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Electrodiagnosis of Weakness: An Interactive, Case ...
Electrodiagnosis of Weakness: An Interactive, Case ...
Electrodiagnosis of Weakness: An Interactive, Case-Based Approach
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Good afternoon, everyone. Hey, Mike. Welcome to our session today called Electrodiagnosis of Weakness. My name is Sandra Hearn. I'm one of the faculty at Michigan Medicine. We have a fabulous teaching team today, and we look forward to working through some really interesting cases with you, showcasing a workup to weakness in the electrodiagnostic laboratory. Presenting with me today are Dr. Eric Ensrud, who's a professor of PM&R and neurology at the University of Missouri. Eric is over there. Dr. Sean Jorgensen is clinical professor of PM&R at Albany Medical College. He's over here on my right. And I will take the larger group over here. And don't worry who you start with. You're gonna get all the cases. We're gonna get a little exercise today, meaning that you'll be rotating every 17 minutes and seeing another case with a different facilitator. We've been running this session for a few years now, since 2018, with a short break for COVID. We try to pick a little bit of a different electrodiagnostic theme each time. I'm gonna ask all our newcomers to join us on the left-hand side of the room, please. Please join us on this side. And this year's theme is weakness. Our fourth presenter, Dr. Rad, is unfortunately unable to join us today. So we've switched up the program a little bit, and we're still gonna show you four cases. None of the three of us has any conflicts of interest to disclose. Our goals today will be to learn to discuss and recognize clinical and electrophysiologic patterns. We'll do the rotating stations as I discussed. And what's fun about this session is you guys get to make the calls. You literally will help us choose nerves and muscles one at a time and build out the test until we arrive at a diagnosis together. And so we'll reveal the data in real time rather than showing you sets of electrodiagnostic tables. I'm gonna ask our newcomers, actually, we're pretty evened out. Sit anywhere you like. As you rotate through the groups, please feel free to engage the other experts as well. As you all know, there are multiple ways to solve a puzzle, multiple ways to plan a study. And so I always enjoy these sessions in part because I get to discuss with you all and learn different things that you do differently. And I find that that helps me refine my technique too. So use Dr. Ensrud, use Dr. Jorgensen, and use each other in small groups as you discuss. Lay of the land, we're gonna rotate every 16 or 17 minutes. We're gonna call this group over here, are gonna be our A and B people. Group C is with Dr. Jorgensen and group D is with Dr. Ensrud. After the first rotation, we'll have the people in the large group stay with me and these two groups will do a switch. At the second rotation, we're gonna flip sides of the room and the group here is gonna split into two and go to those stations. And then these two smaller groups will converge on the side here. And then our final switch will consist of just the two small groups at the end switching. So I'm gonna actually end on that slide, so that's up for you. So know that if you're on this side, you're the A, B group. If you're here with Dr. Jorgensen, you're C, and if you're in the far end over there with Dr. Ensrud, you're D. All right, so without further ado, I'm gonna turn it over to my colleagues at their individual stations to run cases with you and we look forward to discussing with you all. Thank you. And then when pressed, he had difficulties a lot. He has one of the biggest gastro-spiratory concessions. Notably, he has no immune system. He is having an oddness. His shingles are often getting stuck to the roof of his eyes. His gallbladder function should be severe. However, when pressed, he did have some weight loss. His workouts, other than what happened in 2008, He had some pretty seductive, proximal, but more so distal upper lipidus, and just a little bit of lower lipidus, increasing the heat of his body across the lower lipidus. He did have some circulations, not overwhelming, but a little bit of transient deltoid. His tone was totally normal. His sensation was normal to him. And his reflexes were increased in the biceps. Otherwise, normal. And she did not have any other inflammation. It was very, very rare. So the way I try to analyze it, I'm trying to think that these things are so mild. I'm trying to consolidate our data. What do we know right now? What are we thinking? What's the cause of the anxiety? And then trying to take some of the planning into consideration. So consolidating the statistics. This is Digital Fast Forest, thanks for watching. He had no sense of place at all. It's a fine example. That's a different thing to me, that's very different. As far as upper motor neuron, lower motor neuron, I think it's just a number that would really be important. He had some luck. Nothing was overwhelming. Doesn't have any of the nerve involved, which to me is always super important to me, because one of my patients certainly had a sort of some rockiness out there. It's super common in a lot of people. But if there's cranial nerve involved, that's very unlikely. He had a flexor extension, which was actually a pretty significant issue. We checked it. It wasn't something that showed a lot of improvement. But it was pretty substantial when we checked it. Yeah, it changed their differences. There's this yellow stick that follows me, and I have it in the air. It was just for a couple of minutes, and now it's in a little shape I see. And then any miscellaneous things, all sorts of things. So this is kind of just consolidating. We're trying to direction of improvement. I think that helps. But you know what? I'm pretty positive. I'm working on it. Sorry, it's hard to hear. She does have a singularity. She did not associate with the ALS. At the same time, it's not a plural. Well, except that you would expect him to have a Romer, which is a sensory attraction you would expect for a Romer. Right. Which, I'm sorry, does that even make sense? You know, you do that kind of separation. The Romer would be imaginative, you know, maybe the sensory Romer is a little less likely, but that's definitely a potential complaint. I think that has to be applied more. No, and I mean, I didn't put that, that's, I don't have to ask that, I think, no. He didn't say that he had bad afternoon, but he's not trying to lose weight, that's not the point. He said he made a slight mistake. I mean, Lambert Eaton, you know, Why, why, why Lambert Eaton? And there's one thing I think that's really going on with Lisa was that this is her book at this point. Which is not uncommon. Of all the people that come to the office, if you really just try to go through your list someday and you're going to have a bunch of neuro patients come in and ask you, how many of you just don't have any significant pain in this area? There's going to be a minority of them out there. So then I think maybe you can ask them. And I don't imagine a lot of people are out there at this point doing a lot of these things anyway. Like, oh, I can close your body or something and go to the fifth counter. I mean, so if we're going to say, and I don't know that any of you guys need to be more necessarily looking towards the other eyes. To me, the two big things I always look at is the sensory yellow map or sensory motor and the other motor. To me, that's the most discriminating item. So, pure motor, we don't have too many possibilities. If it's a pure motor, we don't know at this point. It's essential. It's going to be some sort of thing that's going to go on after a while. But let's cast that to the side. But the peripheral things that are pure motor, what are they? This game is possibly ridiculous. Well, I mean, that would usually be sensory. So those are usually going to be painful. So things that are pure motor, what are our categories? So, we're leading in sensory motor. Motor neurology is what? Biology. So, it's the science of motor neurology. Well, but that would be motor neurology. So, pure motor neurology. If you think about the motor axon, it's going to be the motor axon itself. But a dead series, usually they're going to have a lot of sensors that they have to pick off. And you can have myelopathies and things that do that. There are certain myelopathic conditions that will have a sensory button. But those should be sensory too. Like hearing, huh? Yes. Well, and so that would fit under motor neurone. Right? Whatever. It's what people call a correlation. So I think, to me, that's one of the really important exercises as you're going through this clinic. This is a pure motor thing. 90% of the things that are going to come in, you know, sensory stuff, we're never going to have. We always care about motor more. Those motors have done a reflection of how severe the disease process is. We were just talking about how much, you know, people come in and say, Oh, I have this thing right here. I have to run this thing. They just don't care about that. So, when someone is pure motor, you really don't have to put the brakes on. This is a different thing. Let's get my pure motor mode. This is pure motor with Kennedy, which you can look at. Kennedy is a disease medical course. Yes, that would be under a motor neurology student. Although they often have a sensory neurology, yes. Yep, Kennedy disease, especially with motor neurology. You can see it in both. They have it in both. It holds up to a motor neurology and a pure motor neurology. Or the biceps. So, but let's just play it out. So, if, let's say we had you looking at a figure 8 ball. Right. Yeah. And we're seeing the same thing. Right. I don't want to touch this guy. Right. Call me. With, pretty much, going to go lower, going to go up. And that is four categories of performance. Oops, got a few more. And then I was wondering if somebody asked... Re-innovation changes everything. In that intraprenual process, because we have a lot of problems, in that sort of a renaissance, super-common, we explain a lot of this, but... It's red if it's out of focus. What's that? Yeah, right. Right. This is real world stuff, you know. Is that significant? We just said, alright now, if he changes, you know, the track... All right, from co-speakers, a two-minute switch point. Alright, so, this is how it works in the real world, you're not allowed to just sit and blast into all this stuff and be like, oh my god, what's happening? You know, so, process. That sounds like a seductive shot. All right, let's do a switch of the groups over there. Dr. Jorgensen and Enstrud to do a switch when you can. It's more widespreadable, but it's a disorder of motor nerves, right? He's only got one nerve. That's the one part of the motor stress that's important to him. For this person, right, he should know that this is a workaround, not an exercise. It's a physical exam of losing kind of one nerve at a time. What's the pathophysiology? Say again? One more time. Demyelination. Okay, yeah, so there's failure of conduction across these different sites, right? We're seeing conduction blocks with minimal axon loss. And so the clinical correlate for that is that she's weak without a whole lot of atrophy. And then the time course is very chronic, right? We see some level of re-innervation in some of the muscles without active re-innervation. He's electrodiagnosed again. Acquired motor neuropathy with conduction loss. Our group stays here, so don't worry about that. There's involvement of multiple distal motor nerves in a non-myotomal pattern. Electrophysiologic involvement of bilateral upper limbs. There's no evidence of sensory involvement or active axon loss. Clinically, these findings suggest multifocal motor neuropathy. At this point, we're seeing her 10 years out, so we don't know the exact time course of that loss. So this is what happened to her subsequently. She had the electrodiagnostic study around May, saw neuromuscular neurology. She was tested for anti-GM1 antibodies, and they were negative, but clinically, this was consistent enough with multifocal motor neuropathy that she was treated with IVIG. At a three-month time point, she reported 80% subjective improvement. Different physician examining, but wrist extension went from three to five and finger extension from one to four, so significant motor improvement. And then at about a year later, she continues on IVIG. She has mild weakness of the hand intrinsics at around four out of five, but is stable. She has a little bit of symptom flare prior to the next IVIG infusion, so they're holding her dose stable. And she was diagnosed with cutaneous lupus, and she underwent further workup. So it's probably some level of immune-related dysfunction for this patient. So a little bit on MMN. How often do you see? This is the only one I've ever seen, but I've only been in practice for about seven-ish years. Okay. I am going to jump us to the next case in the interest of time. The goal for these sessions is to let you guys run through numbers and thinking and whatnot, not necessarily to go deep in the disorders. Case two is a snowboarder. This is a 20-year-old man with bilateral hand weakness. He was snowboarding about 18 months ago accident. He fell on his two wrists. One side fractured. One side not fractured. One side casted. Really, they felt about the same to him. His wrists hurt when he fell on them. Six months later, he had some recovery, but he describes he just was never quite back to normal. So I said to him, well, tell me when you were at your very best, what could you do? And he said he could lift weights at the gym. Okay, so 12 months prior to me seeing him was his best. Sometime in the last nine months, he got worse. He started to have insidious hand weakness, loss of the hand intrinsic mass, some vague paresthesias in the upper limbs, mostly to the bilateral thumbs. Really? I said thumbs? You sure it's not your pinky finger? He said thumbs, but vague, and then no pain. On exam, he had extensive atrophy of the hand intrinsic muscles, most pronounced over the first dorsal web spaces and dorsal interossei. His hand looked kind of skeletal, you can see all the way, the metacarpals really well. One out of five strength for fifth and second digit abduction. Everything else in the hand was very weak, distinctly less than three out of five. Finger extension, okay sign, thumb opposition, anywhere from a flicker to a little bit of movement. And then proximally, wrist extension, elbow, shoulder, normal, and no fasciculations. The primary exam was diminished to light touch over bilateral thumbs, and normal through the remainder of the hands and forearms. Reflexes were two plus and symmetric, no Hoffman sign, and no ankle clonus. So we did the differential for hand weakness on the prior case, so I won't ask you guys for that again. Is anyone thinking of one or two things that you do want to throw out for this patient? Differential diagnosis, just one or two things. It's a weird pattern, right? It's quite severe, it's very motor, much more so than sensory. The sensory stuff's vague. He has a lot of hand intrinsic weakness. Ulnar nerve. More than that, it's, yeah. Thumb opposition's also weak, okay sign's weak. It's almost like the whole hand. It is symmetrical. Say again? Interior interosseous nerve, yeah, so the okay sign was weak. Yeah, ideally I should give you kind of one joint at a time. I didn't write it down for you, but ideally I should test that and tell you. So let's look at the electrodiagnostic study. Where do you want to start on a case like this? Ulnar nerve, ulnar sensory? Yeah. Are you very curious to find out if there's sensory involvement? I am. To me that's the big divide right now. Am I looking at a motor only disease? Am I looking at a disease that affects the motor but not the sensory nerve conduction such as a radiculopathy or an intraspinal lesion where there are sensory symptoms and signs and loss, but the sensory electrophysiology is normal? Or something else where the sensory is down? So here's our... Sorry, that was Searle. Okay, here's our ulnar sensory on the right. This gentleman's 20 years old, latency's 3.2, amplitude's 38, and a conduction velocity of 56, looks very nice. Where do you want to go next? Media? Also very nice amplitude. Good amplitude, good latency, good conduction velocity. We are not seeing sensory electrophysiologic abnormalities whether looking at the upper plexus and thumb or whether we're looking at the lower plexus, ulnar nerve. We're not seeing it. I did not do radial, but that's a good thought. Did I do median D1? No. Are not yeah, yeah, where are you going to go next? Motor Which one owner? Amplitude 0.7 millivolts You can see there's some technical difficulty here because it was higher on the proximal stem. So that's a technical factor Latency is normal. No slowing of conduction velocity across the forearm or elbow Axonal loss. Yeah, where do we need to go next? Yeah Not really all of it was quite atrophy no neck pain Yeah, I think so I think so Maybe FDI a little bit more. It's hard to say now, but it was it was very atrophy. It did not look split Left owner Very similar Somebody wants to see median which is good, right when we see abnormalities, we have to find abnormal with normal And lo and behold, we still have a low amplitude not as low as owner Okay, but it's not good. So contralateral side Very similar so it is quite symmetric, isn't it? What are you thinking nice very nice What do you want to do for needle So active denervation, decreased recruitment, increased amplitude. to the other side. So all this sort of pattern. Triceps is also affected. biceps normal you're thinking a spinal cord lesion that centered around c8 and c7 right good No neck pain. So here we might do, I think I did opponent's policies on one side. and cervical paraspinals were normal. So that's a good strategy, right? What you guys are looking to do, I can tell you're looking to make sure that different peripheral nerves are affected, but the myotomes are consistently around C7, C8. This isn't a very clear, clean, one-level lesion, right? This has got a little bit of spread to it there. Okay, so let's move on. Let's put it together. This is kind of the full study as done. But the things to point out are, if we think about the myotomes, which myotome is the most affected? C8, right? C8 is overall worse. Sure enough, between the median and Ulnar studies, which one is more C8? Ulnar is more C8. The median, recording the thenar eminence is more T1, right? So that aligns with this pattern. And sure enough, if we look at our recruitment column, our weakest muscles are C8 on both sides. C7 is also affected on both sides. T1 is affected to a degree, but not as much as those ones. So this is a little bit of a, it's a focal lesion, but it's got a few myotomes wrapped up in it, hasn't it? MRI, you're saying? We'll get there. It is interesting, right? The sensory is not quite aligning, so we'll get there. Yeah. Where does a lesion localize? This is most likely an intraspinal lesion. It's intraspinal because our motor electrophysiology is normal, and our motor electrophysiology is not, and it's myotomal, at least in the motor presentation. Go ahead, please. What'd you say? I'll get there. It is a little bit funny, right? It is an odd pattern. Now, what I will share with you, though, before we get there, is that the, yeah, I'll continue for now. Right, so you're thinking if the anterior portion of the cord is involved, right? The anterior horn cells, as opposed to the full cord. Yeah. He did not have, he did not have Hoffman or hyperreflexia. Okay, so a chronic and active lesion. So, putting it together, there's evidence of severe bilateral intraspinal lesions at C8, with some involvement of C7 and T1. Electrophysiologically, these lesions may localize to the C8 anterior horn cells of the spinal cord, or nerve roots. On the right, where more detailed study was performed, there's additional evidence of bilateral C7 involvement. It looks chronic and active. This is imaging. And so, this is the MRI of the cervical spine in neutral position. You can see the cord and the nice, white CSF around the cord. Just a quick signal to my colleagues, we're gonna switch in two minutes. We're gonna switch in two minutes. So to consolidate our data, we saw primarily a motor process. We didn't see any evidence of conduction block. And the needle showed abnormalities of smirks over space and time. Really, I wasn't aware of anything at all. So when I've taken all this together, that's the bottom line. Some of the processes, here's what you can get. Pure motor, almost free motor. And we have some open motor ordering around it. It's soft, but it's active. And we do have subcranial nerve movement. And safety, we're thinking, is interstitial. So what do we have? It doesn't, right? But how do we admit it? We have circles at both sides. You would actually know, but if you don't test, you don't know, right? It doesn't get into my brain. It doesn't matter what you see. If you see a strong clinical event, it doesn't matter. It doesn't matter. I'm not telling you how to get it. But you better be ready to write off. So we've got several people who have had this for a very good amount of time. What's this? But don't try this at home. It's not. You know what it is. So I don't think he doesn't have a lot of room to do it, right? And so that's to do the O.H. in your system. Just true weakness would be really important. We're out of their stuff. We're out of their stuff. There's nothing tricky about this. We're American. We all have a right to know who we're on with. We have to give them what they owe us. Don't let that throw you off. Debt flexors and extensors are an underappreciated thing, and they tell you. This is no longer something that you can explain. Otherwise, you could explain most of this by asserting the real world. And I've seen many people in debt flexors and extensors know what they're actually doing, and it gets them. But if you looked at this patient, that was never justified. It's hard to work out, you know? And those systemic sides, too. How many people who have applied to make a lot of these things all the time have said, even though the guys have been working out, they have already collapsed? How many of them said, where? Not in my part of the country. No one has said that. How many people are going to wake up now and say, you know, some of us just lost a good thing, and now you're going to bail us out? As always, the AIA and I will be on the platform next to you. And our webinar is called Strike Out Loud. And a temporary low-stage plateau. as well, so you can debate whether you're going to be able to get a response or not. So in short, the research is still pretty scant because it's pretty rare. Cervical collar has been shown to work in small case series, but it's very restrictive to be living in a cervical collar. So at the end of the day, the clinical history is one where it progresses for a while, then it plateaus. So it might be that you kind of do what you can to try to limit flexion for that period of time. But they don't get worse for life. It's not like ALS. All right. Let's switch. Thank you all. Well, you know, I think I have my answer. But in all, I think the whole model affects a little bit more. You know, I tend to do more in my... Yeah. It affects the lower motor neuron much more. So the anatomy of the spinal cord, the lower motor neurons work on the anterior portion of my hand. So if the anatomy is that the cord is being shoved up against the front of the spinal canal, and that the anterior spinal arteries, branches are being compressed, and they're rendering ischemia to those cells, then you're going to have failure of the ventral cord. And then you'll have the motor findings much, much more than sensory. Yeah. Hey. Nice to meet you. I go to MSU in Boston. And a lot of my friends from undergrad talk about you. And they're like, I learned so much about neuromuscular stuff because of you. So I was like, nice to put a face to the pain. Okay. So where are we here? What period? You guys had Sandra's two tastes, right? Probably PM and R boards. That would be a tough question. Yeah. So where did you... Oh, is it? Thanks. Alright, come on, turn around. Hey, everybody's better? Come on over. Alright, we have more. Thank you for watching. No trouble with that? No. She only worked out that had been done on the floor. Thank you so much. He did have the simulations when he was president of the legislative committee, but his tone was totally different. So I had to support him. I didn't do any censorship for him, but I censored fine art. I'm going to try to jump off. What have we seen so far? Give me a couple of feet on this. What does that mean? So, weakness with what? Because I did a lot of discriminating. Weakness. And what was it? It's important to mention that, oh, okay, well, I'm just going through my kind of normal routines, actually. Get the grips. All right. So, first of all, this is not a public meeting, as you see. It's kind of hard to put something together if you have to draw two motors. Pure motor and motor engine, I find it's like multiple possibilities, I mean, the pure motor and the motor engine, I mean, they're rare, but, LNN is the most common engine of motor neural engines, so, you know, it's something you have to come up with. So, primarily motor and EN is a very specific thing, you won't see it a lot, but, it helps you. That helps you a lot, you've just, it's not even triple X's that are any different, I think. It was lower. There was also 3 plus pi 6, which isn't hard, but it is perhaps an up-and-down bit, so maybe it fits. That's also a very easy way to kind of, you know, just throw out a bomb. This is all over the side, so you have a big group of things all over another. If it's both, that's actually very small. But, you know, 3 plus pi 6 by itself, So that's a significant contribution, this is definitely something, next question. If he has this much weakness, with no sleepings of it... You guys are 3 plus 5 so it's not that bad. So not much to learn. We'll keep that in mind. Again, pure motor is very specific, start by start, and then at the end, you have the motor itself, the body, and then you have the actual nerve itself, the motor itself, you have the junction, and then there's the junction of the ship muscle itself. There's the core, that's all there is. Not the cripple cells. No. But then of course, you could have sensory motor processes, of which there are zillions, where the sensory just isn't very clear. in process or something, but again, this one is very... I'm telling you man, you guys all saw it, Stan's just worried for himself, you're gonna tell me what you want. No longer the threat of what are being But, but, but before, just like spraying stuff out there, what are, where is your thoughts? Is this a pure motor process? I'm not telling you what the right answer is, but I'll tell you, this is one of those big decision choices. Alright, well, so they propose it to them. To the rule, if it's under 50, it's not going to work. So we've got a big little motor there. So, it's either a deduction block, which you'll hear a lot, or it's actually lost somewhere in the formula. Well, if it's just a deduction block, you're still going to start with some deductions. I thought I was going to be okay. This is not normal. So this is not normal. We're not arguing about little hairs now. This person has a serious thing going on. That's a serious thing. I don't know. Can you talk to someone in the previous group today? So we should get some sensory stuff. So proximal and lateral? For both of you? It's kind of like glass. You have to... This is plastic on the right. We don't have any marbles, right? This is going backwards. We're going to do it especially if we, if we, do we feel You know what happened? Yes. You know what happened? It folded, right? So it folded, so this is all short, right? So, right, so this is all thin. It's all thin. So two different things have happened. So it should solidly analyze all of our critical electrodiagnostics. So try and put it a little lower, okay? And when you hear that, I mean... or to not allow them. So we're not looking for somebody who has absolutely no clue. I didn't see any deductions by particular experience. And then when we're with clinically, then we go back, we get some of what we're doing. We have some creative learning process. I don't know if this is either a brain or a systemic. Well, we know it's got to be related to the brain because we have tons and tons of those things going on. So, this did not need to be created by us. All right, Dr. Ensard and Dr. Jorgensen, we should switch in one minute. Again, go back to your lab and look. It's very rare to have cure weakness and it's very bad. There's no good things, there's no good dying things that actually present as cure or cure symptoms. So, sets of complaints, bring them to my office and the voters will be able to reference it. If the voter tells me there's a problem with that, I'll bring it to court. Next question's in extensors. Alright, if you're thinking ALS, that's a very important thing. Just number one, it can tell you it's a symptom. Number two, it's bad. Nice to meet you. Thanks for your participation. Good luck. What's going on? You know, you're just collecting all this data. It's coming out of your head, right? You know, they're telling you stuff. You're examining it. It's all up in the air. What's happening here? What's the gist of what's happening? Let's keep solid. What's this big impression that's happening? What's the crust of what's happening? So he's kind of, but before I jump, before I, I mean, you're right here, but I'd say let's, let's just, like I said, consolidate. So this is a picture of, say, I would have weakness subjectively in the Lord. Right, so we don't have sense for any And we're going to try some things for free. So he had to sit there, that's right, he had to act. So he's got a little host of action next to him. He can tell him what he wants, I don't think he does. They really shout it out. Should we have a tax filter function? I mean, we should probably have something. So that's helpful too. No, they have lots of sensors. So the differential are those big fours. So if someone comes in with K moderate, you are not going to see people. We've all seen the same thing. Somebody don't tell me they'll be dragging their leg, they can barely walk, they're crawling across the corridor. I have no burden here. Right? This is what drives everybody. But we care about you. Why? They've got no bone, and they're like, I don't know, I don't know, I don't know. So sensory does not tell you anything. A motor, a little bit of damage, a lot of damage, a lot of damage. We are aware, we creep out on the motor sensors, they creep out on the sensors. So that's something that's interesting. But what if you're a motorist? Then check them. Have these four. Alright, so now, like you've done already, you're going to walk up to me, you're going to turn me down, you know, you're not just going to blast this punching game, you're going to put me down. Set, oh yeah. And I'm going to tolerate it, and you're going to have to accept it. I'm going to put the important stuff first, in case it's all you get. And I'm just going to get seven more inches. Uh, it's a low amp. Why don't you give us a low amp? Awesome. What else would you see? If that was the case, if this was what we did yesterday, on the August induction law, what else would you see? Well, I don't know if you would see the induction laws we've lost in the years, but what else would you see? Now, so as you said, it's the opposite of what you said. And this tells you, this is not a trivial amount, this isn't like an impossible number. This is a 20-figure amount of tax on real cars. You should probably look at it. No. And that's important to know. Oh, a little bit of induction is fine, but the difference is a lot of stuff, right? And no induction of lie. I can't make a solution of anything. Oh yeah, that's good too, right? Yeah, yeah. All the walls. Yeah, so that's just the ranch. I don't think we have to separate it. They had the same machines. Yeah, yeah, yeah. That's correct. Now again, it's not separated. There's blood on the roof. Something's done to this guy. Something's hurt this guy. There's blood on the track. God's trying to follow it, right? Is that going to change the years? No. Should you say change the years? Should we shift from we're all pure muscle motors? Pivot and say no, now we're sensory motors? So you're saying you're saying I still think this is primarily a motor thing and maybe this is just something special? Maybe we'll have to explain later. So you're saying to improve it. Now with that, we need to improve something. What do you guys want? I don't know. I agree. So the interpretation and the reason that that's said is because I don't know. I don't know. I don't need to. But you're right. Not that I know of. I don't know. And this is another point. I want to bring up the sudden onset and the immediate process. So what do we want to do? Should we just go crazy and do all four legs? I don't know. I don't know. We should do it. We should definitely do the plan. Here's the important thing. So what do you want to do? So we're at the point where we're thinking about a good spine position and moving with this point. It's harder to see but we know how to get out of this slow motion position. I don't know. She has a patient I saw in the infirmary who was assuming a voice. So let's now consolidate all of our... It's definitely emotional. We're going to get that out of the way. It's concerning how far we're going to force this way. We don't support the wall. So, AOS is one, GitOps is another really tough one. Yeah, so if not, yeah, you're right, you're right, but let's say something different than a tear in the heart. No, that's painful. That's a tear. That's painful. So, you know, you're not going to take your little man along with you. I don't want to keep you from staying in this room. But you're right, that's the other page we need to look at. In a series of swirls, we're getting over a lot of the things we need to look at. And these are exactly the thought processes that we're learning on, when is it occurring, and what are the consequences of what you guys perceive by it. The perineal nerve involved in telekinesis is either in the head, or it's everywhere. It's in the head, it's in the system, it's in the systemic cell. There's not many things that come to your reach without it being in your system. So I think this talk has been a result of that. America and we all have a right to have an environment that includes people from ALS, AIDS, diabetes, and everyone else. So don't be thrown off as you were. And you shouldn't be. So don't get thrown off by that trivial and probably unrelated sense of intent everybody talks about. Netflix is an extension. We all look at the tongue for attributes. We're just, as soon as we walk up to the U.S. Ambassador, he was in that class with me, and he said, uh, you know, it actually takes a circle completely And then we're going to suspend the service. Nobody's going to get a job and lose money. Not in my part of the policy. But, you know, that's how you, you know... Now, we've got a scene on the hunt, did you watch this? Did he get thrown off by the little squirrel that ran across the trail? No. Alright, you got me. Thank you. So hopefully you have a seat at one of them. And if you haven't already had a seat at one of them, you might be quite glad. And it's not enough if you seat at one or two more. Yeah, I would say it's probably more safe. Thank you.
Video Summary
In this video, the speakers discuss a case of weakness in a patient. They highlight the importance of differentiating between pure motor and sensory motor processes. They also mention that weakness without sensory involvement is less common. The differential diagnosis for weakness includes motor neuron diseases, peripheral nerve diseases, neuromuscular junction disorders, and muscle disorders. The speakers emphasize the need to consider the sensory findings in addition to motor findings in order to narrow down the differential diagnosis. They also explain the importance of performing a thorough examination and conducting electrophysiological studies to assess nerve conduction and determine the location of the lesion. The speakers mention that in this case, sensory findings were normal and there was evidence of atrophy and weakness in the muscles. The electrophysiological studies showed reduced motor amplitudes but normal sensory findings, suggesting that the lesion is likely located in the spinal cord or nerve roots rather than in the peripheral nerves. They discuss the possibility of a C8 anterior horn cell lesion as a potential cause of the weakness. Finally, they mention that imaging studies, such as MRI of the cervical spine, can be helpful in localizing the lesion and confirming the diagnosis.
Keywords
weakness
pure motor
sensory motor
differential diagnosis
motor neuron diseases
peripheral nerve diseases
neuromuscular junction disorders
muscle disorders
sensory findings
electrophysiological studies
lesion location
C8 anterior horn cell lesion
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