My name is Daniel Simmons, I'm a neurologist and clinical neurophysiologist out of Boise, Idaho. That's my health system right there, St. Alphonsus. I'm always looking for good people, so if anyone is interested in Boise, it's a great place to live and work. We'll be talking about basic nerve connection physiology and different anomalies, and this series of talks actually grew out of some whiteboard chalk talks that I used to give to technologists when I was in academics. We had trainees coming in every few months. The goal is to kind of move from algorithmic thinking to more of a nuanced, conceptualized thinking to help you plan your nerve conduction studies and understand what am I supposed to be seeing and what's axonal versus demyelinating versus conduction block from a conceptual level and not just trying to remember, okay, if the proximal is down and the distal is up, then that's conduction block. So hopefully we do that today. The first part of the talk will be about that portion, basic nerve connection physiology. Then we'll look at some anomalies, and then we'll do some cases. So I'm joined today by my colleague Morgan Jordan. Dr. Jordan trained where I did at the Brick Army Medical Center in San Antonio. We both had seven years there, and Dr. Jordan is now a neuromuscular fellow at University of Florida in Gainesville. So I'll invite her up, and we'll get started. Hi, everyone. This is a little bit high for me. Thanks for coming so early in the morning on the last day. Okay, so I'm going to do the first part, and then I'll hand it back over to Dr. Simmons. And I do just want to thank him for inviting me and also give him credit because he created these slides, and these slides are what taught me nerve conductions. So they're amazing, and I just want to make sure that everybody knows that it was him and that I'm not this talented with PowerPoint and things. So we'll start with big picture nerve anatomy. So I think we all know the center of the nerve is called the axon, and the axon is responsible for conduction or transmission of the nerve signal. The axon's surrounded by the myelin, which can be thought of as insulation. So really what it does is it helps speed the conduction along. So it helps with efficiency of the signal that's being sent down the nerve. A bunch of nerve fibers together are called a fascicle. And then when you have a bunch of fascicles together, we call it a nerve. You can have sensory fascicles and motor fascicles together, and we call that a mixed nerve. And you can have all sensory fascicles together, and that's a sensory nerve. When you have all motor fascicles, that's called a motor nerve. So with a sensory nerve, it starts with a sensation in the limb. So that signal from the limb gets transmitted up the nerve towards its final destination where it's perceived in the brain. With a motor axon, it starts with the planning of motor movement in the brain, and that signal gets sent distally where it results in movement of the limb. So when we set up our nerve conduction studies, we take our stimulator and we send a current down a nerve. So whether it's a motor nerve or a sensory nerve, that signal gets transmitted in both directions. So if we're going to set up a motor nerve conduction study, we'll take a motor fascicle. And you can see we have about five axons there that are surrounded by the dark blue myelin. So that's going to be how it's depicted for the rest of the presentation. And we're going to record the signal distally. So we set up our recording electrodes on the muscle belly. So we'll take our stimulator and we send a current down the nerve, and you can see that the signal goes in both directions, but we're recording distally in the muscle. So that recorded response is called a CMAP, or a compound muscle action potential. And what that is is it's really a summation of all the axons that we stimulated in that motor fascicle. So this is why you want to make sure you're super max when you're doing your nerve conduction studies, because you want to stimulate all the available axons that are in that fascicle. So when we do our sensory nerve conduction studies, we're stimulating a sensory nerve, and we typically use our ring electrodes to record. We send the current down the nerve with our stimulator, and the response that we record is called the SNAP, or the sensory nerve action potential. And similarly, it's a summation of all of the axons that you stimulated. So now that we talked about what normal looks like, we'll go into the different types of nerve injuries, and we'll start with axonal. So like I said, the CMAP and the SNAP are a summation of all the axons that you stimulated in your nerve conduction study. So the size of that response is reflective of the number of axons that were available, and size is measured in amplitude and area. So if you lose axons, you're going to see reduced amplitude and area. Malarian degeneration is the process of degeneration of the nerve that occurs after you injure an axon. And that occurs in both directions, and it occurs all the way down the length of the nerve. And that process takes three to ten days, depending on whether it's a motor fascicle or sensory fascicle, and how long the nerve is. So in an axonal injury, we assume that the myelin is normal and healthy. And like I said, the myelin helps with the speed of the transmission. So if the myelin is healthy, and you have a pure axonal injury, you're going to have normal conduction velocity and latencies, and those are how we are measuring speed in our nerve conduction studies. So say we have an axonal injury of a motor nerve, it's a mid-segment injury, we'll get malarian degeneration that occurs in both directions. So after ten days, the malarian degeneration has been completed, and we can set up our nerve conduction studies. We'll stimulate distally, and we record the signal, and that's the CMAP, and you can see we've lost 80% of the axons. So the CMAP amplitude is reduced by 80%. We'll move to our proximal stimulation, and we still only have that one remaining axon, so similarly, the amplitude is reduced by 80%. And we have normal myelin, the myelin of that one remaining axon wasn't injured, so we have normal distal latency and normal conduction velocity. So say we have a distal injury, we'll have malarian degeneration that goes down the whole length of the nerve, and then in ten days, we'll do our nerve conduction studies. When we stimulate distally, we still only have that one remaining axon available, so we have the reduction of the amplitude by 80%. When you stimulate proximally, same thing, you only had one remaining axon, so you have a reduced amplitude, again, 80%, and the conduction velocity and latencies are normal, and this is why you can't localize an axonal injury. It involves the whole length of the nerve after you have malarian degeneration, so you can see when we stimulate distally, reduced amplitude, proximally, reduced amplitude. So one more example here, if we're going to cut the nerve very proximally, you're still going to get malarian degeneration, that involves the whole nerve, so we'll do our nerve conduction studies again, we'll stimulate distally, as you can imagine, 80% reduction in the amplitude, we'll stimulate proximally, an 80% reduction, the myelin was healthy and intact, so we have normal distal latency and conduction velocity. So to recap, if you injure the axons, you're going to have reduced amplitude and area, and that's going to occur along the whole length of the nerve because of malarian degeneration, and you're going to have normal conduction velocities and latencies, or maybe slightly slow. It's a common misperception that any slowing is due to primary demyelination, but in fact, you can have mild slowing from a pure axonal injury, so we'll try to explain why. So I said we were stimulating a motor fascicle with individual axons, but each of those axons actually have their own individual properties, including their max rate of conduction. So say we have a CMAP, which is the compound muscle action potential, like we said, it's the summation of all the individual axons. So you can see they're all represented somewhere along this waveform, and the onset latency, which is used by the computer to calculate conduction velocity, is really only representative of the fastest firing fibers. So if we have an axonal injury that injures 80% of our axons, but we're left with only the fastest firing axon, you can see that our onset latency and our conduction velocity is going to be very normal. But what if we injure all of the fastest firing and we're left with the slowest firing? You can see that it still falls within that, where that CMAP would be, but your onset latency is pushed back quite a bit, so it's going to be mildly slow. It's going to show up as red on your machine. So axonal loss can cause mild conduction velocity slowing. But what's considered mild? Typically we say not less than 75% of the normal values. So in the upper limbs, if it's less than 38, in the lower limbs if it's less than 30, assuming normal temperatures, then you can assume this is a demyelinating injury, pure demyelinating. But if it's kind of in this intermediate range, it could be just an axonal injury, but it could also be demyelinating, so you can't really say for sure. So this chart is kind of helpful when looking at your conduction velocities to kind of reference back to. Yeah, all of these could be trauma and injury because you can have a partial dissection of the nerve. Yeah. So this, we would see this. No, no. You don't know. We don't have a way to say for sure. But this is just saying that you can have a range of conduction velocities that could be due to solely an axonal injury. So we don't know if it's the fastest fibers, if it's the slowest fibers. We don't know what piece of the nerve or what those, the individual axons that are left, we don't know what those properties are, but if it's within that range, it could be just axonal. Does that kind of make sense? Yeah. All right. So recapping again, axonal injury causes reduced amplitude and area, and that's along the whole length of the nerve, mildly slow or normal conduction velocities and latencies. And remember that it takes three to 10 days before our Eulerian degeneration is complete. So what happens if we do our nerve conduction studies before it's complete? So say we have a mid-segment injury, but we only have a little bit of Eulerian degeneration, so it hasn't affected the length of the nerve yet. And we're going to do our nerve conduction studies at 24 hours because we were asked to. So say we stimulate distal to the site of the injury. From our stimulation point to where we're recording, everything is intact still. So that's going to look normal. When we stimulate proximal to the injury, we have to bypass this area of axon loss. So you're going to see the reduced amplitude by 80%. Conduction velocity and latencies are normal here. And we call this pseudoconduction block. And we'll talk about conduction block in a little bit, but that term pseudo means not really conduction block, but it can look like conduction block. So how do we tell the difference? So what do we do in this situation? You have to repeat the study after 10 days. So allow enough time for Eulerian degeneration to occur, and then you can prove whether or not this is conduction block or was this an axonal injury. Ideally you wait 10 days before you do the study, but we don't always have that option. That's what we have for axonal injury, so now we'll move on to demyelination. So remember myelin is the insulin, or not insulin, insulation. So it helps with the speed of the conduction of the nerve. If you lose the myelin, it makes sense that you'll have slowed conduction velocities and latencies. That's how we're measuring speed when we're doing our nerve connections. The amplitude and area are normal. The axon is intact. If it's an area of focal demyelination, you can use your nerve conduction studies to localize the lesion, which is different than the axonal injury that we just talked about. So I showed this picture earlier where the signal is sent distally and travels up the nerve, but that's not exactly how the signal gets transmitted. So myelin actually surrounds the axons more like this, where it's separated by these nodes where the ion channels live, and the signal actually jumps from node to node, and that's what allows for this efficient transmission of the signal. If you have demyelination, you lose that ability to kind of bypass a large chunk, and it goes very slow down the nerve through the area where there's no myelin there. So let's look at some examples. Say we have a mid-segment injury, and this is a demyelinating injury, so you can see kind of where that dark blue myelin is missing there, but the axons are intact here. So if we stimulate distal to the injury, you can see that everything distal to where we stimulated was normal, so the latency is normal, the amplitude is normal. When we stimulate proximal to the injury, we have to go through that area of demyelination, and you can see how things slow down there. So that's represented by our conduction velocity, and remember your conduction velocity is calculated based on your distal site and your proximal site. So in order to see that slowing, you have to be able to sandwich the injury like we were able to do in this picture. So examples of this are a fibular nerve injury at the knee or an ulnar neuropathy at the elbow, which we see quite commonly. So imagine a distal demyelinating injury. If our most distal site is still proximal to that injury, we'll still have to bypass that area, and you can see it moved very slow there, so our distal latency is going to be prolonged, amplitude's normal. We'll stimulate at our proximal site, and you see we still have to go through that area of demyelination, so the signal did take longer to get through, but our amplitude's normal and our conduction velocity's normal, and again, that's because the conduction velocity is calculated from our distal site to our proximal site, and between those two areas there was no injury. Example is carpal tunnel. In carpal tunnel, your most distal site of stimulation is commonly more proximal to where we expect the injury to be where the carpal tunnel is. So say we have a proximal injury. Our distal site did not have to bypass any injury, so everything looks normal, and say our most proximal site is still distal to the injury, and everything distal to that site is normal, so our conduction velocity's normal, amplitudes are normal. So this does occur, and the common examples are multifocal motor neuropathy, where your demyelination and conduction block is often very proximal and more proximal to where we typically stimulate with our nerve conduction studies, and early Guillain-Barre syndrome, which typically starts at the nerve root. So to recap, myelin helps with the speed of transmission, so you lose the myelin, you have slowed conduction velocity and prolonged latency. Amplitude and area are normal, because that's representative of the axons, and if it's focal, you can localize the lesion with your nerve connection studies. So you can see in demyelination, it causes the slowing of the signal, because we don't have the ability to kind of bypass that area of myelin. But sometimes, things can slow down so much that the signal stops moving through. It just kind of leaks out or is blocked, and we call that conduction block. So what conduction block is, it's due to demyelination, but it causes a failure of transmission, so it acts like fewer functional axons. The axons are not actually injured, but the signal's not passing through. So because of that, we are going to get reduced area and amplitude proximal to the lesion, and the key here is that you have to stimulate proximal to it in order to see this reduction in amplitude. Because the axons were not injured, there's no valerian degeneration, so it's not going to be seen at all sites of stimulation like you would in an axonal injury. So some examples, so say you have a mid-segment injury, this is a demyelinating injury, but there's conduction block. So you stimulate distal to the injury, everything looks good, your distal latency is normal, your amplitude's normal, and you stimulate proximal to the injury, and you can see things slow down, and 80 percent of the signal did not make it through, and that's conduction block. So you can see the conduction velocity is slow because that slowing was in between our distal and proximal site, and then we also have that reduction of amplitude by 80 percent because 80 percent of the signal didn't get through. So this is kind of the picture that we just showed for demyelination with conduction block, and if you'll remember, it looks exactly the same as the one that we showed with acute axonal injury, which we called pseudoconduction block, and we said repeat the study in two weeks. So after two weeks, the demyelination with conduction block is going to look the same. You'll still see the reduction of the proximal amplitude, but with an acute axonal injury after two weeks, you've allowed time for valerian degeneration to occur, so you're going to have that reduced amplitude at all sites of stimulation. So say you have conduction block with a distal injury, and this injury is more distal than your most distal site, so you have to stimulate there, and then you're going to see the latency was slow because it's demyelinating injury, and then you also didn't get 80 percent of your signal through, so the amplitude is reduced by 80 percent. When you stimulate proximally, you have that same area of conduction block, so still only 20 percent of that signal is getting through, so you're going to have the reduced amplitude, but your conduction velocity is going to be normal because you weren't able to kind of sandwich that area of injury. So we see this in carpal tunnel syndrome, right? So your most distal site is more proximal than the injury. So what can we do in these cases? Ideally, you would stimulate proximally to that, and sometimes that's possible and sometimes it's not, but in carpal tunnel, you can sometimes stimulate in the palm, and this looks like an acute or a non-acute axonal injury, right? So you're seeing that reduction in amplitude at all sites, but that's because of this functional loss of axons, right? You can't get the signal through, and the way to prove that is to then stimulate proximally here. So there you were able to stimulate more distal to the injury, and you see that normal amplitude. If it's an axonal loss, valerian degeneration has affected the entire nerve. You're not going to be able to have that normal amplitude. So recapping, conduction block is due to demyelination, and it's essentially a failure of transmission. So it will look like fewer functional axons, but if you are able to stimulate distal to the site, you'll see that normalization of the amplitude there. What about sensory conduction block? This one's a little bit trickier, because snaps are smaller than our C-maps, and they're more prone to temporal dispersion and phase cancellation, which are normal and physiologic, but makes it harder to say is this conduction block or not, especially if you're looking over a long segment like this. So if you stimulate your C-map at the, or your snap at the wrist and elbow, you may see this reduction in the amplitude, and that could be normal. So if able, if you're able to stimulate closer together, you may be able to see some sensory conduction block, and the example there is in carpal tunnel syndrome, if you can stimulate at the mid-palm compared to the wrist. You may see that normalization of the amplitude if you're kind of past that site of injury. So to summary, axonal injuries cause reduced amplitude. It occurs along the entire site of the nerve. So anywhere you stimulate, you're going to see that reduced amplitude. Conduction velocities and latencies will be normal, or maybe mildly slow, and if you do your nerve conduction studies before 10 days, it may look like conduction block. Demyelination is going to cause slowed conduction velocities and latencies, so our measures of speed, but our area and amplitude will be normal, and you may be able to localize these injuries with your nerve conduction studies, depending on where the site of injury is. And then conduction block, you will see a reduced area and amplitude if you're able to stimulate distally. If you stimulate proximal to the conduction block, you'll see normalization of the area and amplitude. So I'll hand it over to Dr. Simmons. All right. Thank you, Dr. Jordan. Let me go to my, let's see. Okay. So we've done this talk before. I revamped it a little bit. So hopefully if you've seen this before, you like the updates. We'll have more time for questions at the end as well. So feel free to ask them as we go or wait till the end, either way. All right. So I'll be talking about some common anomalous innervations. I say common here because there are tons of anomalous innervations and not all of them are relevant or useful. So we're going to be talking a lot about Martin-Gruber anastomosis because this is what you'll see. Without a doubt you will see this. We'll talk about the accessory perineal and then some other less common ones that are important to know about and sometimes quite questionably relevant but you can impress your attending or your trainees if you know about them. So I'm going to walk through some cases with you. This is a 60-year-old female with progressive hand weakness and these are her nerve conduction studies and this is a talk about common anomalous innervations. So you can guess what this is, I imagine, unless I'm trying to trick you, which am I? So what do we see here? Is this a Martin-Gruber anastomosis? It looks like one if you just looked at the waveforms. If you didn't take into account the history, the exam or any of the numbers, these waveforms could look like an MGA. But what do we see here? The latency is prolonged, the amplitude is reduced and there's some slowing. And remember this patient came in with progressive hand weakness. So what is this? Could be, yeah, could be multifocal motor neuropathy, could be that. Anybody else? Well, if you had entrapment at the elbow, I think the conduction block would be the next one down. So it should be between the elbow and below and above. That's a good thought. So I was going for CIDP here but MMN would work, would look the same. All right, so just to show you that this is not an MGA, if you get this pattern, most of the time it's going to be an MGA. But that clinical context matters. All right, here we have a different 60-year-old female with progressive hand weakness and these are what her nerve conduction studies look like. It's a little bit different. So what are we seeing here? We have this drop in amplitude, approximately, and we have some slowing across the elbow. So what is this? Ulnar neuropathy at the elbow with conduction block, right? Also progressive hand weakness. All right, so this is not an MGA. Now we have a different 60-year-old female with bilateral hand paresthesias. This is her study. Is this an MGA? I hear a vote for normal. I think that's what I heard. Normal. Are you worried about this, this drop in amplitude? It's one millivolt. It's pretty small. There's no change in waveform. There's no slowing across the elbow. So this is normal and you'll often see this with an ulnar motor study. They're just due to physiologic temporal dispersion. You'll see a loss of amplitude about 10% or one millivolt. If it's within that range, then I usually don't worry about it, but this is something you can see normally. Okay, we have another 60-year-old female with hand paresthesias. So I heard either Martin Gruber or MMN. Again, looking at the waveforms, you can't really tell. This could be a conduction block at the forearm. It could be a Martin Gruber. So we'll get into this, but you have that loss of amplitude. There's no slowing. So this is finally your Martin Gruber anastomosis. All right, so lots of things can look similar, and it's important that we know how to prove that it's Martin Gruber before we actually make that diagnosis. We don't want a misconduction block, but also that clinical context matters. All right, so the way that I remember Martin Gruber is that it's M to U, so Martin M Gruber with the U median to ulnar. That's how I remembered it in residency. That's how I remember it now. All right, so here's a schematic. We have the median nerve that goes to the thenar muscles and the ulnar nerve that goes to the rest of the hand muscles, hypothenar and thenar, and the intrinsic hand muscles. And then the Martin Gruber anastomosis are these crossing fibers that come from the median nerve and anastomosis with the ulnar nerve. All right, so this is something that you will see. It's a normal anatomical variant. It doesn't cause any symptoms. It can be clinically relevant in cases of like nerve transfer surgery or nerve injury, traumatic nerve injuries, things like that. But most of the time when we see it, it's not clinically relevant. It's just to, we just need to understand what we're seeing. It's only motor fibers, and the most common muscle is the FDI. That'll be the most common innervation pattern we don't always see it when it's in the FDI because we don't commonly record the FDI. Maybe you do routinely, but I don't usually unless there's a reason to. So it's the most common innervation. When you should suspect an MGA. So like I said, you can allow for about a 10% drop in amplitude between wrist and below elbow or about roughly a millivolt. So when we see more than that, you've either stimulated submaximally in the proximal region, you have co-stim distally, or there's conduction block, or you have an MGA. And that conduction block in the forearm is going to be pretty rare outside of CIDP and multifocal motor neuropathy. So when you're, when you're seeing this, most of the time it's going to be a Martin Gruber anastomosis. Okay, so there are three components that you need to take into account when you're trying to predict what you should see on a Martin Gruber to try to understand what these waveforms are telling you. Number one is which muscle is it innervating? Is it the FDI? Is it a thenar muscle like the adductor pollicis or the the flexor pollicis brevis, the deep head? Or is it a hypothenar muscle like the ADM? So the reason this matters is that we also have another set of muscles that are supplied by the median nerve, and depending how close you are, how far away you are, and where you're recording, where you're stimulating, that can factor into your waveforms. Okay, so the second factor is the stimulus location. Are you stimulating median at the elbow, median at the wrist, ulnar at the elbow, ulnar at the wrist? So all that will depend on what you see. And then the third factor is where am I recording? So am I recording APB? Am I recording FDI or ADM? All right, so we'll go through some of these permutations to talk through what we expect to see. All right, so for the first example our MGA is to the ADM. Now this isn't as common as the FDI, but for the first example those crossing fibers are supplying the ADM, and we are in this example recording ADM. All right, so what we'll see when we stimulate the ulnar at the wrist, we're stimulating both the crossed and uncrossed fibers, and so we'll get a larger than normal CMAP amplitude, or I guess I should say a normal CMAP amplitude that includes all those fibers. All right, when you come up to the below elbow site, we're no longer stimulating those crossing fibers. We're stimulating only a portion of those muscle fibers, and so we get a loss of amplitude. Same thing as we go above the elbow. All right, and if you notice this pattern, the way you confirm that this is a Martin Gruber anastomosis, you leave the recording electrodes where they're at recording ADM, and you go to move your stimulator to the median, stimulate at the wrist, and we shouldn't see anything here because we're recording hypothenar. There aren't any median muscles in the thenar and the hypothenar eminence, so we get no response. But when we go to the elbow site, we're now recording those crossed over fibers, and we should get a CMAP here. And if you notice, the amplitude of that CMAP that we get is roughly the difference between the CMAP, the ulnar CMAP, at the wrist and then below elbow sites. All right, so we still have our MGA to the ADM, but now we're recording APB and stimulating median. So what will we get here? Remember, we're recording median, thenar muscles. Our MGA is to the hypothenar eminence. When we move to the elbow, we're stimulating those crossing fibers, but we're not recording them. Okay, they're stimulating the ADM, and so we're going to see a normal study. We're not going to know that there's a Martin Gruber here. All right, now if we stimulate the, so we're still working with the same MGA, innervating the ADM. If we move our recording electrodes to the FDI, what will we see here? When we stimulate the ulnar at the wrist, we are stimulating those cross fibers, but we're not recording them. Okay, when we go up to the below elbow and above elbow sites, it's going to be normal. Okay, so now we have our most common innervation pattern for the MGA, where we're innervating the FDI. So if we record the FDI, what will we get? We're stimulating both crossed and uncrossed fibers. When you move up to the below elbow site and above elbow sites, we're no longer stimulating those cross fibers. We're just the uncrossed fibers, and so we get a portion of that CMAP. All right, so you'll get this typical Martin Gruber pattern. To prove that, here's the difference between the last one I showed you. When you stimulate the median nerve, you have a conduction. Remember, we have our, we're stimulating these thenar muscles, and those thenar muscles are going to be picked up by the FDI electrodes. So we get a small CMAP here, even though we're stimulating median, where those electrodes on the FDI are going to pick up a little bit of that. Okay, so we have a small CMAP. When we go up to the elbow site, we get a bigger CMAP, because now we're stimulating not only the thenar muscles, but also the crossing fibers to the FDI. And the difference between the two median stimulations is about 3.7. That should roughly equal the difference between those top two traces, all right, because you recover that amplitude. Okay, and this is the reason that we don't see Martin Gruber anastomosis in 15% to 30% of our nerve conduction studies, even though that's the incidence, because we routinely record the ADM, at least most people do when they do their ulnar studies. Okay, so this is still an MGA to the FDI, recording ADM. Now, we are recording both crossed and uncrossed fibers, but we're not recording those crossed fibers, because it's going to the FDI. It's too far away to record. All right, so we go up to our below and above elbow sites, and everything looks normal. We don't see the Martin Gruber anastomosis. Does that make sense? Now, when we record the APB with our median motor study, here's what we get. So, when we stimulate the wrist, it's only those median fibers uncrossed. We get a normal response here. Now, when we go up to the elbow site, we're stimulating both the thenar muscles through that uncrossed pathway, but also these cross fibers that go to the FDI are going to influence that CMAP, because they're close. The FDI is close to where you're recording. All right, so we're going to get a higher CMAP amplitude at the elbow. All right, so how do we prove this? I go down to the...we leave the electrodes over the median, over the thenar muscles. We move to the ulnar at the wrist, record, and now we're recording both the crossed and uncrossed fibers to the FDI. So, we're going to get a higher CMAP there. When we go to the elbow, we're no longer simulating those crossed fibers, and so that CMAP is going to go down, and the difference between those two should equal, roughly approximate, the difference between the top two. All right? So, this last situation is going to be very similar to what I just showed you, but just for completeness, we'll show you this is now an MGA to a thenar muscle, either the adductor pollicis or the flexor pollicis brevis. All right? So, this is recording FDI. You get that usual Martin Gruber pattern. All right? And then when you stimulate the median at the wrist, you'll get a small CMAP because you're stimulating those fibers, those thenar muscles. And because you're recording FDI, that's close to the thenar muscles, it picks that up. When you go to the elbow, you stimulate those crossed and uncrossed fibers, you'll get an increase in amplitude. It's exactly the same as when the MGA went to the FDI. When we're recording ADM and the Martin Gruber is to the thenar muscles, we won't pick it up. It'll look normal. All right? Now, for recording thenar muscles from the median, you will still see the same pattern that I showed you before with the FDI. It'll look the same. And we prove it the same way. All right? Okay. So, case five. We have a 60-year-old female, again, with bilateral hand parasthesias. This is what we get. So, how do you put this together? The distal latency is normal. There's a small drop in amplitude, and then there's a bigger drop in amplitude. But there's no slowing. The waveforms look reasonable. I mean, there's no change in the morphology. It's just smaller. So, what do you do with that? You think, it kind of looks like conduction block at the elbow, but the conduction velocity is normal. Check your measurements. It's still coming out as normal. So, let's say that this is a Martin-Gruber anastomosis. If you check for this, you stimulate median at the wrist, and then stimulate at the elbow, and you get a response there. So, what's happened here? Does anyone know? So, the question is, how... So, this is a Martin-Gruber anastomosis, and the question is, how are you measuring around the elbow? So, what I do and what I teach my techs is that you find the medial epicondyle, you measure to the olecranon or that angle of the elbow, you measure the 10 centimeters across, and you stimulate there. But what is your distance from the medial epicondyle to that distal site, that below elbow site? The optimal distance, according to textbooks and cadaver studies and anatomical studies, is three centimeters. Does anyone use three centimeters? One person. I use four. Anyone use longer than three or four? Two inches, so it's about five centimeters. Okay. So, this... Here's the reason why three centimeters is best. So, here's your median nerve, and if you have a really proximal Martin-Gruber anastomosis, those crossing fibers... So, anatomical studies have suggested that this really doesn't happen in less than three centimeters. It happens after. But the proximal Martin-Gruber anastomosis, it'll happen three centimeters or more. Okay. So, if you have this very proximal crossing and your distance is more like five centimeters, now you're incorporating those cross fibers into that below elbow segment or that stimulation. All right. And the result is that when you stimulate below the elbow, you're including those crossing fibers, so you can get a higher CMAP, and then when you go to the above elbow, it's lower because you have excluded those crossing fibers. All right. So, this can mimic conduction block at the elbow. So, if you ever have a situation like the one I showed you where it looks like conduction block, but it's not slow and you weren't really expecting it, check for the Martin-Gruber anastomosis, and consider if you're not using a distance of three centimeters or less than to change your distance. You can still use the 10 centimeters or however what the longer one is, you know, the one across the elbow, but you could bring it more approximately. All right. What was that? Yeah. So, the degree of elbow flexion should be between 90 and 130, something like that. Question? Can you sometimes have an axonal injury on or around the elbow without slowing? So, the question was, can you have a axonal injury at the elbow without slowing? And I think that would be really uncommon. I think you can have a axonal injury that is non-localizable because there's a diffuse degree of slowing, but I think it depends on the mechanism. If you have entrapment under the cubital tunnel, the humor ulnar arcade, you're more likely to get some axon loss and conduction block. If it's at the retrocondylar groove, you're more likely to have some more diffuse slowing. But to have axon loss alone without any degree of slowing, you just have normal conduction velocities, I think that would be pretty unlikely. But if that's your suspicion, then check for the Martin- Gruber, and at least you've proven that it's not that. All right. We have another 60-year-old female with bilateral hand paresthesias. So, you were probably thinking carpal tunnel syndrome, and you'd be right. The distal motor latency is 4.9, so it's prolonged. But a few things stand out to you. One is that this amplitude here is too high, and so you go back and check, and the waveform doesn't seem like there's co-stimulation, and then this velocity is too fast. We really shouldn't have anything above 75-ish physiologically, so either if you get this, there's either a measurement error, there's what I'm about to show you. And then you have this proximal positive deflection. So, the positive deflection usually tells you that the electrode is off the motor point for some reason. So, you really shouldn't have this unless you've moved the electrodes in between the distal site and the proximal site, but you haven't. So, this is a clue that this is what you see with a Martin-Gruber anastomosis with superimposed carpal tunnel syndrome. So, the three things you get are the higher amplitude proximal CMAP. You get that positive deflection with the proximal waveform, but not distal, and then you get this spuriously fast conduction velocity, and spuriously just meaning that it's an artificially fast. All right, so let's walk through this. So, this is a normal subject with a Martin-Gruber anastomosis, no carpal tunnel syndrome. When you stimulate the median nerve here at the wrist, you get your normal CMAP and normal distal latency. When you go to the elbow, you're now stimulating those crossing fibers, and we're assuming this is going to, let's say it's going to the FDI. All right, so you stimulate the median fibers to the thenar eminence, those thenar muscles, and then also to the FDI, and that's what gives you your higher CMAP. So, if you look at the tracing on the bottom, I've, in that blue dotted line, that's the FDI CMAP, and because it's not right under your electrode, you have this positive deflection, and then the CMAP from the FDI adds to the CMAP from the APB, and that's why you have a higher amplitude, but because those, because these are getting here at the same time, you don't see that positive deflection from the FDI. All right, so you miss it. It gets canceled out. You don't see it, and then the separation between these two onset latencies, the distal and the proximal onset latency, that's the time that it takes for that impulse to go that distance. Okay, so keep that in mind. I'll come back to that in a second. Right, so the question was, does the opponent's policies contribute to this? Yes, there's, when you're stimulating the media and you're stimulating the abductor policies, opponent's policies, and the superficial head of the flexor pollicis brevis. So all of those muscles contribute. All of those muscles, though, are right under your electrode. So those aren't giving a positive deflection, it's the FDI that gives you the positive deflection. All right, so when we have carpal tunnel syndrome, we have slowing across this segment, all right? So when we stimulate distally, we just have a rightward shift of our distal latency in our waveform, which intuitively makes sense, all right? When we stimulate proximally at the elbow, we have those crossed and uncrossed fibers, and the crossing fibers from the FDI reach the electrode before the median CMAP does. And so we get a rightward shift of the median CMAP, whereas the ulnar CMAP and its positive deflection stay the same. And so now we've uncovered this positive deflection. Does that make sense? And so that's why we see it, all right? So the two waveforms on the bottom summate, and we see them superimposed. Okay, so we have that positive deflection now. Okay, and then if you remember, the separation between those latencies reflects the time that it takes to travel that distance. Because the latency is marked the same here, proximally, but distally it's moved to the right, now that separation is less. And so that means there's less time to travel the same distance. Less time, same distance. That's calculated as faster, okay? So it's not truly faster, but because of the way that the latency markers are marked here, it's an artificially fast conduction velocity. All right, when you compare that to the previous one, you can see how there's a difference there. Okay, so hopefully that makes sense intuitively. All right, here we have another 60-year-old female with progressive hand weakness and numbness. These are our studies here. So how do you make sense of this one? So what do we see? Now, if you just looked at the waveform and didn't look at the numbers and you had the history, you could think this is a patient with CIDP, right? There's multifocal conduction blocks. You wouldn't want to make that mistake, though, because that's not what this is. So you notice there's a drop between the wrist and below elbow. So there's the appearance of conduction block in the form, but you remember this could be the Martin-Gruber anastomosis, which statistically is much more common. But then there's also another conduction block or the appearance of one across the elbow, and that is accompanied by this slowing across the elbow. So how do we resolve this? We check for the Martin-Gruber anastomosis. So we stimulate median at the wrist and then median at the elbow, and we get a C-map there when we stimulate the elbow representing those crossing fibers. And that 3 millivolt C-map is equal to the difference between the wrist and the below elbow site. So this is a Martin-Gruber anastomosis in a superimposed ulnar neuropathy with conduction block. Does that make sense? Now, one thing that we didn't see, so if this was CIDP, if you stimulate median at the wrist and elbow, you will not see this C-map here. Latency should be prolonged. You beat me to it. So latency should be prolonged, and then if you see conduction block, there should be some slowing associated with it. So you shouldn't have, in the context of CIDP or any other demyelinating neuropathy, you really shouldn't have normal conduction velocity and conduction block. So I said we talk a lot about Martin-Gruber. That was the end of the Martin-Gruber part of it. So you know that this is not a Martin-Gruber anastomosis. So what is this? This is a 55-year-old male with unilateral foot drop. So we look at his fibular EDB. I call this the perineal where I come from, but you can call it the fibular. These are his nerve conduction studies. I'll remind you this is a talk on anomalous innervations. So is this the accessory perineal nerve? So this is also my attempt to trick you. So what do we see here? There's conduction block across the fibular head along with some slowing. So this is not an accessory perineal nerve. This is not what you would see. The waveforms are not what you would see. Now we have a 55-year-old male with burning dysesthesias of both feet. We do the fibular EDB study. And this is what we get. So this looks different from the last one. In the last one, the proximal waveforms were higher, or the distal waveforms were higher and the most proximal was low. That's conduction block. This is the opposite pattern. The distal one is low. The more proximal ones are higher. So assuming that you're technically correct so that you're not submaximal or supermaximal, these are true waveforms. There's nothing physiologic that would give you this pattern except for anomalous innervation. All right. So what we do is we stimulate behind the posterior ankle, behind that lateral malleolus, and we see the recovery. We see that C-map there where there shouldn't be one usually. And I'll show you how this works. So here's our EDB muscle. And then the innervation starts with the sciatic and then goes to the common fibular, then the deep fibular, which supplies the extensor digitorum brevis, the EDB. Then we have our superficial fibular, which usually supplies the peroneus longus and brevis. And then in some cases you can have an extension of that superficial peroneal nerve to innervate a portion of the EDB. And that's what we call our accessory fibular nerve. So when we stimulate anteriorly where we normally stimulate, we're only stimulating a portion of the nerve or a portion of the muscle because it's dually innervated. And so we get a smaller C-map. When we go up to the fibular head, now we're stimulating both segments of the muscle. And so we get a larger C-map. Same thing when we go to the knee. So that's what accounts for that pattern. Now to prove it, you go to behind the lateral malleolus, stimulate what you think is there, the accessory fibular nerve, and you get a C-map there. And that C-map amplitude should approximate the difference between the distal site and the proximal sites. Okay. Now we have a 40-year-old female cyclist with progressive left-hand weakness. I don't want you to get too hung up on the clinical scenario here. I had to set something up where we have to check the dorsal ulnar cutaneous. So that's why I'm showing you this. But this is a ulnar ADM study. And you can see that there's some mild slowing. The amplitude is kind of diffusely down. It's not focal. There's some mild slowing across the elbow but also on the forearm, not really localizing for you. So then you do the ulnar digit 5, and it's kind of low. The latency is a little bit increased. Conduction velocity is slow. So the question then is, is this localizing to the elbow or the wrist? And based on these, you can't really tell. So we have a vote for wrist. That's possible. You'd think those latencies are pretty prolonged. But could that just be axonal slowing? Possible. So you check your dorsal ulnar cutaneous and try to resolve this. If the dorsal ulnar cutaneous, or DUC, is absent, then you think, well, that favors the elbow localization because the dorsal ulnar cutaneous comes off proximal to the wrist. So an ulnar neuropathy of the wrist should not involve the DUC. But then, so you do this. You don't get a response. And then the tech that you're working with is very savvy. And they recall something that if you stimulate the superficial radial nerve, maybe there's an anomalous innervation here. And that's indeed what happened. So I've seen this one time. And if I've seen it more than that, I've missed it. But this was actually picked up by my technologist. And I probably would have missed it. So the diagnoses here are an ulnar neuropathy. And I didn't go far enough to really localize it for you. But that wasn't the point of this. We have anomalous sensory innervation of the dorsum of the hand. So normally, the dorsum of the hand is applied by two different nerves, the dorsal ulnar cutaneous, which is a branch of the ulnar nerve, and the superficial branch of the radial nerve. So when you stimulate here, just by the ulnar styloid here, you should get the dorsal ulnar cutaneous response. But in some people, the entire dorsum of the hand is innervated by the superficial radial nerve. So you won't get a response if you're recording that and stimulating at the ulnar, dorsal ulnar cutaneous spot. But if you move across to the superficial radial, then you'll get a CMAV. So how common is this? Not really clear. One publication I saw said it's quite low. I don't know what that means. There was another study that looked at this and found it in four of 44 subjects. That's just about 9%. The reason we don't see it that often, I think, is we're not really doing this study a lot. We don't have a reason to most of the time. So best practice, if your duck is low or it's asymmetric or it's absent, it's really easy just to go over to the superficial radial nerve and stimulate. It takes two seconds. So just keep that in mind if you're not getting this study. I think this is the last case. We have a 65-year-old male with bilateral hand parasites involving digits 1 to 3 while driving. Sounds like carpal tunnel syndrome to me. And you do the median, and you don't get a response. So the first thing you do is you check your cables, right? They're plugged in, stimulator's working, not getting anything. And then you do your digit 2, and it looks like carpal tunnel. You have an intact response here, which surprises you because you have absent CMAPs. So normally in carpal tunnel, it's the sensory responses that are the first to go. So this surprises you, and then you do your mid-palm stimulation, and you have a completely normal amplitude here. So there's conduction block, but your snap amplitude is totally normal. CMAP is totally absent. So what's going on here? So what I'm showing you is an example of an all-ulnar hand. This is probably very rare. And if you look at the diagram there, you have our, in blue, you have the median nerves supplying the thenar muscles. You have the ulnar nerve in red. And then in between the two, it's a distal communication between ulnar and median nerves. And that is called the Ritchey canoe in ostomosis. And so when you stimulate your ulnar, you get a normal CMAP from the thenar eminence. And it's prolonged. All right, so the Ritchey canoe in ostomosis refers to any connection between the median ulnar and the palm. It's motor fibers prevalence up to 70%. Now, we are not seeing an all-ulnar hand in 70%, but some degree of communication based on cadaver studies or anatomical studies, 70%. Most of the time, that is not relevant to us, and we probably wouldn't pick it up. So the all-ulnar hand is thought to be very rare, but it's important to consider, in the case I just showed you, where you have your thinking carpal tunnel, absent CMAPs, but your sensories are intact. So anytime you have a low CMAP and intact sensories, you can think about this. Or if you have an ulnar neuropathy of the elbow and you see wasting of the thenar eminence, that's also a clue. Okay. So we have about 25 minutes, and I'll pull up some cases to go through with you. And I apologize for the temperature in the room. I know it's freezing cold. Let's see. I'm right there with you. All right. So I'll invite Dr. Jordan to come back up and go through some warm-up questions, and I'll do some additional cases after that. All right. So we'll do a few warm-up questions, and then Dr. Simmons will come up for the good stuff. So just to orient you guys, this is a radial-to-EIP study, and the normal values are listed at the top. So what's standing out to us here? Anyone can shout it out. What's that? Yeah, I think you're giving us an answer. What stands out as abnormal? Yeah, oh, yeah, yeah. CMAP. Yep. Good. So you're localizing it. I'm super impressed. But this is, yeah, what do we think here? What do we think the pathophysiology is? You said the CMAP amplitudes were reduced, right? Yeah, axonal loss, yeah. Because we see the reduced amplitude, the latency looks good, the conduction velocities look good and we see the reduction kind of along the, all of the sites that we stimulated. All right, so here's a, I call it a fibular, fibular to EDB. And again, normals are at the top. What do we see here? See slowing here? Yeah, very good. Okay, so what's the pathophysiology of this lesion? I heard a lot of answers. I'm sure someone got it right. Yeah, we see the slowing there. All right, median to APB study, what do we see? Right, yeah, the latency looks good, but we see that reduced amplitude here, so conduction block and any time you see conduction block, you want to make sure that you're, you don't have any technical errors. All right, here's an older to ADM study. Anything standing out? Conduction block. Yeah, and how did you know that? What made you suspicious for conduction block? Yeah, and then we can see the, mm-hmm, good. The other thing here, this is mixed and you didn't really see what the additional information with mixed was, but you'll notice that the, even the amplitude at the wrist and the below elbow was also low so you have some axonal loss there too, but with this degree of change here, you also have conduction block there. All right, so an older to ADM, anything stand out? Yeah. Good. All right. Okay. That's just to get you thinking, warmed up. Okay. So case one, these are, I used to have theoretical cases and I looked back through my records and I found some actual cases. So these are all real cases from the past year or two. So we have a case one with foot drop. So this is a 36 year old female with a history of a fracture of the right foot after a fall about four years previously. She wore a boot for several months and her pain got better. And then she lost about 50 pounds over about a year and a half. She started insulin for pre-diabetes and then three months ago she began to have some new pain and weakness in the right leg. And she had some uncomfortable paresthesias in the lateral lower leg and dorsum of the foot and some intermittent zingers, as she called them, from knees to toes, or from knee to toes. On exam she had difficulty dorsiflexing her foot and toes, dorsiflexion meaning bringing the foot up. And she'd seen several people and including some pain doctors. She was in a lot of pain. She was on opiates every day. And one of those providers said, you have CRPS. And the part of the history I didn't tell you was that she actually did have CRPS in the other foot, but that had gotten better. So she was scheduled to go in a lumbar sympathetic block, which I don't know a lot about the procedure, but it's fairly invasive. And then she saw me and I had some questions about this, and so we did some further work out. So this is her perineal fibular motor to the EDB. So amplitude looks okay. She's 36, so it's a reasonable amplitude. But there's some conduction velocity slowing. Is anyone bothered by the amplitude change from fibular head to popliteal fossa? Co-activation? Possibly, okay. Well we've got some slowing here and so there's a small loss so you know there's some slowing there's a little bit of loss of amplitude so you're kind of thinking now could this be conduction block and she does have weakness so we can do the tibialis interior same nerve just different muscle the two proximal sites of stimulation are the same as the EDB and here what do we have here we have a clear loss of amplitude approximately and so what does this tell you conduction block yeah along with that slowing and you can see on the waveform that there's a clear loss of amplitude okay I think we just oops so we talked through this but assuming the absence of technical errors what's the best explanation it's conduction block the fibular head all right so this is that mid segment demyelinating injury with conduction block where we showed you distally everything looks okay all right that's our 5.5 amplitude latency looks normal and then when we go proximally to the lesion we have a block of about half of those fibers and so we get a lower amplitude that's that 2.6 all right so how can we be sure that there's not superimposed axon loss the amplitude itself 5.5 is normal so do we know about axon loss and how can we figure this out any thoughts well EMG yes yes EMG very sensitive to axon loss but before we start that is there anything we can do so what I would say is that you can perform the study on the contralateral side and EMG is very sensitive but it's not quantitative so if you do any nerve conduction on the other side you can get a sense for what percentage is of axons are lost all right so needle EMG can help determine this to you so on the left side her amplitude was 7.4 so is there axon loss maybe I would say you can probably take this and say yeah there's axon loss the difference between the 5.5 and 7.4 it is not meeting that threshold at 50% difference so you're not quite sure once you get the EMG that'll show you fibs and positive waves in fact she did have axon loss and so the difference there most likely is axon loss just for fun here is her ultrasound of the fibular nerve on the I should have put these in different order but on the left side of the picture is the right cross-sectional area that's the abnormal side it was 19.9 millimeters squared and on the normal side it was 8.5 so there's an enlargement there but more than that on the right side there's the perineal nerve fibular nerve there's the fibula and then there's this bone spur right next to it okay and longitudinal section the longitudinal view we have the nerve coming through it's highlighted in blue we have the fibular head and then there's that bone spur here's a video of the nerve can you see my mouse oh yeah the nerve is here and as I'm moving the stimulator and not a stimulator the probe you can see the nerve coming right over this this spur this sharp and when I put my probe over this that was where the pain was and that would send a shocking sensation down the leg so sent her back to her orthopedic surgeon and they shaved this off and she got better immediately after the surgery she was pain-free this is after years of having pain in that leg so a good example of how electrodiagnosis can really change the course of someone's clinical trajectory okay so case two we have some hand paresthesias a 37 year old male presents with bilateral hand numbness tingling and pain he worked on a production line initially intermittent symptoms now more constant and it involves a thumb index and middle finger and daytime triggers include smoking and driving looking at his phone so sounds like carpal tunnel right so which electrodiagnostic abnormality typically occurs first in carpal tunnel syndrome so it's actually in that order that I'm showing you usually demyelination precedes axon loss and sensory precedes motor right that's a pretty reliable progression in carpal tunnel syndrome okay so when we do a routine antedromic digit to sensory study or recording at the digit to or stimulating at the wrist so I'm going to come back to this diagram in a second so this was his digit to study what's the path of physiology is it demyelination is a conduction block is it axon loss is it some combination of the above you can shout it out if you'd like to or you can commit in your head okay so I would say not enough information all right it's a question here response e that I didn't show you so is there demyelination I think we can say yes with certainty the conduction velocity is slow enough that this is definitely demyelination all right is there conduction block well maybe but we don't know that yet is there axon loss maybe the amplitude is low 7 mill microvolts is it a combined demyelinating axon loss we just don't know yet how do we figure this out well like I showed you if we have a block that's distal to our most distal site of stimulation we may only be stimulating and we're stimulating all the fibers but only a portion of those fibers may be getting through the block all right so that can look like an axon loss lesion so if we come more proximate more distally like dr. Jordan was telling us we can stimulate in the palm bypass that block and see how many fibers we can stimulate all right so this is the rationale for doing a segmental digit to study it's the only way to distinguish axon loss from conduction block this is what we did here and so you'll see the mid palm responses on the top and the amplitude goes from 7 to 16 so that's there's definitely some conduction block there and you can see the difference that 19 meters per second that's the carpal tunnel that's the wrist segment and then the 63 is from palm to fingers and so average it was 29 the whole distance but this parses out that focal slowing so does it matter that we can do this does it matter that we can distinguish axon loss from conduction block I think it does this helps you confirm the diagnosis you can confirm that focal slowing it's a better marker of severity it better product it's a you know you can define prognosis for the patient if they have sensory loss because of axon loss that's going to take a lot longer to recover and maybe it doesn't recover but if there's conduction block there and they have sensory loss you can reassure them that that's probably getting it better with surgery and then this study can be helpful in the context of polyneuropathy which I didn't spend any time on but if you have slowing here and your digit to study and the person has diabetes they have a neuropathy then you can do this segmental study and see is there uniform slowing across the whole segment or is there segmental slowing that only involves the wrist and that's something that this can help with all right case three is a person with neck pain 55 year old male presents with one month of neck pain and right arm weakness every time he turns his head to the right he gets a shock of electric pain rating from the shoulder into the thumb I mean he has some numbness of the lateral forearm the thumb and the index finger you know it's a weakness in the right arm when attempting to biceps curls and has difficulty opening a heavy door with the right arm so it's kind of cluing you in there's some proximal weakness their biceps infraspinatus routine nerve conduction studies are expected to be what show demyelination conduction block axon loss normal goes back to what you're thinking this clinically might be it sounds like radiculopathy right pinch nerve in the neck typically we have normal results here for radiculopathy but this is what we came up with so we've seen this quite a bit now so what is this this is the ulnar ADM there's a lot of numbers here the amplitude is in the middle there so assuming we have no technical errors what explains the pattern that we're seeing we have a loss or a drop in amplitude between the wrist and below elbow site we have no slowing Martin Gruber anastomosis that's right okay which ulnar muscle is most commonly involved FDI is most commonly involved that's a different question from which will you most commonly see right you'll most commonly see the ADM because most of us are doing ADM and not FDI right remember that that's why we don't see it as often as it occurs right and we can confirm this by stimulating leave that leave the amplitude or they leave the electrodes where they are and then stimulate meeting at the wrist and meeting at the elbow all right case for is a burning feet 73 year old female presents with constant miserable burning pain of both feet for one year she has some mild gait imbalance but no weakness exam shows some ankle a reflex here absent vibration of the toes mild weakness of the toes do her Searle and it's absent tibial motor those amplitudes are low she is 73 but should be at least 1.1 on based on age-based norms and the conduction velocity is kind of slow so the question is what's the path of physiology so I heard a vote for D I heard a vote for axonal so I think a lot of people here would say D mixed demyelinating and axonal and the reason you would say that is because amplitude is low so there's some axon loss that's that's clear the conduction velocity is a little bit slow okay does that mean it's demyelinating I would say no all right maybe there's a little bit of demyelination but the vast majority of polyneuropathies are going to be axonal okay so when we say that something's a demyelinating polyneuropathy we're referring to a primarily demyelinating polyneuropathy where you have very slow conduction velocities prolonged distal latencies so this is a reminder that you can get mild slowing just from axon loss alone if you just by chance lose most of your fastest fibers if you think about it if you if you're losing 90% of your fibers most likely you're gonna lose your fastest ones all right and you're left with the slower conducting fibers and so what you're measuring is these fibers that are left over that happens to be slower and so you can get a mild degree of slowing with just a purely axonal polyneuropathy and so I prefer to stay away from this mixed demyelinating axonal term because it doesn't really help you all right now there are some cases where you have clear demyelination and you have clear axon loss and sometimes you have to decide which is primary which is secondary but most of the time if you have something like this where it's mild slowing it's most likely going to be axonal okay and there's that chart again all right happy to take any questions or feedback Yeah, so the question is, for Kerpel Tunnel Syndrome, he usually does the comparison studies, medium versus ulnar, medium versus radial, which is better to do a segmental, a digit two segmental versus a comparison? And I would say if your question is conduction block, if you're trying to understand is this, am I seeing low amplitudes because of conduction block or axon loss, then the segmental is the only way to answer that. I use both, depending on the situation. So if the median motor, if I start with the median and it's prolonged, so then my pretest probability is Kerpel Tunnel Syndrome. I've done the median motor, that's prolonged. That's in line with what I'm thinking. And so then I just want one more study. And so then I'll do the digit two, the segmental digit two. That tells me is there axon loss, is there conduction block? And it confirms the study. It's very sensitive. The problem with the digit two segmental is it's technically challenging. So when you're stimulating the palm, you have to work at it to get the right, you know, the baseline to be right and the latencies. It's using the onset latency to determine the conduction velocity of the segments. And the onset latency for a sensory potential is not that stable. Sometimes it can be hard to see. So it requires averaging. I usually average five on each site. When I'm doing a Kerpel Tunnel evaluation and the median motor is initially normal, then that's taking it into the mild category. And in that situation, just my personal preference, I do the CSI, the Robinson Index, where you're adding up the peak latency differences between the digit one comparison, the digit four comparison, and the transcarpal study. That's just how I do things. I think that's also a very sensitive test. Does that answer your question? Yeah, I think that's a great question. The question was, after a carpal tunnel release, patient has recurrent symptoms, and how do you know is it recurrent carpal tunnel? A lot of times those sensitive comparison studies, digit four, digit one, transcarpal, those latencies don't get back to normal. And so I tend not to do those studies. I will do the digit two and see, I think potentially the digit two segmental can help you there. The peak latency at the wrist should return to normal. The median motor latency should return to normal after a carpal tunnel release. What I think is very helpful is ultrasound. If you can see a persistent entrapment, or if there's been an incomplete release, if scar tissue has over time encroached on the nerve, you can see that, and that can be helpful too. But you're right, the comparison studies, those sensitive comparison studies, may remain abnormal indefinitely just because of the way that remyelinates. The remyelinated portion of the nerve is not as good as the original, so there's always gonna be a little bit of slowing there. Other questions? Yes, sir. So the question was, after a ulnar nerve transposition, if you have recurrence of symptoms, it's challenging to measure the distance, to comment on is there a recurrent nerve injury? And yes, it is very challenging. And what I would suggest is before doing the ulnar study, you can map out the course of the nerve with submaximal stimulations and actually draw it on the patient. And then do your, I would suggest doing inching studies across the elbow there. So you know exactly where the nerve is going. You have to be careful because sometimes these, whether it's just a decompression or an anterior transposition, you may also have some subluxation depending on the elbow flexion. And so you have to make sure you're in the same position the whole time, the patient's not moving and subluxing that nerve. But you can use submaximal simulations to map out the course, draw on the patient where it's going and then do your measurement. And when I measure, I use just a homemade measuring tool because a tape measure kind of bends and folds that can throw off your distances to you. And so I cut an old cable from an EMG electrode and I put with a permanent marker every two centimeters, a mark. And I use that to kind of form to the patient's elbow. Just a tool that you can use if you'd like to. Does that answer your question? Yeah, the question was for Richie, can you, you have, you can potentially have wasting of the thenar eminence along with some ulnar motor loss, and that can mimic a T1 radiculopathy. And so, yeah, I think that's an example of where the electrodiagnostics fall short. Unlike Martin Gruber, there isn't a good way to confirm electrodiagnostically that that's what you're dealing with. I think the needle exam helps, although you're kind of limited in terms of which, how many muscles you can record. I think you can fall back on the clinical exam, clinical suspicion imaging helps, but that's a tricky situation. The question is, do you stimulate mid-forearm? I think you could try if you were trying to. Surface stimulation or needle stimulation? Yeah, surface versus needle stimulation. I've not used needle stimulation to try to stimulate the median nerve. I think you'd have to be pretty hard pressed to very precisely localize a lesion in the forearm. It gets pretty deep there. And so you're traveling through a lot of tissue. And I think you'd have to be careful about actually injuring the median nerve if you did a needle electrode. So I don't routinely stimulate in the forearm. I've tried it before. It's just not very easy, because it's so deep. All right. I think we're out of time. Thank you for your attention and attending.

nerve conduction

axonal injuries

demyelination

conduction blocks

nerve anatomy

nerve physiology

axons

myelin

conduction velocity

onset latency

response amplitude

Martin-Gruber anastomosis

accessory peroneal nerve