next lecturer, we will go ahead and get started. We will skip through kind of some of this front matter. Again, we're gonna keep everybody video and audio muted. If you have any questions, my name is Sterling Herring. You should be able to track me down. Click on participants and I should be up near the top. Sterling Herring, you can double-click my name and you can send me a message directly and we kind of ask them as appropriate. That kind of helps us keep noise and background down. It also helps us kind of keep some control over what's being said in an AAP-sponsored setting. So I apologize for the kind of roundabout way of doing it, but it's how it has to be done. Any questions about this lecture series in general? Again, there's a lot on the website physiatry.org. I keep getting muted somehow. If you have any questions about the lecture series in general, please reach out to us directly or there's a lot on the website physiatry.org slash webinars. You can reach out to Candice there directly, cstreet at physiatry.org or track us down on Twitter. Give us just a second. Looks like we're about ready to go. We're excited to hear our next lecture from Dr. Tina Wang who is out in California at Loma Linda and UC Riverside. Welcome, Dr. Wang. Hi, thank you. Can you hear me well? Yes, we can hear you. All right. Thank you for having me. Thank you so much for joining us. You should be able to share your screen. All right. Okay, can you see that? Yes, I can. Perfect. Okay, so this limits what I can see from you guys as long as you're okay with it. Hello, are you muted there? I'm muted, sorry. Yes, everything looks great. All right, are you ready for me to start then? Yes, fire away. And if any questions come up, they'll usually send them to me and then kind of at set-aside time, you know, at the end or whenever. You're welcome to interrupt anytime and just unmute and jump in since I can't see you all's screen. Perfect, thank you. All right, fantastic. I'm gonna get started. So thank you for having me today. The lecture, my lecture is on myofascial pain. I am attending physician at out of Loma Linda. I also get the residence from Loma Linda School of Medicine, our PNR residents and medical students and a lot of different specialties. I have a private practice where I treat patients with fascial disorders and I do a lot of research out of my clinic private practice as well. So today we're going to define what myofascial pain is. We're going to go through the research that supports these different definitions and then lastly we'll talk about the treatment options available for myofascial pain. So what is myofascial pain? It includes a broad definition of all muscle pain and it does include the specific definition of myofascial trigger points as well. And that is how I got into myofascial pain and why it matters to you is I was a dancer and I had severe foot pain which I figured I knew how to treat it and I didn't. I wrapped it up. I thought maybe there was a fracture in there and I so happened to be at a interdisciplinary dancers health day and there was an old-school physical therapist who trained with an even older physical therapist out of New York City Ballet and they had passed down traditions of myofascial release and she literally did a 10-second release on my foot and a week of excruciating pain went away and it had been chronic before then. It went away completely gone and that is how my interest in myofascial pain started. It was really working with dancers, working with myself and being introduced to this concept of myofascial pain. And what we see is studies that estimate the prevalence. They can range anywhere from 23% to as many as 93% of the population and this includes trigger points as well. And trigger points are thought to be involved in all sorts of pain syndromes including tension headaches, low back syndromes, pelvic pain, your itises, your bursitis, your arthritis, your tendonitis, all these things that we see in outpatient musculoskeletal clinic. So then it becomes really important in our own health and the health of our patients. So trigger points, are they real? And there was a Delphi review of all the experts out there, the pain specialists, and they really questioned if trigger points were real. And they made a point of stating that it's not that they deny the existence of myofascial pain or these tender points specifically but really the pathophysiology behind it. Is it true? Does the science really support what we think is going on in the muscular processes? And when we look at the evidence, Stoop and colleagues out of Switzerland, they used the Pedro scale to review the studies from 1978 to 2015, 230 studies using the Pedro scale to check internal validity. What they found was that the average quality was less than six, less than moderate to high quality evidence. So the evidence is poor. They did make a point of stating that, you know, a quarter of it seems to be good evidence. So really what is happening with myofascial tender points, trigger points, pain, what's going on in there? And to really understand, we have to go back in history and look at the history of how myofascial pain and trigger points was discovered in the Western civilization. And that starts with Dr. Travell and Simons. Dr. Travell was a rheumatologist and she was really the pioneer in this field. And she was able to so effectively treat JFK's pain that he appointed her White House physician. And her protege was Dr. Simons, an aerospace specialist. And together they collaborated, published papers, and wrote the Sentinel landmark book out there. So these two were really the pioneers in the field that led way for how the field has grown. And according to Travell and Simons, myofascial tender points or trigger points are specifically characterized by three clinical findings. That would be a top band, a hypersensitive spot, and referred pain. You may hear your attending physicians talk about other phenomenon that they might see, such as referral patterns, observed twitch response, and reduced range of motion, painful range of motions. Those are clinical symptoms that came later by other researchers that helped to characterize trigger points. So trigger points should not be, they should, they are different from other types of points. They are distinctively different. Acupuncture points are defined as energy meridians, the flow of energy. Similarly, pressure points come from the Shiatsu tradition of energy flow. In martial arts, they have their points, and these are typically vulnerable areas where neurovascular bundles run shallow. And then fibromyalgia have very specifically defined tender point areas, and these are all different. So let's explore the theory behind the myofascial trigger point, because you're often tested on this. Whether or not the research supports it, it's tested. So clinically, myofascial trigger points are easily identified as painful areas in the muscle. There are microscopic changes that occur in the muscle fibers, causing a contraction and chronic shortening of the muscle fiber, and this is usually thought to be due to overload or incorrect loading of muscles. Then there came the integrated hypothesis. This was first presented in 2004 by Drs. Gerwin, Domerholt, and Shaw. And what is going on is that there are micro lesions in the muscle fiber, which cause the sarcoplasmic reticulum to release quite a big load of calcium. And this load of calcium causes contraction of the muscles. And this contraction leads to a top band, as well as compression of capillaries and local ischemia. It prevents adequate oxygen delivery, proper healing, and there's pulling of noxious metabolic waste. And this leads to a self-perpetuating cycle that they termed energy crisis. And so this energy crisis then leads to changes at the motor endplates. Acidic pH develops, and acetylcholine esterase activity is decreased. So then there is an increased amount of acetylcholine. There are releases of pro-inflammatory mediators, CGRP. Those then also affect the motor endplate. And what we see is an increase in activity in the area of the acetylcholine. And when we stick an EMG needle in there, we see many endplate potentials. And this process then self-cycles and continues this noxious cycle. And this is thought to be the theory behind trigger points. Down the road, there can be neuroplastic changes that occur at the dorsal horns of the neurons, and then central sensitization. So we've talked about the basic myo part of myofascial. What is the theory behind the muscle origin of these trigger points? Now let's talk about the fascia portion of myofascia. And this is really where the science has gone in recent years. So here is a diagram, a very simple diagram, of fascia. Note here that there is skin, and between the superficial fascia divides the subcutaneous tissue, the two fibroadipose tissue layers into two components. And this really permeates the entire body. And there are skin ligaments that connect the superficial fascia to the deep fascia. And this forms a three-dimensional network in the body. There's also the deep fascia, which envelops all the muscles of the body. And the characteristics of this deep fascia changes according to the body region. So under the anatomically, all the muscles are surrounded by fascial layers. There's the epimysium. And then the muscle fiber bundles themselves are separated by the paramecium. And the individual fibers are surrounded by the endomysium. And these are all different deep fascial layers and continuity. So what is the evidence that fascia is a contributor to pain? The first step is to look at the innervation. So fascia was originally thought to be an inert tissue, purely mechanical. If you took it away, no big deal. Well, is that really true? And Carla Stecco, what looked at, she's an orthopedic surgeon out of Italy. And what she did was she took soft tissue from hip replacements, and she looked at the innervation in the various tissue layers. And she looked at 11 patients and two cadavers. On the left axis, the y-axis, you'll see those are density of nerves. And focus on the diamonds. And note that the skin has the highest density of innervations. And this is followed by the superficial fascia, as well as the ligaments that surround the joint. Note that the traditional tissues that are thought to be the cause of pain, pain generators, the capsule, and the muscle, they have the least number of nerves in them. So in another study by Schilder and colleagues out of Germany, they found 12 volunteers who offered their body up for science. And they use ultrasound guidance to inject isotonic saline. That was their control versus hypertonic saline. And they injected into the various layers, the deep fascia, the superficial fascia, and the muscle. And what they found was that they were able to induce pain in all three layers. But there was much more pronounced pain response from the fascia, the deep fascia, and the superficial fascia. They also mapped out the area of pain after hypertonic saline injection into these areas. And note how in the deep fascia, there's a much greater pain level as well as a greater area and dispersion of that pain response, that referred pain all the way into the anterior of the torso. So we've looked at the innervation. Yes, there's innervation. And when we inject, there is a reproduction of pain. Well, what kind of fibers are in there? What kind of pain fibers? And so in this paper, you see a also out of Germany, you see these different fascial layers from a rat thoracolumbar. And you can see that the deep fascia is actually divided into sub layers. and all these sub-layers have different nerve density, and they've stained these nerves. And what they found was that these nerves have the presence of substance P, and they postulate that then they are C-fibers. And we'll talk about that, what are C-fibers? So this is a classic anatomic dissection by Dr. Willard out of New England and Dr. Fleming. And it shows you the extensiveness of the thoracolumbar fascia, how thick it is, and its communication with the various ligaments around. So it is not an insubstantial tissue that is inert in our body. So C-fibers are these free nerve endings that end in your deep fascia and your superficial fascia, and they are unmyelinated. So that means when we go in to do our EMG studies, they will not show up in many of these sensory action potentials that we're looking at. So the patient can describe a lot of pain and a lot of dysfunction in these nerves, but we can't pick that up objectively on the EMGs. And this is as opposed to the faster fibers, nerve fibers with myelination. So these studies show that there is a high number of nerves and they're likely C-fibers, but what else is going on to cause pain and dysfunction in these tissues when patients have myofascial pain? And in this study by Weinkauf out of Mannheim, Germany, their medical school, they injected growth factor, nerve growth factor specifically into these areas. And they showed that there was an increased pain response that peaked at three days. They also injected citrate to see if the pH changes would cause pain. And recall in the myofascial trigger point theories, these were all things that they felt contributed to these trigger points. So they injected citrate and yes, they were able to also see that there was a pain response from drop in pH in this tissue. So these studies suggest that there may be peripheral sensitization that's occurring. And we know indirectly that if we're injecting growth factor, there may be nerve sprouting. But is there really nerve sprouting? Are there nerve changes that are occurring? And to take a deeper look at this phenomenon of peripheral sensitization, this study was conducted by Hoheisel and Dr. Mintz. And what they did was they inject, they inflamed the thoracolumbar facture through irritating injectates. And they were able to see that there was no change in the density, overall density of nerves. But what they did find was that distribution of density of those nerves changed. And the outer layer decreased in the number of nerves and the inner layer of that thoracolumbar fascia increased in the number of nerves. And they also stayed positive for substance P. So presuming that these are nociceptive fibers, C fibers. In addition, and further studies down the road, they looked at spinal segmental innervation into the dorsal horn. And they were able to see that traditionally these sensory fibers that went to specific segments, specifically in this case, they looked at L3. They were able to show that after noxious stimuli, there were new connections that formed at multiple spinal levels into the dorsal horn neurons of these animals. And not just more levels, but other deeper areas of tissue started to form these connections. So we know that these studies show there's peripheral sensitization, there's changes in the nerves. But what specifically is going on in the fascial tissue itself? Is that changing? And Antonio Stecco out of Italy, NYU, John Hopkins, he's there now. They looked at the sternocleidomastoid of patients with neck pain compared to patients without neck pain. And they found a significant increase in the loose connective tissue. So loose connective tissue under ultrasound is that stuff between the bright fibers in black, it shows up black. It's extracellular matrix. And they show that it was the extracellular matrix that increased rather than the dense connective tissue. So in Stecco study, oh, so this study just showed that they saw that increase in fascial tissue as well in rats. And the Steccos were able to show that it was increased in humans as well. And they treated these patients with manual therapy. And they were able to show that the thickness of the tissue drop, that extracellular matrix, the glycosaminoglycans, that thickness and tissue dropped. And when that dropped, the pain level dropped. And so they concluded that the thickness of the tissue itself was associated with the pain level. So where does this increase in loose connective tissue come from, this extracellular matrix? And again, we thought that fascia, this dense fascia, this D fascia was inert. And Carla Stecco found fasciocytes. She found these cells and she coined them fasciocytes within the fascia. And her histological studies show that these cells were responsible for the production of hyaluronan, the gliding stuff. So where is hyaluronic acid located? Where is hyaluronic located? It's located between the D fascial layers. It's located within the muscle fibers between the layers of the D fascia in the muscle. And they're responsible for gliding. So you might ask, if there is more extracellular matrix, there's more of this loose connective tissue, shouldn't there be more gliding? And so Antonio Stecco asked that question and he teamed up with engineers and did a mathematical modeling of the behavior of hyaluronan. And the traditional thought that more hyaluronan is better did not pan out. In fact, what the mathematical modeling showed is that as the density and numbers of the hyaluronan molecules increase, there was clumping and the viscosity increase. So no longer was hyaluronan responsible for gliding, it was causing stickiness of the tissue, a lack of glide. And so we saw this in humans. Dr. Lingavin is a medical doctor out of the NIH and she looked at 121 human subjects. That's a lot of people. And she looked at 50 without back pain, 71 with back pain. And what she found under ultrasound was that look at the layers above and below the red line. That sheer glide in folks with low back pain decreased by 20%. So she found in humans with low back pain, the gliding between the deep fascial layers decreased by 20%. So we've talked about the fascia part. We've talked about the muscular part. How do they tie together? And so in this mathematical modeling with Carla Steko, she worked with a computerized model. This is a tibialis anterior. In this model, she showed that changes in pressure in the muscle of tibialis anterior, specifically on this slide, she looked at other muscles as well. There was movement and displacement in the surrounding deep fascia. So movement pressure changes in the deep fascia directly affect the surrounding, sorry, in the muscle, directly affect the surrounding deep fascia. And it does so in a directional manner. So this may be one of the missing links between what myofascial pain is between the muscles and the fascia. In this study by Margalef, who looked at the trigger points in specific, so they found specifically trigger points in humans, they found that in these areas, there was in fact an increase in that extracellular matrix content, the glycosaminoglycans. So these studies show that perhaps they're not two separate things. Maybe they are interrelated and influence each other. A brief aside about central pain. It's outside the topic of this lecture, but I do want to say that it also is not separate from peripheral sensitization. They go together. If there is peripheral sensitization, it starts to change the input into the dorsal horns. Then it starts to change the brain, specifically the insula, and then the output starts to change and it becomes a cycle. So really understanding what phase of pain response the patient has developed and what to treat and what aspects to treat is important. So this is what my research is in. I collaborate with Antonio Stecco looking at the dense connective tissue and the extracellular matrix, attempting to quantify normals and quantifying abnormals. And specifically, we're looking at the iliacus fascia. I'm also studying palpation techniques and manual therapy techniques to look at its effect on the deep fascia. So let's dive into treatment. What's the best evidence for treatment of myofascial pain is extremely limited. And there are many trials that are listed in the Cochrane Review, which show that there are no superior effects for any particular treatment. So what does that mean? It means they all work, but not one better than the other. Dry needling is a very, very popular technique, especially among physical therapists. Travell performed dry needling as well, but the tradition of dry needling amongst physical medicine rehab docs is with a hollow beveled needle. And that's how Travell did it. And it's passed on this way. Oftentimes, our physical therapy colleagues don't do that. They use acupuncture needle, which are solid filament needles. So does trigger point dry needling work? And in this meta-analysis, yes, it works great. Six to 12 months dry needling is very effective, but not more effective than other techniques like manual therapy, like laser, like wet needling. Trigger point with lidocaine is the standard technique. Travell and Simons, they recommended manual therapy with a combination of stretching and procaine or lidocaine injections. Many other injectates have been used and studied and none show superiority. So being safe is important. Shockwave therapy is also a very effective and popular intervention and is very popular in Europe. And that's also been shown in this systematic review to be extremely effective, but again, not much better than dry needling, trigger point injections, laser therapy. So this is from a presentation by Wolfgang Barmeister out of Germany. He's a private practice PM&R doc, and he uses a lot of shockwave therapy in his practice. And here you see an elastography, ultrasound elastography. So when you look at the B-mode ultrasound, that's the black and white figure, you don't see a lot of difference between the two. But when we put the ultrasound elastography on, that shows us a computerized model of the stiffness of the tissue. And I use this a lot in my practice as well as my research. So on the top here, you see that dark part in all that red, and that represents stiff tissue. And after shockwave therapy, you see a softening of that tissue in orange and yellow. So it gives us an estimate of the stiffness in there that we may not see on B-mode ultrasound, but a manual therapist may be able to palpate that. Another favorite and often overlooked modality that I commonly use is heat. Heat is fantastic, and it's so underutilized. The last study before any recent study was in 1984, looking at heat and diathermy. And as you can see here, the graph from it, 30 minutes of heat is extremely effective in treating myofascial pain. And then the next study done in 2020 demonstrates the same thing, very effective for neck and plantar fascia pain. So how long do you heat? This is a very, very standard graph out of the textbook, anywhere from 15 to 30 minutes. You need about 15 minutes to get that deep tissue to heat up, and 30 minutes is pretty standard. Stretching is also a very simple, but often overlooked intervention. This study was by Dr. Langevin, and she taught a rat how to stretch. So if you look at the figure in B, she taught the rat to hang on to the edge of the table, and they stretched this rat very gently for 10 minutes every day after inducing injury, and this time with carrageenan. They'll use various injectates into the deep fascia. And in the A and B are the saline controls. And in C, that's the carrageenan without any stretching, and you can see a dense increase in that loose connective tissue. There's a thickening of that fascia with more of that black layered lay down, versus D, with the rats who receive just light stretching, 10 minutes every day, they did not develop the same thickening in that fascial tissue. Fascial manipulation is a sequencing technique and trademark technique developed by the Stekos, and it uses diagnostic treatment as sequencing along fascial planes, and in this study, they treated, these were low back pain patients, they treated everything except the back, and they were able to show effective decrease in pain levels after two to four treatment in these patients. When compared to a combination of massage, electrotherapy, and laser, those were equally as effective. So all of these interventions are extremely effective for myofascial pain. So what might be occurring during these manipulation processes? And in this study out of NYU, they examined five patients prospectively with lateral elbow pain, and they used a proton T1P relaxation mapping technique to look at the content of the loose connective tissue, the glycosaminoglycan, as well as the unbound water. So in GAGS, the water is bound, and when they're unbound, they're considered free water. And what they showed was that the free water content, as you can see in the pre, that's the red and yellow stuff lighting up, the free water content decreased in the patient's post-manual therapy. So they postulate that perhaps it's the loose free water content that we're palpating and treating in these tissues. So clinically, how do you integrate all this new knowledge? Well physical examination and history are crucial. Recall that study out of Mannheim, Germany, where they injected the 12 healthy volunteers. Well they also characterized the type of pain these patients were feeling, or these volunteers were feeling in the various layers. And the original study looked at the superficial fascia, the D fascia, and the muscle. And draw your attention to the superficial fascia on top, and the characteristic description of the pain when the hypertonic saline was injected into the superficial fascia is burning. So your patients may describe burning if their superficial fascia is the source of pain. In a follow-up study, they were able to reproduce these results, and in the D fascia, patients will describe stinging or cutting pain. The muscles will have the classic throbbing, beating, aching pain. So this is also where I am doing my research, is attempting to quantify what layers contribute to what percentage of pain in patients, in a given patient, in a group of patients. And it's really exciting material. The future of fascia and the research is wide open as we try to understand how all of these different layers and aspect of fascia tie together in a clinical situation. All right, any questions for me? That has been fantastic. Thank you very much. I'm not seeing any questions come in yet, but I think this has been a blind spot for a lot of us. I think it's something that we see a lot in terms of patients coming in the clinic, and I'll say pain patterns that don't fit a lot of the molds that we commonly are taught. And so I think this has been a fantastic review of research and literature in a very clinically relevant setting. So I appreciate you filling in that blind spot for us. A couple of questions coming in, give me just a second. I've pulled it up too. Yeah, thank you for having me give this talk. And it was supposed to go much longer. I think I took out a lot of the technical details. Looks like, so we have a question here about evidence for percussive therapy, like Theragun and that sort of thing. It's been popularized among athletes and the public, kind of like we saw cupping several years ago. Any thoughts on that? Yeah. That's an excellent question. And there are a lot, this field of fascia is so wide open and it's so multidisciplinary. And a lot of the therapists, the physical therapists, physiotherapists around the world are looking into this. And what we find is these American percussive devices, so, and I see the OMM question too. So I'm going to tie this together. And I know you're a DO by background too. So layered palpation is extremely important. And in a lot of these manual therapy techniques, even if they are not of osteopathic origin, like the fascial manipulation, there is layered palpation. So with these Theraguns, they're fine if they're in skilled hands, if that practitioner can feel the layers of what they're going after, fine, great. But when the lay person takes these Theraguns and starts bashing their bodies with them, they're probably causing a lot of fiber breakdown. So they're probably causing more damage, more of this noxious stimuli. And then recall in that integrative theory, now you're going into this vicious cycle. So I suspect that's what most lay people are doing with that Theragun. They're really damaging their tissue. And they've also looked into, this is an area where they definitely need more research and they're looking into, but the frequency of that vibration is important. So we're seeing that lower hertz seems to have this relaxing response on the nervous system, the parasympathetics, whereas at these higher frequencies, especially with these American-made products, you're probably overstimulating the nervous system where all of this all these C fibers are, and you're assaulting the nervous system. So I don't think there's anything wrong with the approach. It's just, it has to be thoughtful and really looking at how you're using it and why you're using it. OMM is fantastic. I do a lot of osteopathic manipulation, layered palpation. And there are a lot of DOs who, especially foreign osteopaths who are looking at layered palpation and how it changes things. In my practice, it's phenomenally effective. And that's also what I'm looking at in my research is if we come at the tissue in different angles, in different layers with layered palpation, how are we changing that fascial tissue? Because those are questions that even us in the fascia world, even though we believe in what we're doing, we know that we have to demonstrate that there are objective changes. Do you want me to just go through all these questions or do you want to? Yeah, if you don't mind. I mean- Okay. Yeah. I'll just go through them one by one. So what's the difference between a trigger point and a tender point? So that's the debate among people who don't believe in trigger points. So then they'll say the trigger point is not real. It's a tender point. Then I'll hear people say that a tender point is different from a trigger point because the triggering needs X, Y, Z, and therefore it's tender and not a trigger point. Or they'll say the tender point is a latent trigger point. And that is a Travell and Simon terminology. So latent versus active triggering. So these are really nuances looking at the older literature or traditions too of what is passed down to you and your terminology of them. I don't use any of those terminologies and I'm typically really inflammatory by the things I say, but I'm not going to go on record to say them because I've learned. The more I learn, the less I know. But a lot of my residents hide and they don't use any of those words with me because I'm more interested in these specific components and this layered component. So what is really, and as you start to look at myofascial trigger points and really osteopathic lenses, what are the stressors in the patient's life? Are they humped over in this upper cross, lower cross way? Are they eating junk? Are their hormones all out of whack? What's going on that is underlying this entire view of the patient? And so I try not to label these painful areas by these terms as much anymore, but those terminologies are very traditional terminologies that you may hear your attendings use, but there's not much science backing up those terminologies. How about patients who undergo surgery and the fascia is cut off? It's really bad and there is research and that's where a lot of Carla Stecco's research is going as an orthopedic surgeon. It's amazing to have a surgeon in the field who's interested in looking at histology like that. And it really depends on the layer and what she looked at specifically was C-sections. So when you go in to do a C-section, it looks fantastic on the outside because the OB-GYNs are really doing a great job to make sure it's aesthetically pleasing, but underneath the tissue is a mess, an absolute mess. And many, many of my patients, that's one of the first things I ask is, have you had abdominal surgery? Because it will show up years later as pelvic floor pain. And that pelvic floor is absolutely in continuity with the torso. So now we have back pain, pelvic pain, all from a big surgery that was no big deal. No big deal. Everybody has these many years ago. And you add additional insults after another and it turns out like this. So with surgeries, you have to know what layers they're cutting through. Are they getting into the deep fascia? And how do you treat these? This is a really neglected area in phys med. And I somehow end up with all these patients in my practice or even in the hospital because no one knows what to do with them because it is really fascially mediated pain post-surgery. So your cardiac patients, your abdominal patients, and there are ways to treat them. It's just really tricky trying to access them in a very conventional medical system. Do we always need ultrasound to locate trigger points? No. Absolutely not. That's DOs and their layered palpation and that feedback. No. What's the evidence? None. We don't have evidence. I'm trying to show that in one of my studies that it's real and that it's reproducible. But that is a very, very controversial topic, especially with the more PhD-oriented folks in fascia. They just keep telling us clinicians, you got to prove it. We don't believe you. But us clinicians, we absolutely feel like we can palpate things and treat things effectively. And the patient will give you that feedback. So you resolve the densification in there and they'll say, my pain's gone. And we'll feel that. We'll feel the change in quality of tissue. Do you infiltrate trigger points? What drugs do you do? Do you describe? Okay. Awesome. Really controversial. So I am, I'm trying to figure out the best way to answer this without offending anyone. I feel like that when we treat trigger points, the classic trigger points into the muscle tissue, I think that in some instances we are treating a pathology that is partially responsible for the pain. I don't think that it attributes to 100% of the pain. And I think that there is much more that we have to treat beyond just the trigger point itself. We have to treat the fascial contributions. We have to treat the kinetic chain contributions. We have to treat the sympathetic, parasympathetic inputs. We have to treat nutrition. We have to treat movement, the concept of not, of this gym, right? You sit at the desk all day, you stress out, you stress out about deadlines, you stress out about the kids, you drive them to this and that. And then you're going to go hit the gym really hard for an hour, 30 minutes. That entire concept has to change because we as humans have to move. And I'm putting together a book on this, on what is the history of fascia, myofascial pain, and what is the history of human movement and where did that, where did that change and why do we have these myofascial pain syndromes? And you have to know that this is all very, very controversial because we don't have hard science with it. And a lot of it is taking our clinical experience and trying to prove that what we experience with the patient is real, is true and demonstratable on a scientific level. Do I prescribe any oral medications? So in my private practice, it's very integrated and I give a lot of magnesium. Magnesium is fantastic and I give a lot of heat. And I'll give heat before doing any injections, before giving any oral medications. And you'll find that with these types of myofascial pain, most medications really don't work. And if a patient is telling you the medication is not working, like a traditional NSAID or gabapentin, those typically don't work. And I don't start them unless the patient is absolutely over the, you know, just absolutely needs a crutch, then, you know, it's always a negotiation. But if a patient is telling you that's not working, it's probably better to just take them off all that stuff because now you're dealing with all the toxicity from the breakdown of those medications. Any other questions? I'm not seeing any more, but thank you so much. Again, this has been a really enlightening talk. We appreciate you joining us today and sharing your background, both clinically and kind of what you do.

myofascial pain

trigger points

prevalence

pain syndromes

pathophysiology

fascia

treatment options

diagnosis