My name's Daniel Simmons, and we're going to be doing the talk on planning nerve conduction studies. Let me pull up my slides here. There we go. So I'm from Boise. That's where I practice. I'm an employed neurologist there, a clinical neurophysiologist. If you don't know where Boise is, that's in Idaho. Some people think it's in Iowa. It's not. It's the home of the Blue Turf, the next Heisman winner, I think. How many of you are technologists and residents, fellows, attendings? Well, this talk is going to take you through how I approach, how we approach nerve conduction studies, trying to move from an algorithmic, memory-based approach to an intuitive understanding of why we're choosing the studies we're choosing and hopefully provide you with some tools that you can use, that you can take home. The disclaimer here is that every lab, every attending physician is going to have different preferences. And so take what you learn and see if it works in your setting. And if not, that's OK. There are lots of different ways to do this. That's part of what makes it fun. I'll let my colleague introduce himself. But this is Dr. Fulham. With Brooke Army Medical Center, that's where I trained and that's where we met. But I'll let him tell you more about himself when he talks next. All right. Yeah, that's not, oh, it's gotta be on, there we go. Nope, turning it on doesn't help, okay. Turn that off. All right, I'll use that. Okay, so I'm gonna talk about upper limb nerve conduction studies first, and then, go ahead. Can the lights be higher? Oh, yeah, that's a, let's see. As soon as our AV person comes back, I will ask him to dim the lights. All right, thank you. Okay, I have no disclosures. For the techs in the room, this is a CNCT checkpoint opportunity, so. Oh, nice. Is that better? Oh, those lights, yeah. Okay, so we got some dim lights. All right, so take note of the highlighted items. Those may come up in the CNCT checkpoint questions that you can get credit for. Okay, so why not this? Why don't we do this? Right median motor, right ulnar motor, right radial motor, median sensory, radial sensory, ulnar sensory, and just repeat everything on the left side. Why not that? That'd be more efficient, right? You don't have to think about it. You just do the same thing for every patient. You've got it covered. Well, this should be intuitive, but yeah, it's uncomfortable, and it's expensive if you do this for patients. Also, the problem of false positives. So the more tests you do, the more the opportunity is for false positives. I'm gonna talk about that in a minute. How many of you know this table? Yeah. So this is the maximum number table. You can find this on AANEM website. But this is basically a guideline, like if you were to get audited for some reason, to say for most cases, 90% of cases, this is the maximum number of nerve conduction studies that would have to be done to answer the question. It's a rough guide, but it kind of is helpful. So I think we need to talk about false positives. So that's any positive test in an asymptomatic or normal control. And the way we define this is by a reference range in a control population, so mostly volunteers who are asymptomatic. And so we have this way of calculating the mean. We take the standard deviation or a couple standard deviations. We arbitrarily define that cutoff value based on the number of standard deviations from the mean. So for example, if we were looking at median motor amplitude, we would take 100 healthy people with no symptoms. We'd measure their amplitudes or their median motor study. And we'd say beforehand, we're gonna define abnormal as two standard deviations below the mean. So this is a histogram showing you all the different values of those 100 patients. Most people are kind of in that six to 10 range, and there are some people above and below. We fit it to a standard curve and take the mean, take the two standard deviations below, and then we define our cutoff value as four. So we're gonna say anything less than four is abnormal, even though a proportion of our subjects fell into that range and that was normal. So that we're defining this cutoff value there. And by definition, that's gonna give us a 2.5% false positive rate, just statistically. Okay, so if we do a bunch of tests, and we just say, if only one of those tests is gonna be, if we require that just one of those tests to be abnormal to make our diagnosis, then the false positive rate for each test is additive. Okay, so if we do something like this, where we're, for example, evaluating carpal tunnel syndrome, we just do every test we can think of, we're gonna have a false positive rate of 15. That's way too high. If we say, I'm gonna require that two different tests are abnormal before I make a diagnosis, then it keeps the false positive rate low. So the take home here is that there is a possibility of error, just based on that false positive rate. And we only want to do the minimum number of tests required to make our diagnosis. We want to avoid reliance on a single data point. And we always wanna strive for at least two independent data points for diagnosis. Error happens, it's part of nerve conduction studies. You really can't get away from error. Okay, so I'm gonna take you through some cases. And again, this is how I think about things, is how I approach them. There are lots of different ways that you can do this individually. All right, so we have a 40-year-old female presenting with bilateral hand parasthesias for a year. It's the thumb, index, and middle finger most affected. The symptoms wake her up at night. Gets worse with driving, holding a phone. She's dropping things. No neck pain or weakness in the hands. So what does it sound like? Sounds like carpal tunnel, right? Pretty, pretty easy case in terms of what the clinical diagnosis is. So this is her nerve conduction study. Did the median motor first. Is this consistent with what you were expecting to see? And the prolongation of the median motor latency there. Everything else looks okay. So that's taking us down the path. And then this is the digit two, or the index finger sensory, the antidromic sensory. And the abnormal values are highlighted there for you. So the latency is prolonged. The conduction velocity is slow. The amplitude is low. Are we done there? We've done two studies. They're both showing us this is, there's some slowing across the wrist in the carpal tunnel. Who would stop there and say we're done? So the question I have for you is that amplitude of nine, what do you think about that? It's low, so what does low amplitude mean? That means axon loss, right? Most of the time, axon loss. Or could it mean conduction block? And how would you determine that? So how you can determine that is by simulating the palm. This is called the segmental sensory study. You can do it on digit two or digit three. Basically, you are, if you think the block is at the wrist, at the carpal tunnel, and you're stimulating proximal to that in the wrist, then you are stimulating before those blocked fibers. So if there is a block, you can resolve that by stimulating past the block in the palm. And we stimulate in the palm, you're surpassed that block, and you're stimulating all the fibers. All right, so if your amplitude recovers, if it goes up to normal in the palm, then you've confirmed that you have conduction block. Okay, is anyone doing this routinely? Yeah, so this is the only way that you can differentiate axon loss, sensory axon loss, versus conduction block. Let me show you here. And just to make a note that when you do this segmental study, you're looking at the velocities, and it breaks down the velocity of digit two to palm, so that distal segment. In her, it's 58. The palm to wrist segment was 27. And then the average velocity across those two segments was 37. So it really breaks down where that slowing is. You can prove that it's segmental slowing across the carpal tunnel. So this is how that works. So if you get a pattern like this, where you have a slow conduction velocity, and your amplitudes are the same at the wrist and the palm, you know it's demyelination only. If the amplitude increases in the palm from the wrist, then there is conduction block there, sensory conduction block. And if the amplitude stays the same, then you know you have sensory axon loss. And so, like I said, it's the only way to distinguish these two. And really recommend averaging at least five waveforms in both the palm and the wrist, because we're looking at that conduction velocity. And that's determined by the onset latency of those potentials. Onset latency varies a lot. There can be a lot of variability in terms of where that latency falls. So by averaging at least five or so waveforms in each place, you get a more accurate conduction velocity. All right. And in her case, the ulnar motor and sensory studies were normal. So the conclusion is that this was a moderate severity, median neuropathy at the wrist. And I said bland grade three. I used a bland grading system. This goes back to a paper from 2000, 2001, where it correlates severity with outcomes to carpal tunnel surgery, which is why I like it. It's worth reading if you haven't looked at that. So we would say there's evidence of sensory conduction block at the wrist, which carries a better prognosis than sensory axon loss. So that's important for the patient to know. And there's no evidence of sensory or motor axon loss. All right, case two, we have a 78 year old male with numbness and weakness in the hands, onset more than a decade ago. And it's the entire hand, it's numb. And it's constant, there's no triggers, no neck pain. So this is his initial nerve conduction study to the median motor recording APB. So his distal latency is prolonged, 6.8. Amplitude is low, 3.9, 3.7. That conduction velocity is a little slow. So take a look at that and think about what you would do. Is this helping you? And then what would you do next? So sometimes when you have axon loss, you can have some mild slowing from axon loss. If your normal value for your median motor is 4.5, and if you have a completely axonal dependent slowing, that latency shouldn't be above 5.7 or so. And this is clearly be above that. So there is some demyelination here. This is clearly demyelinating. All right, so who would stop there? Does anybody stimulate the palm? We've got one taker. Does anybody have the, I mean, given the dogma that you should never stimulate the palm? Haven't heard that, okay. So blank slates here then. Okay, well, in this case, we did stimulate the palm and the amplitude jumped up to 5.2. So what does that tell us? It tells us, it's similar to the prior case, there's conduction block. So that weakness that he's having of his hands, maybe he can get some back if we do a release. Whereas if it's axon loss, then maybe not. So it can make a difference prognostically to have this information. The problem is this is controversial. It's controversial whether or not you stimulate in the palm. And I'll explain why, but that's what I would do in this case, and I don't do it all the time, but if you have a low amplitude at the wrist, you can try to stimulate in the palm. So you have to be really careful about this because where you're stimulating, where I have my stimulator placed here in the picture, that's about where the recurrent thenar branch is, and it's close to that deep branch of the ulnar nerve. And so you can easily get co-stimulation if you're not careful. So you have to be very careful about this, start with very low currents, make very small increments, and if you notice any change in the waveform, go back because you may have co-stimulation. And so if you have something like this where at the wrist it's low, but then you go into the palm and it's much higher, that's conduction block, that has a good prognosis. If the amplitude is the same at both places, it's axon loss, that's prognosis is much worse, and at least a longer recovery that you expect. And if you have a change in the waveform, you call it co-stimulation. Now, I say when in doubt, if you can't tell, if you're not sure if it's co-stimulation or if it's the median, then just throw it out. Just delete that portion of your nerve conduction study, keep the rest of the median, and then move on. Because this is easy to get wrong. And this is why. So Dr. Larry Robinson, if you are familiar with him, this is a really great paper from 2007 that goes through a lot of different studies for carpal tunnel syndrome. This is his hand that he's stimulating, and he doesn't have carpal tunnel syndrome, no symptoms, but it's his own hand. And he's showing you here, that top tracing is that palmar stimulation. And you can see how the waveform looks the same as the others, it's just higher amplitude. And so his point here was that it's dangerous to stimulate in the palm because you might get a higher amplitude, waveform looks the same, and you can't really tell. But one thing I would point out here is that if you notice that the stimulation, the milliamps here, it was 100. And at the wrist, it was 34, and at the elbow, it was 48. So he's cranking up the current here to make a point. So I think you can do this, but you just have to be very cautious about looking for those changes in waveform. All right, and again, if you can't tell, if you're not sure, just take that off. All right, so going back to our case here, do the median digit two sensory study, and it's absent. So check palm and wrist, make sure there's no conduction block, and it's absent. So we said earlier, we wanted at least two data points. This is another data point, it's an abnormality, but it doesn't really localize to the wrist. It doesn't really, it says, yeah, the median's absent, but is the slowing at the carpal tunnel? We don't really know. So where would you go next? Yeah, so the suggestion was to look at the ulnar motor and sensory to see, is this an isolated median, or is this a more diffused polyneuropathy? Which I agree with, and we'll do that, but to get that second data point that localizes to the carpal tunnel, you can do this study, the median ulnar motor comparison. This is a really simple study to do. You're basically taking advantage of the fact that the second lumbrical sits right on top of the interosseous. Second lumbrical is median innervated, interosseous is ulnar innervated. You put one electrode there, you stimulate first at the median, and then at the ulnar, and you compare the latencies. And this is a motor study, so we're looking at onset latencies, or distal latencies. And the reason this is helpful is that even when you have absent sensories, even when you have a very low median CMAP, these studies are often preserved. So this is a really good tool that you can use when your sensories are absent, and it's not a hard study to do. Okay, so we did ulnar motor and sensories. Those were normal, so we've isolated it to the median nerve. And the conclusion that this is a very severe median neuropathy at the wrist, land grade five with motor conduction block across the wrist, if you believe that waveform, and evidence of sensory axon loss. Okay, case three is a 28-year-old female with three months of hand paresthesias at night, and thumb and index finger most affected. No daytime symptoms, no neck pain. Starting off with the median APB, latency looks pretty good. The waveforms look good, amplitude's normal, conduction velocity's normal. So if this is carpal tunnel syndrome, we know it's in that mild range, because the motor study doesn't really start to become affected until it's at least moderate severity, alright? So just curious, what would you do next? What's your next study? If you do the median motor, you're thinking carpal tunnel, what's the next step for you? Sorry, talk a little bit louder, they've got a fan going on. Digits two and four, okay. Yep. Anybody else want to do something different? Sorry? F waves? F waves, okay. How would the F waves help you? Yeah, so you can get, right, so you can kind of use it as an internal comparison. The F waves will be prolonged, the latencies, or they could be prolonged. Sometimes you get a reversal of the ulnar and median F waves. If the median's longer, maybe that tells you there's some slowing, but it doesn't really tell you where, and chances are that if the median latency here is normal, the F waves would probably be normal to you. Okay, so what I would do, I'll just tell you, is I'd go into the digit four, and I like to go straight from the median motor, if it's normal, to a digit four, because it sets me up for something that I'll tell you about in a second. All right, so her digit four comparison, this is a ulnar median comparison, looking at the anti-geomic sensor response to the digit four, recording the same spot, stimulating two different places. We're looking at peak latency differences. The difference here is .4, which is right on that border of normal, the upper limit of normal. So then, what I would do is the median radial digit one comparison, and in her case, it's just above that upper limit of normal, .6. All right, again, looking at the differences in peak latency, and now you're thinking, where is it going? This is a lot of studies. You said, just use the minimum studies. How about this one? Median ulnar palmer comparison. This is an orthodromic study, where you're stimulating the palm, recording at the wrist. Again, looking at peak latencies, and this is, again, just above that upper limit of normal that most people use, .3. Okay, so I've done a bunch of studies. Anyone use this, the combined sensory index? I see one hand. So this is called the combined sensory index, or CSI. It's also been called the Robinson index. Dr. Robinson, who I mentioned earlier, came up with this. And basically, you take the, he called these studies the ring diff, thumb diff, and palm diff, so you're taking the difference between the peak latencies, and you add them up. So you take .4 plus .6 plus .4, and that gives you an index value of 1.4. And normal is less than one millisecond. And this is a really sensitive test. So we're adding peak latency differences. In my opinion, it's reserved best for mild carpal tunnel syndrome. So in that case where you're thinking carpal tunnel, the median motor is normal, you know it's less than moderate severity, because that motor is normal. And you don't want to use it for a severe carpal tunnel, because you may have absent sensories. And if it's in the moderate range, if you can answer the question with just two studies, like in the first case I showed you, where the median motor was abnormal at digit two and two was prolonged, you're done. In this case, your median motor is normal, and you need something else. So because these are all comparisons side to side, or median ulnar or median radial, it's resistant to cold temperatures, so that's a plus. You should always warm your limbs, but if for some reason they're cold and you can't get them warmed, this is resistant. They've tested this under cold and warm. When you use an index value like this, you avoid that false positive problem, all right, so it avoids that. And then taking the index value is more sensitive, using the CSI is more sensitive than relying on any one of those individual tests. So I like to use this when my median motor is normal, and I'm thinking carpal tunnel syndrome. All right, so the conclusion here is that this is a very mild median neuropathy at the wrist, bland grade one. Okay, case four. We have a 38-year-old male with numbness and paresthesias of the fingers for six months. The numbness involves the ring and small finger of the left hand. I'm just realizing, oh yeah, that is the left hand, isn't it? Yeah. Mild weakness noted for the last two months, intermittent discomfort of the medial elbow, and no neck pain. So what are we thinking here? Ulnar, yeah, I'm not trying to trick you. This is, yeah, should be thinking ulnar neuropathy. That's our pretest probability, right? So just a note, it's important to have the elbow flexed and the arm abducted, because that pulls the nerve tight, and you have better measurements there. When the elbow is straight, the nerve is slack, you have some redundancy, you can have some inaccurate velocity measurements across the elbow. How many people use the ANEM reference values for this? We got one, a couple, three maybe. So that conduction velocity less than 43 across the elbow, that's pretty slow. I think most people would probably use a higher value than that. And a drop of 15 meters per second, I think most people might use 10. But I think the reason that these are low, that these values are more conservative, is because it's recognizing that there is a ton of error possibility in the measurements around the elbow. So it's really important to get that right. So here's his waveforms. This is ulnar motor recording ADM. So any thoughts on this? Kind of unimpressed. I'm seeing unimpressed faces. So I'll give you a second to look at that. What do you think about this drop in amplitude? Maybe it was technical. Not really convinced. 0.2 milliamps, millivolts. I think what you said was a drop in velocity. Yeah. Yeah, yeah. Yeah, so there's that drop in velocity too. So you're seeing there's a correlation here. You know, if you were convinced this patient had carpal tunnel syndrome, I probably wouldn't do anything further with this. But remember that your pretest probability is that this is an ulnar neuropathy. All the symptoms, the exam, well, if you're a tech, you don't do the exam, but the symptoms at least point you towards ulnar neuropathy. So I do think in this case, this is worth chasing down. So how can we do that? Everybody's favorite, inching studies. All right. So when we do the inching studies for this case, you see that that drop in amplitude isn't just technical. There was definitely something that happened between the medial epicondyle and two centimeters proximal. So those are very stable waveforms. And then that corresponds with some focal slowing there across that segment. So when we do conduction studies, do inching studies, we're looking at a 0.7 millisecond difference between the two. I'll talk more about that here. And then in this case, you can also do sensory inching. I don't do it a lot. Not inching, but sensory across the elbow. And in this case, it shows some slowing, some focal slowing across the elbow. And there was also a drop in amplitude across the elbow. There's two drops in amplitude, right? One is normal, one is abnormal. So when we go from wrist to elbow and we have that drop from 30 to 9, that's your normal drop. That's temporal dispersion, phase cancellation. And you expect that sensory response to be lower, more proximally. Because as it runs down that nerve, it flattens out. All right? So that's expected. But when you go above the elbow, you go from 9 to 3, you don't expect more than a 20% or so drop across the elbow. So there's sensory conduction block there, too. When you do this, it's really important to average your responses, again, because those onset latencies are more variable. And so that'll give you more accurate waveform. So the conclusion here was that there's a mild ulnar neuropathy of the elbow with primarily demyelinating physiology, localized to the retrocondylar groove at the medial epicondyle. I'm going to talk more about that in a second. And that there's sensory and motor conduction block at the elbow. No evidence of axon loss. Okay. So what was initially kind of an unimpressive study actually becomes really impressive when you get down to it with the inching studies. So I want to take a sidebar here and talk about inching studies. You know, I jokingly said that they're everyone's favorite. I think they're time-consuming. They're technically challenging, a little bit tedious. The patient's looking at you like, am I going to be done soon? But I think it does have its place. So why do them? Like in this case, you can detect focal slowing over a case, over what would otherwise have been diluted over a longer distance. And you can localize more precisely. And what I mean by that is, is it distal to the medial epicondyle or is it more proximal? And I think there's mounting evidence that this distinction really matters. So cubital tunnel, distal, versus retrocondylar groove, more proximal. All right. I want to talk about a study that goes back almost 10 years ago. This is a study that looked at 86 arms with ulnar neuropathies. Every patient had inching and ultrasound to try to precisely localize where the problem was. They found that 76% localized to the retrocondylar groove. That is not the cubital tunnel. That's like right behind the medial epicondyle and just proximal to it. Most commonly, this was demyelinating. And most commonly, the mechanism is chronic leaning on the elbow. So it's a chronic compression. It's not a fixed point of entrapment. It's chronic irritation. All right. And the most common segment was that medial epicondyle to the proximal segment just next to it, the two centimeter segment. 17% were localized to the cubital tunnel. This was distal to the medial epicondyle in that segment. And most of these were axonal in physiology. And the mechanism here was entrapment under that humeral ulnar arcade, that fascial compartment of the FCU muscle. All right. So does it matter? I think it does where this localizes to. All right. Some technical points. If you want to do this correctly, it's helpful to map the course of the nerve with some preliminary submaximal stimulations to know where exactly that nerve goes. There's a significant portion of people that have their ulnar nerve sublux out of the groove when they bend their elbow. So you measure from the medial epicondyle. You go down four centimeters and then up six centimeters. So it's a 10-centimeter distance. And you're marking two-centimeter increments along the nerve. All right. And it's really important, really, really important to use just supermaximal. When you go back and do your actual measurements, your stimulations, to use just supermaximal stimulation. If you start off too high, that latency spread or the current spreads proximally or distally along the nerve, and your latency can move. And we're looking at 0.1 millisecond increments in latency. And so just a little bit of latency spread down the nerve from a too high of a current can really make your results different. So start low. Make sure you're submaximal when you start out for each stimulation. And then very gradually, I'm talking like less than 5 milliamps at a time, increase your current. And when we look at inching studies, we're looking at the latency difference between all the sites. We're not looking at conduction velocity. The latency difference is what you want to focus on. And normal is less than 0.7. And then look at any changes in amplitude or area that might give you a signal that there's conduction block between two segments. This is a case I had last month where there's really significant conduction block. She was very weak in her hand muscles. And it localizes very nicely to this segment between the medial epicondyle and the 0.2 centimeters distal. And so this, like I showed you before, is most likely corresponding to the cubital tunnel, which is usually going to be an entrapment mechanism. So that's the spot there. And on ultrasound, there was this flattening of the nerve right in that location. You can see, let me show you. So where the Xs are on the ultrasound, that's the humeral ulnar arcade. That's the fascial portion of the FCU muscle. And then just approximately to that, the nerve swells up by the medial epicondyle. Here's a longitudinal view where distally to the right, you have the compressed nerve. And the X in the middle is where that entrapment is. And you get this abrupt swelling of the nerve from that point. And that's just distal to the medial epicondyle. Go ahead. Yeah, yeah so the question is, yeah, yeah so he's asked questions about the where the swelling is and where the slowing is. I think it depends on the mechanism. So we know from carpal tunnel that when you measure the cross-sectional area there's in it if there's a fixed entrapment point that that cross-sectional area is going to be small because it's it's entrapped and then it swells on both sides of that entrapment and if you have a mechanism like this where this this so the swelling is is this is more proximal it's in there it swells the swelling is proximal to the medial epicondyle but the entrapment is distal if you have a case of like a retrocondylar compression from habitual lean on the elbow there's no point of entrapment there and so in that case the swelling does correspond you it's most most swollen where it's most irritated where it's been leaning that's usually going to be retrocondylar groove and so the point of maximal slowing there is where there's most swelling because the mechanism is different. In this case where you have an actual entrapment in where the the cross-sectional area is low is small that's going to be your point of maximal slowing. Did I answer your question? Yeah yeah so I think you will right right and I think in this case there was some swelling throughout the nerve it wasn't localized to just one segment the conduction block here was clearly at one segment but the slowing was multiple segments but I think from from people who do correlation studies between ultrasound and inching studies there usually is pretty good correlation between where's your slowest point and where's the swelling but not always. Alright thanks for that question. Okay so I mentioned sensory inching studies this is something you can do who's ever done this before sensory inching yeah that's pretty pretty tedious really have to average those I would say use caution they take a long time very technically demanding if your amplitude of your snap at the wrist is low then don't even bother because you're gonna have super low amplitudes up at the elbow really need to average those and again use just super maximal current because if you use too high of a current that that current's gonna spread distally and it can mess up your latencies and there's really not room for for error here. The peak latency interestingly enough the difference required is the same as a motor study it's 0.7 and that was based on a study that was done in 2019 and any amplitude reduction between those segments of more than 15% is indicative of conduction block. More sensitive than doing the routine just across the elbow study but definitely more time-consuming. Has anyone used this the mixed nerve study? So this is an orthodromic mixed nerve study where it's a comparison study it's a median ulnar comparison you have you do this in the extended arm position and you are you are recording in the same spot for each stimulation so right here in the if you see on the diagram where the electrodes are the median ulnar nerves that come right next to each other in the arm and so you can record both just with the same set of electrodes. It's 10 centimeters proximal and the recording electrodes are placed between the biceps and triceps muscle bellies and you stimulate down at the wrist and median or ulnar and those the distance between those should be similar or the same and this gives you a small sensory potential or a mixed nerve potential and you're looking at the difference between the peak latencies. So if you're thinking ulnar neuropathy you're expecting your ulnar sensory or your ulnar mixed nerve response to be longer a longer latency than the median and the there's a little bit there's not consensus on what the cutoff value should be. I think it's I use 1.1 is definitely abnormal and if it's less than 0.9 it's it's a normal and in between it's probably borderline but there isn't a lot of consensus on that but this one I think is very useful because it's not very hard to perform it's not that technically challenging you can usually get pretty good responses it's a whole lot easier than doing the sensory inching. It doesn't give you that precise localizing value. All right case 5. 55 year old diabetic male with two years of progressive left-hand weakness and atrophy there's constant numbness of the ring and small finger reports this funny bone feeling at the elbow chronic neck pain. So this is a guy you're like he's got everything right he's got polyneuropathy probably it's got the ulnar neuropathy it's got neck pain could be radiculopathy like where where do you even go with this one pretest probability because of this hand localization you're thinking probably ulnar. So let's start with that so this is your ulnar study and there's a little bit of slowing and the distal latency is a little bit slow amplitude is low and conduction velocity is slightly slow but not clearly localizing so the question is like you know he's diabetic could this just be all diabetic neuropathy could that explain everything that we're seeing that's the question I'm asking and that's why these are hard what's that possible And that's right, and that's why we do the test. Yeah, so we need more data. So look at the FDI, and the results are similar. Didn't really help us. So what to do next? Ulnar digit five is absent. We still don't know what we're dealing with. Polyneuropathy, ulnar neuropathy, something else. Polyneuropathy plus radiculopathy. Dorsal ulnar cutaneous is also absent. But then we go to the other side, and it's normal. So this is telling us something, that this is not a polyneuropathy. Maybe he has a polyneuropathy, but that's not the cause of his absent sensory responses, because it shouldn't be asymmetric like this. So we've learned something here. So now we're thinking ulnar, and a radiculopathy wouldn't cause you to have absent sensory potentials. Do the medial antebrachial cutaneous study. Who would have done this? Yeah? Yeah? The reason, and this is just a free recommendation, that if you have a low or absent ulnar digit five sensory response, go ahead and check the MAC, the medial antebrachial cutaneous. Because a lower trunk or medial cord plexopathy can present kind of like an ulnar neuropathy. That's just a good practice point. We go over to the median motor, and we've got a little bit of slowing here. So distal latency is a little slow. Conduction velocity is a little slow. Who's calling this carpal tunnel? Yeah, warm. Yeah, so let's assume that he's warm. He's sweating. OK. OK. Remember, this could be polyneuropathy, right? So whenever you see that prolonged median latency, don't automatically assume it's carpal tunnel. It could be polyneuropathy. This is a mild degree of slowing. Same thing with the motors. Our digit two response, the latency is kind of on the border, 4.0. Maybe a little long. This is a 14-centimeter study, so maybe kind of borderline. Conduction velocity is mildly abnormal, mildly slow. OK, so here's another situation where the segmental study really helps you. So we were wondering about that median motor latency. Is it prolonged because of carpal tunnel? Is it prolonged because of a polyneuropathy? He's diabetic. So when we do the segmental study, if this median motor was prolonged because of carpal tunnel syndrome, the sensory should also be similarly affected, right? Because usually, sensories are more affected than motors in carpal tunnel. When we do this segmental study, it shows that there's no focal slowing across the carpal tunnel. If you look at these segments, the top segment here, the conduction velocity, it's not the top segment here, the conduction velocity. Can you see my mouse? Yeah. Digit 2 to palm is 47. Palm to wrist is 42. Not much of a difference. There's no conduction block. So we can conclude from using these two studies in combination that he does have a polyneuropathy, and there is no median neuropathy at the wrist. OK, but we're concerned about the ulnar neuropathy. And this is what I was explaining before with this segmental study. So this box on the top, this is what he had. This is telling us polyneuropathy. If it looked more like the bottom study, then you would conclude that there was carpal tunnel, that there was median neuropathy at the wrist. Even though, if we had just done the wrist stimulation, we would have got 45 as a conduction velocity. So you wouldn't have been able to determine the difference. But by throwing in the palmar stimulation, doing the segmental, it gives you a lot of information. So the summary of this case was that there were low amplitude motor responses, no clear focal slowing across any segments. The ulnar sensory was absent, but it was intact on the contralateral side. There was a normal MAC, mild slowing of median motor, and sensory studies with normal amplitudes. So number one, there is a severe non-localizable, unfortunately, ulnar neuropathy with primarily axonal physiology, sensory and motor loss. And we also know that there is a sensory motor polyneuropathy, but no evidence of carpal tunnel syndrome, even though his distal latency on his median was prolonged. All right, this is the last case here. 64-year-old female presenting with intermittent numbness of the right hand. Numbness involves the first three fingers and the thumb. Poorly defined parathesis of the lateral forearm. No defined triggers, intermittent sharp shooting pain from the neck into the right arm. This is her median motor study. Looks pretty good. This is the digit two study. It's robust. Amplitude and velocity latency is normal. I think I have a typo there. That latency one shouldn't be 3.8. Radial, did the radial because there was parathesias in the thumb. That was normal. Did the lateral antebrachial cutaneous because there were parathesias in the forearm that looked normal. So this patient had radicular pain. Radicular refers to the root, the nerve root. Usually shooting pain from the neck into the shoulder, the arm, or the hand. Often the parathesias are not well localized. They don't have a clear demarcation between the different peripheral nerve dermatomes. Can be exacerbated by weight bearing, neck positioning, but not always. So our nerve conduction studies are often normal in radiculopathy. But it doesn't mean that they're not useful. So we have two goals when we're spacing a patient that we think has radiculopathy. Number one is to make sure that it's not something else. So it's not carpal tunnel. It's not ulnar neuropathy, et cetera. But number two, and most importantly, we are trying to establish that these sensory potentials are intact in the region of parathesias. So if their parathesias are in the pinky finger, then we want to do a digit 5 sensory study. If it's in the forearm, we want to do a sensory study there. It's laying the groundwork for the interpretation at the end. So even though these studies are going to be normal, it's important to pick which ones you do to lay that groundwork. So why are the sensory responses intact in a radiculopathy? This is our spinal cord here. We have our green is the sensory nerve. DRG is a dorsal root ganglion. That's where all the cell bodies are. The red is the motor nerve, and their cell bodies are in the spinal cord. We have the root, plexus, and nerve. So the nerve needs its cell bodies to stay alive. So if there is a problem at the root level where this icon is here, it's not disconnecting the cell bodies from its nerve. And so the nerve is going to stay alive, even though there's a root injury. So the disconnect is between the nerve and the brains. There's going to be some sensory symptoms, but the dorsal root ganglion and their cell bodies are still connected to the nerve in the periphery. So those sensory nerves remain intact. And if we have something beyond that, that's when we're going to have low sensory potentials. So we have lots of options for, in the upper limb at least, for what you do in these cases, depending on where the sensory involvement is. So don't get stuck in a rut of just doing digit 2 and digit 5 and you're done. Think about where are their paresthesias, where is their numbness, and do a study there. You're laying that groundwork, because then someone's going to come in, do a needle study. Maybe you do the needle study, not as text. And they're going to make that diagnosis. So the conclusion is, depending on EMG, so we don't know what the diagnosis is here, but we're at least laying that groundwork for the EMG to make that interpretation. So I'll end with this. Avoid the test everything strategy. Remember, false positives are real, and it's a problem. Select tests based on symptoms and location. And remember that two abnormal tests are better than one. So we can take questions at the end. I will hand it over to Dr. Fulham. All right, good morning everybody. Like Dr. Simmons says, I'm Tim Fulham. I'm a neuromuscular specialist. It's actually active duty Air Force, so I'm down at Brooke Army Medical Center in San Antonio, Texas. And today I'm gonna talk to you guys about lower limb and generalized complaints. At least I know from working with residents over at Brooke Army Medical Center that when it gets to lower extremities and people are learning these, this is where most people are kind of like, they try to avoid coming in for those studies as much as possible and feel a lot more comfortable with the upper extremities. But I think with time. With the lower extremities, you find that the nerve conduction studies and planning can be a little bit more straightforward, I think, than the upper extremities. I have no disclosures. The only thing I do have to say is that these opinions are my own, not those of the Department of Defense or Defense Health Agency or anything like that. And just take note of any of the highlighted items that I kind of put throughout the study here. So just to kind of lay the groundwork for lower extremity, I think it's important just to kind of think about a couple things going into it. And one is just being aware of any anomalous innervations that you may come across while you're doing these studies. So we have pictured here is kind of the normal layout where you have the common perineal nerve on the lateral aspect of the leg going across the fibular head and dividing into the deep and superficial perineal nerves. And oftentimes, when we're doing the perineal motor study, we're recording over the extensor digitorum brevis. So in most folks, when we do this recording, we get similar waveforms that we're kind of familiar with here on the left where you have similar amplitudes at all the stimulation points at the anterior ankle, the fibular head, and then also above the fibular head. But one thing to be aware of is in a certain percentage of the population that you can have this additional connection for the superficial perineal nerve gives a branch to the extensor digitorum brevis. And this is called the accessory perineal nerve. And this can cause a unique finding when you go to do your routine perineal motor study where, if you pay attention here to the waveforms on the left, you can see that there's a change in kind of the shape of the waveform as you move to the proximal stimulations and also a slight increase in the amplitude. You can see here it went from 3.9 to 4.4. So this could mean one of two things. It could either that you under-stimulated at the ankle or that this patient does in fact have an accessory perineal nerve. And so if you were to just stimulate behind the lateral malleolus and between the lateral malleolus and the Achilles tendon, you can see this extra negative response, CMAP response that you get, which kind of confirms the finding of the accessory perineal nerve. So just something to be aware of. So if you're doing a routine perineal motor study and your amplitude increases or the waveform changes when you move proximally, it's important to just remember the accessory perineal nerve and go ahead and simulate behind the lateral malleolus just to check for that anomalous innervation. Something that Dr. Simmons talked about briefly at the end of his study is, you know, the sensory studies are really our great localizer in nerve conduction studies. And so we have here another schematic, you know, you have the spinal cord, we have the ventral root, and then in the, pictured in blue, and then in the red you have the sensory component of the nerve going through the dorsal root. I think it's really important to pay attention where the cell bodies are here. So for the anterior horn cells, those are located in the spinal cord, whereas the cell bodies for the sensory nerves are located in the dorsal root ganglion, which is in the intervertebral foramina, so outside of the spinal cord proper. So while they're in degeneration after you have nerve damage, it goes from the site of injury back to the cell body. So in this case, if you injure something peripherally, so like neuropathy or trauma, you're going to have degeneration shown here with the dotted lines of the peripheral nerve back to the dorsal root ganglion and all the way back to the anterior horn cells for the motor component. So you may see lower motor action potentials, and you'll also see that the sensory responses should be lower absent as well if your injury is past the dorsal root ganglion. But when we think about radiculopathy or things that are proximal to the dorsal root ganglion right here, again you have your degeneration that just goes back to the cell body. So now you're still, you could potentially see the lower motor amplitudes, but your sensory responses will be preserved because that peripheral portion of the wire was spared from the damage. And so where we're stimulating, we're still able to get a signal. So given that localizing value of our sensory responses, it's important to kind of know in your head our framework of where we can get sensory responses in the lower extremities. So you can get a lateral femoral cutaneous nerve study on the lateral thigh if that's where the numbness is. If it's the lateral aspect of the distal leg, going on to the dorsum of the foot, you could think about doing a superficial perineal nerve study. If it's on the medial aspect of the calf, you're thinking about doing saphenous. And then if it's the posterior calf or bottom of the foot, you're looking at soral or your plantar nerve studies to localize this to pre or post ganglionic. So with that, let's go ahead and jump into a couple cases. So for the first case, it's a 42-year-old male that was referred for persistent foot pain after an ankle fracture, which they suffered five months prior to referral. They did note that they had a cast in place for the first six weeks after the injury, but it was since removed and they've had persistent pain despite participating in rehab and following all the normal recommendations. They note that the pain on the foot, right foot, is worse with movement and any sort of weight bearing. So when we're thinking about unilateral foot pain or numbness, you can obviously think about one of the more common reasons people are referred, which is actually non-neurologic causes to orthopedic issues, like plantar fasciitis or tendonitis in the foot. Obviously tarsal tunnel syndrome is something that comes to mind, especially when you see unilateral foot pain or numbness. And then you can also think about S1 radiculopathy or even mild peripheral neuropathies as a potential cause for the symptoms. I'm a motor person, so I always start with my motor studies first. And so in this case, I started with the right tibial over the abductor hallucis. And here, really, it's just a normal appearing tibial motor study. So normal distal latency, normal amplitudes, and normal conduction velocity. And in this case, the F-wave response was also normal. Moving over to the right sural sensory, just thinking about posterior calf, bottom of the foot. And here, again, we have a normal peak latency, normal conduction velocity, and normal amplitude. And finally, moving down into the foot, did a medial plantar mixed nerve study on this patient. And here, again, even though it's highlighted, the 5 is a normal response for a medial plantar mixed sensory in terms of the amplitude. And the peak latency and conduction velocity look reasonable. So in this case, part of our differential that we talked about was peripheral neuropathy. And in this case, I'm pretty comfortable in saying that this patient does not have large fiber polyneuropathy. So if you're able to get a normal tibial abductor hallucis with a normal F-wave, a normal sural, and then some sort of distal sensory response in the foot, then you've effectively ruled out large fiber polyneuropathy in a patient with just three nerve studies. And so the two options outside of the medial plantar study, which tends to be more reliable than the lateral plantar. The lateral plantar, think about it being about a third of the amplitude of the medial plantar. So if you're looking for something that's 5 or 6, then the lateral plantar, you can anticipate being 1 or 2 milliamps. So it's going to be a much smaller response, so less reliable to grab. But the other one that's useful to kind of know is the dorsal sural sensory study, because sometimes people have had prior ankle trauma, ankle surgeries. And so if you want to go to the lateral aspect of the foot, this dorsal sensory study is another option to get a distal sensory response. So in this case, we have one patient that we've ruled out the large fiber polyneuropathy. But again, we're still stuck with the unilateral symptoms. So we need to start looking a little bit deeper. And so in this case, we finished up and did the medial and lateral plantar studies. And we see that on the right side, he has amplitudes of 5 and 9 for the lateral plantar. So actually, the reversal of what we typically see for the amplitude pattern for this. And the good news is they only have symptoms on one side. So we have another good side for comparison. And then when we go over and do the lateral plantar, the medial lateral plantar studies on the left-hand side, I put a line here just to show you. You can see there's some skewing in the latency responses here as highlighted here at the boxes. And so you can see that the peak latency from the medial plantar response on the right side was 2.9 as opposed to 2.6 on the left. And on the lateral plantar, it's 3.2 as opposed to 2.5. And the most glaring difference is the amplitude of 5 for the medial plantar on the right and 20 on the left, which argues for potential of distal tibial neuropathy as we see with tarsal tunnel. Again, as Dr. Simmons had alluded to, you always want to try to have two data points to be confident in your electrodiagnostic conclusions. So in the case of tarsal tunnel, you can do distal motor comparisons as well as these mixed sensory comparisons, which we just showed. And these ones, you're just stimulating the tibial nerve and recording over the abductor digiti quintipedis on the left-hand side there. And then, or you can just do your typical distal motor response over the abductor hallucis. And here you can look at the latency differences from side to side. I apologize on this one on the machine, it was flipped. So the left is on the top now and the affected side, the right, is on the bottom. You can see that there's a significant latency difference between side to side. So greater than 0.5 being abnormal for the abductor hallucis, the latency difference was 0.6, and on the right, it was 0.9. So at this point, we were comfortable saying that this patient had, you know, finished up the routine studies, so the perineal motor and the superficial perineal sensory studies were normal on the right. And the EMG of the right lower extremity, excluding any foot muscles, was normal. And so our electrodiagnostic impression is that this patient had a right distal tibial neuropathy affecting the medial and lateral plantar nerves, primarily demyelinating in nature given the peak latency changes, and this can be seen as tarsal tunnel syndrome. For our second case, it's a 45-year-old that was referred for evaluation of five years of low back pain with intermittent radiation to their left leg. The patient describes radiating paresthesias, mostly moving from the buttocks down to the posterior calf and bottom of the foot, aggravated by any sort of running activity. And there was no clear weakness, but they did feel like calf raises were more challenging than they previously experienced in the past. So in this case, starting on the affected side, the left tibial motor study, a recording of our abductor hallucis. And again here, the distal latency looks preserved. Amplitude is reasonable, it's 4.4, but there is a decrease in the conduction velocity with a normal F-wave latency. So something just to pay attention to. In this case, it did go ahead and do a perineal over the EDB, and this study looked normal. So kind of looking at the conduction velocity here over the tibial nerve being low, and then the preserved conduction velocities in the perineal motor nerve makes us think this is more of a focal-related pathology as opposed to something diffuse. And then again, our great localizer doing the serosensory study given their distribution of the patient's numbness, and we have a normal peak latency and a normal amplitude. In this case, you know, H reflexes are something I don't do all the time, but in certain cases they can be incredibly helpful, and I think knowing when to use them comes to just understanding what we're actually looking through the H reflex. And so this is just a little pictorial depiction, so if we're looking over our recording point over the soleus and our reference over the Achilles tendon, when we send the signal back up through, what we're doing is we're assessing the tibial nerve through the sciatic nerve through the lumbosacral plexus, and then it's going to go through the dorsal route and back out the S1 nerve route, and back down to create this reflex response. So this is the equivalent of our Achilles reflex, it's a monosynaptic reflex arc. The duration on your stimulator is set high at one millisecond, and you start at very low stimulus intensities, and what you can see is the H reflex response, the amplitude is over here and will gradually increase as you go up, but it reaches a threshold where once the actual motor response comes in, it'll start to decrease after that. So this is the normal response that you should see in a normal H reflex, and doing side-to-side differences can be incredibly insightful. So just knowing the pathway that we just went through, your H reflex is going to be abnormal in pathology at the tibial nerve, the sciatic or lumbosacral plexus, and then S1 radiculopathy, and obviously if it's a more diffuse process, like a peripheral neuropathy, it could be abnormal. But it should be normal in things like tarsal tunnel, because the pathology is distal to where we're recording over the soleus. And then any sort of perineal or femoral neuropathies, you wouldn't expect the H reflex to be abnormal, and for any radiculopathy outside of an S1 radiculopathy, it should be relatively preserved. So in this case, given the fact that the patient had symptoms going down the back of the leg and to the bottom of the foot, and we had a pretest probability for S1 radiculopathy, we did go ahead and do an H reflex. And here it is on the left, and you can see that there's a really poor, inconsistent response of the H reflex listed over here with a low amplitude of 0.4, whereas compared to the contralateral side, the right, they have a very robust H reflex and significant increase in the amplitude of 1.3 as compared to 0.4 on the affected side, and the latency is 34.4 milliseconds on the unaffected to 39 on the affected side. So that greater than 1.5 millisecond side-to-side difference is really the clincher here for the abnormal H reflex in this individual. Then one last study just to kind of look, we had that abnormal left tibial response and looking at, if you remember, the amplitude is around 4, and here on the unaffected side, you can see the amplitude is 10, which again goes along with the S1 radiculopathy. And in this case, the EMG confirmed chronic denervation changes in the left medial gastroc as well as the CRD in the S1 paraspinal, which led to the final electrodiagnostic impression of a left S1 radiculopathy, which was chronic without active denervation and relatively mild. Our third case here is a 20-year-old with type 1 diabetes that was referred for lower extremity pain and paresthesias. This patient noted that her feet would change color, mostly at the bottoms, to a dusky blue when she was moving throughout the day. And she had pins and needles present for at least the past three years, that started in her toes but is now up to her distal thigh. She did not have any weakness, but she did note that she fatigued relatively easily when trying to walk longer distances, and her pain became unbearable as she walked for longer periods of time. So again, this patient is 20 years old, and moving to the first, the right tibial motor nerves and symptoms are relatively symmetric. You can see a severely prolonged distal latency of 8.3, reduced amplitude of 0.3, and a reduced conduction velocity of 33 meters per second. Again, this is a more chronic period of time that this was happening. Looking at the F-wave response, you can see the normal less than 56 in the lower extremity in this patient was 68, and you can see the very low amplitudes and inconsistent responses of the F-waves. And looking at the EDB on the same patient, so the distal latency is preserved in this case at 4.7. Amplitude is borderline, but normal at 3.6, but conduction velocity again is low in the mid-30s. And in this case, on the perineal motor study, the F-wave was unobtainable. In looking at the sensory studies, the serosensory response, the amplitude is 8 in this case, but the peak latency and conduction velocity were, well, peak latency prolonged and conduction velocity reduced, consistent with some slowing. So in this case, we have slowing in all of our motor nerves that we've studied so far, low amplitude tibial motor study, and then a slowed serosensory response bilaterally. So at this point, I think we're relatively convinced that we have a diffuse process affecting this patient, so a polyneuropathy. And so the goals of the nerve conduction study, once you establish polyneuropathy, is to, one answer, is it symmetric or asymmetric? Is it length-dependent or not? What's the primary pathology? Is it axonal or demyelinating? And sometimes the answer can be both. And then also, is it the motor or sensory fibers that are being involved? So in this case, we already had the serosensory responses bilaterally. You know, for amplitudes less than 1, it becomes much harder to kind of use the 50% rule side to side. But in this case, we can see that both tibial responses are less than 1 milliamp in size, so relatively symmetric, and the slowing appears to be about the same bilaterally. In this case, I moved up and did the right arm as well. And here over the abductor pollicis brevis, you can see now the distal latencies and amplitudes are preserved, but we still see some borderline slowing of the motor sensory response. And then the superficial radial was essentially normal. And in this case, the EMG just showed chronic denervation distally to the medial gastroc and tibialis anterior. So here we have a length-dependent, mostly symmetric, motor greater than sensory polyneuropathy with both mixed axonal and demyelinating features. This is very common in diabetes, and so especially uncontrolled type 1 diabetes for longer periods of time, you often can see significantly prolonged distal latencies, conduction velocities in the mid-30s. And this is why these are often confused with things like CIDP or other inflammatory neuropathies in that people don't always appreciate the demyelinating features you can see with it. So our next case is another younger patient. Again, I'm a military neurologist, so I see a lot of younger patients. So this is a 26-year-old that was referred for evaluation of intermittent tripping and some numbness in their bilateral hands and feet. They were noticing a lot of errors when they were trying to type, but no major changes in their handwriting. After longer periods of standing, they would get paresthesias in their feet when in formation, and she felt like she was tripping when she was more tired or after running even short distances at this point in time. The only other history is repeated ankle sprains during her teenage years, and she had one documented during her basic military training as well. So for this 25-year-old, you start at the right peroneal EDB and the tibial over the abductor hallucis, and you're kind of scratching your head because this 26-year-old has no responses. You move on to check the sensory responses as well. Again, they just had some mild numbness, but zero sensory responses in the right leg. So if you have absent responses on your initial distal motor and sensory studies, it's really important to just to start to move up the limb or the body to try to get some idea of the pathology. You can't – length-dependent processes will often result in severe distal axonal damage, and so you may not be able to see the primary type of pathology unless you move more proximal. So in the legs, the advantages that you have is for the peroneal motor study, you can record over the tibialis anterior. The advantage here is that you have two simulation sites, both below the fibular head and then also above the fibular head, so you can also get a conduction velocity. You're not stuck with just a distal latency, but you can also do a tibial motor recording over the soleus and get an amplitude there as well, especially if you have something that's asymmetric in the lower extremity that's affecting the calf. So in this case, we did go ahead and record over the tibialis anterior, and in this case, we are able to get a response. You can see that the amplitude is 3.2, but the conduction velocity is significantly slowed at 24 meters per second. It's important to point out here that this could be focal demyelination at the fibular head because it is a compression site, so we'll need more information if this is a focal demyelination or more diffuse. So then the only other option then in this patient is to move up to the arms. In the right median motor, you can see a severely prolonged distal latency of 9.2. In the median motor study with a conduction velocity, again, in the high 20s consistent with diffuse demyelination. And then looking at the superficial sensory response, since we weren't able to get any sensory responses in the lower extremities, again, we can see prolonged peak latency, slowed conduction velocities, and a relatively low amplitude. Does anybody know what's going on with this patient? Yeah. Yeah. So this is a length-dependent symmetric sensory motor polyneuropathy with primarily demyelinating with secondary axonal features. And that lack of conduction block and the uniform demyelination is consistent with likely hereditary demyelinating neuropathy like we talked about with CMT. And so it's really important when we're looking at these patients in the lab, if you're seeing the distal atrophy, you know, any sort of foot deformities like the pes cavus or echinovarous formation of their, the deformation of their feet, to be suspecting this and don't be thrown off by absent sensory and motor responses, even if they are younger. The other big clue to these is the discordant sensory responses. So these patients often don't complain about sensory signs or symptoms. You know, you don't know what you have until it's gone. So if you never had it, you don't miss it. And so even though they have profound sensory findings when you check them, they don't often have that as a major presenting complaint. It tends to be the weakness that brings them in. And then one final case here. So this is a 59 year old referred for an eight month history of weakness. The symptoms came on relatively abruptly over a couple of weeks and they've been gradually worsening since. They're having difficulties going up and down the stairs at home and getting out of chairs. They don't have any numbness or tingling anywhere. They are having some issues swallowing and actually had two admissions to an outside facility over the past three months where we're treated with plasma exchange and IVIG with no clear diagnosis, but presumed myasthenia was the thought. Acidic colon receptor antibody, LRP4 and musk antibody testing had all been negative by an outside facility. And this was the first time he was having electrodiagnostic studies done. And so here starting in the lower extremities, the left perineal motor study here shows just a lower amplitude, but normal distal latency and conduction velocity. And the left tibial also had a low amplitude. There were some technical difficulties that were the patient's body habitus getting the proximal tibial motor response. So that lack of a proximal tibial motor was felt to be technical in nature and was made noted by the EMG in this case. Looking at the sensory response, it looks robust. So normal amplitude, normal conduction velocity for a 50 year old. And then in the left upper extremity, again, we can see in the left ulnar motor study a relatively low amplitude of 3.9 milliamps, but normal conduction velocity. And then our motor, our median motor also shows a, it's normal motor response, but borderline for at 4.7 with a relatively normal conduction velocity. And again, the sensory responses are robust. Pay attention here. This was a person with big hands, so they used 15, so don't pay attention to the peak latency. The conduction velocity was normal, so there's no slowing across the wrist. And only digit 5 was good. So what next in this case? Just to summarize, we have generalized weakness with no sensory complaints. And so far we have diffusely low CMAP responses and normal and robust sensory responses. When we're looking at the differential for pure motor disorders, you know, a lot of people jump to pure, you know, primary muscle disease. In the EMG lab, we're often recording over distal muscles. So to have low CMAP responses from a primary muscle disease is relatively rare actually, because most acquired myopathies are going to be in a limb girdle pattern of weakness. So your weaker muscles tend to be your shoulder and hip girdle as opposed to your distal hands and feet. When we think about isolated motor neuron disorders like ALS, this is really the importance of the physical exam. Was there hyperreflexia noted? Do you see fasciculations? Is it asymmetric in nature? That's typically what you're going to see with more motor neuron type disorders. But if you're seeing somebody with proximal weakness with low CMAP responses, you know, neuromuscular junction disorders are something that you have to at least keep in the back your mind and consider if you need to do short exercise testing or repetitive nerve stimulation. And I think just going back to the pathophysiology here can really help understand why short exercise testing can be such a useful test in this clinical scenario. So here we have kind of the normal neuromuscular junction with your presynaptic neuron with the synaptic vesicles filled with acetylcholine. And then kind of our input or go signal is the incoming calcium, and the off is the outgoing potassium. And so depolarization of the motor neuron will cause influx of calcium into the synaptic terminal. That calcium allows the acetylcholine vesicles to dock and ultimately release the acetylcholine, which then binds to the acetylcholine receptors, and you get the, you know, comic book POW action potential happening in the muscle and contraction. In postsynaptic disorders such as myasthenia, we have to think about where's the pathology. So here we're thinking about internalization and blocking the acetylcholine receptors at the postsynaptic portion of the neuromuscular junction, so on the muscle. So again, we have calcium come in, which is normal, unimpeded by myasthenia gravis. The acetylcholine can dock and release, but because there's less receptors available, you have potential for failure and a lower contraction of the muscle and intermittent contraction failure as a result of that blockade postsynaptically. For presynaptic disorders like Lambert-Eaton, now the pathology is here at the voltage-gated calcium channels. And so when the nerve depolarizes, there's less calcium that's able to get in, and therefore there's less acetylcholine that's able to dock and release. And so we have less acetylcholine in the postsynaptic junction and less of a CMAP response. So in the lab, we can take advantage of the fact that it takes about 100 milliseconds for calcium to leave that presynaptic terminal. So 100 times 10 is 1. So if you can... Oh, it's 1,000. So if you stimulate the muscle or you have that nerve fire more than 10 times a second, so if you do like isometric exercise, that stimulates about 20 to 25 times per second that that nerve's going to fire, then calcium can start to accumulate. So you get these little bursts of calcium that are sticking around in the presynaptic junction. And now you can restore the normal amount of docking and release of acetylcholine into the neuromuscular junction and restore the CMAP potential potentially in the lab. So in this case, when we see the diffusely low CMAP potentials, if you just have the patient exercise that muscle that you're recording for 10 seconds and re-stimulate, if you see a greater than 100% increase in the CMAP potential, that's highly specific for something like Lamberty and myosinic syndrome, so a presynaptic neuromuscular junction disorder. So that's what was done in this case. You can see here in the perineal recording over the EDB, you can see the amplitude goes from 1.4 to 2.8. From here, we go from 2.2 to 5.4 in the tibial motor study, and then the ulnar motor study going from 3.9 to 7.5. So clearly fulfilling that 100% increment, highly consistent with a presynaptic neuromuscular junction disorder. Three hertz repetitive nerve stimulation is going to be abnormal in both presynaptic and postsynaptic disorders, and this was the case here in this case as well. An EMG in this case was unremarkable. So electrodiagnostic impression is that we have evidence of a presynaptic disorder of the neuromuscular junction, as can be seen with Lamberty and myosinic syndrome. So I think key points for me that I kind of think about with lower extremities is that the legs are often affected first by length-dependent processes. In this case, we're often thinking about neuropathy. And so you can utilize those proximal recording sites, such as the perineal over the tibialis anterior, the tibial over the soleus, or an upper extremity to garner more information if you're kind of not striking out on the more distal or routine studies. Always include a sensory study in the distribution of the patient's most bothersome numbness or tingling when possible, especially if below the knee. And this maximizes the localization for pre- versus post-ganglionic disorders, specifically radiculopathy. And then always remember, if you're seeing those diffusely low CMAP potentials with normal sensory responses, always consider just doing some testing for post-exercise facilitation with 10 seconds pre- and post-exercise. We have references here. And take any questions. All right. Thank you. Oh, that's a little loud. We'll take some questions. Before we do that, I want to just encourage you to use your phone, get in the app. There is an area to leave feedback. You can rate the session. There's just four questions. It says, rate the session, rate the content, what influenced your rating, provide ideas. Any feedback you have will be helpful to us. We try to make this relevant to the people that we're trying to reach here. This session was mainly for technologists, although I think it's helpful for residence fellows and any faculty who are wanting to get back into nerve conduction studies. But this really helps us plan for the future. We try to update this every year, so that would be appreciated. Well, thank you for your attendance and your attention. Any questions? So, yeah, so typically what will happen is, you know, if you just see one low C-MAP, you're not going to jump right into the exercise, but if you go through the rest of your kind of routine studies and everything's low, you can open back the other study and just open up another channel and just have them exercise for 10 seconds, you know, reestablish your, make sure the C-MAP's still the same, you're going to put your stickers back on, C-MAP's still the same, exercise them for 10 seconds, and then see if it improves. Now, sometimes you have the advantage of, you know, if somebody was in the hospital or they're referred specifically for LEMS and they're asking for pre- and post-exercise testing that's different, but in this case it was something that was kind of a clinical unknown, so oftentimes you're having to go back and reestablish and do it again. I had a patient several years ago that had a diagnosis of myasthenia for a decade, and he came in and he was on steroids and mastodon and had the double vision, and the first thing I noticed was that his C-MAP's were low, and you really shouldn't have that with myasthenia, although he was pretty end-stage, and I did the, you know, the exercise and they jumped right up. Any other questions? Okay, well feel free to come up after, you know, we're happy to take questions in person as well. Have a good rest of your day, enjoy the meeting.

nerve conduction studies

ncs

clinical neurophysiology

algorithmic approach

intuitive understanding

carpal tunnel syndrome

CTS

ulnar neuropathy

polyneuropathy

segmental sensory studies

anatomical variants

tarsal tunnel syndrome

Lambert-Eaton syndrome

electrodiagnostic principles

CTS

carpal tunnel syndrome

nerve conduction studies

nerve conduction study

ncs