Hi, welcome to the next episode of Lessons from the Lab. My name is Devin Rubin and I'll be hosting this episode with a wonderful guest that we'll have on in just a few minutes. This has been, this is the end of the week for me. It's really been a great week. It's been a challenging week. We've seen lots of interesting patients in the EMG lab and in clinic. And for those of you who are college basketball fans, this week is the Jimmy Valvano week. There's been some basketball games in memory of Jimmy V. He was a great college basketball coach many years ago who died of cancer. And I was watching a game earlier this week and they played Jimmy Valvano's speech at the ESPYs, the first ESPYs, and he gave a very, very emotional and impactful and moving speech just a few weeks prior to his death. And in that speech, he talks about that there are three things that everyone should do every day. And he says the three things are, everyone should laugh, everyone should think, and everyone should cry or be moved to tears. And I think it's really a thought-provoking speech. It's something that I think is actually true. And if I think about my past week in the EMG laboratory, and even today, I certainly laughed. We work with our colleagues and our techs and we try to have fun. Even though it's busy, it's stressful at times, we really try to have a good time. So we had lots of laughs this week. I certainly thought, and we have challenging patients. And sometimes the more I do, the longer I do this, the more I realize that I don't know or that there are new ideas or thoughts that come up that need to be answered. So I did a lot of thinking this week. I didn't cry, but I certainly have been moved. We see challenging patients, some have very severe diseases, and when we hear their stories and we see them, they do move our emotions, at least to me. We do our best to try to help them. And really, that's part of what this educational program is about. It's trying to improve our skills to help make better diagnoses, more accurate diagnoses, and ultimately to help our patients. So I encourage everyone to listen to Jimmy V, to laugh, to think, and to move yourself to tears every day, if not multiple times a day. So with that, I'm looking forward to having a wonderful guest, and she may make me laugh, she may make me think, she may make me cry, but let's get to it. Well, welcome to the next episode of Lessons from the Lab. It's a great pleasure to introduce my guest, Diana Kwan. Dr. Kwan is a professor of neurology at University of Colorado. She's a neuromuscular specialist and EMG-er, and she's also the current president of AANEM. So welcome, Diana. Thank you. How are you? Excellent. Yeah, I think last time I saw you was in Phoenix and you were being inaugurated. So how does it feel to be in the White House now? The AANEM White House. It feels great. Yeah? I love it. Yeah, it's super exciting and I'm working on planning the meeting for next year, and I think it's going to be a really fun meeting in Savannah. Yeah, it was such a great meeting in Phoenix. It's just, you know, I think every meeting gets better and better, and especially now that we all can be together, and it was great. I wish I had time to rest during the meeting because there's so much going on. I don't know if you felt that way. Yeah, there was. There were a lot of people there, and it was such a great venue, too. Yeah. Yeah. So, well, I know it's Friday. It's Friday afternoon for me. I hope you've had a good week. Yep. It was busy, as always. Yeah. It's nice that the weekend's coming on. We were really busy. We had lots of interesting patients in the EMG lab, and it's exhausting, but it's a lot of fun. But I've been looking forward to this all week, to talk to you and learn from you and present you a case. Okay. So, I don't know if you've been looking forward to it, but we're going to have some fun. I'm scared. This is not a board exam, so there's nothing to be scared of. So, you know, part of this educational program that we launched with AANEM about a year ago, as you may know, is really to kind of learn from each other and for the viewers. This is on YouTube, but also it's on the podcast, so some people will be just listening. But really, the goal is just to kind of talk through how we approach a certain clinical situation in the EMG lab. And, you know, as I've learned, and we all know, that we don't always approach it exactly the same, but it's good to kind of get perspectives from others and have others hear about each of our perspectives of how we approach a case. So, I thought I would present a patient that we had about a month ago in the EMG lab. I'll just give you the brief presentation, and then we'll just kind of see how you would approach this. Sounds good. So, I, so the patient is, I'm actually, I think I'll actually just share my screen here. I just have a one slide, but I'll, of the history. So basically, it's a pretty straightforward history. She was a 62-year-old woman. She's very active and healthy, didn't have any medical problems. She played tennis on a regular basis, and in July, she began to note some weakness in her left hand and her leg. And she basically said it was, it came on gradually, it had been progressive over the course of a few months, and then she thought maybe it had stabilized. She wasn't sure. She didn't think it was progressing as quickly a month or so ago. And she didn't note any atrophy, but she had twitching in her arms and her legs, so probably fasciculations is what she was describing. She didn't have any pain. She didn't have any sensory loss. She didn't have any bulbar symptoms, no ptosis or diplopia or speech disturbance. And so that was basically it. And on her exam, so she was seen by one of my colleagues and sent to the EMG lab, but her exam, you can see in the table, but I'll just describe it for those who are just listening. She had moderate weakness in distal and proximal muscles, primarily in her left arm and leg. In some of the distal muscles, her MRC grade was one in her thenar muscles, it was two in her finger extensors, and then the rest was kind of five minus or four in the left arm. And similarly, in her left leg, she had moderate weakness proximally and distally, more distally in her dorsiflexion and plantarflexion. But then she had some patchy weakness on the right side that she wasn't aware of also. And her reflexes were brisk. She was hyperflexic. She had crossed adductor responses. And her sensory examination was completely normal. So that was basically the history and the exam. So I guess my first question is, I imagine you've seen patients like this before, and how do you approach this patient? I guess from an electrodiagnostic standpoint, or do you think this patient needs an EMG and what would you do? Yeah, so I do think she needs an EMG. And so did this lady come to just the lab, like she'd been seen by a neurologist before? Or was this just someone who came at 10 o'clock for an EMG? Yeah, patients here, our EMG lab is so much fun. So they just knock on the door and say, I want to just have an EMG. No, so she was seen by another physician at Mayo earlier that day. So in our practice, the patients come in, depending on if we're in clinic or in the lab, they often see one of my colleagues, and then they're sent for the EMG later that day or the next day. But we examine the patient. We take our own history, of course. And this is what I noticed as well. Okay. Yeah. So yeah, obviously very concerning because there's this weakness, but there's no sensory symptoms. So it's kind of a pure, pure motor situation. And the hyperreflexia with that always makes you worried that maybe the person has ALS. So that would be my big concern. But I think there's other things that it could be. It could be a combination of different problems. Like maybe she has something going on in her spinal cord, or maybe there's a muscle problem with, maybe she's just hyperreflexic. So I think the EMG is definitely helpful in that regard, trying to distinguish among those different possibilities. And every once in a while, you might get a patient who has some ridiculous issues without a lot of pain or noticeable sensory complaints. So I think it's always worth looking at that possibility. Yeah. Yeah. And I agree. And I guess maybe I can ask, even though we're going to focus on the electrodiagnostic approach, do you do other testing in someone like this besides an EMG? Well, we typically will do MRI imaging just to see what's there and make sure that there aren't other potentially contributing or treatable issues that could help the patient. So MRI, like make sure there's no cervical stenosis, cord compression. Yeah. Yeah. And every once in a while, you discover, oh, the person also has multiple sclerosis or something too. So that's not super common, but every once in a while, we find things that are unexpected. So an interesting question, I'm going to just slightly change this scenario because someone asked me this at a meeting a couple of weeks ago. So if this patient, if you knew the MRIs were normal, so nothing, no compression, and the patient had bulbar involvement, so had a spastic dysarthria or a mixed spastic and flaccid dysarthria in addition to the arm and leg weakness, do you think the patient has to have an EMG? This was kind of asked me, and that's why I asked it. You know, we do EMGs on almost every patient, but do they have to have it? Like, do you know the diagnosis without the EMG if they had the bulbar involvement? I think you probably kind of do. You know, so I think there are maybe some scenarios where the patient's like, no way, I'm super needle phobic and I do not want an EMG. I would feel reasonably comfortable following that patient knowing that the MRI didn't show anything and saying I'm fairly confident that you have Lou Gehrig's disease and we can just follow you and see how things go. I think if the clinical situation did not play out as expected, I probably would kind of push the patient to have a study. But, you know, we probably do what you do, which is we just kind of automatically do the EMG. Yeah. And I'm not advocating that we shouldn't do an EMG. We would do it too. But I think we had this discussion in our EMG lab yesterday that there are a few diagnoses that you can make when you walk into the room and within one minute when you talk to the patient. And I think ALS sometimes is, if you hear that spastic mixed dysarthria and you look at them and they're atrophic and they're fasciculating, there's not much else that's going to be. Absolutely. I agree. So, but we would still do it. And I think there's, to me, there's other reasons for doing it too, besides looking for another diagnosis, but looking for subclinical involvement in other areas that the patient may not have objective weakness and things like that. Yeah. Yeah. And I think it's such a serious diagnosis that I think most patients would really want as many tests as possible to be sure that that's really what is going on with them. Yeah. Yeah. So, so what do you, so back to this patient. So how do you approach this patient in the EMG lab? What do you, like, what, how, what do you do? Well, we would examine the symptomatic, the most symptomatic limbs. So in this case, we'd probably look at the left upper limb because that looks like that's the weaker side. And then in the leg, it looks like it's the left side that's weaker as well. So we would probably do a left arm and left leg. We do nerve conduction studies to just ensure that there's no significant conduction block, make sure there's no compression neuropathies that, you know, may be amenable to treatment and just make sure that there's nothing else that this could be. So we would, you know, we would just do some basic nerve conduction studies in both those limbs. And then we would probably focus on the, on the needle exam. And when you do the nerve conductions, and again, there's different approaches, and in the arm, would you do two motors and two sensories, or do you just do one motor and sensory, and an arm and a leg, or how extensive do you spread the nerve conductions? Yeah, so I think we would definitely focus on the weakest muscles, so we would look at, say, here in your hand, and the thumb is weak, and we'd definitely do a median motor. We'd probably see that the amplitudes would be low, and then we would do the sensory to make sure that there was that dissociation that we expect, so we would want to make sure that the median sensory looked pretty solid, and kind of similarly in the leg, you know, we would probably take a look at the, I assume that the toe extension is probably weak as well, so we definitely do fibular and maybe check the fibular sensory as well to just kind of make sure that that looked consistent with a pure motor syndrome. And do you do repetitive stimulation in these patients? Yeah, we would not in this case, because every once in a while, especially if the patients are more rapidly progressive, the neuromuscular junctions are just kind of unstable, and then you get the abnormal REP stim, and you're just confused, so I don't think it's super helpful in this situation. Yeah, I agree, and I think that's an important point. A number of years ago, that was part of our protocol. We would do like at least one motor and sensory, often two in the arm, and baseline repetitive stimulation, but I agree that I've seen patients with ALS, and they have decrement over 10%. I've seen up to 20% decrement occasionally, which is rare, but some degree of decrement I don't think is all that rare. And at one point we thought, well, does that help with prognostication if they have more decrement? Is that a more rapidly progressive disease? And I don't think the data really bears that out. I think there have been studies looking at that, and it doesn't always correlate with rapidity of disease or prognosis. I don't know if you feel that way or... Yeah, I think it is difficult when you're dealing with the individual patient. I mean, sometimes we see trends and we think we can predict things, but I've been wrong many times in my career when I thought that things were either gonna be slow or fast based on patterns, different types of patterns, but so I stopped making predictions in that regard. Yeah, right, right. And that's the question the patient's always asked too, right, which is the hardest question. Yeah, what's the time course? So, okay, so we would do a pretty similar approach to what you did. I'm gonna, if you don't mind, I'm gonna just kind of show you a couple of the nerve conductions and see what you think about them. So I'm just gonna kind of click through here. So we, I think we started with the leg here. And so here's the fibular motor. And just for the viewers who are listening, it shows a low amplitude of 0.22 and the conduction velocity is 37, which is a bit slow for us. There wasn't conduction block. So does this, do you get, are you bothered by the slow conduction velocity when you see that in this situation? No, I'm really not. You know, I think we can see a little bit of slowing of conduction velocity, especially with this degree of axonal loss, so. Yeah, yeah, I agree. I'm okay with that. And then we did a tibial motor, which has an amplitude at the knee of 0.9 distally. It's 1.9. And so nothing too surprising there. I think so. Yeah, I, and it does look like, you know, the proximal is a little smaller than the distal, but we often see that behind the knee, it's just kind of hard to get that maximal stimulations. Yeah. Especially in a larger patient. Yep, yep. And we allow, I think most criteria for conduction block, you need more than 50% drop in amplitude at the tibial nerve, so. So then we did a SERL, not the superficial fibular. I don't know if, is that wrong? To do a SERL? No, I don't think, yeah. Okay. I mean- You can critique me. Yeah, no, we don't always do the superficial fibular either. I think, you know, if the patient doesn't have any sensory complaints, then, and we saw what you just showed me, we wouldn't necessarily do. And we usually do the SERL just kind of as a screen for sensory neuropathy. And if that looks completely normal, we'd probably just quit there. Yeah. So this SERL is nice and normal. It's nine, amplitude nine. And this patient was 60, I think 62. So then we went up to the arm and then we did what you said, what you do too. We did the median and ulnar motor and sensory. So here's the median motor. Remember this patient had a really weak thenar muscle on it. And yeah, looks, it's very low for those who can't see it, but no block or dispersion. So here's a question for you. I'm always telling my techs, you know, don't change the, don't change the sensitivity. And they still do it anyway, because they're like, I can't see it. I can't see where to put the markers. So like, you know, we typically will have the median motor recordings on a sensitivity of maybe two millivolts per division. And we try not to change that. What do you tell your techs? No, we do change it so we can see the waveform better. This amplitude is 1.6. So if, and we, our default is two millivolts per division. So as you can see, that would just be like less than one division, be really low. Right. And so we do change it. So it kind of fills the screen. To me, I think the only risk is it's going to change the onset latency or the latency markers. So if I'm really worried about like, you know, a distal demyelinating process, you have to be careful about that. But I, our techs will do that. We want to see the waveform so we can see the morphology pretty well. Right. Yeah. And I think in this situation, yeah, even if this, so when you blow this up, the latency marker from baseline's going to be shorter and it doesn't really matter here, right? Right. Yeah. So that was the median, very low. And then do you do F-waves in these patients? Sometimes we do. If the, if the routine, you know, nerve conduction shows a big enough amplitude. Yeah. I guess, you know, if it's like more than one, we'll, we'll try that sometimes. We probably wouldn't bother in the peroneal or in the fibular nerve, but I think in the other nerves we would try. Right. So this is the median F-wave. It's kind of interesting. Are you sure it's an F-wave? Well, no, I'm never sure of most things, but I don't know, what else could it, what do you think it is or what could it be? I don't know, it looks, they look very similar. There's not a lot of variability. And so I would wonder if maybe that's actually an A-wave. Yeah. Yeah, I think it could be, again, for some people can't see this, but there's this reproducible waveform, late response on three out of eight traces. We do eight, the others don't have it. And I guess to me, an A-wave would be there almost every time. It's not always, because they sometimes drop out, but I think it'd be there more often than not. So I think this probably is an F-wave. Okay. But if it is, it's kind of interesting. And I don't know if you see this when you do F-waves in patients with ALS, when they're really big and they're the same F-wave multiple times. So like F-wave persistence. Yeah. I think, especially when those amplitudes are pretty low, the F-waves can look a little, they don't look like your average F-waves. Yeah. And what I always tell, especially our trainees when they're big F-waves, that's not a good thing. I think early on when people are learning and training and they get some F-waves and they're big, they go, oh, these are great F-waves. I can see them nicely. They're really big. But a large amplitude F-wave may mean that there's a neurogenic process with re-innervation. So that one motor unit that's re-firing is innervating many more muscle fibers. Right. And so it's almost like, this F-wave is almost as big as the M-wave. Exactly. Yeah. And the persistence to me tells me there's very few motor units left. Right. So this is a bad F-wave. Yeah, it's not a good situation. It's horrible, right? Yeah. Do you do motor unit number estimates? We do not. No, we don't either. But this is, I remember Jasper Dalby, he was into motor unit number estimates and said that a simple way to kind of estimate the number of motor units is by the F-wave method, by just taking the smallest F-wave and divide it into the M-wave and that gives you a rough estimate. So here, if you do that, then the number of motor units can be really low. Right. That makes so, I mean, that makes a lot of sense to me. Yeah. So anyway, that was the median, the Ulnar motor, kind of similar, low amplitude 2.5 and no block or dispersion, wouldn't you agree? I do agree. Yeah, it looks. And then the Ulnar F-wave, I think it's an F-wave. Yeah. These look a little different, right? They're a little better. I mean, in the sense that maybe there's a few different morphologies there, possibly. Maybe this thing right here, you can see it, that might be an F-wave, yeah, but still pretty big, high amplitude. Exactly. And then lastly, we did two sensories in the arm, the Ulnar and median antidroma can, those look really good. They do. So nothing surprising to you? No, yeah, I'm just getting more worried for the patient as we go here. Yeah. So what do you do? So you do a needle exam, I assume. We do. So how many muscles and what would you do in this patient? We would probably just do kind of a standard root screen because I think I remember from the table, the amount of weakness was, or the distribution of weakness was fairly widespread in both, more so in the arm than the leg, I think, but it was encompassing kind of all nerve roots. So we'd probably do maybe about five muscles. In a limb? In a limb, yeah. And then actually, if, even if there are areas that aren't super weak, we'd probably wanna look at those too, because sometimes you can see some subclinical changes. If there's been reinnervation, you might not be able to pick that up clinically, but if you put your needle in there, you might see stuff. Yeah. So how many limbs do you need? Like how extensive would you wanna see findings to be confident that this is a diffuse motor neuron disorder? So we would, and so assuming that we know that there's really nothing on the MRI scan, and that we're not worried about concomitant impingement and structural disease, we, I would probably go ahead and just, cause we're sometimes on autopilot, we'd sort of do five muscles in the arm. And if that looks pretty compelling, we see a lot of fib and sharp activity and a lot of chronic denervation. We might in the leg, if we get to two muscles that are of different myotomal levels, and we're seeing the same exact types of changes, we might do three muscles in the other limb. And then we might take a peek at like thoracic paraspinal as well, just to sort of complete things. So if we play a game, kind of like name that tune, if you have two muscles in different nerve roots and nerve distributions in the leg, and two in the arm, and two in the thoracic paraspinal, so six muscles, and they all have fibrillations and they have big motor units, is that enough? Can you, and there's no other spinal cord compression. In a needle phobic patient, like you said at the beginning, can you, do you think that's sufficient to do two or three muscles in a limb and not do a whole screen of, like a root screen? You could probably quit there. I mean, you know, at the beginning we had kind of talked about, could you even not do an EMG? And I think if you were pretty confident clinically based on what you were seeing, you're seeing kind of that combination of upper and lower motor neuron signs, there's no structural explanation for it, and no sensory symptoms, you know, you get your needle in there, you do your nerve conductions, you see what we see here, you do a few muscles, you could probably be pretty confident about the diagnosis. Yeah, and what about bulbar muscles? Would you do those in this patient? Or when do you decide to stick some of the bulbar muscles? We'll do them if the patient's symptomatic, but if, you know, their speech sounds absolutely clear, we see no fasciculations, they're not the most pleasant, so sometimes we'll skip that. Or the same way, if the patient has a limb presentation, they don't have bulbar involvement, I think while one could stick those looking for subclinical involvement, I think the likelihood it's gonna help in the diagnosis is pretty low, but I think the opposite, when we see patients with bulbar ALS, then those are the times we would, of course, stick some of those muscles. Yeah, you mentioned fasciculation, so what do you think about those? Are they important, or do they count as evidence of denervation? I, you know, I tend not to value them, if that's a term that could be applied here, as highly as I would fib and sharp activity, because I think a lot of times we're seeing fasciculations and they don't necessarily indicate, you know, an aggressive or malignant motor neuron disease, whereas fibs and sharps, I think, tend to get my attention more. Yeah. So. May they help, oh, go ahead. Yeah, I mean, a lot of times the patient will tell us about fasciculations, or we'll just see them clinically, and we get our needle in there, and maybe we might see them, we might not, if they're not happening in the area that, you know, that we're examining at that moment. Yeah, I think fasciculations, I think there's something interesting about fasciculations, because oftentimes I'll see them, and then I put the needle in, and they're not there. I think when they see the needle come in, the fasciculations hide. Yeah. They're like, ah! But really, I think oftentimes we don't grade that there are fasciculations present, but I think sometimes that reflects how much time you leave the needle in the muscle. And if we're rushing through a muscle or we see some fibrillations, it's a quick exam, and we don't let the needle sit there for a minute or two, we're gonna miss those. And I think if we were, in these patients, if we were to let the needle sit there for two minutes in every muscle, then many of them will have fasciculations. So I think it's under, they're under-called often because people aren't spending the time looking for them. Yeah, I agree. Yeah. But the allergy criteria, you know, one of the criteria counts, equates fasciculations as the same as fibrillations if there are other neurogenic motor unit changes. And I was never really all that comfortable with that, but I, until I had a couple of patients where they just had profuse fasciculations and big unstable motor unit potentials without fibrillation potentials, and that patient had went on to develop denervation and had ALS. So I think there's something to that. Yeah, I agree. There is something to that. I, you know, personally, I always feel a little more confident when I actually see the fib and sharp wave activity. Yeah. Yeah, I agree. So, well, this is what we did. This is a little, this is just our table. And so we did not do all five muscles in the arm, but this patient had pretty obvious findings with fibrillations and reduced recruitment and long unstable motor unit potentials in pretty much every muscle. So our approach in this patient was to do the anterior tibialis, the medial gastroc, and the vastus medialis, and then in the arm, FDI, pronator, teres, and deltoid, and then we did one thoracic paraspinals. And I think because of the diffuse nature, changes everywhere that, you know, like going back to name that too, and I think we can name that too, and that degree of, that number of muscles in this patient. Yeah, I agree. Yeah, but I think that sometimes, you know, I'm sure in your practice, you'll see a patient that has just arm involvement and doesn't, and it's one limb. And in that situation, we may extend the needle exam and test more muscles in an unaffected limb to look for subtle involvement. So, okay, so do you think this patient has ALS? Assuming that- I'm pretty worried, yeah. So how do you write your report in this? If you do the EMG and it's not your patient, I'm just curious how your interpret, what does your interpretation say, the wording? So I was always trained with kind of a standard line that, you know, the patient has evidence of an acute, or actually they have evidence of a chronic because you've got these kind of, you know, bigger and longer motor units suggesting kind of reinnervation. And then you also have the fib and sharp activity, which is kind of more active denervation. And so there's kind of a combination of chronic and ongoing denervation, which we would say is consistent with a motor neuropathy or neuropathy. And we would say, you know, that I can't completely exclude the possibility that maybe there's multilevel radiculopathies, but I think that a lot of times I will leave that out if, you know, there really isn't any sensory complaint and I'm, you know, reasonably confident that there's not radicular disease. So if you, when you write that report and it goes to a non-neurologist, I don't know if you ever get patients with ALS that are sent by Family Medicine or somewhere else. Yeah, every once in a while. Do they, will they understand that? Will they read between the lines and say, this is ALS or will they call you or do you call them? Yeah, so they don't understand. I would say that the majority of them wouldn't necessarily understand that. And we would probably, I would probably just pick up the phone at that point or send them, we have, we use Epic, so I'd probably Epic chat them and be like, you know, this patient would probably benefit from a neuromuscular office consultation and we'd be happy to look at this person because we're a little concerned about them. Yeah, I think, and I'm not going to get into the EMG report wording and writing, but I think it's interesting with the electronic medical record now. And, you know, my approach is as much as possible to put in the interpretation of what I think the patient has, no matter whether it's ALS or myotonic dystrophy or something like that. So in the past, I used to say these findings, there's evidence of a progressing neurogenic, diffuse neurogenic disorder consistent with a diagnosis of ALS, but then patients now get those reports about an hour later, because it goes into their portal. Yeah. So it's uncomfortable to do that. And I've changed my wording a little bit to just say consistent with a progressive motor neuron disorder, which is the same thing, but it's kind of nonspecific. As you know, there are other motor neuron disorders. I think it would still scare a patient, but, you know, I don't really beat around the bush. And I like to just kind of say, this is what this patient likely has, if I'm confident in that. Right. Yeah. I think the other thing, just from a pure electrodiagnostic standpoint that it can look like is an axonal polyridiculopathy. Right. You know, that's gonna have low, if it's truly preganglionic, the sensories will be spared on the conductions and there'll be fibs and neurogenic units diffusely. So, you know, I think in that situation, the hyperreflexia argues against that. And the lack of sensory symptoms. But sometimes for me, if the patient doesn't have clear hyperreflexia, I think it's ALS, but I'm not sure. I may put motor neuron disease or an axonal polyridiculopathy. Right. Do you do that? Yeah. So we do that sometimes. And, you know, a lot of times, well, especially if the patient comes from another physician and we see something like that, we would definitely contact them. Because I think you're right. Like, I tend not to be that specific in the actual EMG report, but I will be very specific with them on the phone or in kind of informal messaging. And, you know, it is kind of problematic as the patient does see that. And sometimes they have no idea that, you know, they think they have like a pinched nerve. So. Yeah, it can come as a real shock. And, you know, I think the, being able to see your own medical record is good, but it's also bad when you can see it so quickly and before we have time to talk to the patient. So, yeah. So I think it's crafting that report and the wording is really important. So, and one more question and I'll let you go after that, but what about ultrasound? Do you use ultrasound in the assessment of, like for fasciculations or not really? We don't. And not because I don't think it potentially is useful. It's just that I myself was not trained in ultrasound. I kind of came of age before that was a thing that people did. And so I know some of our younger faculty will occasionally use ultrasound, although typically not in this particular situation. It'll be more in people where we're concerned about, you know, focal lesions or enlarged nerves and that sort of thing. Yeah, I'm similar. We probably came of age at a similar time, but I think we're still kids. So we can always, you know, I'm using more and more ultrasound and we are in our practice, but not so much for ALS. And I know there are studies that have shown that ultrasound's better than needle EMG for detecting fasciculations, just because it looks at a wider area of the muscle. So I see the value in it, but I think I'm of the same school of thought as you that I'm more interested in looking for fibrillations, motor unit changes. So, you know, I agree that I think there's a role, but I'm still a needle person. Yeah, me too. Yeah. Yeah. So, well, I really appreciate the time you've taken. This is really terrific. It's nice to kind of hear the different perspectives. I think my take-home points are we do things very similarly and, you know, the importance of thorough nerve conduction studies to exclude other causes and then a really careful needle exam. And it's great to know that we practice similarly. Yeah, it is. It always feels good when you find out that other people are kind of doing the same type of thing as you're doing, so. Yeah, and I think that the slight difference is, you know, whether you do three limbs in this patient or I do two and several muscles, I think there's no right or wrong way of approaching these patients. I think all different variations are valid. So, you know, I think for the listeners and the people watching that, that hopefully this gives them some guidance, some information about what we're looking at, but to know that there are various ways of approaching these patients and making the diagnosis. Absolutely. So, well, thanks. I hope you don't have to go home and shovel snow. I will later, but so far it hasn't come down yet. I'll probably be shoveling a lot tomorrow morning. Well, I'll be thinking of you while we're- Yeah, sunbathing. Sunbathing, yeah, in December here, so. Yes, yes. All right, Diana. Well, thanks again and have a great weekend. Thank you. Thanks for tuning in to this episode of Lessons from the Lab. This was a terrific conversation with Diana Kwan. It's great to discuss the approach to motor neuron disease. It's nice, as we said at the end, that we have similar approaches to these patients in what we're looking for and the types of studies that we're performing to help support lower motor neuron involvement in patients with suspected ALS. She made me laugh. She made me think. And I am a little bit tearful that she has to go home and shovel some snow and deal with the snow while we're in the 70-degree weather in Florida. So everyone should do the same, should laugh, should think, should cry, and should learn. And hopefully all of you learned a bit during this episode and I look forward to the next one. Bye-bye.

motor neuron disease

evaluation

ALS

nerve conduction studies

needle examination

fasciculations

EMG reports

diagnosis

ncs

amyotrophic lateral sclerosis

MND