of, you start to see these changes in folks when they feel like they've got the right team. We just had a, I got a text from my COO, she's also our nurse, a patient wrote us like a note that just said like she finally feels like things are on the right track, like after two years of, she is 24 years old, does not have pelvic pain, she has cervical facet dysfunction. But she was sensitized and she needed a little bit of different handling than just like let's do blocks, right. So you see these sort of subjective changes in addition to some objective measures like scales, right. It's also, I think it's important to weigh both, right, so you make sure that things are moving along. And sometimes people are in a situation where you have no choice but to intervene because like that woman I talked about who couldn't sit, we could wait and try all these things but she also was in a really tough spot so we had to intervene a little bit more urgently. Sure. I just wanted to add to that like for the central sensitization part. I think our biggest role comes in education. I think we follow this patient for quite some time. So I think every follow-up visit is an opportunity to talk to them about their diagnosis. I think with pelvic pain most patients are lost in what's causing their pain. So the more the models, the anatomical models that you can show and tell them where this pain is coming from helps them to understand the process that I think is the biggest step towards healing or progress towards healing. And they develop a trust with the physician who is really caring for them and that makes a difference to downregulate the central sensitization as well. Guys, I want to thank you for shedding light on what I think all of us agree on as being a really, really difficult topic, right? These patients tend to be some of the most complicated patients and there is a lot of crying in the room on both parts, right? Mahula, I'm just going to echo your sentiment about this being physiologically and anatomically complex. In translational medicine, one of the things that is understood by urology PhDs in the lab is that the animal model for interstitial nephritis is taking a rat and putting a hot probe in its rectum, okay? And if you think about what this means and what this may mean with regards to this discussion, what it suggests is that if you have an insult anywhere in a somatic region, there's a communication not anywhere around S1, S2, S3, and S4, right? So there are marked and visible changes in another location innervated by the same nerves, right? And so it makes us think and it should make us think and wonder about what we're doing and especially with interventions. One of the things I do with my patients before we get to STEM is that I try lateral branch blocks for one of the reasons that you mentioned. Lateral branches are part of the clunios, right? They become the clunios, but there's some evidence that there's a retrograde influence into the somatics within the spinals, right? So you can actually create a modified conduction through the pedendals. We have evidence from EMG and GON data that suggests that this may be helpful. But what I also do is I'll do, not concurrently because you guys are going to talk about billing, but also doing a ganglion of impar block as well. So you get somatic and parasympathetic fibers. The question is, well, what happens if that doesn't work, right? Spinal cord stimulation, even with small ends, each patient is variable as well because with spinal cord stimulation, these leads, putting them in may be easy, keeping them in is difficult, right? Because with DRG, I mean, what levels do you do for DRG? Again, independent of billing, bilateral L1 and S2. Okay, yeah. So the sacral DRGs I've found to be really, really challenging to keep in. Putting them in is easy, but keeping them in and keeping them from migrating has been really difficult. I've had to have a neurosurgeon or a general surgeon in the room to triple loop and suture these so the sacrals don't move, and they still move. They move. Yeah, they move and they also fracture. Pretty readily, but now, I mean, there's a different conversation. With the new anchoring system that is being, well, it's not new, but with us pushing for anchoring with these, it's a little better, but you're right. There's no question about that. I mean, I would echo that and say that I think that the other thing here is that the revision rate is high, and also, as someone who does a lot of neuromodulation, I'm still skeptical about the long-term outcomes. Right. Just because I haven't, it seems to, I see a lot of patients who go elsewhere and get those, and then they come back to me to take them out. What do you do, and this is my final question. What do you do when you've done your CBT before you get to injections, before you get to SCS, and then you do those things, and then it doesn't work? They fail, the things that you've done. Like, what's then the end game? Do you guys go back to CBT? Do you recycle some of the interventions that you've already done? What's the plan? I think this patient population is so unique. They're incredibly challenging, and I think that, not because they're inherently challenging people, per se, although sometimes there's a personality element to this that we really haven't talked about, but I think fundamentally, it's knowing when not to do anything else. Right? You're likely to be like, guess what? Like, I don't think you need serial trigger points for the rest of your life, or serial hydrodissections, or serial stim. Like, maybe you just need to sort of plug away at PT and make incremental gains. We have this, just as sort of an analogous example, we see these patients now that are hypermobile, right? And these are typically 30-year-old, mostly women, in their 30s. They've had one sort of insult, like viral infection, trauma, something, and now their lives went from being high achievers to being, they can't keep their eyes open and go to work, right? There's no solution for that. Right now, there's no gene therapy. There's nothing we can do about joint hypermobility syndrome that's curative. And there's going to be a hundred doctors out there that are going to give them solutions that don't make any sense. Hey, let's fuse your cranium to your C1, C2. Fine, right? Like, you can do it, but now you're like, trying to drive. It doesn't make any, it makes sense for a very small subset of people. Some of these folks, the best advice I can give them is, you're going to have to modify your life to allow you to be as functional as possible. It's almost like, when I trained, we used to tell our MS patients the energy conservation strategy, like, do some, don't do too much, don't do too little. It's the same sort of thought, like, unfortunately, because otherwise, we just end up with these, I get patients all the time that get referred to me, they have a DRG, a peripheral nerve simulator, and a pump, right? And none of them's working, and you're sort of like, okay. And you've done everything, someone else has done everything, so do you repeat it all? I wanted to get your thoughts on decompression can be helpful, but also this big question of is it really just that that's not the primary site of pathology, but for some reason stimulating there helps pain. You know gluteal pain that for some reason I haven't identified where the primary pathology is and I just wanted to get your thoughts, all of your thoughts on it, because it seems just so strange that there's this whole new entity that is causing so much pain, or what's reported to be so much pain. The original basis upon which this whole new entity began was because pain docs wanted to find a way to put spinal cord stimulators in people's paraspinal muscles and and this is, and so in order to do so they were doing what's called peripheral field stimulation, not peripheral nerve stimulation, because it was nowhere near where the clunial nerves were, but they were calling it clunial neuralgia and putting it in on anybody with axial low back pain, and this group of people got, many of them got better for a month or two months or three months, but most of them it didn't, and that set us back as a field a decade in peripheral nerve stimulation, which is a legitimate treatment option for a variety of things. That was the first, that's where clunial neuralgia came from, but many of us started blocking the clunial nerves where it's actually found and identified and discovered that, well, some of these people actually do improve. It's a small group, but, and it's not everybody with axial low back pain like, like a lot of people were using that technique for. Now, in, pain docs can use their, what we do for good and evil, so now it is commonplace for pain docs to use peripheral nerve stimulation along the lateral border of the sacrum right next to the SI joint and call it clunial neuralgia, and that's what I'm stimulating, but in fact they're stimulating the lateral branches of the, of the sacral nerve roots of the dorsal rami of the sacral nerves and treating posterior sacral ligamentous pain. But that over utilization always comes at a cost to those of us who are wise about the utilization of our services. Dr. Desai talked about how he's about to tell everybody that we're not going to have SIRF anymore because of over utilization. So I think we accidentally figured out that clunial neuralgia is a real, oh, wait a minute, not because of over utilization. I take that back. I shouldn't have said that. That is a reasonable treatment option for that disease. Nevertheless, we've lost a lot of things due to over utilization over the years and that could happen again, but somehow stumbled into the fact that there's probably a real entity. I think I'll respectfully disagree a little bit with Dr. Nagpal. So in the 1980s, there was a lot of investigation. Dr. Main and others were looking at trying to understand buttock pain, SI joint pain, lots of anatomical dissections, lots of diagnostic blocks. We know a lot more about how to do diagnostic blocks, but they were injecting 3, 4, 5 cc's along various targets and as a result the specificity was low, right, you could get some sensitivity but specificity was low and that they did a bunch of catabaric work back then too to help us understand this idea that this might exist and there's anatomical and pathological data that shows that the nerve can be dilated, it can be atrophied in the osteofibers canal and then dilated outside of it as a compensatory means. Despite all that what I just said, I still think that this should not be the first diagnosis we think of but rather something that's a little bit of a diagnosis of exclusion. That's one thing and I think it's just it's something we should keep in mind in our differential without necessarily always jumping to it first. The second thing I would say is that, and I think this echoes the point that was made just earlier with the last question, is that sometimes we stimulate somewhere and we get a benefit that is unexpected because it's activating things that we don't 100% understand yet, whether it's sort of sympathetic nervous system or other fibers where there's a lot of crosstalk. And I think that's possibly what's happening in some of these patients, right? Where just because we're doing cloneal, we're getting some sort of central nervous system change which is giving the person pain relief without necessarily it being the cause of the pain. Any other questions? Otherwise, we'll adjourn for the next. Thanks everyone. Thank you.

deep gluteal pain conditions

diagnosis challenges

treatment challenges

early diagnosis

anatomy of deep gluteal structures

case study

evidence-based management

pelvic pain complexity

personalized treatment plans

muscular pelvic pain

neuropathic pelvic pain