Okay, well, thank you very much for returning and for any other new people who have joined us and so so this is the second part as I mentioned of our two-part discussion about basics of nerve conduction study and needle EMG. So this section focuses more on as I mentioned on a needle EMG basics and also specialized studies that Dr. Aaron Eisenberg is gonna give. So he is a neurology faculty at the University of Toronto. He's also the fellowship director for all fellowships plus the director of the neuromuscular fellowship. So it's like a big umbrella and also the small one. Also runs a rapid neurology clinic. He's a director of that at the Sunnybrook Hospital in Toronto. So that's Dr. Eisenberg. Hi everyone, thank you Kian for the opportunity to speak again. This is great. Before we go any further, maybe I just want to get a sense of how many people how many people in the room are physicians? And how many people are techs or training to be techs? Okay, so it's a good mix. So this is very basic stuff, but I think it's always good to review the fundamentals for everyone no matter how long you've been doing this. So we're really going to be focusing on the the EMG part and then very briefly afterwards in the last 10 minutes, I'll talk about repetitive nerve stimulation and I already hit the button. Sorry. Yeah, I just want to make sure I know how I'm using it and then I'll talk about repetitive nerve stimulation and blink responses. So our objectives today basically we'll start with a very basic approach to EMG which really can be divided into spontaneous and voluntary activity. And we'll spend like I said most of the time on that. I included short and long exercise studies which we may or may not have time to get into but the slides will be in the package for reference anyways. And I don't know if I said this at the beginning, but I have no relevant disclosures. So what is EMG? We often use the term to refer to the entire test that we do but it's actually the second part of the test the needle EMG and that's analysis of spontaneous and voluntary muscle activity with the use of a needle electrode. And so the equipment needed I'm sure you've all seen these machines before it's it's fairly straightforward. You need a computer and a EMG head box and amplifier. So this is the actual EMG software. And then you actually need some very basic equipment like a needle electrode and cable and then alcohol swab and gloves. And I think Kian spoke before about the different types of needles that we can use and these are the two basic types. And it's actually important because it affects the way you interpret your waveforms. We in Toronto, we actually use both. A concentric needle, I don't know how well you can see this, but it actually has two parts to it. So it has like a straight kind of metal core and then a surround kind of it's almost like a hypodermic needle that you would get an injection, but there's metal inside of it. So there's actually two parts. So the inside is the reference electrode and the outside, sorry, the inside is the active electrode and the and the outside is the reference electrode. So everything is all in one. Whereas with a monopolar needle, it's just a single electrode and then you need a second sticker as your reference electrode. So concentric is obviously easier to use because you have less stickers and everything's referenced more closely. So this is this is what a concentric electrode looks like. It's just a single needle into the muscle. Whereas the monopolar has a second electrode, but it actually changes the waveforms that you see. So because, and I don't think I have a great picture of this, but there's an excellent picture in the Preston textbook. Because the the monopolar electrode has kind of a round almost pyramid tip at the top. The pickup area, so like kind of the area of the muscle that it looks like is like a sphere all the way around the tip of the needle. And so if you turn the needle side to side, what you see on the screen and what you hear doesn't change at all. But the concentric electrode is kind of, it kind of has a beveled edge. So it's almost like it has a directional teardrop pickup area. So when you turn the needle, it actually changes. So it's actually a little bit more complicated and a little bit more technical doing, oops, something just disappeared. Is Chester still here? Yeah, no problem. So I'll keep talking. Anyways, so so it's actually a little bit more complicated and sometimes requires a little bit more nuance when using a concentric electrode. The other thing, and this is probably the most important thing, is that the waveforms that you get with a concentric electrode are actually smaller. So for people who switch back and forth, we often say that when we use a concentric electrode, everything looks like a myopathy, because all the motor units are kind of shrunken down. And I'll talk about why that is. So it's just good to be mindful of that. We actually still use monopolar electrodes quite a bit in Canada. I like them. They're great, but they're also cheaper. So they're a lot easier to use. I think I lost power. There we go. Okay, so I'm not gonna go over the actual how-to of EMG. This isn't like an EMG workshop. And to be honest, to really, really learn how to do EMG, you need hands-on training over months and, you know, many of us do fellowships, of course. But in one slide, the skin needs to be prepared with an alcohol swab. And then really there's two parts to the needle exam. So at first you put the needle and you put the needle into the muscle and you move it around with the muscle at rest. And you just listen for insertional and spontaneous activity. So really there should be no spontaneous activity, except for one exception, in normal muscle. When the muscle is not moving, it should be fairly silent between needle movements. Of course, there's exceptions to that in various different diseases. Voluntary activity is the second part where you actually get the patient to activate their muscle and you analyze the motor unit action potentials at lower and higher activation. So these are really the two parts to needling each muscle. And then we go muscle by muscle. So insertional activity is what you hear when you actually move the needle through the muscle. And I'll play a video for you in a moment. We have lots of videos to kind of illustrate everything we're talking about. When you move a needle through a muscle, the muscle fibers, which are muscle cells, they actually depolarize. And so you hear this kind of crisp and crackling sound. It's very, very brief. It's almost essentially time-locked to the time that you're moving the needle. And it's actually important to get insertional activity. It's part of the way that you know that you're in a muscle as opposed to fat or some other tissue. But it can be sometimes misleading because if someone has a myopathy or an end-stage neuromuscular disease where their muscle has kind of atrophied or there's fatty or fibrotic replacement, you don't always hear normal insertional activity. So I'm going to try the video now. The advancer seems to not be working again. Okay, so let me see if I hit it twice. So I might need you, Chester, to play the video. So if you kind of hover the mouse over the bottom, it should... Is it possible to get like a mouse up here to... Sorry, guys. So just to talk about insertional activity briefly. So if you were to put your needle electrode in in the calf, for example, of a patient with a muscular dystrophy where they have fatty replacement, you'll hear a little bit of insertional activity, but it'll be decreased and that's because there's actually decreased muscle there. So insertional activity, I would say 95-99% of the time is it just really tells you that you're in muscle and it helps kind of keep you, especially in some muscles that are very small and there's a lot of other structures, it's actually very useful to know that you're in muscle and not approaching a vascular structure or something like that. But rarely you have to be mindful that when you don't hear anything, you may actually be in muscle and it just might be diseased muscle that's just not making as much noise. Okay, sure. Sure, yeah, if you have a question. Yeah. No, it's okay. No problem. It sounds like we have audio at least. But ideally we have both. But I will say that like, it's really like, okay, so I think we're, yeah, so I just got to go backwards. So this should be insertion. Okay, so now if I hit it again, no. So I think normally like, I have to hover the mouse at the bottom of the screen. Go forward. No, you have to go. Yeah. So if you like. Okay. Every time you hear that crackling, it's just moving the needle. So it's super brief, right? It's over within 300 milliseconds of when you stop it. So pretty straightforward. This is what you hear whenever you're doing a normal DMV. Okay. So that's insertional activity. Spontaneous activity is any sound that the muscle makes when it's at rest, okay? So it can tell you, it's actually very, very useful. So it can tell you information about the localization or distribution of a problem. So for example, if someone has an L5 radiculopathy and you needle a bunch of different muscles in the leg, it'll be the L5 muscles where there are spontaneous discharges. So it can tell you kind of what the pattern is. Or if it's length dependent, you'll only find spontaneous discharges in muscles in the foot and the calf. But as you move up the leg, they might be gone. So it can tell you about where the problem is or what the distribution is, but it can also tell you a little bit about the type of pathology. So there are some discharges that you can hear that can be seen either in muscle or nerve disease, but then there are some that are really much more characteristic of either or. So for example, myotonia or myotonic discharges are much more characteristic of myopathies, whereas fasciculation potentials, for example, are much more characteristic of neurogenic disease. So attention generally should be paid to both morphology, so the appearance of it, but also the firing pattern and stability. And with EMG in general, you're always kind of using sound and visual, but the sound is far more important. So if you only had one, I would always go with sound. So spontaneous, so this is the motor unit, by the way, just to put everyone on the same page. So this is the alpha motor neuron, the cell body that sits in the interior horn of the spinal cord. And this is the axon that comes down and all the terminal axons that innervate these tiny individual muscle fibers. So each one of these is a motor unit, okay? So a spontaneous discharge can come really from a problem or even a physiologic phenomenon, anywhere down this axis, okay? So the first kind of place that we often think of is the motor unit action potential, which is when anywhere basically along the cell body or the axon itself, there's a discharge. This is where voluntary activity comes from, but in terms of spontaneous activity, this is where we get fasciculations, which we all get sometimes, muscle twitching. Myokymia, which is another kind of muscle twitching. It's quite common in normal people in eyelids, but in other diseases we see. So if you get twitching in your eyelids, that's often myokymia. But in other diseases, we see it in other parts of the body. Cramps, Charlie horses, which we all get, are very commonly a problem with them or coming from the motor unit action potential. And then much more rarely neuromyotonia, which is associated with very rare diseases. And we can also get muscle fiber action potentials, right? So we can actually get them coming from the muscle fiber itself. So this is fibrillations, positive sharp waves, and plate spikes and so forth, okay? So these are kind of the two main places that the discharge can be coming from, either the entire motor unit or individual muscle fibers. And we'll talk about that in a second. So this is the only kind of spontaneous activity that is normal, okay? Anything other than this is not normal. This is end plate noise and spikes. So this is when you're doing an EMG and your needle is actually close to where the nerve inserts on the muscle. And there's two things you can hear. You can hear end plate noise, which is kind of a hissing seashell sound. And then you can hear end plate spikes, which are muscle fiber discharges, which look a little bit like fibrillation potentials. And they're kind of more like crackling oil. Turn the volume up a little. Can you turn it up a bit more? Sorry to be high-maintenance. We'll maybe play it one more time. Oh, so it's this one. So I don't know if it's, that sounds painful to me. I have that conditioned response. But once you do it enough, you'll start to realize what it sounds like. It has a very kind of hissing, crackling sound. And this is non-pathological. And it doesn't mean you did anything wrong. In fact, if you're in the right spot, if you landmarked well, you're gonna hit end plate. But you just, you need to move away from it. So fibrillation potentials are abnormal spontaneous activity. And these are muscle fiber action potentials that are firing spontaneously in the setting of denervation. But you can also see it in muscle disease and even in some neuromuscular junction diseases. And they're characterized by a very regular firing pattern. So you'll hear this kind of over and over again. It's the regular firing pattern that really tells you that this is an abnormal spontaneous discharge as opposed to a distant motor unit or end plate noise or something else that you shouldn't misinterpret. And so this is where sound and the audio really, really comes in. It's a really important distinction. Some people, very often, as soon as they see fibrillations, will say this is denervation. This is a neurogenic problem. And that's not necessarily the case. We see these also in muscle diseases. And like I said, even in rarely very severe neuromuscular junction diseases like botulinum toxin injections, or sorry, Botox infections, sorry. And so basically the way I think about fibrillation potentials is that when a nerve is plugged into a muscle fiber, it's almost telling the muscle fiber to stand at attention and to wait for instructions. But as soon as the nerve is unplugged or there's a problem where the muscle is not seeing input from the muscle fiber, sorry, from the nerve, it starts firing on its own, okay? So we'll play that now. So you can see that has a very, very regular pattern and it's almost so regular that you can predict it. So if you start tapping it out on the table, you're gonna find that you're in sync with it. I find that people who play music often pick this up a little bit faster because they're used to kind of doing this. Fibrillations can actually speed up or slow down, but they should kind of speed up or slow down with the same interval. And you'll hear what we mean as we see more. But it's that very characteristic regular firing pattern that is what tells you that's a fibrillation. A positive sharp wave, we'll talk about this in more detail, but really in terms of the pathology, in terms of what it means, it essentially means the same thing as a fibrillation potential. So much so that in many EMG labs, when we actually do our reports, we'll have fibrillations and positive sharp waves in the same column because I don't really care if they're positive sharp waves or fibrillations. They mean the same thing. They mean that the muscle fiber is not seeing input from the nerve one way or the other, either chemically or physically, and so it's firing on its own. They just have a different morphology and therefore a different sound. So rather than that like straight up and down appearance, they have this initial downward deflection followed by this kind of hump here. We won't talk about exactly why it looks different because that's probably controversial and I think for our purposes, unimportant discussion. But for our purposes, it really means the same thing, but it just has a different sound. So the main thing you'll probably hear is it has like a lower pitch sound. And the reason it's lower pitched is that it has a longer duration. Generally speaking, the duration of any waveform, whether it's a spontaneous discharge or a voluntary discharge, the wider it is or the longer duration it is, the lower pitched it is. But we don't care about that. It's the regularity. The thing about positive sharp waves that's a little bit tricky is that unfortunately the distant motor units or voluntary activity, which are a common kind of mimic of abnormal spontaneous activity, have the same kind of appearance. So that's why I always tell people, especially fellows in residence, don't worry too much about what it looks like on the screen because that can be misleading. You have to focus on the regularity. So those two discharges we just talked about, by the way, remember in terms of thinking about where the discharges can come from, either the motor unit or the muscle fiber, those come from the muscle fiber. Myotonic discharges also come from the muscle fiber. So they can either have a brief spike or fibrillation morphology or a positive wave morphology. And they have this very characteristic waxing and waning amplitude and frequency. And sometimes described as like a dive bomber or revving engine. And as soon as you hear it a few times, you'll know exactly what it is. It's the kind of thing that even if you're not in the same room as the EMG, if you hear it, you'll know what the disease is. So they're classically associated with myotonic dystrophy type one and type two. They can also be seen in non-dystrophic myotonias, so channelopathies. But you can also see them in other chronic myopathies like inclusion body myositis. Truly in any very chronic myopathy and rarely and it's very challenging. Sometimes we can see them in very chronic neurogenic diseases. And that always throws us for a loop because if you see a patient with like, you think has ALS and then you see a few myotonic discharges or kind of discharges that look like myotonia, it can throw you off the scent a little bit. So, oh, that's okay. So this was almost certainly myotonic dystrophy type one. I can't remember anymore what it was. So it has that really, really kind of characteristic revving sound. Complex repetitive discharges, so are basically continuous depolar. So this is a muscle biopsy, okay? And these are all muscle fibers, so muscle cells. And these are also muscle fibers, but they're obviously not normal. So they've kind of all atrophied and they're all near each other. So this is group atrophy. We see this most commonly in neurogenic disease, but you can really see it in any chronic neuromuscular condition, including myopathies. And so what a complex repetitive discharges is, is when it's an individual muscle fiber that has a discharge that kind of hops to the next muscle fiber and it forms this circuit. And so you get this super, super repetitive discharge that has a very characteristic machine-like sound. It almost sounds like you're in a factory. And again, it can look like fibs, it can look like positive sharp waves, and it's actually comprised of those, but it's a CRD. I find CRDs are actually, they're interesting the first few times you see them, but then they're kind of annoying because they're really loud and they get in, and they don't tell you anything other than something has happened here at some point in the past. It doesn't tell you if it's neurogenic or myopathic. It doesn't tell you if it's like an S1 radiculopathy from 30 years ago or myositis. So as soon as I hear them, I record them for the fellow and then I try to get away from it. And they're very loud and they take up a lot of space. But they're interesting. So they do mean that something has happened, but it does not mean that something is actively happening. And I'd say another common thing is, I've seen some reports where CRDs are taken as a surrogate of active, spontaneous, abnormal, spontaneous activity or active denervation. That should not be done because it does not mean that. Actually, before we play the video, oh, can you go back, sorry. I'm being really high maintenance. And I probably will continue to be high maintenance. So next slide. So before you play the video, these are the kind of waveforms that were triggered. And you can see, this looks like a fibrillation. And essentially it is, it's the same electrical discharge. And you see this thing here, that looks like a positive sharp wave. All that this tells you is that these discharges are coming from muscle fibers. But when you play the video. So if you didn't have the video, if you didn't have the sound on, or you weren't really listening, it would just look like fibs and positive sharp waves. But it's not just that, this is a CRD. And if you hear enough of it, you'll get used to it and probably not find it terribly interesting. So those are all the discharges that come from the muscle fiber. So now we're gonna move to the discharges that come from the motor unit. So these are fasciculation potentials. We all experience these, especially in our calves, some of us more than others. And this is spontaneous involuntary discharge of a motor unit. Can be really anywhere from the actual cell body or down the axon itself. But the issue, so what actually happens is when the discharge happens, it travels down and the entire motor unit fires. And this is called the motor unit action potential. So it's really all of these muscle fiber action potentials added together. So this is what it looks like when you activate your biceps. If I put a needle in my biceps and I started to activate it, I'd see a bunch of these. The computer doesn't know whether it's a fasciculation or it's just a single voluntary discharge. But fasciculations kind of take on the same appearance. So they have a very irregular kind of popcorn-like sound. And they can either be benign or physiologic. And then they can be seen in almost any neurogenic disease. Of course, when seen in the right setting and in abundance, they're concerning for motor neuron disease or ALS. So I think we have a video. Good. Good. So popcorn in your microwave. So, and these, in order to really know that these are fasciculations and not voluntary activity, you have to put the needle in, take your hand off the muscle, and make sure that the muscle is at rest and just listen. That's really the best way to check. In reality, often when there's fasciculations, you don't even need to do that. They're so abundant that they'll just make themselves apparent. Doublets and triplets are kind of on the spectrum of fasciculations. So these are fasciculations firing in groups of two or three. They can be seen basically in any of the conditions that we see fasciculations in, but they can also be seen in tetany and in hypocalcemia. And I think I have a video here. So you can see there's two fasciculations kind of locked together. And further down that spectrum is myokymia or myokymic discharges. So these are just group discharges of the same motor unit. Same kind of idea as a fasciculation, but we don't really see this as often. And certainly this isn't really like something we would consider a normal variant. This is usually seen, unless it's in your in the eyelid, it's usually seen in the context of a disease, most commonly in radiation injuries, but they're kind of like clumps of motor unit action potentials. And this is, we're still talking only about spontaneous. This is, you know, muscle fibers, motor units firing on their own. So they kind of look like rippling movements of the muscle. They often look like fasciculations, but they're kind of like sequences of twitches, and like I said, often seen in radiation and sometimes in demyelination and hypocalcemia. So they have this kind of characteristic marching sound. So the only thing I want to point out is that you can, like, these waveforms look much more narrow, right? And that's just because I changed the sweep speed here. Normally it's 10 milliseconds, and this is a hundred. So I just kind of clump them down, and just for the purposes of showing these groups. One thing I've learned, especially with trainees, is that if there's a waveform, it's spontaneous, and you're not sure what it is, it might be myokinia. That's one of the ones that people often take a while to kind of narrow down. They have to rule out other things. So that's kind of a helpful thing. And then cramps, I don't have a video of it because it's just continuous activity. It's basically this, it's a charley horse, it's the same thing. And we can see it in a number of neurogenic diseases as well. This is due to involuntary contraction of a muscle. But it comes from the nerve, not the muscle. So the charley horse, the classic cramp that you get in your calf, or any kind of muscle that you have in your legs, or anywhere after activity, if it's a true cramp, that's actually coming from the muscle. There's other kinds of cramps, but that's often not a true cramp. That's myotonia, or a contracture, or something else, and that can actually come from the muscle. But the cramps that 90% of us all experience are just plain old neurogenic discharges. I also don't have a video of neuromyotonia. I can tell you that I've been practicing nine years now. I've only heard this once, and that was when I was in fellowship with Kian. So it's not common, and you usually only see them in, you know, very rare cases. But it's a very, very high-frequency discharge of a sequence of motor units all kind of clumped together, and it has this kind of characteristic pinging sound. So we see this in very rare diseases like Isaac syndrome, Morvan's, Korea, and so forth. So that's all the spontaneous activity. So just, it's good to keep in your mind that spontaneous activity can come from, remember, either the entire motor unit, or it can come from individual muscle fibers. Okay, so now we're going to talk about voluntary activity. So everything we just did is the first part of the EMG, when you're just moving the needle through a quiet resting muscle. Voluntary activity is definitely more technically challenging, and this is, this is, I tell residents that this is why, this is one of the big reasons we do fellowships, because you need a year to train your ear, I think. Not everyone does, but it's helpful. And so voluntary activity is, you're actually looking at the motor unit action potential, the morphology, so the appearance, the stability, and the firing pattern, as the person is activating the muscle. And this is also the part of the EMG that's a little bit more uncomfortable, because they're, you know, activating the muscle when there's a needle in it. And so the basic discharge that you get is called a MUAP, and that's a motor unit action potential, as opposed to a muscle fiber action potential, which we were talking about before. So this is just an example of normal voluntary activity. And you can see on the screen, there's, there's probably two muscle motor unit action potentials. I'll just, I'm just gonna call them MUAPs firing. They look a little bit different, and you can measure their duration, you can measure their amplitude, and also something called their firing pattern, which we'll talk about. Now, I've actually used a different screen here to actually measure these parameters. So this is kind of like a quantitative EMG, sort of, but the reality of it is that we don't do this 99% of the time. We, we use our, we, I think we call it pseudo-quantitative EMG, where we, we look at the appearance of it, and we listen to the sound of it, and that's our way of judging the, the size and the firing pattern. So we'll talk about the kind of different parameters of morphology. So the first thing is amplitude, and you measure amplitude from the lowest to the highest point. Amplitude can vary greatly. So anytime you actually move the needle through the muscle, and you look at voluntary activity, you're gonna look at a population of motor units, right? You're not just seeing one, you're gonna look at, ideally, 20, but sometimes more, sometimes a little bit less, and you're kind of averaging, averaging them out in your head, and seeing, in general, do they all seem to be around the same kind of normal pattern, or are they larger, are they smaller? A normal amplitude should usually be anywhere from a hundred microvolts to two millivolts, more or less. In a population, in a given muscle, some might be a little bit bigger, some might be a little bit smaller, and that's fine. It's not exactly a bell curve, but there's definitely a distribution, but that's kind of the range, and so it reflects the number of muscle fibers in a motor unit, but perhaps more importantly, how close your needle in the muscle is to the motor unit that you're measuring. So the closer that you get to a motor unit, the taller the amplitude gets, so that's another kind of important part of the training, and it can also reflect the size of the individual muscle fibers. Duration, which I think of the two as kind of a more reliable and useful parameter, is measured kind of from the initial takeoff to the return to baseline, and again, it can be anywhere from 5 to 15 milliseconds, but again, you'll get a distribution, so having a few 4 millisecond duration motor units in a muscle is not concerning, as long as there's some other ones that are 10 and 12 and 8, but if all of them are 4, or most of them are 4, that's going to make you a little bit more concerned, this might look more like a myopathy, and vice versa. If you have a bunch of really, if you have like a few that are 15 to 20 milliseconds in duration, one or two, but everything else looks like it's normal, then that's fine, but if they're all that wide, you're going to start to think more about a neurogenic phenomenon. So this is more related to the number of fibers in a motor unit, which is really important for denervation and re-enervation, we'll talk about that in a second, and also the synchrony of muscle fibers firing, but the thing that's really important about duration is that it's a little bit less related to how close your needle is to the motor unit, which means that it's kind of more of a robust parameter, so it's a little bit, it's a little bit more forgiving in terms of technique, so it's really, it's really helpful, especially early on. Rise time isn't really a parameter that we measure, but it's extremely important for judging when you are close enough, so you should only judge a motor unit when your needle is close enough to it, when it's in focus enough that you know that you're getting kind of a good representation of it, and so we use rise time in order to judge how close we are to a motor unit. So rise time is the distance from the bottom to the top peak, it's actually a duration, right? So rise time generally should be less than five microseconds. Let's say this was the rise time, for example, so it's kind of like the slope a little bit. If the rise time is kind of looping like this, this isn't a motor unit here, but I'm just trying to give you an example, it would make you think that that motor unit is too far, so I shouldn't actually judge the morphology yet, because it's not in focus. I don't have a good look at it yet. And then there's also phases and serrations, so we talk about polyphasia, it's the number of times that it crosses the baseline. I think I'm gonna try to speed up a bit, just because, oh Chester, I think the clock stopped. Anyways, I'll keep going. Oh, okay, so maybe I was never using it to begin with. That's okay. So, and this is really about the number of muscle fibers and the synchrony of muscle fibers firing. So it's a lot to keep track of, right? But it's not like each EMG that you look at, you're judging, okay, that one's, you know, two millivolts, and that one's half a millivolt, and this is duration, you're, it's more of a gestalt. It's definitely a gestalt when you're doing this. So in terms of the morphology, so in an acute, so we can actually map the morphological patterns to different diseases. So in a neurogenic condition, when it's very acute, all of these morphological patterns look normal, and I'll kind of show you why. So this is what happens. In an acute neurogenic process, some of the axons have been severed, but the remaining motor units look totally fine. So each one of these is gonna generate its own motor unit action potential. So these motor units are gonna look totally fine. So the only thing that's gonna be affected is recruitment pattern, which we'll talk about afterwards, but the actual motor unit itself and all of the morphological parameters are normal, okay? But in a more chronic neurogenic pattern, you start to get reinnervation, and that actually changes what the motor unit looks like. So this is actually kind of early neurogenic reinnervation, but it gives you an idea. So this axon's gone, right? Damage has been done here, and so all of these muscle fibers have been denervated, and they've been kind of orphaned. So what starts to happen is reinnervation from adjacent motor units. So this motor unit, which previously kind of looked just like this, starts to reinnervate these muscle fibers, and with time, it's probably gonna pick up more of them. So you can see what's happened here. It's started to grow, and as it starts to pick up more of these, this thing is gonna grow more. More of these individual muscle fiber action potentials will be incorporated into this motor unit action potential. It'll become wider, and it'll become taller, so the morphological pattern will change. And so that's why what happens is your amplitude gets increased, and your duration gets increased, and your phases get increased. So in very simple terms, neurogenic reinnervation, chronic neurogenic units look large. In an acute myopathy, the opposite happens. So nothing actually happens to the wire or to the nerve, but muscle fibers actually die or are diseased or kind of taken out of the equation. So each individual motor unit loses muscle fibers, so this is the motor unit action potential down here. It shrinks because there's just less going into it. So the duration shrinks, the amplitude shrinks. It can become more polyphasic, though, because they're not in sync as much. So that can happen in acute myopathy. Chronic myopathy is without question the hardest EMG, especially when people are learning, because it can kind of do both. You can get very large motor units and very small motor units. So IBM, inclusion body myositis, is a classic example of like the most challenging EMG for a fellow. A very common disease, and it's often referred for ALS as a question as well, so it's really important. So you get this kind of mixed pattern in these chronic myopathies. So the thing that really becomes helpful is recruitment pattern, which is the last thing we're going to talk about. So before we get there, I'm just going to show, oh, and I have examples of all these, sorry. So this is, again, oops, sorry Chester, do you mind playing this? So this is a normal motor unit, just to remind you what it looks like and sounds like. And before we move forward, so I'll just show you, like, so this is each... That video has two parts. He didn't play it twice. So each of these like little squares is 200 microvolts, right? So a whole screen is 2 millivolts. So you can see these are all kind of like one and a half millivolts, a nice kind of normal size. And in terms of duration, they're all kind of like, I don't know, 10 or just under 10 milliseconds. So these are all like very normal looking motor units, which is a good example. Now before I even start it, you can see that these are smaller, right? They're shorter, but also look at how like, we call this clippier, crisp these look. The duration is like super, super short. Some of these are like, they're polyphasic, but some of these are like less than five milliseconds, okay? So do you mind playing it, Chester? It sounds like static almost. I guess it was a short video, but you get the idea. They're very, very small. The thing I'll say about myopathy is that neurogenic disease is not subtle most of the time. It's very easy to recognize, relatively speaking. The units look big. There's lots of fibrillations. It's a much easier kind of pattern to learn. Myopathies are much more subtle. I guarantee you that I really had to search to find this video because many of the patients I have with myopathy, it's just not that apparent. I don't know if you find that, but it's just, it doesn't always, it's a much more fickle EMG. Okay, so then last thing we'll talk about is firing pattern, and really we're talking about recruitment. So there's kind of two things. There's activation and recruitment pattern. So activation is just how much the muscle is actually firing voluntarily. So for example, let's say someone has a stroke and they have weakness of their right arm. The EMG should not be abnormal from that. That's an upper motor neuron lesion. The EMG should be mostly fine, except they're weak, so they can't activate the muscles as much, so you're not gonna see as much on the screen. Or let's say someone dislocated their shoulder and they have lots of pain in the arm, and every time they move, it's causing pain. They're gonna activate it less. You just see less on the screen. So that's not really an EMG abnormality. It's just that you're not seeing as much to interpret. Recruitment is very different. So recruitment is the ability of the muscle to appropriately bring in or recruit motor units or MUPs with increased activation. So as the patient activates, there's kind of a pattern that those units should come in, a normal pattern. And in a normal situation, at the lowest level of activation, one motor unit action potential will fire at 5 Hertz. And with increased activation, approximately each new MUP will be added every 5 Hertz or so. And we call this the firing frequency. So if the frequency is 5 Hertz, there should be one. If it's 10, there should be two motor units and so on, approximately. It's really, really hard to see this visually, but we can listen to it. So I think this was me, and I don't think it was my tibialis anterior. There's one motor unit. I'm gonna play that again. So I'm gonna go back. And Chester, don't start the video if you don't mind for a second. So you can see that at the beginning, I was firing at approximately 5 Hertz. I was firing at the lowest level of activation. And then as I started to increase my activation slowly, my muscle or whatever recruited another motor unit and it came into the screen. And if I had have activated more, more motor units would have been recruited. So do you mind playing now? And try to listen when you hear that second unit come in. So this is the first one. Okay, go ahead. Oh, you haven't been playing it? I was. That's one. There's the second one. I think I tried to bring in a third, but it's hard. So this is firing at approximately 10 Hertz. I know it says 33.7 Hertz, I would ignore that, because there's all this other stuff on the screen and it's picking up all this stuff. So this is kind of a very classic normal pattern. Okay. In neurogenic disease, there are loss of the number of motor units, right? So there's less motor units to call on for help. So think about it as if the muscle has a job and the motor units are like workers. So you have less workers to call on, and so you have to ask more of them, right? So the recruitment is reduced, but each individual motor unit has to do more, so it has to fire faster. So this is what it sounds like. So we'll start at probably a one. I think there's more. Yeah, right, so. And I'm just changing the sweep speed here. So I just, I went from 10 to 50. So we can play it again in a second, but you'll notice that as the activation increases, it's that one motor unit that's just firing more. This is probably like a bad C7 radiculopathy or something like that, where the person has lost a lot of motor units. And you'll notice, actually, the morphology doesn't actually look bad. They're not that tall, right? They're not clipping the screen, but there's way reduced recruitment. So this is probably like a relatively acute situation. So you'll notice that as this person starts to activate more, there's only one, maybe two motor units to help out. So it's doing everything it can. It fires as fast as it can. And this is classic reduced recruitment. Maybe in the interest of time, we'll actually move forward. In myopathy, there's a loss of muscle fibers within each motor unit. So the motor units get smaller and they generate less force. So there's the same number of workers, but they're just capable of less, right? So with each level of activation, you need to bring in more workers, more motor units in order to do the same level of work. So we call this early recruitment, not increased recruitment. There's no such thing as increased recruitment, or if there is, it doesn't apply here. And the reason we call it early and not increased is that this ratio does not change. The number of motor, the firing pattern, so the frequency on the screen with the number of motor units is still five to one approximately. It's just that everything's firing so much faster. Of everything that EMG-ers learn, I'd say this is the most challenging, is judging early recruitment. Because number one, it's very subtle, and even in myopathies, you only really see it if someone has just the perfect amount of weakness, like a medium amount of weakness, or you only see it clearly. And it's subtle, right? The other thing is is that you can only really judge early recruitment if you are actually the one doing the EMG, if you're actually feeling how hard they activate. Because you have to be able to judge, okay, how hard are they pushing, and how much activity do I usually see on the screen when they do this? So if someone's really resisting me when I'm checking their biceps, normally I know what that looks like on a screen. I hear that all the time. This is way more than that. So a very classic example is you'll put the needle in the muscle, and I start with their arm on the bed lying straight and pronated, and then all I get them to do is supinate their hand and maybe lift it up like an inch off the bed. So they're barely activating their biceps, just enough to lift their forearm like a centimeter off the bed. And the screen fills up with activity. Which is normally what it would look like if they were reefing on you, if they were really doing a bicep curl. So that's what early recruitment looks like. So with that said, I still tried to show you a video of it. Imagine this person's doing almost nothing with their biceps. But you don't know that that's abnormal without correlating it to how much they're doing, like how much resistance they're giving you. So that's EMG, and I'm at 50 minutes. So maybe I'll very quickly, I'm just gonna do a repetitive nerve stimulation. Is that okay? I can do it in five minutes because it's important. And blink studies are self-explanatory. So repetitive nerve stimulation is used in the evaluation of neuromuscular junction disorders. And it's basically a series of stimuli at lower high frequency, and you get these C-maps. This is back to nerve conduction studies, right? So this is like a median C-map, it's just five in a row. I'm gonna do very, very basic neuromuscular junction physiology, although I'll try to go quickly. So this is a schematic picture of the motor unit, right? This is the cell body, the axon, the terminal, and the muscle. So the neuromuscular junction is kind of important for mediating this electrical, chemical, electrical pathway between the nerve and the muscle. So an action potential comes down, and then there's a chemical jump to the muscle, and the muscle has an electrical discharge. So that's the electrical, chemical, electrical connection. So blowing up this kind of nerve terminal, neuromuscular junction area, what happens? The action potential reaches the terminal, calcium enters the nerve terminal, acetylcholine is released. So this is the chemical part. Acetylcholine binds to the receptors on the muscle, the sodium channels open, and ultimately, you get an end plate potential, and that's what leads to, talk about safety factor in a second, that's what leads to contraction of the muscle. So very briefly, these acetylcholine molecules binding to the sodium channels on the muscle is what generates this end plate potential. It's kind of like a trigger for the muscle to fire. It's an electrical trigger, and it has to be above this red line called the threshold. That's like kind of the threshold for what the muscle needs to hear in order for it to fire. And this distance here is key. It's called the safety factor. The end plate potential is higher than the threshold. There's a redundancy built into the system, and we all need this, right? Because that's why that when we are kind of exercising and firing more and more and more, the muscle can keep going because this will go down, but it's still above the safety factor, still above the threshold. So this difference between the end plate potential, which is the electrical signal generated by this whole thing, and the trigger or the threshold for the muscle to fire is a redundant buffer that's built into the system. So at low frequency stimulation, what has happened is, so sorry, I need to go back a second. So you'll notice that back here, there was a more acetylcholine ready to be released in the primary store, okay? Before anything had happened. But once it's released, there's less ready, right? So when the action potential comes down, sorry, when the action potential comes down and this is released, there's gonna be less of these receptors bound to, and so the end plate potential will be reduced, right? You're generating, and that's natural. There's nothing pathological about this at all. You've just used up the initial primary store of acetylcholine, but it's still above the safety factor, so the muscle fiber still contracts. We don't feel or see a difference when we do any testing. Competitive nerve stimulation is basically all testing of the neuromuscular junction is all about exposing an abnormal safety factor, that difference between the end plate potential and the threshold. So this low frequency, two to three hertz RepStim is typically used for myasthenia gravis and other postsynaptic disorders. And high frequency stimulation is usually used for Lenz and botulism or postsynaptic disorders. The truth is we rarely actually need to use this. Any motor nerve can be tested, but RepStim is definitely more sensitive in symptomatic and or proximal or facial nerves. So if someone has ptosis and diplopia as part of their myasthenia gravis, it's much more likely that you're gonna get an abnormality in the facial RepStim as opposed to the median RepStim. So you have to do baseline, one minute wrap. Okay, I'll do two more minutes. The technical factor is very quickly you have to do a baseline nerve to make sure it's normal. And this is the procedure. So you perform a baseline RepStim at two to three hertz with five to 10 stimuli. And remember, as you go naturally, acetylcholine with each successive stimulation, the release will be decreased. But because it's above the end plate potential, your muscle fiber action potential and your compound muscle potential look the same. So you're not gonna see any difference. You don't notice this because of this redundancy here. As long as these bars are above this line, you'll generate a normal RepStim. I'm just gonna move forward quickly. In myasthenia, the situation is different because you've got these antibodies binding these receptors. So when that happens and this is released, there's less of an electrical signal generated. So this is the same. The acetylcholine release is the same, but it generates less of an end plate potential and it starts to dip below threshold. So you don't get as many firing with each successive stimulation. And so some muscle fibers fail to meet threshold and that's why we get a decrement. And that's what this looks like. So the first one's fine because there was enough in the primary store, but with each successive stimulation, there's less acetylcholine released and the waveform goes down. If there's a 10% decrement at baseline, you get them to exercise for 10 seconds. When you exercise, more calcium is pumped in, which moves more of these acetylcholine molecules down, which basically almost restores the primary stores. That's kind of what happens. And so you get something called post-exercise repair or facilitation. So this is at baseline, they exercise for 10 seconds and you lose that decrement. It goes from 32% to 8% in this situation. I'm gonna move forward because I wanna wrap up. I just wanna show you very briefly in presynaptic conditions. The problem is that calcium is not in LEMs, for example. Calcium is not entering the cell. So when an action potential comes down, there's very little, if any, acetylcholine released, so there's nothing generated. So the end plate potential is below threshold, nothing happens. I'm just gonna move forward. So what you can actually do, so this is a perfect example, and this is actually from fellowship at Brigham. This is a patient, this is an ulnar study, where at baseline, they had a very low amplitude response. I think it was 0.3. But when you, and then this here is after exercise. So this is an ulnar at the wrist, below and above elbow, and then this is after exercise. When you exercise, it pumps more calcium in through whatever channels are left over, and then it starts to release more acetylcholine. So really, this is the ideal test of choice for LEMs, where you get this post-exercise increment. So here it goes above, I think this increased by 3,000 or 4,000%. I think in the interest of letting Dr. Choi have time to speak, I'm gonna wrap up there, but I will be available after if there's any questions. Sorry about the delay. That's it, thanks. Chester, I think, I have more slides, so it's not the presentation won't finish. Thank you very much, Dr. Eisenberg, and sorry for the technical issues, hopefully, and thanks to Chester for troubleshooting and getting us through them. So the final speaker is Dr. Joseph Choi, who is a neurology faculty member at Georgetown University and also the neuromuscular chief at the Mid-Atlantic Kaiser Permanente, and Joe is gonna talk to us about some study pitfalls and troubleshooting some of them and so forth. So Joe, come on. Thank you for the invitation. So my talk, more or less, focuses on how not to screw things up. So, are we having, it's not uploaded yet. So ideally, obviously, if you do everything technically correct, you get good data, there's no problems with anything, but obviously, in the real world, we're gonna have some pitfalls and troubles along the way. So the goal of my talk is just kind of talk about common things that happen in the EMG lab and how to avoid it. Largely, it pertains to nerve conduction studies, not EMG, because most of the pitfalls are in the nerve conduction study. So one of the things, I guess, so things that are most commonly seen on the EMG lab, for example, is cold temperature, and it's probably a bane of most people that do nerve conduction study in the lab, whether you're a tech, physician, whoever's doing it. When it's cold temperature, as it was covered earlier, there's a slowing of nerve conduction velocity and distal latency, and that is a pathology, whereas cold temperature is not a pathological process, it's just, that's a normal physiological response. So when you have cold temperature, you really have to watch out that, you know, what you're recording is not, is it true pathology or not? So, meaning, if you do a hand study and you're evaluating for tingling on the hand, for example, so EMG labs, we get, you know, specific questions like carpal tunnel eval versus tingling on the hand versus something as forelimb study, and you're like, what are you looking for, which is not an ideal situation. So when you're doing it, it's really important that you actually have proper temperature, because if you're doing it on the hand, if you have a cold temperature, guess what? You're like, oh, there's a long distal latency, patient has a carpal tunnel, then you do an ulnar study, and you're like, well, there's prolonged distal latency in the ulnar studies, well, patient has an ulnar at the wrist, and they end up walking out with two diagnoses they don't have, which may or may not get surgery or other treatments for. So it's vitally important that we have to be mindful of temperature. It is the, one of the most common errors that happen in the lab. For example, like, early after graduating, I remember getting a, you know, relatively young man with two kids. He was diagnosed with, he said some neuropathy that doctor didn't know, but it was demyelinating. He didn't know he was gonna see his daughter's graduation. He was, like, petrified. I examined him, and I talked to him. He just has tingling. He has a completely normal exam, but he was diagnosed with demyelinating disease. When you touch his hand and legs, he's just cold. He's got good reflexes. You know, based on exam alone, this is gonna be a normal study, but the person that did it didn't really control for temperature, so feet were cold, slow distal latency, slow conduction velocity. Hands were cold, slow everywhere, so these things really do happen quite a bit. If you talk to a lot of people that treat CIDP, there's a lot of patients that don't have CIDP that get diagnosed by error, and they keep getting treatment, so it's really vital. I guess we're still having problems? Is? Yeah. It's not for the U.S. patient. It's, there's a, and it says Joseph Choi, AA, for today. If you put it up, I could tell you which one to open. All right, so there's some, so in a minute, when we get the, illustrate the point, what happens with the nerve conduction study, so I will get to, there's a visual representation of one of my residents. She had normal hand temperature. We recorded the distal latency and the peak latency, and you could see how it's, if the onset is, time zero is here, it's normal, kind of comes up early. Then I put her hand in ice bath for about five minutes, and then it was about 10 degrees cooler, and you could see the latency actually get prolonged to a point where one becomes normal and cold hand becomes abnormal, and it is kind of vital that we actually have to be very mindful of it. I'm trying to figure out how the progression on my talk goes, so I could just keep going until I get my, some visual over here. The other topic that I'm gonna cover is when there is a, what looks like a partial conduction block. It's kind of hard to explain without visuals. It's kind of like when you do a nerve conduction study, you get a big amplitude, then you do a successive simulation, and there's a drop in amplitude, which looks like a pathology, and you think this is a conduction block, but there's various sorts of things that could happen that would cause what the visual representation you're getting, what looks like a partial. Yes. Sorry. The flash. Is that working? Oh, okay. We're really having a. Okay. I gotta log in. Yeah, sorry for the technical difficulties. Yeah, it's kind of hard to describe what I'm trying to say without a visual. Yeah. Sorry, I gotta put the computer over there. I actually shut it down earlier. Trying to save battery. Can you not log on, or is there? In the system that was uploaded? Oh. It was updated again this morning. Thank you. Oh, here we go. Great. Can I control it with this or are you going to have to advance it for me? There you go, I got nothing to disclose. So quickly cover things, we're going to talk about temperature, we already did, technical errors, anomalous innervations that can happen, which is a, if you don't recognize it, which you could diagnose as an abnormality, age and height, we'll briefly cover, which kind of, you could say somebody has a slow conduction velocity when they actually don't, there isn't, you know, somebody that's 80 years old and they're slowing, so that's something to be accounted for, and we'll cover some things in the ICU as far as what to do from a technical standpoint. All right, so we talked about that, so this is what I was trying to illustrate. So this is my resident's hand on normal temperature, you can see the onset right here and the peak onset, and this is after, in an ice bath, and then you can see the prolongation. So this could be normal versus it could be pathology, or misdiagnosis of pathology, even though all it was is cold hands. I mean, this is probably one of the most common causes of error in the EMG lab, so that's why I put it first and I can't stress that enough, because everybody that does EMG, we get patients on a regular basis that have an abnormal study, but when you correct for temperature, they have normal studies. Okay, so best way to warm it up is cold water bath, and this is something I learned during fellowship because when I was a resident, I saw people use hair dryers, use all sorts of things, but when the temperature is really cold, meaning they're more than 10 degrees or close to that, you really need a warm bath because you need to get the core temperature up. If you get the skin temperature up with a hair dryer, it's going to cool down, but the nerve underneath is still cold, and you're still measuring cold nerve, and that's going to cause you to have abnormal data, which is all technical. So if it's really cold, I would say use a water bath. Between heat lamps and hot air, meaning air dryer, you got to plug and unplug. I don't think anybody wants to waste time anyway. Hot packs, I found it to be somewhat helpful. On the arms, you want to basically have the temperature anywhere above 32 and legs over 30. Obviously, if you have a normal study, nobody really cares what the temperature is, but if it's abnormal, it's vitally important that you actually record the temperature because if you didn't, you never know if the temperature was the issue for the nerve conduction study. You can't correct for it, but this is what pitfalls, I mean, there's a range for it, and you correct, and then it's borderline, you don't know what to call it. So better bet is just warm up the limb and just move on from there. So this is what I started doing when I was practicing. So I would have my front desk person that checks in have this little handy thermometer and shoot it on their hand. If it's cold, give them a warm pack, and last thing, it's time to go to the bathroom because how many times have you sat in the room and you're ready to start, you put all the recording leads on, they go, I got to go to the bathroom, and you got to unplug everything. It's an issue, so it does help with the bathroom, but again, I do help find out that if you record temperature before they come in, it really does help. If it's really cold, you could tell the patient to go to the bathroom and warm up the hands before they come to the lab and give them a warm pack. So temperature monitoring system is really helpful. You just basically put the probe on, the temperature gets downloaded into the data, so you don't have to worry about it at all. It's always being recorded. You could always look up every time something is slow. The other thing I have done often is I basically treat the limb that I'm testing like something precious. I get one of the pillow cases, I wrap it up, I put a warm pack after I warmed up, that way it stays warm. There's nothing worse and more disrupting EMG or nerve conduction testing when you have to take them off everything and try to warm them back up. You know, time, EMG labs are getting busier and busier, so you just have to be more efficient. And if you're evaluating for something like a focal neuropathy, it does help to test other nerves, meaning if you're doing a carpal tunnel, do an ulnar nerve also. That way, if it's a cold temperature, everything's going to be slow. But if temperature's normal, if they have carpal tunnel or median compression at the wrist, it's going to be normal just for the median nerve, but not the ulnar. So things that are helpful using a palmar comparison or a lumbar interosseous comparison because you're doing kind of similar location for median ulnar versus median ulnar, it's kind of the same thing. So temperature plays less of a role. And if you really have a hard time getting somebody's temperature warmed up properly, I would really recommend doing comparison studies. That way, at least you can be more confident about it. All right, so this is something that happens periodically where you, this is a distal simulation at the wrist, elbow, above the elbow. And then you get this low compound action potential, and you're like, what the heck's going on? You go over here at the below of the elbow, and you're like, increase, increase. You're like, did I do something wrong? What's going on? So when you see this pattern, a couple of things, these are the four common things that could happen. A, you submax stimulate it here. B, you excessively stimulate it at the wrist, meaning you co-stimulate it, adjacent nerve. For example, if you're doing a median at the APB, maybe you stimulated some ulnar because you were a little excessively stimulating or increased the duration or the intensity so high. Third, you have an anomalous innervation like a Martin Gruber. That's why there's what looks like a conduction block. And the last thing is actual true conduction block. The reason I drew this line over here is because this is technical error on our part. This is just normal anatomy that we just maybe need to sort out. And this is the only thing that's a true disease. So if we don't do this portion and double check this, they end up with a disease diagnosis and all of a sudden we're chasing our own tails again. And one thing always to do, when you see this and when you're trying to sort this out, you could always go back to the basics. What's the exam show you? Because if it's a conduction block, they're going to be weak. If this is one of these things, they're going to have normal strength. So it always goes back to the initial because remember, electrodiagnostics is considered an extension of an exam, not replacement of an exam. So always keep that in mind. All right. So I'll cover submax stimulation first. This is when at the forearm or the elbow, that's when you submax stimulate it. This is commonly more seen on those guys with huge muscular forearms and you're trying to put that probe in, you're jamming it in, you gel again, you crank it up and you just keep doing it. It tends to be not this big of a difference, but that's kind of common reason for submax stim. Now the question is how do you try to avoid not doing a submax stim? One way of doing it is this is a stimulation point here, here, here. So this is the same intensity. So what I would do is put it at a moderate intensity or low to moderate, and I will start from one end and I work my way across without changing the intensity. You could see how the amplitude is tiny, a little bit bigger. See how big it jumps up? I mean, this is a relatively a thin person, so it didn't take much, but this is the same intensity, but just moving it across. So if you find that spot that gives you the biggest amplitude, then you're going to go for the supermax stim. You don't want to start random places and start cranking it up. This is when you get co-stimulation because you're stimulating other nerves nearby. For example, if you just put that stimulator here and you stim, you get some median, but if you go high enough, you're going to get the ulnar over here, and obviously thenar has median and ulnar, so you're going to get co-stimulation. So it's really important that you kind of figure out where the location of that nerve is before you increase. So this is once you find the spot, then you just keep increasing the intensity until you get maxed in. When you think you hit max to make sure you're in the right spot, you increase by 10% to 15% more. It seems a little bit obnoxious to the patient, but you just want to make sure that you're on the right spot, plus you stimulated all the neurons on the site. So that's how you're going to get your supermax stimulation. Okay, so we're going to talk about now co-stimulating, meaning stimulating adjacent nerves, so you get two different nerve muscle pairings, so you get a falsely elevated CMAP amplitude. So this could happen, again, maybe I should have used a different muscle. So this would be more typical if you used a APB on the median nerve, because the median nerve, APB, obviously there's median, and there's also ulnar. As I was kind of discussing earlier, if you stim it right around in between median and ulnar, you could co-stimulate both. But by the time you get to the forearm, between the forearm where the median nerve travels and ulnar, it's pretty far, so you've got to be really obnoxiously high before you co-stimulate at the forearm. But at the wrist, if you put the stimulator at the wrong place, you could easily co-stimulate median and ulnar. So you have to really be mindful that you don't co-stimulate. All right, so how do you reduce excessive stimulation? Again, stimulate over the intended nerve. Watch for any abrupt changes in morphology, meaning when you co-stimulate, you go from one morphology that looks like APB muscle, all of a sudden the morphology abruptly changes. So you have to pay attention to what the morphology looks like. If there's a rapid change, you have to say, did I co-stimulate? What did I do wrong? The only thing interesting is when I was starting early, I realized you also get a little bit of a morphology difference if the patient's tense up versus relaxed their muscle because the recording area is basically, it looks at the shape of the muscle on their knee. So when I was doing a nerve conduction, the morphology kept on changing. I just didn't know why. I was like, am I doing something wrong? I realized the patient's like, I'm relaxed. They're like so tense while they're getting stimulated. So be mindful of that. That's the only other times I've noticed the morphology changes when they tense up from relaxing. So the other thing is watch for resultant muscle movement, meaning it happens commonly when you're doing a perineal study. So when you do the proximal stimulation behind the knee, instead of going a little more lateral, you go more medial, then you stimulate the tibial. So you should be, when you're doing a perineal, the ankle goes up and out, but when you do a tibial, it's down and in, so you have to watch out which direction the foot is moving. Same thing with if you're doing a hand, APB, you should go up, but you shouldn't see all nerve muscles activate. So that's another way of knowing when you're co-stimulating or stimulating a wrong nerve. And last thing, you could somatose record from two different muscles and nerves, but that's a lot more work, and I'm not sure how many people actually do that. I rarely ever do this. You just have to, if you do the first three, I think you could easily reduce the excess of stimulation. All right, so this is your anomalous innervation. This is normal anatomy, and this is not a pathology. So when you see this pattern, the first two I do is, did I submax, meaning submax here? Did I excessively co-stimulate over here? And if that's not the case, I'm going to say, is this basically a Morton-Gruber or some sort of anomalous innervation? If that's the case, then you could see this pattern and not mistaken for a conduction block. So this is a kind of a classic Morton-Gruber in the arm. So this is the pattern you're going to see. You're going to say, I get this really nice, beautiful amplitude, and I get to the forearm, I cannot get this amplitude up, and you're cranking it up, higher intensity, longer duration. It's just not working. So what the patient could have is this Morton-Gruber anastomosis. So this is a median nerve. Let me just see if I can... Median nerve here, this goes over this way. This is a normal ulnar nerve going over this way. What happens is there's a fiber from the median nerve crossing over the dotted line and going to the same muscle that ulnar innervates. So when you do that, you get extra fibers that you get at the wrist, but you don't get at the forearm, and you could get this pattern. Now the question is, how do you actually prove this in the lab? So the three most common are FDI study, ADM study, and APB study. Mind you, just about many patients that come in in the lab for the hand study, you end up doing these two, FDI, especially if you're doing ulnar at the elbow study. So these three are common studies that we do in the lab, and it is the three most common from Martin-Gubrin asthmosis. So this is the initial pattern you get. You get this nice amplitude here, and then you get a lower amplitude on the forearm and more proximal stimulation, which these are about the same. Then like I said, you try to do the submax, co-stem, that's not the case, then now how do you prove it? So when you did the study, this represents here the fibers coming from the median and ones that are from the ulnar, and these two are basically more proximal to it, so you don't get the fibers from the median that's crossing over. That's why you have a low amplitude. So how do you prove it is, you stimulate at the median nerve, and being that there's no fibers going to that, or at least minimal, because there's some co-stimulation here, you get this little tiny blip. But when you stimulate median nerve at the forearm, you get the crossing fibers now, so you're going to get this little amplitude popping up. So if you add this amplitude to this amplitude it should come out to about the same as there because you're accounting for the fibers that are crossing over. Does that make sense? Okay so this is the same concept again crossovers here so obviously if you do the wrist versus forearm you get a bigger amplitude at the wrist and this time again you stimulate at the median nerve sorry and then you stimulate the median nerve at the forearm to get this amplitude again add these two together and you get this amplitude and and the last this is the median nerve recording from the APB so this is like when you're doing a routine median nerve study for a carpal tunnel eval and then this is what happens here you get this you stimulate at the wrist and you get none of the fibers are crossing over then when you stimulate at the forearm you get that fibers from the median that goes crosses over to the ulnar to go back to the APB muscle so this is the opposite of what we saw before you get a higher amplitude at the forearm because the crossing over from median to ulnar by the way Martin Gruber and Aston Moses all median to ulnar crossover and it's only motor not sensory so you don't generally find MGA on a sensory study mind you you don't get done with your proximal stimulation of sensory studies anyway but always remember MGA it's meeting to ulnar only not the other way around because if you go the other way it's a different anastomosis and that's even more rare so again how do you prove it now you just got to jump over to the ulnar nerve and then you get a nice big amplitude because you're getting the fibers that are crossing over and then you do the proximal stim and obviously you get the same pattern and it's really important that you check for these things because you know when you when I was training I would get this pattern I thought I screwed up somewhere you know did I under stimulate here did I co-stimulate I would kind of get stuck on the first two cycles and then I was like oh yeah I forgot about the third thing I have to look out for which is a Morton Gruber so remember if you're doing a median nerve study your proximal is bigger amplitude if you're doing an ulnar study you get more proximal that's lower amplitude so distal is higher so it's the pattern you're looking for but again when you're doing it you always have to go through the thought process when you see a drop in amplitude you can't correct you're gonna say did I sub max at the area that's low did I co-stimulate in the area that's high or is there a Morton Gruber or some sort of anomalous innervation that you're missing and now you have to figure out how to prove that because if you don't go through this then you're gonna say patient has a pathology and this is even more rare but you can't have a proximal Martin Gruber so meaning instead of being more further out it's more proximal so this could mimic somebody with ulnar neuropathy across the elbow one way to try to avoid it is when hopes that really chomped so are you telling me I gotta go nope keep going back keep going go okay thank you I'll just go from here so one way to reduce it is doing so most of us use 10 centimeter as the difference from proximal to the distal stimulation across the elbow some people use five and five meaning five proximal and five distal from the elbow but if you look at cadaver studies and other studies from EMG labs if you use about three that's distal and seven proximal you tend to avoid the proximal Martin Gruber and the other thing that does help using a three centimeter the distal stimulation is the further you go into the forearm the ulnar nerve dives in deeper into the muscle it's harder to get up maxed in on those patients anyway so I used to use five and five and then I just eventually switched the three and seven measure me three centimeters seven centimeters because I got sick of dealing with the drop in amplitude on the forearm and wondering if I did something like is there a Martin Gruber I kept on you know checking for things that wasn't there so I would generally recommend three and seven to make the ten centimeters across the elbow rather than five and five so accessory perineal nerve this is the one that you see in the legs so normal would be where this one nerve innervates all of the EDV muscle but portion of the population has this accessory nerve that comes on the posterior side so the EDV muscle is duly innervated by portion from the deep and portion from the superficial so what happens in this patient when you stimulate at the ankle you get a low amplitude because you're not getting the accessory nerve that's coming through but when you go on the fibular neck because it's up here you're doing common so you get both the superficial and the deep so you get this high amplitude so this is the same concept as what you find in the arms so when you see this pattern you stimulate not the anterior of the leg you go to the posterior side behind the lateral malleolus and you stimulate there typically where the sural nerve would run and you get a nice amplitude again you add this and this I mean this and this together you get this amplitude so always keep that in mind so pitfalls just to kind of go back if you see any changes in amplitude you can't seem to correct always ask yourself sub max then excessive or coast in here anomalous innervation whether it's a Morton Gruber and the arms or accessory perineal in the legs and last thing is the pathologies the conduction block you know if you see this you could say all patient could have you know multifocal motor neuropathy because there's a conduction block in any typical site so those are the things that we just have to really think this is more common than this so you have to think this first before you go over here whoops can we go back one can we go back one I think I went over all right so we'll just kind of cover the rest of a little more quick I think something you could all read basically when you're doing a nerve conduction study basically by four years of age they have an adult value so if you have a teenager it's not really a major issue doing a nerve conduction study I know some people just don't like doing it on younger patients but you know you expect normal conduction plus I didn't just the latency and so any other thing is some of the younger population you might see a by four morphology which because they're still myelinating so you might see like a by fit that kind of comes together later in age but if you see that on a younger person meaning somebody closer to this age don't be too alarmed that's kind of a normal pattern this is probably a bigger thing where you get an older patient and then you get this borderline conduction velocity older you get and I mean obviously we have a lot of older patients that are coming in that are 70 80 years old so you remember there is some normal slowing of conduction velocity because you tend to lose a little bit of the faster myelinated fibers as you get older so you have to account for some slowing so you know notion of just writing there's a demyelinating disease is that's another pitfall so you have to be careful in older patients the other thing is several nerve studies as you get older there's absent and healthy patients when you're over 1780 it reaches close to 40% when you go over eight years old so if there are symptomatic you know you could probably say maybe it is neuropathy but with that said when you're at this age category you always have to kind of say this could be normal for age versus it could be a feature of an external neuropathy so keep that in mind when you're doing this because I think nowadays in our healthcare system there's more patients that are getting more diagnostic tests than ever before I feel like there's less history taking exams there's more diagnostic testing so I think we have to be a little more vigilant about making sure the data is correct when they leave so basically taller the patient you get some slowing it's not a pathological so long it's just a normal thing you see because the nerve diameter basically tapers as you go further this becomes really an issue on a tall and elderly patient so this is really something you have to account for but if you get somebody that's particularly tall that's 70 years old and your motor studies are like borderline you don't know what to call it keep this in mind and you could always consider correcting for it I see you I don't think anybody generally likes doing nerve conduction EMG in the ICU because of the artifact basic things watch out for obstructions interference is the biggest thing the sensory studies are a mess sometimes you can't unplug things in the ICU obviously so you have to keep that in mind grounding is really important when you're in the ICU patient can't activate so you have to work around it and positioning is all what's also challenging oh the other thing is might be always be thinking what are they asking and when did the symptoms start because the timing of the nerve conduction abnormality EMG abnormality does change if something changed yesterday our study is not going to do anything so doing a study that early is not going to help them at all so for the EMG studies in the ICU keep a focus question and obviously these are the questions that they typically ask so make sure you design the study appropriately and most experts recommend one leg one arm do a motor and sensory do a f-wave meaning make sure there's no prolongation meaning like demyelinating disease to say why the patient's so weak and needle one proximal one distal muscle you know is it a myopathy is there a neuropathy so if you do this I think you are able to at least get a sense of what's going on if one arm one leg and you do this and if it's completely normal chances are if you do it at the right time it's going to be a normal study even if you do it later so this is the general recommendation safety ground ground ground generally best places between stimulator and the recording and obviously make sure it's not a wet skin sorry but a little fast because of the time pneumothorax is something that scares all of us when we're doing needle studies but when you look at all the data it's pretty rare at least that are symptomatic mind you without that said true incidence is unknown you know unless the patient has says I'm short of breath and they get an evaluation you don't know who has a small pneumothorax that you cause you don't know about but if you're gonna put a needle in anything that's you know obviously paraspinals higher up anything around the scapular you know always ask yourself if it's vital to the diagnosis and only other thing I could say before that is make sure you use a smaller needle not the long ones and kind of know where your landmarks are so you don't go too deep infection risk it's really low you don't have to use prophylactic antibiotics for valvular disease patients don't go through an infected skin but the common things been common but with that said it's really not much of an issue no evidence to say needle stick is much higher increase or infection and most of the study says you know preparing the skin before doesn't really change but I think all of us obviously always clean bleeding risk with the needle EMG so this is a people with dual anti platelets anticoagulation I know some EMG years never like doing anticoagulation but the data doesn't really support that you have to avoid it absolutely so if you look at two different studies looking at a lot of patients two out of close to a hundred had some symptomatic hematomas this is for dual anti platelet but they're all small and typically asymptomatic another group did another study with hundred muscles I on a range of you know one point six to four which is pretty high but it's again pretty not common but with that said you don't want to be willy-nilly about sticking a needle when somebody's an anticoagulation so use a small gauge needle avoid deep muscles because you can't really compress those sites and if they have a hematoma it could be larger than you think and avoid muscles that has arteries and veins nearby obviously for obvious reasons they just don't clot as well take home message cold temperature biggest thing to look out for when you have what looks like a partial conduction block or a low amplitude in certain spots check for Martin Gruber sub max over stim elderly patients just remember that you could have a bit of a slowing conduction velocities a little bit of slowing just the latency you could always do the calculations and just make sure that it's it's normal I see you focus questions watch for artifacts pneumo thorax infection bleeding risk is really low but obviously just due diligence and limit the number of muscles tested if you if they're on anti-coagulation sorry I kind of rushed a little because of the time thank you very much and again sorry for the technical issues and thank you for going fast and catching up I think my thing was done pretty nicely so we're around for questions we had hope to leave some time within the session but we're around if you need to ask any questions and if not then have a nice day and enjoy the rest of the meeting

needle EMG

muscle activity

morphology

firing patterns

recruitment patterns

motor unit action potentials

neurological conditions

nerve conduction studies

ncs

technical errors

temperature impact

submax stimulation

anomalous innervation

diagnostic accuracy