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Lower Extremity Neuropathie
Lower Extremity Neuropathie
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lecture series. Tonight's lecture is sponsored by the AMSSM Online Fellows Education Subcommittee, the AMSSM Education Committee, as well as the AMSSM Fellowship Committee. I am Julie Creech-Organ. I'll be your moderator today. And today we're gonna learn about peripheral neuropathies of the lower extremity with our guest speaker, Dr. Gary Ho. So the purpose of tonight's program and all the program within our series is just to serve as an adjunct to your individual program education, to help you learn and meet and interact with some of our wonderful AMSSM members, as well as sometimes other invited guests, and also to assist you in the CAQ preparation. A couple of ground rules throughout tonight's presentation. We do ask that you mute your computer or device's microphone and turn off your camera during the presentation. If you have any questions that might arise during the presentation, please feel free to submit those in the chat function. I'll be monitoring those throughout the talk, and then we'll have a time to discuss those with Dr. Ho at the conclusion of the lecture. Also stay tuned for looking at that chat box at the end of the lecture, we will have a link for an online survey to help us customize and better serve you with these lectures and these presentations. So it is now my pleasure to introduce our speaker for this evening, Dr. Gary Ho. Dr. Ho received his medical degree from Georgetown University and then completed both his family medicine residency and his fellowship training in sports medicine at the Fairfax Family Practice Program. He served as a team physician for several professional as well as collegiate organization, and is currently a team physician at George Mason University. Dr. Ho is also the past director of the Inova Fairfax Medical Campus Sports Medicine Fellowship Program, and past medical director for the Fairfax County Public School Systems Athletic Training Program. He regularly volunteers at the medical tent for major sporting events and has several published works, including numerous book chapters and journal articles. As a fellow of the American Medical Society of Sports Medicine, the American College of Sports Medicine and the American Academy of Family Physicians, Dr. Ho holds a number of academic appointments and is board certified in both family medicine and then has his certificate of added qualifications in sports medicine. Additionally, as if that wasn't enough, he has credentialing as a musculoskeletal ulcer stenographer and point of care ultrasound, and in the management of concussions and other traumatic brain injuries. Dr. Ho teaches internationally and has special interests that include musculoskeletal and neuromuscular ultrasound, running medicine, martial arts and combative sports, orthobiologic therapies, office procedures, concussions, point of care ultrasonography, mechanical peripheral neuropathies, and academic medicine. As a key faculty member of the National Capital Sports Medicine Consortium, he enjoys teaching and mentoring medical students, residents, and fellows in sports medicine. Dr. Ho currently lives in Vienna, Virginia, and serves in the community as a sports medicine physician in North Virginia and Fairfax, Virginia. So it's without further ado that I will give the screen on over to Dr. Ho. All right. So let's see. Thanks a lot, Julie. I'm gonna go ahead and see if I can share my screen. And, okay. Can you guys see my slides? Looks great. Great, awesome. Well, thanks a lot for that kind introduction, Julie. It's my pleasure to be with everybody tonight. As Julie was reading all that stuff up, I was remarking on some familiar names in the participants list. And so hopefully we'll have a little bit of fun tonight. And without further ado, we'll go ahead and get started. So I have no relevant financial disclosures. So what I'm gonna try to accomplish in the next 40, 45 minutes or so is to have a nice discussion about peripheral entrapment neuropathies as encountered in sports medicine with a focus in those that occur in the lower extremity. I'm gonna build on the really excellent talk that Dr. Dan Cushman gave a few weeks back focused on upper extremity neuropathies. But there were a lot of important points and general concepts that I think will bear fruit for us to reiterate and emphasize, especially for the fellows on the call as they prepare for their CAQ exam and board certification exams. So we'll touch upon some of these general concepts with how we approach mechanical peripheral neuropathies because they will ring true whether it's upper or lower extremity neuropathies. And then in the second half of the talk, we'll shift our focus to the sonoanatomy and the clinical approach to select lower extremity neuropathic injuries that we see in sports medicine. So the first little pearl that I'd like to highlight is as far as easily testable materials. And one is they like testing lists and classifications and definitions. And so this is the sonon classification of nerve injuries is something that will serve the fellows and anybody recertifying in sports medicine well to remember and I'm not gonna spend too much time on it, but so the sonon classification is one of several classifications that looks at nerve injury as a spectrum of severity, but also has important implications with not just how we communicate with each other, but also prognosticating recovery for the patient. So you got three main categories, you got neuropraxia, axonomesis and neurotmesis also sometimes referred to as neuronomesis. And so the most mild form of nerve injury in this classification is the neuropraxia. A neuropraxia represents essentially an impaired conduction across a nerve segment, but the axon continuity is preserved and the surrounding connective tissue sheet is also preserved. And a prognosis is usually very good to excellent and recovery can be expected to be full, although how long it takes varies depending on the nerve injury specifically. Axonomesis is a little bit more severe. It's kind of represents a spectrum of intermediate levels or severity of nerve injury. And in this type of injury, you have damage and compromise of the actual axon. However, the surrounding connective tissue sheet in this myelinated axon is reasonably preserved. How much or how little it's intact will depend on how severe the nerve injury is, but because the surrounding connective tissue sheet is still there, it allows the disrupted ends of the axon to regenerate. And this connective tissue sheet serves as a scaffold in order to guide that regeneration so that the injured or torn ends have a way to grow towards each other and reconnect. That's to be contrasted with neurotmesis, which functionally is analogous to a complete transection of that nerve axon, where you have disruption of the axon as well as the surrounding connective tissue sheet. So the reason why this is more severe is because you lack that connective tissue sheet in order to guide those little buds from the injured ends of the axon to grow towards each other. In fact, without that connective sheet, axonal regeneration usually happens in a very haphazard manner, and recovery is rarely ever full and often incomplete. The other thing I'll mention is axonomesis is the one that's most variable in its prognosis, and therefore it's also the one that's most dependent on other factors. And it's important for us to remember other aspects of our training, whether it's primary care or other general medicine concepts because the general medical health and the metabolic health and condition of the patient will have significant contributions as to a patient with axonomesis and their propensity to recover. And I'll make mention of that in a bit. So at this point in the fellowship year for a lot of fellows, you guys have had usually pretty good training and good practice in getting a good, complete clinical history. But a couple of little important points that are relevant to peripheral trapehneuropathies that I'll try to point out because I think they're important. One thing is that, classically often think of neuropathic symptoms, numbness, tingling, burning, that kind of dysenthesias type of symptoms that we often see in nerve injuries, but it's important to keep in mind that not all nerves are the same and that some nerves are more sensory, some are more motor, but a lot of these mixed nerves because of the heterogeneous nature of some of the smaller fibers that make up these peripheral nerves, you can get symptoms that are not classically neuropathic in nature. You can get achiness, you can get dull pain, you can get stiffness, you can get exertional fatigue, for example, and where these symptoms might actually mimic other musculoskeletal injuries. So it's important to keep this in mind because nerves can mimic other conditions such as tendinopathies and arthropathies. So I always encourage people to keep peripheral neuropathies on their differential diagnosis, especially when people don't respond to their initial therapeutic plans. The other thing I'll make mention is that we often think of symptoms of nerve entrapment radiating distal from the site of injury or the site of entrapment, and that's fairly typical, but it's not the only radiation pattern. So for example, if we were to use a classic example of carpal tunnel syndrome where you have entrapment of the median nerve at the wrist, most of us are pretty familiar with symptoms referring and radiating distally along the hand and the fingers. However, symptoms can also radiate proximally where it might actually radiate in this same example, perhaps nerve entrapment at the wrist, but the symptoms may actually radiate proximally or centrally, and this is called the Veillé phenomenon. And it's not just a symptomatic kind of observation. It also represents certain pathophysiologic processes. And the reason why I mentioned that is because nerves are funny. You know, they go two ways. And because of that, you can encounter a nerve, which starts in the central nervous system going all the way to, in this example, your fingertips, but that nerve can be entrapped in more than one place, but primarily present with symptoms of one entrapment. This is a phenomenon called double crush, and it's another pearl I'd like to share with the audience because it's one that you should keep in mind so you don't get fooled. So in that same example of carpal tunnel syndrome, you know, perhaps somebody presents with a median nerve distribution, numbness, tingling, burning in the hand. However, they can have entrapment in the carpal tunnel, but they might also have entrapment, say, at the elbow. But if you forget to look at the elbow, you might miss that other entrapment, and that's why it's called double crush. And more often than not, I mean, it depends, but it's more often that the more proximal lesion is actually the primary lesion. And if you neglect to actually assess for and treat that additional proximal lesion, you might be incompletely or suboptimally managing your patient. So that's just another pearl to keep in mind. I mentioned this earlier, how important it is to remember to at least have an eye out for the patient's general medical history and their general metabolic health, the examples, diabetes, hypothyroidism, various nutritional deficiencies, et cetera. And these are important, and if it's not within your typical chosen scope of practice to manage these, definitely partner up with somebody who can help you not leave these stones unturned. And the reason why is because not only do they put patients at a greater risk for having nerve injury, but also can complicate somebody's recovery and hamper their prognosis. A great example I'd like to share with you is I had a patient not that long ago who I was treating and was getting some response to some of the procedures we were doing, it was suboptimal. And I decided to put my old primary care hat on, check some labs. It turned out that she was subclinical hypothyroid. We replaced her thyroid hormones and got her therapeutic. And all of a sudden her response to our treatments for her peripheral neuropathy was significantly better and more optimal. And so that's just another opportunity to do better by your patients. This next slide kind of reminds me to remind you guys that don't forget to examine the spine and the entire extremity, okay? As an example that shared earlier, that double crush, this is one of the reasons why is because you might have a symptom presenting, you might have a patient presenting with symptoms of carpal tunnel syndrome, but that may actually have a cervical radiculopathy. And with that cervical radiculopathy, you don't want to miss that pathology. So I always start all of my peripheral nerve exams with the spine. And then I make sure I examine the entire extremity. Another pearl to keep in mind is that you want to make sure you undress your patient so you don't miss any important clues. And muscle atrophy, like in this upper left-hand corner, is usually, you know, can be pretty obvious and that usually connotes a more severe injury. But sometimes muscle atrophy can be more subtle and it's important for you to look, otherwise you won't find what you're not looking for. The other thing is to examine the entire extremity and look for other clues, you know, in addition to positive symptoms, such as pain, numbness, tingling, burning, those things. But you also want to look at the other things that nerves do and remember that these nerves often go to the skin and they have vasomotor and pseudomotor functions. So a lot of times you'll see discoloration in the skin, you might see some changes in sweating and so forth, which can provide valuable clues as to what you're actually looking at by way of peripheral neuropathies. It's also important to remember to look at the patients globally. You know, in sports medicine, we're in the business of motion, right? So a lot of our athletes with peripheral neuropathies and intravenous neuropathies often have a significant contribution to their pathology by their biomechanics. So looking for anatomic malalignments, that goes without saying, and I'm not gonna go too far into that, but just to remind you to keep in mind that you gotta look at the full kinetic chain. Other specific aspects of the physical exam, most of us are familiar with this Tonell's sign or Tonell's maneuver, where you use your finger, the tip of your finger to percuss over the area of a nerve and look for the reproduction of symptoms, right? And so on the left, you got a cubital tunnel and a cubital tunnel version. On the right, you have a tarsal tunnel version of that. You can also look at provocative compressions and neural tension. Of course, those neural tension signs are gonna be specific for the particular nerve. And there are some pictures throughout tonight's talk that will demonstrate what some of those might look like. And then the last important pro I'd like to emphasize when it comes to general aspects of peripheral neuropathies is that because we're sports medicine docs and we're looking at athletes who are in motion, many times they're not symptomatic unless they've done something to make them symptomatic. So it's often, we come across this all the time, patient comes to the office, their exam is pretty negative in the room. Well, take the opportunity to have the patient perhaps perform the provocative activity to flare up their symptoms and then re-examine them because when you look at them post-exercise, your physical exam might all of a sudden be more positive and more fruitful. By extension, looking at diagnostic testing, there are a lot of different tests that we can get for peripheral neuropathies. Plain film radiographs, MRI, CT, bone scans, even some vascular studies can be useful, but the majority of these are gonna be mostly exclusionary. The exception could be an MRI. MRI is the ones that's most likely to be diagnostic. Case in point here, the picture in the upper right-hand corner is a coronal slice across the ankle. And as you can see here, this demonstrates a ganglion cyst that is abutting the medial and lateral plantar nerves. So in the right clinical setting, I think that can be fairly diagnostic. Additionally, there are specific sequences and contrast protocols using MRI that can be more specific in looking at nerves, such as MR neurography. And that's what's being shown at the very bottom here, looking at the sciatic nerve, the right and left side MR neurography. And you can see very clearly the difference in the nerve caliber from left to right in this companion case. Musculoskeletal ultrasound is obviously something that I do a lot of, but it's also very useful when it comes to the resolution and the ability to diagnose soft tissue problems, like nerves. And so we'll be talking a little bit about that. And here's an example here. This is actually from, I don't know, 14 years ago. This is looking at a superficial coronal nerve. On the top picture is the asymptomatic side and the bottom picture is the symptomatic side. You can see there's a difference when you compare left to right, you've got a thickened and edematous nerve, as well as the presence of this neuroma. And it was fairly easy to make that anatomic diagnosis there. And then lastly, when it comes to diagnostic modalities here, basic ones initially. Don't forget to remember to at least think about the metabolic health of the patient. And if you need to, don't be afraid to order some labs in order to screen for them because they may play an important part in your management strategy. A little bit more about ultrasound here. So what I have here now is a few pictures of what a grayscale image is of what a nerve should look like and maybe what it shouldn't look like under ultrasound here. On the upper left-hand corner, you have a short axis image of a typical nerve. You've got this cluster of grapes. You see all these round fascicles. These cluster of grapes are a honeycomb appearance of this nerve and short axis here. Okay, some people call this a bundled or a clustered tessellate fascicular pattern, but that's what that looks like there. Compare that to the symptomatic and abnormal nerve on the center of this top center of the screen here, where you notice a couple of differences. You notice that the nerve is enlarged. It's larger. It's more hypoechoic. And in that hypoechogenicity, that darkening, there's an obscuring or effacement of that normal cluster of grapes fascicular architecture. Okay. In the lower left-hand corner, you have a polyfascicular and a unifascicular nerve and long axis. And this is what it should look like. You can have this multi-layered or compact fascicular, which is different from compact fibular. It's a compact fascicular appearance of the long axis of this nerve. I often, visually for me, it looks like a bundle of drinking straws. That's kind of how it looks like to me. And then in the bottom center, you see a more abnormal nerve here, where it's thickened. It's enlarged. You get that same hypoechogenicity that I mentioned earlier, and you get that effacement, that kind of blurring out of that normal compact collinearly fascicular appearance. The other thing you'll point out here, you notice it in the same image, but a lot more obvious in the image in the lower right, is you can see a caliber change in the nerve as well, where the nerve caliber is much smaller at the point of entrapment or compression. And then in the segments that flank that, either upstream or downstream of that nerve, usually the proximal portion of that nerve entrapment is a lot more swollen. And sometimes people call this like the dumbbell sort of appearance when you get swelling on both sides. But that's how it might look like. And then in the upper right hand corner, you can see there's several different types of pathologic nerve appearances. I will point out that actually sometimes nerves look completely normal under ultrasound, even though they can be a problem. So it's important to maintain that index of suspicion. The other thing ultrasound can be helpful in doing is looking at the muscles that are innervated by the nerve that you're suspicious of. And this is important because it can give you important clues. The nerve may look normal, but if you check out the muscle that the nerve innervates and it doesn't look normal, you should continue considering nerve pathology in play here. So in this picture in the upper left hand corner, you can see a normal gastrocnemius and soleus muscle in this calf right here compared to the picture right next to it, which is fairly abnormal. And so normally the muscle on the short axis should have that relatively dark hypoechoic starry night appearance. And what you see here, you see a lot of hyper echogenic obscuring of that normal architecture. And actually in this case, you can even see a decrease in the actual size here. In the upper right hand corner, you can see other examples of fibro fatty atrophy in the rectus femoris muscle. And this picture also illustrates the grading pattern. And I'm not going to go over the grading pattern, like in the lower left hand corner, I think that illustrates it really well, but there's several different grades when looking at, when you talk about describing how bad or how much of fibro fatty atrophy you're dealing with, with denervation changes in a neuropathic patient. Other things that ultrasound could be helpful for is looking at neural hyper vascularity. So hyperemia, you know, as you know, inflammation often is picked up with increased vasculature in the soft tissue. We're familiar with this with tendons. Well, the same happens with nerves as well. Of course, your ability to be able to pick this up is very operated dependent, but it's also device dependent and different machines are going to have different capabilities when it comes to your ability to assess microvascular changes in the nerve. So, but newer technologies, such as microvascular imaging have proven very useful, but again, it'll depend on your device setup. And then for ultrasound, the last thing I'll mention is elastography. I'm not going to spend too much on this, but you know, this is growing in popularity as we look to use this technology to assess the relative stiffness of nerves as another indication when it comes to pathologic processes. This is still, its adoption has been relatively slow since its inception in neuromuscular and musculoskeletal ultrasound, mostly because of costs and its availability. But that is changing pretty rapidly. So, so be on the lookout for that to appear in your toolbox someday. And then another diagnostic modality that is often associated with peripheral neuropathies, of course, is EMGs and nerve conduction studies and electrodiagnostics. And Dr. Dan Cushman did a really nice job providing his brief overview of this. And I'm just going to point out one important aspect, and that is that EMGs and nerve conduction studies can be falsely negative if done too early. So if you're performing it within three weeks, sometimes even four weeks of the onset of symptoms or pathology, it may be falsely negative. So, so make sure you keep that in mind when it comes to timing of this, of this diagnostic modality. The last thing is just like physical exam, you know, if an athlete is not symptomatic at the time of getting his EMG, his EMG or nerve conduction study, it may also be falsely negative. So again, I, I make it a point to try to advise my athletes to provoke their symptoms prior to getting this test if I, if I've ordered this, or, you know, get on the phone and have a nice conversation with your colleague who's performing this so that you guys are on the same page with, with, with doing this test after provocative maneuvers. All right, so this next slide provides a kind of a snapshot overview of some of the non-operative treatments in our toolbox when it comes to managing these, these patients. And when I first started giving talks on peripheral neuropathies, we used to talk about three R's. And so the three R's were rest and relieve, rehabilitate, and if it didn't get better, you would refer to a peripheral nerve surgeon. But let, you know, over, over time, you know, over the years, because of technology like ultrasound, we've gained more and more tools that allow us to help people, help patients as sports medicine physicians. So we added a fourth R, and that was release. And that was to, to reflect the ability for us to hydro-dissect these non-operatively and dis-entrap some of these nerve entrapments without surgery. And then in more recent years, we added a fifth R, and that is quote-unquote regenerate as we, as we start to see increased adoption of orthobiologics and regenerative medicine techniques. And of course, nerve has not escaped interest when it comes to an opportunity to use these treatment modalities. So just kind of expanding on some of these, of course, with, with the rest, relieve, and rehabilitate, two of the, two of the, the three basic R's, you know, we're going to correct biomechanics, look for training errors, you know, we're going to use bracing and orthotics as needed, depending on what the patient needs for their function, whether it's because of sport or because of their, their daily lives. We're going to rehab, rehabilitate their strength, their muscle endurance, their proprioception, and then we're going to employ a very specific rehabilitation that are directed at the nerve. So a myriad of various neuromodulation techniques, neuromobilization techniques, as well as nerve glides, which we'll, we'll talk a little bit more about. And then there's medications that can be used. And then when it comes to release, what we're talking about here is percutaneous hydrodissection adhesiolysis neuroplasty, which is the full name of that procedure. We often say hydrodissection for short, but if we're, we're actually meaning to release the nerve from its entrapments and adhesions, then we're not just putting fluid in there, you know, we're not just pulling apart tissue planes. We're actually doing that for the purpose of lysing adhesions and disentrapping the decompressing of the nerve. And so, so that's, that's what that release stands for. And then when it comes to regenerate, like I said, the use of PRP, platelet-rich plasma, other platelet-derived techniques and other orthobiologics, you know, has remained a very keen interest of myself and many others when it comes to how useful they may be when it comes to addressing peripheral neuropathies, more specific for the degenerative neuropathies. But I think it's important to keep in mind that we're probably modulating more than we are regenerating with a lot of these, because basically there are intrinsic regenerative and reparative processes, and we're modulating those processes. We, you know, we, when we're using these orthobiologics, they are not being used in a vacuum. We're working with the body, and most of that regenerating is actually done by the body. So I, I like to prefer to think about these as more orthomodulants, as we are modulating the regenerative process, and I use that same language to be very transparent to our patients. So why the utility of nerve glides? And if you notice in this video on the left side of the screen here, you can see this is a long axis image of the median nerve at the elbow as this subject is flexing and extending their wrist. You can see how much the nerve moves. So a lot of peripheral nerves will have a certain, a pretty wide ability to, to, to slide and glide, and it's thought that with entrapments that these, the nerves ability to glide is compromised, and it's not just the gliding between the nerve and its surrounding soft tissue environments, but also the gliding between different elements with inside the nerve as well. So for nerve glides, we're aiming to try to re-establish that healthy biomechanical function of the nerve. So in this picture right here, we have an example of a nerve glide for the sciatic nerve. On the right of it, you see a still picture of, of somebody demonstrating what a, a superficial peroneal nerve glide might look like, and at the bottom here are two positions for femoral nerve glide. And so some patients, you know, are going to be more able to do this on their own, while others are going to require some more in-person instruction, such as the, working with a skilled physical therapist or occupational therapist. And then when it comes to hydrodissection, I'll just share this video. This is actually the, the first hydrodissection I did, probably about 14 years ago now, and it was of the sural nerve. And just as I mentioned before, it was a good example. This case was a good example of how nerves can mimic other musculoskeletal conditions. This was initially diagnosed and treated like a Achilles tendon problem. But when we looked, we actually saw a swollen nerve. And so you can see this very thickened and hypoechoic sural nerve here in long axis. And on the right, you can see it in the short axis. I usually start off by mapping the nerve and drawing on the skin. It gives me a good idea of where I'm going. And then I start the procedure by also scanning to use a power Doppler to, to get a full inventory of the surrounding blood vessels in order to avoid iatrogenic, iatrogenic injury to the vasculature and for the utmost of safety. And then what I do is I bring the needle alongside the nerve injecting fluid to create some space, some working space. And then I use the hydrostatic pressure, that fluid to peel off layers and layers of soft tissues as I approach and get closer and closer to the nerve, eventually getting right to the plane, right at the nerve and inject fluid to, to push the surrounding soft tissues off of the nerve. And as I do that, I make sure I continue to work around the nerve. And this is what I want to end up having. I want the nerve floating in fluid in a halo or donut of fluid. Notice that the nerve is round and circular in shape, and that's what I look for. And then what I do is park the needle on top of the nerve, turn my, my probe 90 degrees, and then, then I extend that donut or halo of fluid into a cylinder to hydrodissect that segment of nerve. And once I'm satisfied with that, I move on to the next segment. You can see here on the screen now is a segment of this patient's cerebral nerve that is less pathologic. You can see the nerve is not as thickened. You can see that the surrounding soft tissues are just falling off the nerve as opposed to having that sticker peel back sort of animation that happened when it was adhesed. And of course, there are surgical treatments for a lot of our intrepid neuropathies. And I'm not going to go over all the procedures here, but it's important to keep this to mind and, and know when we've reached our limits, but also know that, you know, there are some patients that are, are probably earlier surgical candidates, and it's important to, to keep that in mind. And this is just a case I'll share with you guys from when I was a fellow. This was a patient with a multi ligamentous injury of the knee. And as part of our stage surgical procedure, he, you know, we also needed to address his common peroneal nerve because after his injury, he also had foot drop. And what you can see here, this is a lateral aspect of the knee. You can see the torn posterolateral corner here, but you also have this common peroneal nerve. This is the fibular head. Here's the neck. You can see how erythematous swollen and edematous it looks. And so, so, you know, surgery really allows us to really see that nerve. All right. So the last thing I'll mention when it comes to general nerve aspects before we jump into nerve specific, lower extremity specific neuropathies, is that there are a lot of different trends out there. And I've made mention of some of these with platelet release, lysate, PRP, things like that. And much of this is actually pretty intriguing. And a lot of the data is, is emerging. And some of it's pretty promising. But obviously it needs a lot more study. And for the sake of time, we're not going to dive too much into, into these, but certainly can discuss more if the audience wants during the Q and A. So we'll turn our attention to selected lower extremity neuropathies. All right. That's what you came for. So here we go. All right. The first one we're going to look at is the ilioinguinal nerve. The ilioinguinal nerve arises from the lumbosacral plexus. Okay. Which, which resides with inside the psoas major muscle. So you can see the psoas major muscle here, and you see all these nerves that come out the side. On the right side of the picture here, you have the psoas major muscle depicted as partially resected here. And you can see all those nerves of the lumbosacral plexus from inside that psoas major muscle. Well, the ilioinguinal nerve is among the first that to come off of it from the superficial aspect anyways. And it comes from T12 to L1, leaves the psoas major muscle. And as it leaves the psoas major muscle, it quickly goes into the abdominal wall. And as it travels from the posterior to anterior direction, as well as from the superior and infradirection, it wraps around the abdominal wall, makes its way into the inguinal area, and then towards the pubis here. As it does so, it spends most of its time traveling between the innermost and the intermediate muscle layers of the abdominal wall, namely the transversus abdominis and the internal oblique as depicted here. As a nerve travels and gets close to the ASIS inguinal ligament area, it begins to surface. And as it surfaces, it can be perhaps between the external oblique and internal oblique and ultimately to the skin to innervate the inguinal canal, the skin overlying the inguinum, as well as the pubis and the external genitalia. Okay, ilioinguinal nerves can be injured either ectogenically from abdominal or inguinal hernia surgery. But from a sports medicine perspective, they often get injured as a victim of sorts from abdominal strains and tearing of the abdominal musculature, such as the external oblique. Case in point, this is often seen in hockey players, and that's where this gets its other common name, which is called slapshot groin. Patients will present with pain in the lower abdominal wall and the groin. Sometimes it refers down along the inguinal region to the pubis and external genitalia. It's often worse with hip hyperextension. And you can sometimes get tenderness and a to nil sign about the ASIS and the inguinal ligament where it starts to pierce that fascia as it surfaces to go subcutaneous. Treatment, you know, there aren't a whole lot of nerve glides you could do for this, but certainly medications, topical medications, if people are wanting to start really conservatively, but injections can be particularly helpful. And of course, we highly recommend to do that under ultrasound. And this is what it might look like. So you can see here, this is a kind of a mostly an axial plane image. Here's the ASIS here, external oblique, internal oblique, transversus abdominis muscles here. And you can see in that tissue plane between the internal oblique and TA, you can see these nerves here. And what's highlighted here is the iliohypogastric and ilioinguinal nerve. And I think this is important to keep in mind because it's not just these two nerves that sit there. There's a subcostal, for example, and there are several communicating branches. And really these fascial planes are often home to not just individual nerves, but really a nerve plexus. So when we do injections or hydrodissection neuroplasticity, we're often aiming to actually hydrodissect that tissue plane, as demonstrated here. As you can see, external oblique, internal oblique, TA, and then this is an in-plane needle guidance, and using the hydrostatic pressure to separate those tissue planes to free up that ilioanguinal nerve right there. The next nerve we'll talk about is the obturator nerve. This is a fun nerve. It does a lot of things. Comes off of L2-3-4, again from the lumbosacral plexus, leaves the psoas major muscle, and what's interesting is that as soon as it leaves the psoas major muscle, it goes right into the greater pelvis and sits on top of the kind of the rim of the greater pelvis, as shown here. So this is an image from medial to lateral, as you can see here. Here's the psoas major muscle. Here's your obturator nerve as it travels, and it hugs the outer wall of that bowl that is our, uh, our pelvis, moving towards this hole in the pelvis, this big gaping hole that we call the obturator foramen, which is covered by the obturator membrane, as well as covered by the obturator externus muscle and internus muscle. There's a little opening in the anterior most aspect of this obturator foramen called the obturator canal, and that is where the obturator nerve leaves the pelvis here. As it does so, uh, it actually gives off a whole bunch of branches. So here's a picture right here. This is a cadaver picture looking from inside the pelvis. This is posterior on the left, right is anterior. You can see this fan-shaped muscle that's the obturator internus, and you can see highlighted in green here the obturator, uh, nerve traveling along the pelvis and exiting the obturator canal. As the obturator nerve leaves the obturator canal, it gives off a whole bunch of branches, articular branches, etc. It's two terminal branches, though, that go down the thigh are called the anterior and posterior division. Um, and, uh, as far as where they travel in the thigh, you can see here as that nerve divides, you get the anterior division, the posterior division. The anterior division is often seen, uh, between the, uh, adductor longus superficially or anteriorly, uh, and then the adductor brevis. Well, behind the adductor brevis, between the brevis and the adductor magnus is where the posterior division is. So when you're in the thigh, proximal thigh, and you want to know where these nerves are, the anterior division is going to be right anterior to the adductor brevis, and the posterior division is posterior to the adductor brevis. And, uh, they also collectively innervate the, these adductors. So again, that's that posterior division there, uh, and, uh, it actually gives off terminal branches all the way down to the knee. And so the obturator nerve is actually the nerve, one of the nerves responsible for hip pathology presenting as knee pain, so that referral pain pattern, uh, and it's one of the things that can fool you. So, so that's the nerve responsible for that. Um, yep, so this is just more pictures kind of showing that anterior division right here. The other thing to keep in mind is if you notice this tissue plane, okay, this is where the adductor longus is, but it's also in the same tissue plane as where you eventually, further down, we'll find the sartorius. And so what's interesting about that is that it will, the anterior division of the obturator nerve gives off communicating branches that communicate with, uh, the saphenous nerve, which we'll talk about later, in this sub-sartorial plane, uh, and we'll return to that in a moment. So there's some pictures showing what that might look like. And so, uh, people can injure this in a number of different ways. You can hurt this by trauma. You can certainly hurt this by certain limb malpositions, et cetera. Um, I already mentioned, uh, about the nerve mediating symptoms from hip pathology, going down to the knee. Um, but we also see this, uh, uh, from injury, uh, using the same mechanisms as most adductor strains. Uh, and so a good classic board exam question for the fellows is that they might describe a patient who looks like they have an adductor strain, and, uh, they might ask you to think about what nerve, uh, could mimic this. And the, uh, one potential candidate for that is the obturator nerve, or perhaps you have an athlete who's had a lot of groin and adductor strains, muscle strains, and have healed well, well from them, uh, in the past, but now they've got scarring from that, that actually entraps the obturator nerve, and now you have a peripheral obturator neuropathy. So, so that, that's a, uh, potential, uh, cause. Uh, so patients will present with pain in the region, can radiate up and down. Uh, it can sometimes be numbness, tingling, burning, but sometimes it can be a little bit more subtle and more achy in nature. Diagnostic testing. Uh, so certainly you can do, uh, um, MRIs and EMGs for this. Here's some MRI pictures. Up in the pelvis, you can see here's the obturator nerve from inside the pelvis. Here's the bladder right before it leaves the pelvis. And then in the thigh, you can see the anterior and posterior division, uh, uh, sitting anterior and posterior to the, uh, adductor brevis, respectively. You get a very similar image to this, uh, under ultrasound. As you can see here, adductor longus, brevis magnus, anterior division, posterior division, and the accompanying, uh, cadaver slice showing the same anatomy there. So, um, manage this, uh, conservatively, uh, with, uh, rehab, stretching, muscle strengthening, um, nerve flossing, uh, injections, uh, hydrodissections, and then, uh, surgery if all fails. Uh, this bottom one is an example of a nerve repair of the obturator nerve following injury either genetically from a hip surgery. And that picture is a, uh, example of what a nerve glide might look like for the obturator nerve. The next nerve we'll talk about is the, uh, saphenous nerve. And the saphenous nerve, uh, is the terminal branch of the femoral nerve. It comes off L234, uh, leaves the, uh, um, the lumbar, uh, the lumbosacral plexus and the psoas major, uh, and then it travels towards the groin, leaves, uh, leaves the pelvis through the femoral canal, gives off its muscular branches, and then continues down the thigh as the saphenous nerve. So, femoral nerve turns into the saphenous nerve. As it travels down the thigh, uh, it actually travels deep to the sartorius muscle, as you can see in this picture right here. Uh, and, uh, we often call this a sub-sartorial plane. And in that sub-sartorial plane, it's not the only nerve. You got the saphenous nerve, you have the nerve to the vastus medialis, the medial retinacular nerve, uh, and you've got communicating branches with your obturators. So it's really, you know, to simplify things, it's a sub-sartorial plexus. But the saphenous nerve itself will then cross from the, uh, anterior to the posterior medial aspect of the thigh as it travels closer to the knee region through what's called the adductor canal, which is formed by this green roof, this aponeurosis, uh, aponeurosis, which some people call the vassal adductor membrane, okay, but that's the roof of Hunter's canal or adductor canal, and the saphenous nerve travels through that on its way to the knee. At the knee region, the saphenous nerve gives off infrapatellar branches and then sends its terminal crural branch, also known as the sartorial branch, down the medial aspect of the lower leg and ending up as the medial cutaneous nerve of the foot. And so you can get symptoms that radiate there along its entire course. People can injure this by blood trauma. I see this a lot as a martial artist getting low leg kicks in the area, which is very popular in certain full contact karate tournaments, can injure this nerve, turf sports as well. And then this is, this next animation kind of shows a bit of that referral pain pattern, but often people present with kind of anterior medial knee pain here, and the infrapatellar branch is usually the branch that's the culprit. So most of the diagnostic testing is exclusionary. Ultrasound can be helpful, but usually the nerve is, it's difficult to see it as swollen. Sometimes we'll see it as swollen, you can see pathologic changes, but often I think I make good use of ultrasound guided to nails or provocative compression to make, to help make the diagnosis, and then confirming it with a diagnostic block or injection. You can treat these conservatively, nerve glides, myofascial release, injections, hydrodissection, and then surgery if needed. And this is what an injection might look like here. Again, you target it by looking just deep to the sartorius muscle, find that femoral vessel, and then find that, that plane and hydrodissect that tissue plane with all the nerves. Okay, the lateral femoral cutaneous is a very popular nerve that I get asked to lecture on and talk about. And it comes from L234, okay, it leaves the psoas major, and then makes a beeline straight to the ASIS as it hugs the outer aspect of that, of that pelvis, sitting on top of the iliacus muscle. When it approaches the ASIS and inguinal ligament, it normally exits the pelvis by going under the inguinal ligament, and then on top of the sartorius, and you can find it between the sartorius and the tensor fasciae latae muscle. And I say usually, because as you can see this in the slide in lower left hand corner, I've given seven examples of some variable anatomy. So what it does as it traverses this is highly variable, but a good place to pick it up is actually between sartorius and TFL. Okay, so here's, here's what it looks like, and you can get a positive tennels over here and get symptoms, and often patients present with fairly classic well-demarcated anterior lateral thigh discomfort, numbness, tingling, or burning. Often this occurs in the context of weight gain, or tight garments, tight belts, equipment, you know, I see it in police officers who wear their duty belt a little too tight, again rapid weight gain, also prolonged malpositions, so malpositioning, so not uncommon for new moms to have gotten this, having spent a lot of time in labor in the lithotomy type of position, so that's, those are common contexts in which we'll see it. One thing I'd like to mention though, it's, it's a mimicker, okay, it's a mimicker. So in this diagram you can see here's the lateral femcutaneous, and as it leaves the pelvis it gives off three branches, an anterior branch, an intermediate branch, and a posterior branch, and the posterior branches end up right here over the skin overlying the lateral aspect of the hip, the greater trochanter, so it's a mimicker of hip pathology, and the anterior branch you can see may actually come all the way down to the anterior knee, so it can also mimic knee pathology as well. So diagnosis is usually made clinically, and management, you want to avoid that compression with the tight clothes and the tight equipment, perhaps weight loss or weight reduction might be, you know, recommended, and then injections can be helpful in hydrodissection. If all else fails, it's primarily a sensory nerve, so you can consider ablation, surgical decompression, or perhaps even removing the nerve entirely. So on the right side here is some images of what that might look like, okay, and so you can see, you can find the nerve between the sartorius and the tensor fasciae latae here, and I'll give another example. This is actually, these are pictures of my lateral femmocutaneous nerve that I acquired from a handheld pocket ultrasound device, and you can see here, you can see the tensor fasciae latae muscle and the sartorius muscle, and in between, in that subcube plane, you can make this small multifacicular neural nerve structure, which is the lateral femmocutaneous, and then if I slide a little distal, this one nerve will split into three branches, as you can see here. Again, my sartorius and TFL, and you can make out the three branches of the lateral femmocutaneous, and you can spin on these and look at them in long axis as well. These nerve and nerve branches are much more obvious when they're pathologic, and so you can see they're swollen here, and this is an example of what an in-plane short axis image in-plane injection might look like when it comes to hydrodissecting the lateral femmocutaneous. All right, pudendal neuropathy. This is one that is classically taught when it comes to sports medicine, entrapment for entrapped nerves, okay, because we see this in cyclists a lot, and so this is, it comes off of S234, comes off a different nerve plexus now, comes off through the sacral plexus, which is inside the pelvis here, and as those nerve roots, the ventral rami of those nerve roots come together to form the pudendal nerve, that nerve leaves the pelvis through the greater sciatic foramen or greater sciatic notch, along with the sciatic nerve and the piriformis muscle. It spends a short amount of time, extra pelvic, in the deep gluteal space, in the same, it's the same plane as the sciatic nerve here, where the nerve actually can be found between two ligaments, the sacrotuberous ligament and the sacrospinous ligament here, okay, and then the nerve enters the pelvis again through the lesser sciatic foramen, okay, and as it does so, here it is entering the less sciatic foramen, it enters into this tunnel or canal called Alcox canal or the pudendal canal, which is formed by the aponeurosis of the obturator internus and the fascia, etc. Within that canal, it gives off several branches. It gives off the inferior rectal, anal nerve, perineal nerves, nerves of the extent of gerontenitalia, like the posterior scrotal nerve in this case, or the dorsal nerve to the penis or clitoris. So patients can, can get this compressed more often by repeated, compressed out insults from spending a lot of time on the bike, for example. It can get entrapped in between the ligaments at the ischial spine, but more common in our cyclists, it gets entrapped in Alcox canal because of compression of that ischiorrectal fat, okay, and you can see how that sitting on that seat might push on that ischiorrectal fat compressing on that pudendal canal right there. Patients present with pain, numbness, tingling, burning in the perineal area, perianal area, and the external genitalia, often accompanied with dyspareunia, impotence, and sometimes urinary incontinence. So diagnostic testing can be done, and this is what it might look like under MRI. Here's an ultrasound. Here's an image of the ischial spine, and you can see the nerve right here by the ischial spine. There's the pudendal nerve right there. So management, minimize the pressure on the nerve. So either looking at the, the bike fits, changing the, adjusting the riding position, perhaps changing a bike to a bike, bike seat that takes the pressure off of the, the ischiorrectal fat, maybe it may be advisable. And then finally, corticosteroid injections, hydrodissections can be very useful, and surgery or ablation if all else fails. All right, two more big groups of nerves, and then we're done. So the peroneal nerves. So the peroneal nerves start off life as a, as a part of the sciatic nerve, and the sciatic nerve travels down the thigh, just deep to the biceps femoris, and at the very superior aspect of that popatial space, the sciatic nerve splits, and the common peroneal nerve portion of it travels towards the fibula with the biceps femoris, and as it approaches the fibula, it then goes around the fibular neck, as you can see here. As it goes around the fibular neck, it actually goes through a tunnel called the peroneal canal, peroneal tunnel, which is formed by the aponeurosis of the peroneus longest muscle. As it goes around the fibular neck, it splits, and it splits into a superficial peroneal nerve and a deep peroneal nerve. The superficial peroneal nerve stays in that lateral compartment, just deep to the peroneus longest, while the deep peroneal nerve then basically continues in that same trajectory, pierces the intermuscular septum, and enters into the anterior compartment here. So with the superficial peroneal nerve, it stays in that, in that lateral compartment, traveling from proximal distal, posterior to anterior, until about the mid, mid-leg, or perhaps the junction between the middle and distal third of the leg, where it pierces that fascia to go subcutaneous. While it's in the lateral compartment, though, it innervates all the muscles in that lateral compartment, and then here you can see it's piercing that fascia, leaving that neural hiatus right here, and it further divides into the medial and intermediate dorsal cutaneous nerves at the foot. Well, this division sometimes can happen a little bit more proximal, and if that happens with, if this divides while it's still in the compartment, each of these branches will leave through its own neural hiatus, and I mention that because each of those neural hiatus fascial openings is a potential site for entrapment. Deep peroneal nerve, once it gets into the anterior compartment, it basically moves from lateral to medial of the anterior tibial artery, and it does so, that, that shift from lateral to medial happens right over the anterior ankle, right deep to the extensor retinaculum, and we call that the anterior tarsal tunnel, so you can get entrapment of the nerve there as well and get anterior tarsal tunnel syndrome. As that nerve goes into the foot, it divides into a lateral branch and a medial branch. Lateral branch innervates a couple muscles in the foot, while the medial branch then makes a b-line going over the lisfranc ligament to the skin of the first web space. So patients can entrap these nerves, and superficial peroneal nerves are really common when, if it's a neuropraxia that we see in sports, often due to overly tight ankle lacing or taping or, or bracing, you can get entrapment of that nerve. You can also get entrapment of that nerve by, by fibrosis at the neural hiatus, which is right at about eight to ten centimeters above the lateral malleolus. Patients will get symptoms radiating along, along that superficial peroneal nerve, anterior lateral leg pain, symptoms in the dorsum of the foot, get a positive tunnels over that nerve. Deep peroneal nerve is a little different in that it's going to be, depending on where you entrap it, so if you get a more proximal entrapment of the deep peroneal nerve, you could conceivably get foot drop. So if the nerve gets entrapped, say at that inner muscular septum that we talked about, right after it bifurcates from the common peroneal nerve, you can actually get foot drop because it innervates all the muscles in the anterior leg compartment. However, if you entrap the nerve further down by the ankle, you may have entrapped it after it's already innervated the muscles and you may not get as much of a foot drop, but you can get pain that radiates onto the dorsum of the foot. And then of course, you can get entrapment down by the Lisfranc ligament as well. So you can make the diagnosis by a positive Tonelles and a clinical diagnosis. And then if you have common peroneal nerve entrapment, you can get a positive Tonelles by the fibular neck, perhaps just behind the fibular head, and or you'll see symptoms of both superficial and deep peroneal neuropathy. So you'll see, for example, foot drop, tripping over the toes, etc. Diagnostic testing, here's some pictures. On the left side, you can see an ultrasound looking at that superficial peroneal nerve from distal to proximal. Here's the nerve as it goes through that fascial hiatus, there it is going into the lateral compartment from distal to proximal. On the right side, you can see a long axis and a short axis image of a very swollen deep peroneal nerve by the ankle. In the middle, you can see an MRI mid-leg showing the placement of those nerves, both in the anterior compartment and the lateral compartment. And then treatment-wise, you want to avoid all that tight taping and bracing. You try medications, nerve glides, which is demonstrated here on the slide. And then orthoses, especially if they have foot drop or trouble ambulating. Injections, hydrodissection, or in this case of this lower left-hand corner, surgical decompression. And the last nerve attribute we'll talk about is the tarsal tunnel syndrome, and this is really analogous to carpal tunnel in the in the wrist. It's compression of the tibial nerves or its branches, and it's prone to metabolic insults as well as footwear mechanics. People will have pain and symptoms along the medial ankle to the bottom of the foot and plantar arch, the ceiling burning, worse with weight-bearing, so that's a clue. You can get a positive to NELS here. And then as far as testing, you know, you can certainly get diagnostic testing with MRIs, EMGs, but ultrasound can be helpful, but it's primarily a diagnostic, a clinical diagnosis. Treatment, physical therapy, we're working on foot mechanics, footwear adjustments, perhaps orthoses, and then injections and hydrodissection as shown here can be particularly useful. You can certainly release, you can do a tarsal tunnel release, which can be done percutaneously or surgically. So all right, now we got a couple of pop quiz shots, and then we should have, I'll be ready for some Q&A. So all right, the first question, and I think Andy's going to have a little survey for you guys to participate in if you'd like. And so I'll read the question to you guys. It's basically, let's see here, 50-year-old male, right medial knee pain six months after sustaining an injury while playing rugby. He was diagnosed with a medial meniscal injury, had arthroscopic debridement for it. He recovered uneventfully, but it didn't really help his medial knee pain. He describes it as sort of an aching burning, radiates to the anterior medial aspect of the foot and to the dorsal medial ankle and foot. It's worse when he has a laptop on his lap, and he's just not getting better. So he's asking for the next diagnostic step here. So I'll give you a couple seconds to try that. Try your hand at that, and let's see what we got here. Oh, did I lose that? What happened? Okay, give me a second. Okay, where is? Okay, there we go. Okay, all right. So the answer is answer C. They're trying to drive you towards looking at the saphenous nerve, and it looks like everybody did well there. Okay, next question. 67-year-old woman, persistent foot drop after a fibular head fracture from two years ago. What do you prescribe? Let's give that a shot here. Okay, let's see how people did. So if you chose, yes, everybody chose B, which is your AFO or ankle foot orthoses, so that's good. All right, next one. 20-year-old male soccer player, four months of right groin pain, deep ache just to the side of his pubic bone radiates down the medial thigh while he plays soccer. He's got some paresthesias in the medial thigh as well, especially when he's being active. He's got some weak hip adduction. You decide to order an EMG, which shows a denervation pattern to his adductor longus and brevis. So which nerve do you suspect? So if you chose A, looks like most people got this one right as well. So A, operator nerve, then you were right. All right, we have a 42-year-old cyclist, amateur cyclist, decided to increase his training to compete in 100 miler. He began suffering numbness, tingling in the peroneal and penile area. He's got some erectile dysfunction as well. Which nerve is associated with this sensory dysfunction that he's presenting with? So hopefully this one should be fairly obvious, and 100% of you guys got that right as well. Okay, and of course that is our favorite feudendal nerve. So with that, I thank you for your attention. I know I covered a lot, but I hope it'll be useful for you, not just as you prepare for the CEQ and the boards, but also as you serve your patients in the future. So with that, I will take some questions. All right, Gary, thank you so much. Okay, oh actually, we have a question already. So regarding seeing structural changes of nerve injury and ultrasound, what is the earliest time when we can expect to see these changes? Oh, that's almost a loaded question. I love to say that. I love talking about this. So thank you for the question. The question, as I understand it correctly, is when we look at using ultrasonography, neuromuscular ultrasonography, looking at changes for treatment neuropathy or peripheral neuropathy, what is the earliest that we could see it? You could see it very early. You could see it at the onset of symptoms. You might even see three more grid changes, and this is where it's kind of interesting, is that sometimes people will actually exhibit pathologic changes in their nerves before they get symptomatic, and we'll come across that because I'm in the habit of often not just assessing the nerve that I'm suspicious for before I do a procedure, but assessing kind of all the nerves in that limb, and sometimes you'll see other nerves that show pathologic changes that are pre-clinical or pre-morbid. Now, whether or not that is something that'll become symptomatic or not, it's a little difficult to say, and I think that there's some studies that suggest that some nerves in some people are actually, when they're a little bit pathologic looking, a little bit of swollen, that it might actually be normal for that person, but yeah, so the answer is it can be very early. So the key here is to put the clinical picture together, and I like to say that when I teach fellows that you aren't sonographers, you are sonologists, meaning that, you know, you don't get to turf clinical correlation. You are the clinical correlation, so you do both, and it's really that your clinical acumen and what's between your ears that are, that makes ultrasound more useful. So yeah, the short answer is it can be very, very early, maybe even before symptoms arise. Awesome. The next question is, what do you use, what makes you help decide between using a hydrodissection of an entrapped nerve versus a steroid injection? Oh, that's a great question. So they don't actually, you don't have to choose between the two, you can actually use both. So when people ask me, so there's two answers to this question. So the question is, how do you decide between hydrodissection versus steroid injection? And hydrodissection is a injection technique, and if we're talking about the procedure, and the steroid is something you would consider putting in the injectate. So in some patients, you could choose to put steroid in your hydrodissection solution, so you can do both. So that's one way to kind of answer it, is that you don't necessarily have to choose. But the other aspect, the other way the question could be framed is, when do you do a actual adhesiolysis hydrodissection versus just a perineural hydrodissecting block? Okay, as my nurses used to call it, a mini hydrodissection, because they're all perineural hydrodissecting type of procedures anyways. And I think that the way I decide to do it is that, you know, if it's, you know, if it's early on in the disease process, perhaps the patient wants to try some conservative measures first, and but they're interested in an injection as an adjunct, then I might use it earlier on while using a smaller volume perineural hydrodissecting injection, perhaps with some steroid. But if they fail, or if they're, if they've already had it before, and they need a much wider segment of the nerve freed up from adhesions, then I'm going to be doing the adhesiolysis hydrodissection. And I may or may not add steroids to that. And a third part to that question would be why use steroids versus just fluid, right? And that's a good question. And when you compare them head to head with just steroids versus just something like 5% dextrose, is that the 5% dextrose actually does better alone than with anesthetic and steroid, but the combination hasn't been studied. So there are some biological reasons to add steroid, you might want to consider it to be anti-inflammatory, quote unquote, or probably more likely as an adjunct to extend the block of the anesthetic to reset the nerve. But anyways, hopefully that answers that question. Yeah, that was great. When you decide to use the hydrodissection adhesiolysis, how long would you expect for your patient or your athlete to take before they start to see improvements in their symptoms? Well, that's great. It's a great question. So the question, thanks for that question. The question is how soon after a hydrodissection, and I'm assuming adhesiolysis, the bigger hydrodissection, can you see results? And it can be very early or can be delayed depending on the case. The case, the factors can be the degree of compression, the amount of scarring, the chronicity of it, what type of sequelae, whether it be muscle atrophy or denervation changes. So all those will factor into the prognosis as to the response to your treatment. So it can be a little longer, but it can also be practically immediate as well. You know, how would you assess that? And that would be if you choose to put no anesthetic in your hydrodissection solution and just do D5, where you would not get a motor block, you might actually see results right away. Now, the question is, do the results actually last? And that will also be highly variable depending on the same factors we talked about. But it can be early or it can be delayed depending on the case. To kind of follow up with that, what frequency would you consider repeating your injection if you aren't seeing the results you expected based off of the adhesional lysis? That's a great question. So what frequency can we consider to repeat that? And I think we're going to take it by a case-by-case basis. I like to see them pretty soon though. And usually three or four weeks is usually when I'll see them in follow-up. And that gives me a good opportunity to look at, you know, to see what their response was to the procedure, not just their immediate response, but in their response in the days and the couple of weeks following the procedure. If they had a really good response and at three or four weeks their response is holding, you know, and the response is adequate, meaning they've got significant improvement, say like 80% improvement, I might choose not to repeat it then. But if the response is suboptimal, I might consider repeating it at that time. You know, and I might follow them out to eight weeks and see how it is. And at some point if the 80% starts to drop, I might consider repeating it then as well. But I would say as early as three or four weeks. There are occasionally cases where I will do it every two weeks. And it depends on their previous response. But for most patients, I think in a few weeks after you can repeat it. Perfect. Can you talk about the utility of epidermal nerve fiber density in the workup of neuropathy, both in the lower extremity and just in general? Yeah, absolutely. So the question is, you know, what is the utility of epidermal nerve fiber? You know, basically it's a biopsy study looking at skin, looking for small fiber neuropathy. And it's usually when you have a hard time making the diagnosis. And perhaps your EMGs aren't particularly helpful. You know, your diagnostic images aren't particularly helpful. And that doesn't mean negative. Sometimes it's wildly positive. It's just that it's so positive, you can't tell what's real and what's not. And so whether that, you know, that can be something to consider. And what that is, is you would basically get a small sample from the skin and be able to send it for pathologic studies, looking at the small nerve fibers that go to the skin and look for very subtle changes, pathologic changes in the nerve from a pathology, pathological slide perspective. Sometimes you may need to biopsy the area that you're suspicious for in a control area as well. This is not done that frequently, thank goodness, because as time has gone on, our sophistication with our techniques can be, you know, have allowed us to help make this diagnosis. The other thing to also consider, some people may choose to do a therapeutic trial of a hydrodissection before going with testing for small fiber neuropathy, because it's an extra step and requires another procedure and risks. And if you're going to end up needing to do hydrodissection anyway, which is arguably more or less risky with just 5% dextrose, some people choose to do that. So it's a very shared decision-making process. The other, the last thing I'll say, I'll comment about the utility of looking for small fiber neuropathies in the skin is when people have metabolic neuropathy and you really, you know, you're having a hard time telling, are you having a peripheral nerve entrapment or is this just diffuse metabolic peripheral neuropathy, which is a little bit beyond today's scope. They may still benefit from targeted treatment to peripheral, individual peripheral nerves, but it also helps with prognosticating for expectations from the patient. Awesome. All right, next question is, can you touch on medial entrapment of the saphenous or the obturator nerve in a patient who has had a total knee replacement? And they want to know, would you perform a hydrodissection proximally in the subsartorial plexus or distally along the knee running the risk of an interarticular injection and possible infection? So I'm seeing, I just pulled up the chat and I know this person, and thanks for the questions. So if I could understand the question is to discuss my approach to medial entrapment of the obturator and saphenous nerve post knee replacement and would I perform it in the subsartorial plane? I think the first thing is making a good diagnosis post knee replacement. You can get irritation of nerves and adhesions of nerves that have nothing directly to do with the implant. And in those cases, I would go with what nerves seem to be producing the most symptoms, which I think is what the person posing this question is asking. So I would sonopalpate, sonopercuss, or tenils over the suspected nerves. That's one way to assess things. Obviously look for pathologic changes under ultrasound, but you may not be able to find discrete, obvious sonographic changes or even changes on EMG. But if you get a positive tenils, you might consider going after that with a hydrodissection. So yeah, I would, you know, if they're symptomatic in the subsartorial plane with that, with the plexus and the saphenous obturator nerve, I'll go after it. And I'll go after all the little other branches that Barry and I have discussed many times before. But the other thing also, though, is that you want to make sure you look and see if there's any impingement from the prosthetic itself or any kind of mass effect from soft tissues because of the prosthesis. And if that's the case, you want to target those as well. But yeah, it's a bit, a combination of art and science, but those are the two different scenarios. I hopefully have answered that. Yeah, I think that was great. I'm not sure if anyone else has any additional questions to ask, but we really, really appreciate your lecture this evening. It was wonderful, learned a lot, and I don't know if you have any parting words you'd like to share with us or anything for that matter. Well, thanks a lot for the invitation. I really enjoyed it. I think a lot of great questions. It was good to see some familiar names on the chat as well. For those watching this after we've recorded, I hope you enjoyed it as well. And thanks a lot, Julie. Thanks a lot, Andy. And look forward to seeing everybody next year at AMSSM as well.
Video Summary
In this lecture, presented by Dr. Gary Ho and moderated by Julie Creech-Organ, peripheral neuropathies of the lower extremity in sports medicine are discussed. Dr. Ho, with extensive background in family and sports medicine, elaborates on diagnosing and treating these neuropathies, serving as an adjunct educational resource for fellows, while aiding CAQ board preparation. The lecture touches on the differential diagnosis of neuropathies, from the anatomy and pathophysiology to specific lower extremity cases like entrapments involving the ilioinguinal, obturator, and saphenous nerves, among others.<br /><br />Key teaching points included the differentiation between neuropraxia, axonomesis, and neurotmesis, crucial for evaluating nerve injuries' severity and prognostication. Ultrasound and EMGs are highlighted as diagnostic modalities alongside others, focusing on the importance of a thorough clinical exam and considering a patient's overall metabolic health. Dr. Ho introduces the five Rs—rest, relieve, rehabilitate, release, and regenerate, emphasizing non-operative treatments like nerve hydrodissection and orthobiologics as viable therapies.<br /><br />The lecture also covers nerve glide exercises, appropriate diagnostic tests, and when to consider surgical options. Throughout, Dr. Ho stresses the relevance of understanding the biomechanics of nerve injuries and noting symptoms often mimicking other conditions. He illustrates these points with videos, images, and case studies, providing a comprehensive overview of the treatment and management of sports-related peripheral neuropathies.
Meta Tag
Edition
3rd Edition
Related Case
3rd Edition, CASE 04
Topic
Ankle
Keywords
3rd Edition, CASE 04
3rd Edition
Ankle
peripheral neuropathies
lower extremity
sports medicine
Dr. Gary Ho
diagnosing neuropathies
nerve injuries
differential diagnosis
ultrasound
nerve hydrodissection
nerve glide exercises
biomechanics
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