Good morning, everyone. Thank you for being here. It was early and it was complicated for me to get here. I went to another place and I was in the wrong place, so it was a little bit hectic, but I'm here. So thank you for all for doing that too. And so I would like to thank the AAM for inviting us to give this session. Actually, as you can see, there is part one and part two. This is part one that we're presenting now, and there's another one after the break. So my name is Mohamed Kian Salo-Jeghe. I'm the neuromuscular division chief and EMG lab director at Boston VA Hospital, and also the deputy chief there. I'm also associate professor of neurology at the Brigham and Women's, where I do some EMG and teach the fellows, which is a really fun and lovely thing to do. So I don't have any disclosures pertaining to this talk, but I have had some consultations from Lupin Pharma and Strongbridge Pharmaceutical So, as I mentioned, this first part, 8 to 9 30, is going to be by myself and Dr. Kelly Gwathmey. And so it's going to be on the basic concepts of nerve conduction study and approach to our study. And also Dr. Gwathmey is going to talk about how to do nerve conduction studies, replacements, some information about it after that. Then at 10 o'clock, Dr. Eisenberg and Dr. Troy are going to talk about some specialized studies, repair of nerve stimulation, cranial nerve studies, and blink reflex, and also needle EMG placement and waveform detection. And finally, some pitfalls you have to be aware of when you do these studies, some important technical factors and safety considerations you need to keep in mind. So I hope you can make it to both parts. So as you well know, now how many people do nerve conduction studies here? Okay, so almost half. Okay. And how many are really good at it? There you go. Okay. All right. So as you know, these are very important tools that we use for the assessment of neuromuscular disorders. And there are many of them. I mean, this is probably not the full list. So we have the typical bread and butter nerve conduction studies we do. There are more, less commonly used ones that we can employ. We can even make up your own if you need from time to time. With some caveats, there are late responses, which are similar, but there's some change in how we do it. And Dr. Kwatme, I think, is going to talk about. No? All right. So, and then there's a paired nerve stimulation that, you know, can be done for neuromuscular junction disease. Needle EMG, of course, follows. And then there's some specialized exams that, as I said, we'll discuss today. So this is not, of course, a very in-depth review of what we can do. But as you can see, you know, there are electrodes you always have to use, different types based on what you want to do for recording the electrical discharges. And each has their own application. You know, it could be the ring or the clamp electrodes for the fingers, or the bar electrode for the skin. You know, we have needle that Dr. Eisenberg is going to go over with you. Then we have the, you know, how you put these is basically you have a G1, which is the main active recording, and then a reference G2. And depending on what you're doing, this may change. So we have, for example, for motor study, CMAP, there's a belly tendon montage most of the times, where you put the G1 on the belly, and then the G2 on the tendon. And then there for the sensories, you know, usually just spread these, the bar electrodes already measure that way around 2 to 3, 3 to 4 centimeters, depending on where you are. And also the needle, usually we use concentric, but there are other forms that were used before, not so much now, and will be discussed later. So grounding is very important, and that's, you know, what you want to do to make sure you have the nice waveforms free of artifact. But there are many other technical factors you have to remember. So the machine setting, you know, how the gain, you know, so I can look at the waveforms, and I can adjust that. The sweep speed, again, you want to make sure that your waves are going to be in your screen. And the filter settings are important. We don't usually look at these. I mean, we, I mean, I don't, unless there's a problem. So once you set up, it's all set up on the machines, you click on the study, it pops up, and it's already preset. But if, you know, you're getting something that doesn't make sense, always look at these. Make sure no one touched them or changed them for whatever reason. And for the simulation, of course, we have a red anode and a black cathode on the simulator. And, you know, we can decide to do orthodromic or antidromic, depending on how your lab is doing for the sensories. And then we can do, have to look at the duration of the simulation. Usually, it's 0.1 to 0.2, but you have to be careful. You can increase it, but then, first of all, it's painful, then you may start getting artifacts. But sometimes you have to actually adjust it for, for example, for H-reflexes. And then finally, there's intensity. You always want to start low. I mean, I know some, sometimes, you know, people will begin crank it up to where they think it should work, but that's not the right way to do it. You want to start low and slowly go up. And you always want to be, except for certain exceptions, super maximal. So basically, you want to get the best waveform, you want to go up a little bit more, around 10 to 15 percent on the intensity, and then if it doesn't change, you stop there. Otherwise, you're going to have some artifacts in your study if you crank it up to higher intensities. So the next part, so I'm just going to go on continuing to it. So is neuromuscular localization and how you plan your studies. Just actually, before I forgot to mention, sorry, the timing on the, on our talks is a little bit different. Dr. Gawath may can't attend the second half, so we try to leave some time at the end if you have any questions. So we may have adjusted the timing a little bit. We'll finish on time the whole session, but the cutover may change a little bit, and then also at the end. So as I said, these are extensions after a clinical evaluation when you do EMGs. And it's very important, you know, we especially tell our fellows, our residents, some of them, of course, are rushed for time, and I say you really have to get your own history and exam. I mean, we see requisitions saying, you know, you want carpal tunnel, but you have to pay attention as to who requested it. You know, maybe someone doesn't know exactly how to localize, or someone was told by someone like a PA, told by the doctor, just put in a consult for, you know, and they just put in whatever they think is there. So it's always important to do a good history. So go to the chart, ask the question, do your exam, and make sure that the referring question kind of goes along with the, what your impression is. And if it doesn't, then you have to kind of say that, that what you're looking for, and kind of describe that a little bit. And so with the differential, then you kind of design the study, and then when you're writing your impression on the report, also keep your clinical impression in mind. And if it doesn't correlate together, you want to point it out. Maybe the patient has something totally different you found on your exam, and it may help to kind of point it out to the referring person. For example, we've had people sent for ALS, and they had inclusion body myositis, and you know, we just say, well, there's not motor neuron disease based on the study, but think about this and that, and that really is helpful to them. And if it doesn't really make sense, the findings you have, you can't point that out that, you know, the radial sensory response is absent, but that doesn't really make sense clinically. So they're just aware that, you know, maybe a technical factor or something else happened. And also another key thing is, if it doesn't make sense, repeat the study. If a resident fellow, even a good technician has done it, you have to repeat it yourself. So very important. So as you know, EMG is highly technical studies, and a bit of, you know, change may have an impact on your outcome. So in terms of planning the study, so of course, first we do nerve conduction studies, and we have to decide, okay, how many limbs you want to do, what nerves you want to study, and before you plan it out. And this may change, even may have to go on to other techniques. So EMG, which you plan for 30 minutes, may end up being like a, you know, two and a half, three hour study sometimes. So it's always important to leave some time for that, if you are able to. And, you know, the needle basically comes at the end of, usually follows the nerve conduction study, and it relies on what you found there, and to complement that. But, you know, as I said, you have to sometimes constantly reevaluate what you're doing, and maybe change your plans, and so it's more of a dynamic interactive study than, for example, you're doing EEG, and you have certain amount of setup you have, and you do it. So this is a very important thing to keep in mind while you're planning your studies. So to do a good job, I think we have to have a good knowledge of the peripheral nerve anatomy. That is important for how to localize, and also nerve physiology, which is important to determine why this is going on. So for the pathology that is affecting that nerve for your study, and also helps you determine the timing that happens, and that may be important when you are looking, for example, after trauma or something, whether something is old or something is new, as you're doing your evaluation. So in a very, let me see, so, okay, so in a very, you know, brief review, so, you know, the motor system starts in the cortex substance, the motor neuron, and that kind of extends out as the motor root, and then the sensory, as you know, is a little bit different, and that is actually an important point to know when you're doing, for example, reticulopathy screening. And so, as you know, the cell body of the sensory system lies in this dorsal root ganglion, or dorsal ganglion, which is outside the system. So if there is any disruption between the cord and when you get to this area, so especially the root, so if there's a problem there, it's not going to affect the nerve that is going to the periphery, and that is important to remember. So if there's a damage over here, there's not going to be any Eulerian degeneration going down to the periphery. So what happens now is that you may lose signals coming at that level, so you may lose sensation, for example, in the C5, C6 dermatome, but the sensory response is going to be normal because all the fibers are there, and you shock them, and you record, it's going to be intact, whereas sensation will not be, and that is a key factor we use to diagnose reticulopathies. So these kind of join together, these two, and become the spinal nerve, and you know, based on the level, we have eight cervical, 12 thoracic, on both sides, pairs, five lumbar, sacral, and so forth, and these go to the periphery. Now what happens is that they immediately create two different bramides, so there's a dorsal ramus, goes to the paraspinal muscles, again another important thing we use for diagnosing reticulopathies, so there's paraspinal muscle innervation, again you have to be careful using that word, so basically there is a possibility that there is a reticulopathy, at least getting the roots is involved. So then the rest of the fibers create the ventral ramus, as you can see, and they become the brachial plexus, the lumosacral plexus, and the other nerves, and then basically all the peripheral nerves on the body come from this system, the ventral ramus. So in terms of the physiology, as you know well, the axonal membrane is an active system, it has a resting membrane potential, and when you stimulate it, so it causes a depolarization under your stimulating electrode, and this actually spreads in both directions, so it doesn't care where you want it to go, it goes in both directions. Now what we do then is by setting up the recording electrodes, we capture what we need, so that's kind of the key thing. So this just basically means that where you record is very important, you have to be on the nerve, and how much you stimulate is important for all the fibers to be, that's why we have you do supermaximal stimulation. And then finally, where you place the electrode is key, and for you who do study, sometimes if you change it a little bit, the whole thing changes, the whole amplitude and other factors, and that's actually a point, so we actually ask all our fellows residents to mark where they did the simulation and the recording, so we can go back and check it. That is a kind of a factor that will help us to kind of first educate them, and also then make sure they did a good job. So what you get is pretty much for all of these studies that I mentioned, you kind of get a waveform, and that is a combined or compounded from all the individual action potentials of those fibers that were under your recording, or adjacent to recording electrodes. So what you get is usually some timing kind of factor, so there is a peak latency, so this is the seamless artifact that you get in all when you do a stimulation, that's where you set your beginning point, and then from that you could have a peak latency, which is very familiar, and Dr. Glockin will talk about also in terms of sensory studies, you have an onset latency, that is how you use for velocity, as I mentioned, you have a duration of the waveform, that you know, depending on how you do it, it could be set only for the negative peak, and so actually let me put these up there, so by default, so the negative deflection is the one that goes upwards, and then the positive is the one that goes downwards, as we discussed in these talks, so usually people look at the duration of the negative wave here, coming back to baseline, but you could actually go from the beginning to the end, but you see that at the end, sometimes it's hard to know exactly where to place your cursor, because it's not going to be a clean line, or a clean kind of baseline pass-through, and then we also have the amplitude again, depending on what you're doing, it could be from baseline to the negative peak, or from peak to peak, and that will be discussed further, and also the shape is important for you, and if it changes as you do further proximal simulations, and so what you do, you have are the CMAPs, the compound motor nerve action potentials, so motor response, you have the mixed nerve action potentials, you could have the sensory nerve action potentials, and then finally the motor unit potentials, or motor unit action potentials for the needle EMG, and they, as I said, all follow this kind of thing, so as I mentioned for velocity, you use the onset latency, so remember the peak is not where the fastest fibers are, the deflection is the fastest fiber, so use this, and of course you have your distance that you measure, the time is well the onset latency, and you calculate your velocity. So in terms of the amplitude itself, as I said, if it's abnormal, if it's reduced for SNAPs and MNAPs, so again, sensory nerve and mixed nerve action potentials, it basically means that you lost the nerve fibers. For CMAPs, it's a little bit different, because as you know, for the CMAP, you know, this includes the nerve, of course, and then you have to go to the neuromuscular junction, then go through the muscle fibers, and then get your response, so the amplitude is not just what you shot, and then the fibers that you expect to record, but actually the muscle fibers has to go through these, so any problem in any of these three would impact your CMAP, and then in terms of, as I mentioned in the beginning, that if you have a damage anywhere in the motor system, it will be reflected in the whole course of this nerve, whereas in the sensory, as I mentioned, it's only going to affect the part that is distal to the dorsal ganglion, not over there. So if there's a lesion, as I mentioned, it's not going to be captured on the SNAP proximal to the DRG. In terms of another difference between these measures is in the velocity, so if you shock record over the MNAPs and the CNAPs, the onset latency can be easily used to calculate the velocity, right, of those fibers, and same thing, as I mentioned, for for CMAP, the onset latency is inclusive of these two, junction and muscle, so when we report on the CMAPs, we report the amplitude, we report on the distal latency, but we also stimulate another time, more proximal, and we use that latency difference between these two and the distance between these two to calculate the velocity of the motor fibers, right, so for SNAPs, we usually have to only report on the amplitude and the peak latency or the velocity, you don't have to really put both, you know. So in terms of what happens when there is a damage, so if there's an axonal loss problem, what happens is that you're going to get a reduction in the amplitude, and now you have to remember it's not going to be immediate because the whole process of the valerian degeneration may take some time to get there, right, so for CMAPs, and again, also depends on how far you weigh from the site of the lesion, so to be safe for CMAPs, it's around like maximum seven days, it should have degenerated, if they were to do so for SNAPs, maybe two weeks is enough to make sure they degenerated, that's why they say we'll wait for, you know, three weeks before you do the EMG, which is not really correct, you can get some data when you do an immediate study, and maybe after a trauma or let's say a vasculitic event where you know the nerve was impacted, but what happens is they have to keep these in mind that this may not have been completed and you may have to repeat the study if you do not get your answer. All right, so now you expect the latency to be, good, you expect the latency to be preserved and the conduction velocity in an axonal lesion, however, that is also not correct because remember the onset latency which you calculate, you know, is from the fastest fibers, what if they're lost, so you do expect to maybe get a little bit of slowing of the velocity or prolongation of the latency in an axonal lesion, but it's only up to a point, you cannot be slower than the slowest nerve in that group, right, and so there's a number for that, and if you have that, so if it's slower, then you think there's actually demyelinating process that happened, so which I'll get to in the next slide. So in terms of the needle EMG and axonal damage, so you are going to get, if it's hyperacute, happened like a couple of hours ago, a day ago, you will only see reduced recruitment pattern, as I said, that is important when you have a trauma, you want to see, hold on, these findings related to that or something else, you know, you have to keep these timing measures in mind, so recruitment is the first thing that goes on your needle EMG, that goes on your needle EMG, then if you give it time, depending on how far away, for example, paraspinal muscles, if let's say you have a cord, a root lesion, and maybe within a week, proximal muscles, maybe in a week or two, three weeks, and then even if you go distally, and let's say the legs, maybe a couple of weeks, four or five weeks, for this whole irritability, positive shock waves, and fibrillation potentials to start, so the timing of the lesion is important, also remember, if it's something that is progressing, the damage, that's still, you need to remember that that may actually happen at a later time, so that's the time, and then finally, within months, again, depending on how far away you are from the muscles, away from the lesion, you get the re-innervation, so I get the, you know, the polyphasic long-duration units, slowly they come together, and then finally, they get those long-duration large units, and I think Dr. Eisenberg is going to talk about that a little bit more during his talk. So when you have a demyelinating lesion, as I mentioned, you expect that the nerve is going to be slower, so now if it's lower than 35 in the upper extremity, and 30 meters per second in the lower extremity, of course, you want to make sure the temperature is correct, patient's height, there's some other factors, but usually, these nerves fire between 40 to 80 meters per second, even the slowest one. Now, you know, we have slower nerves, but they do not, like C-fibers and A-delta, but they do not fall into this waveform equation, right? So that's why when you have a small fiber neuropathy, you don't have any changes because it does not affect the nerves we measure, which are the, well, 40 to 80 meters per second. So if something is slower than that, what it means really is that the myelin was lost. It can't just be because of axonal loss, because the slowest cells should still be above that number, right? So that is when you get a primary demyelinating disorder. And then also the latency prolonged by 130%. This is, but this is a good number to keep in mind for the velocity for upper and lower extremities. Now, so before I get to now, remember there is a gray area. So between where they say, if you have a completely normal amplitude and they're slowing not below 30 or 35, then you could potentially have a demyelinating condition, but you have to be careful that if someone is young and, you know, let's say their amplitude, let's say the study there, Dr. Hollis' muscle, it is, you know, five or six, maybe it's normal for your lap, but that's not normal for that person. So there is some amplitude loss there. So I have to be a little bit careful if the velocity doesn't go below that and you were calling it a demyelinating disorder, as opposed to slowing secondary to axonal loss. So another feature of demyelination is something called conduction block. Now, what happens if, you know, there is a demyelination, not in the whole nerve, but let's say in this segment over there, right? Let's say in GBS or CIDP. Now, if there's a segment below that, that is preserved, the axon of course is fine throughout, demyelinating is fine. If you stimulate below it, you're going to get a nice looking response. Let's see if I have those. No. So you're going to get a nice looking response, I'm sorry, down here, right? Now, if you go above it, even though the axon is still there, because these now change and fall outside that equation, because they're so slow, they don't get there in time, basically you get this drop, which is called the conduction block. And this is going to be maintained as long as nothing changes in terms of the axon damage and so forth. So that is a marker of, you know, demyelination. Another one is if it doesn't become that slow, but it's kind of in between, you see the spread of the fibers, and that's called temporal dispersion. And you technically expect the area under the curve, which we don't usually look at, but there is a cursor that can put it there and actually put it on your reports, should not really change that much if it's just a temporal dispersion, but it would change if it is a conduction block. But they have the same meaning. What they mean really is that is an acquired, except with some exceptions, but there's an acquired demyelinating disorder that is causing this. If the myelin was abnormal throughout the whole nerve, let's say in a hereditary neuropathy, the majority of them, just want to underline that, then you would get a uniform slowing without any of the lasso that I mentioned to you. Now, the other thing I remember, as I mentioned to you, if there's the wallearian degeneration has not competed itself, if you go above there, you're going to get a good response again, right? So if you have to wait again for that duration, so if you do have a conduction block and an acute lesion, you may want to consider repeating it after that week or preferably two weeks to see if it was a pseudo conduction block, whereas this was going to kind of go away and this would not also respond because there's no axon left, but did not have enough time to get there yet. So that's a pseudo conduction block. So for needle EMG, of course, we expect there to be no, only reduced recruitment if there is a pure demyelinating lesion, though that doesn't usually happen. There is some damage to the axon to some extent. So you do see some, you know, fibrillation potentials, positive sharp waves, you know, some motor unit remodeling given time, though sometimes you feel that the extent of those is not equal to the amount of these, the recruitment or the amount of weakness, but then that's your call and sometimes hard to say what is, how much is enough, but that you could sometimes sense that after you do these for a while. So the late responses, so I'm going to talk about a little bit more then. So basically these are to look for proximal lesions. So, you know, you are limited in where you stimulate. You can, of course, go and stimulate at the root level, but that is painful. It's not easy to do. It's not that practical if you have to, you can, but another way to look at the proximal segments of a nerve, which you would otherwise not get to with your regular studies is to do late responses. And we have two, one is an F wave, another one is an H reflex and the difference really is in the F wave when you stimulate the motor nerve fibers, as I said, they go in both directions. So you get your C map, which is called the M wave. And if you give it time, there's going to be a smaller wave, which is the F wave. What happens is that the, these discharges go all the way up to the cord. They stimulate some of the motor neurons as portion 5% or so. So it's not going to come down and give you a small response. And every time you do, it's going to be different because another pool gets stimulated. So an F wave, correct F wave would have a M wave and then different looking F waves following that. And that is how you measure the onset, the first one, the fastest one, and that helps you. For the H reflexes, kind of you trick the system with some adjustments in your response and you just activate the 1A fibers that are taking back, for example, from the stretch receptors equal to if you do like an ankle jerk test and these go all the way up to the cord, they stimulate the S1 motor neurons and they come back and cause actually a plantar flexion, like an ankle jerk plus a wave. And that is called an H reflex because it's a reflex test. It goes to the sensory, comes on the motor and checks the whole pathway of the tibial sciatic S1 up and down. So that's another measure you can use. So now how we plan our studies is kind of important. So the way I look at it, and I say this is a very crude, very simplistic look, but that's what I have you know. So basically people coming to us either have a sensory problem or they have a motor problem. And if there's a sensory problem, you think, okay, it could be at the root level, could be in the dorsal ganglion, it could be in the sensory fibers that are going to the periphery, and that's pretty much it for the sensory system. If you have a motor problem, it could be in the motor neuron, in the root level, in the nerve, so kind of similar to sensory, but also you have the two additional neuromuscular junction and the muscle that could also be problematic. So you kind of think about these two localized. So what you do now is you say, okay, if someone has both sensory and motor problems, then it's either at the root level or it's at the nerve level, right? These are the two logical places it could be, or the fiber level. So simplest of all is the reticulopathy. So what you have is there's a root being affected by something, could usually be a disc or an ossifier or something pressing on it, you get a little reticular pain, you have weakness in the distribution, sensory loss in the distribution. But remember, you cannot get full plesia just from one root problem. No muscle is innervated by just one nerve. Now, putting aside the facial, of course, the cranial nerves, so you cannot get complete weakness just from one root problem. It's important to keep in mind. Now, the other one is polyreticulopathy, which could actually give you now pretty severe weakness when you have different roots being affected. Now, it could be, for example, from say, lumbar stenosis, getting multiple roots, but you also have to think about a more diffused meningeal process. So for example, could it be a cancer causing seeding of the meninges? So leptomeningeal carcinomatosis. Could it be Lyme that is now causing, or another infection causing the meninges to be damaged, or any other process affecting the meninges? So now, in that case, you will have diffused pain, diffused motor and sensory issues, and may even get the cranial nerves, if it goes up to the brain, even cause some cognitive changes. So it's a more widespread problem, and you got to kind of keep that in mind when you're doing your study. So of course, as I mentioned to you in the beginning, you want to look for normal sensory responses, right? Normal snaps, but abnormal motor system. Now, your CMAP may be normal, because remember, when you do a CMAP, you have particular muscles, CAT1, for example, in the hands, mostly, and maybe L5, S1, mostly in the legs. So if the level of the damage is not there, you're going to have a normal CMAP, of course, right? But the needle EMG is where the money is for reticulopathy, is where you see the innervation, re-innervation, again, based on the timing I described to you, when it happened. And what you want to look for is that different nerves, the muscles from different nerves sharing the same root level or mitome are affected. So you want to overlap the different root levels from different nerves before I call it a reticulopathy. And that kind of, for example, you want to look at the tibance muscle, which has, for example, an L4, the vastus has an L4, and you kind of superimpose those. You can't just call based on one of them being abnormal in most cases. And then, of course, you can do paraspinal and needle EMG, and that's sometimes maybe the only thing you'll see. But again, you've got to be a little bit careful before you call that. There's some technical factors, and, you know, that prior surgery or something, they may just have these and not really be an ongoing innervation. So we move on to the mononeuropathies. And so, of course, top of the list, we always see our carpal tunnel syndrome, ulnar neuropathy at the elbows, cubital tunnel syndrome, peroneal or fibular neuropathy. These are mostly compressive. Now, some may not agree that is a compressive lesion, but there is some effect on the myelin from outside. And so first, you get some slowing and damage to the myelin. And then in time, it slowly becomes an axonal lesion. And that's how you localize these, because there's focal demyelination. As I mentioned to you, you get slowing across the wrist, you get a conduction block across the elbow, and that's how you localize these compressive or mononeuropathy lesions. If you don't have that, you can't say where the problem is. If it's just axonal loss, like you see down here, so it's enough that it became axonal, or you have a primary axonal lesion, like trauma or vasculitis or something, you can't localize exactly where it is. You can say it's this nerve or that nerve, but where in that nerve may be difficult to confidently localize. If that happens, though, we do needle EMG to kind of find out where it is. So here, of course, we're going to say weakness and sensory changes in that nerve, and any needle EMG changes will be limited to that particular nerve, which you can look for. So as I said, we have to look for focal demyelination before we can say where the problem is. And as I said, also you can get abromalteum, the axons with time and the muscle issues. And also just to stress this again, to do exact localization, need focal demyelination. Needle EMG can just tell you what the most proximal part of the nerve that is abnormal could be. But you can't really say if the abnormal muscle and the normal muscle, the lesion is between them, because it may be a fascicular innervation. Nerves are not just one bundle, they're fascicular, so it may just get that fascicle to that muscle that is more distal, where the lesion could be actually proximal to the normal muscle you check. So I can describe that later if you want me to. So we have multiple mononeuropathies. Of course, top of this is a mononeurodysmultiplex, a vasculitic lesion, very ominous, probably a neuromuscular emergency you've got to address. But there are others that are not as acute, not as obvious. It could be infiltration from, let's say, someone has lymphoma. It could be infection, leprosy, of course, could get multiple nerves and may be relatively insidious and not be that painful. Lyme, same thing. Other granulomatous lesions, like sarcoid, could do it. Some CIDP variants could get multiple mononeuropathies. And finally, some hereditary conditions. But then this is not that long. So if you get that reliably where someone has, and what you see is that someone, for example, has weakness sensory changes and distribution of an individual nerve, then another nerve gets affected, then another nerve gets affected. Now, the problem is sometimes when they get to you, it's been a couple of months, couple of years, so they have looked like a peripheral neuropathy. So first, I have to say how it started is always a key factor. And if it's an individual nerve based on their description, and then another one happened, that's not, of course, your bread and butter neuropathy. And second, if you see a prominent asymmetry, now you can see some in neuropathies, but if you see prominent asymmetry in your studies, then think that these have become confluent over time. It's actually not a generalized polyneuropathy, it's a multiple mononeuropathy with many, many nerves now being damaged. That will change your approach to that patient. So in terms of the bread and butter neuropathy, we see, of course, it's usually distal, symmetric, length-dependent, meaning the distal nerves get affected more than the proximal sensory, more than motor. So you see in diabetes and alcohol and some drugs and so forth. And now, if you have a non-length-dependent generalized neuropathy, meaning that, for example, the sensors are affected more in the hands than the legs, the radial sensory is absent, but the sole looks pretty nice, or if there's a motor more than a sensory involvement, and you have no reason, there's no old reticulopathy, there's nothing else that could explain that, then you want to really think about two things. Is it an autoimmune process or inflammatory process, or is it a hereditary condition if you see this? And so GBS, CIDP, and so forth. So that's a key factor when you're looking at your studies. Another thing, because I work at the VA, when this happens, I'm always going to look for reticulopathy, because most of the veterans do actually have a lot of cervicals, you know, and lumosarcal degenerative disease, and then most of them do have a superimposed reticulopathy. So that sometimes is the explanation we find for motor more than sensory, or this asymmetry sometimes in the motor studies. And then here, basically, depending on what it is, you get weakness in different parts of the body, sensory changes, and you want to look for chronicity changes. Now, seeing fist, cavus, hammer, toe, does not mean equal hereditary neuropathy, it equals a very chronic neuropathy, or some other reason for them to have those changes, of course. But it is a telltale sign, and they also want to ask about family history, and for most diseases, we don't tell the patient, what is your mom and dad have, shock or my tooth? I say, well, they don't know, right? So you got to ask them, well, did they have any problem with ambulation? Did they wear special shoes? Did they have any difference, like, did they have changes in their feet? So sometimes you have to bring out these questions. Did the patient themselves wear special shoes when they were younger? Did they have problems with sports? And sometimes we actually see people come in their 60s, 70s, even higher, 80s, have never been diagnosed, and they have a hereditary neuropathy. So what you do, this is the problem when you're doing studies that it could be a, you know, 30-minute, 15-minute study, or like a three-hour study. And what happens now, you have to do enough nerves to get your answer. So that, to look for demyelination findings, as I mentioned to you, is it hereditary or acquired based on the factors I described, and you sometimes have to do proximal stem, the late responses, and sometimes you end up doing a three or four of them study, you know, and that is something that, you know, you can't really predict. And of course, EMG will depend on the type, where it is, the chronicity, and you see these changes. Now, as I mentioned in the beginning, if it's a small fiber neuropathy, you may not see changes on your nerve conduction study and EMG because they don't fall into that equation. And so there's special tests you can do for those. And remember, if you don't remember anything from this talk, remember that cold nerves are slow. So if you do not see a temperature on your report, or they come and tell you, oh, you know what, we couldn't get the patient warm, two things. First of all, the surface temperature is not your nerve temperature. So you have to wait for at least 30 seconds, a minute, preferably, before we record the temperature, because it's a skin temperature, and the nerve is still going to be slow. The second thing is, we've treated people or asked to treat people for CIDP because they had slow nerves, but no one recorded the temperature. And when you bring them in, you warm them up, it's actually a normal study. So remember that cold nerves are slow, and you always look at the temperature after it has become stabilized. So moving on to plexopathies. So the plexopathies are usually asymmetric in the upper and the lower, or just get one limb. They don't have to be on both sides. In the brachial plexus, of course, we have the famous Parsonage-Turner syndrome, starts with pain, and then it kind of extends to sensory and motor changes, radiation, for example, after someone has breast cancer, and they get radiation for some other reason. In the lower, in the lumbosacral, the same thing, radiation could happen, and it could be a retroperitoneal process, for example, let's say a bleeding, a spontaneous bleeding in the psoas muscle. And also another thing is the lumbosacral radiculoplexus neuropathy, or more commonly known as diabetic amyotrophy, that also could get the plexus. So here, you know, as I said, depending on the type, usually there is a painful process as it starts, and then slowly the patient notices they're weak and numb at that limb. And on exam, you see diffuse weakness and sensory changes, usually in a single limb. As I said, you could get the other one after some time, rarely at the same time, but it could happen, but usually that asymmetry is going to be there. So what you see here is actually, you have to do an expanded study, and now slowly move on to the less commonly done studies, like look at the middle antebrachial cutaneous, look at the lateral antebrachial cutaneous sometimes, so the MAC inside the form and the LAC outside. You have to, for example, do now saphenous nerve studies, which you don't usually do, because now the lumbar plexus requires that for the L4 kind of dermatome. And you may have to do other studies. Actually, side-to-side comparison is always important, because you have a normal side, you have an abnormal side, and the best normal value for the patient is the normal side. It's not what you have on your paper. It's the normal side is what you want to look at. Look for any difference, side-to-side difference, and that is key and can use it actually in plexopathies. And of course, the EMG would show the innervation, re-innervation, again, as I mentioned, the timing is important. And if you see myokymia, so basically continuous movement of the muscle under the skin, clinically or myokymic discharges, which Dr. Eisenberg is going to do a review with you, then you think about radiation. That is highly suggestive, not diagnostic, but highly suggestive of a radiation that causes plexopathy. All right, so finally, we'll move on to the sensors, so a lot of the combined. So the sensor, pure sensory involvement is really two. It could be the dorsal ganglion, right? Or it could be the sensory nerves that are involved, sensory nerve fibers, right? And if there's a motor, then that's kind of the two things you have to focus on. Now, ganglionopathies, like mono-neurotic multiplex, have a limited number of diagnoses, and it's really important to find them and stop them, because once you lose those cells, the neurons, they're not going to get better. So it's an ongoing process, you have to capture it. So things, for example, could be Chagrin syndrome, so you can look for as treatable. Drugs, B6 toxicity, remember B6 deficiency may cause neuropathy, but toxicity, for example, someone was diagnosed with TB, or someone who had exposure to TB, and they put them on high-dose medication, and isoniazid, and so forth, they put them on B6, and they forgot to take them off to B6, or they read somewhere that B6 is good for you, so they're taking high doses, and that's not in their medication. They always ask the patient, are you taking any supplements, and B6 toxicity to do that. Some chemotherapy agents, thalidomide, some of the platin agents that cause ganglionopathies, they got to think about those. Paraneoplastic conditions, autoimmune conditions, both also get the ganglion, and you know, if you do see that, you always want to think about anti-HU and do a cancer screen for the patient. So what you see here is actually that patient has a non-linked append, remember, non-linked-dependent sensory motor is different. This is a non-linked-dependent sensory problem, no motor problem, and they present sometimes with severe sensory ataxia. So if you have involvement of all different nerves, small fiber, large fiber, you know, sensory ataxia, and the symptoms could be, and one arm could be upper and not in the lower, any pattern goes. Pure sensory, then think about ganglionopathy. And what you see here is actually reflects in the nerve conduction studies, so the sensory responses will maybe diffuse, everything may be gone, which may be hard to make the diagnosis. You still have your MAC and LAC if you have nothing further in hand in the proximal nerve to study. And for length dependency, or you see that there is a non-linked-dependent damage to sensories, but nothing in the motor system. So moving on to the motor neurons, I'm sorry, the pure motor kind of involvement, you have the motor neuron disorders, as I mentioned to you, you could be in the nerve, motor fibers, the neuromuscular junction, also finally, in the muscle itself. So of course, the most ominous diagnosis, we can tell a patient now would be ALS. There are treatments, but none of them have been able to reverse it. We'll see what's going on, go to talk, see where we are. But, you know, that's the most ominous, but not all the motor neurons are ALS. You could have infections, it could be polio, could be any of the enteroviruses, of course. West Nile could do this. It could be post-polio, someone had polio when they were very young and they recovered. And when they grew older, 15, 20 years later, those same muscles may start to become weak again. And so you always ask them if they had it in the past. And there are other hereditary conditions getting the motor neuron, of course. So here you get pure muscle weakness and atrophy. And they spread, this is mostly in ALS and the others, they spread in a regional pattern. So remember, the root pattern, the myotomal pattern, same thing here, you get a myotomal involvement or a single root involvement in different nerve distributions. You could get bulbar and respiratory problems. You could get cramps and fasciculations. And if you see upper motor neuron and lower motor neuron symptoms combined, of course, you want to make sure there's no, as I said, I'm at the VA, always make sure there's no cervical reticulopathy that is doing this and causing, for example, core damage. But if you see upper motor neuron and lower motor neuron, simultaneously, then you're highly suspicious of ALS. So what you look for over here is look for sensory responses that are abnormal, that should be, I'm sorry, should be normal. Usually now, some of these, for example, Kennedy's, you may get some sensory involvement also. There's a question whether it gets the ganglion, sensory ganglions a little bit. But so you look for normal sensory responses, reduce CMAPs depending on which levels were involved, of course. And then you want to always make sure it's not a motor neuropathy because that's treatable, ALS really isn't, right? So you want to make sure you do proximal stims, late responses, and look for, if there are no upper motor neuron findings, look as much as you need to to make sure that this patient is not going to get better with IVIG or with some other treatment modality. And then when you're sure about that, and then you kind of say, okay, this is that. Now, the innervation, re-innervation again could be in the mitomal pattern. So if it's in a single nerve pattern and you can't prove it in another nerve distribution with the same root devil, and I keep saying this again, it's important to make sure you overlap these before you call it that this is from the motor root or motor neuron, as opposed to just seeing it in one muscle is not really enough to call it. All right. So now you could also have motor, pure motor neuropathy. And for example, you could have multifocal motor neuropathy, right? So you have individual nerves and you see conduction blocks slowing, you know, individual nerves in the motor component. You could have axonal variance of GBS, and you could also have hereditary conditions that get the motor. And that's why I went back to say more than sensor involvement, you need to think about these if it's pure motor problems. And now here, the difference with ALS is that now it's going to be mostly in a length dependent or in a nerve distribution, right? So it's not going to be in a mitomal distribution. And as I did most of these, except for MMM, which gets individual nerves, you have the more of a length dependent, this some of the proximal muscle involvement. So this will be a spores, proximal is better. And so that's usually, I see, as I said, the other stigmata of chronic neuropathies. So here again, like a motor neuron disease, you have to do enough nerves to look for demyelination. And I went through that already. And then the intervention renovation follows the clinical exam. It's usually in the distribution of nerves or a length dependent pattern. So neuromuscular junction disorders, as I said, also are not only causing muscle weakness and muscle disease. If they're presynaptic, like Lambert-Eaton or botulism, they could have other stuff. They could have autonomic involvement. They could have other features. But in terms of their weakness, they get the neuromuscular junction. Presynaptically, they also have postsynaptic, myasthenia gravis as a junction issues. And these patients have a fatigable weakness. Now, sometimes you get a consult, the patient is tired, end of the day. Do they have myasthenia gravis? I said, that's not really how you do this, right? You have to have fatigable weakness where you do something, you get weak, you rest, you get better, right? And that's what is meant by fatigable. I think all of us probably get tired around four or five o'clock and you don't have myasthenia, hopefully. Most of us, so it's important to remember that it is worse with activity, not as the day goes by. Ocular bulbar issues are also very important. And most patients should have some ocular problems, not all of them, of course, but that is a telltale sign that you get multiple cranial motor nerve involvement without any sensory issues. So it could be ocular, it could be bulbar, it could be speaking, it could be movement of the tongue and so forth. So here we have our slow repetitive nerve stimulation that Dr. Eisenberg is gonna talk about. And also we have the fast rep stim. Now, this is a painful study. So if you wanna do 20, 30, 40 hertz stimulation, it's really painful. So instead, we usually do a, actually you make it a rule. If you see a small motor response, a small CMAP, exercise the muscle for 10 seconds against full force and repeat it. If it goes up by double or more, that means there is a pre-synaptic issue as affecting that muscle, right? So small CMAP, 10 second exercise, repeat. That's the best way to do it. But if you're in ICU or there's like a baby or something that they can't cooperate, then you can do the fast repetitive nerve stimulation. And you always wanna make sure that the muscle nerve pair you're looking at is normal. So make sure there's not like all non-neuropathy looking at the ADM, because if it is and the nerve was denervated, re-nervated, you're gonna get unstable neuromuscular junctions. You're gonna get a drop. Or some other conditions that do get abnormalities of the neuromuscular junction because of denervation, re-nervation, radiculopathy, Kennedy's disease, ALS, all these could potentially cause abnormal decrement. So we wanna make sure that the nerve and muscle is normal. And I would say, if you're sure about that, that these are normal and someone is weak and the REP stem is normal in that muscle nerve pair, is probably not a neuromuscular junction disorder. But the key point is it should be a weak muscle. And also you could consider a single fiber EMG. I think Dr. Eisenberg is gonna talk about that too. But remember, this is a great study in the good hands, but if you're not doing it correctly, if someone has not experienced and they may actually not be very specific study, a lot of technical factors, but it's very good if someone does it correctly, it's a really good, very sensitive marker of neuromuscular junction involvement. So finally, so I'm gonna talk about myopathies, which are, as I said, purely cause pure weakness. Now, we usually think about them as proximal more than distal symmetric involvement. That is correct in the majority of the cases, the inflammatory conditions, endocrine toxic and so forth. But there are forms that are distal more than proximal. And these are, the majority are hereditary conditions. So myotonic dystrophy and other inherited myopathies. Now, inclusion body myoxitis, people talk about proximal. This is really, I think of it as a mid myopathy. It doesn't get the deltoids, doesn't get the fingers in terms of AD, APD and FDI muscles, gets the mid muscles, the biceps, the triceps, the forearm muscles become atrophic. So that doesn't follow the proximal more than distal pattern really. And finally, if you have diffuse issues, it could be a ICU myopathy, could be periodic paralysis that is happening to a patient, usually diffuse involvement. And clinically, of course, depends on which muscle is weak. And based on that, you will determine the pattern and then the diagnosis. And then also the other workup that you may do. Always look for triggers, for example, in periodic paralysis and then also look for mitonia. Again, these may help you with your diagnosis. And on EMG, again, you want to have normal snaps and have normal CMAPs. Usually remember the muscles you do CMAPs off of are not usually involved in a myopathy, right? So now they may be in certain cases, of course, but the majority of them spare the muscles you study for your CMAPs, but the EMG is the key and you see myopathic units and again, helps you with the pattern. And one other thing I want you to remember that if you're doing a screen for myopathy and everything is normal, do not forget the paraspinal muscles because that may be the only muscle, it's the most proximal muscle in the body and they may be affected and you may miss a, or do proximal muscles. Make sure the iliopsoas and some other proximal muscles before you're saying there's some myopathic issues. And you could see a membrane irritability that suggests some kind of myopathy, inflammatory or some of the hereditary conditions, mitotic discharges, again, may lead you in certain directions and diagnoses. So with that, I'm just going to share a few things. So we want to make sure we appreciate any feedback and hopefully be invited back. We can make it a better talk for next time. And please make sure you record what you do here. The stuff you signed up for and you paid for is going to be, of course, reported, but the other stuff that you do on your free time and for free are, you have to kind of go in and register them to get the credits. This is a timeline they put for you over there and during which time they'll report it to your respective kind of societies and so forth. So with that, thank you for your attention. I appreciate it. And I'll leave the questions either end of this session or for me at the end of the other session, if you need to do that. Thank you very much. Thank you. So our next speaker, as I mentioned, is Dr. Kelly Gwathmey. She is an Associate Professor of Neurology at Virginia Commonwealth University. And she wears many hats. She's also the Neuromuscular Division Chief. She's EMG Laboratory Director and also the Neuromuscular Fellowship Program Director. While doing all that, she's really busy with research and extremely productive. And she still has time to give the talk. So thank you very much for accepting. Thank you so much, Dr. Sala-Jage for that kind introduction. And thank you so much for the wonderful turnout this morning. This is great. And Dr. Sala-Jage set me up for success. I see with the first part of this morning's lecture. So I'm gonna cover the nitty gritty upper and lower extremity nerve conduction studies with an emphasis as well on the anatomy. And then my financial disclosures as well really don't pertain to today's talk. It's mostly related to consulting honoraria for myasthenia gravis pharmaceutical companies. So our outline for today looks ambitious. I know we have about 30, 35 minutes before the coffee break. We're gonna start off with the upper extremity nerve conduction studies followed by lower extremity nerve conduction studies and then end with the phrenic nerve. So starting with the median nerve anatomy. So as everyone in this room likely remembers the median nerve is formed by a combination of the lateral cord as well as the medial cord. So the lateral cord coming from C67 supplies those sensory fibers that go down to the thumb, the index, the middle finger the proximal median forearm and the thenar eminence. Now the motor fibers course through the medial cord from C81 and they go down to the distal forearm and the hand. So recall that the median nerve as it comes down the arm innervates first the pronator teres then gives branches to the flexor carpi radialis flexor digitorum superficialis and palmaris longus. And remember from medical school if you went to med school that the anterior interosseous nerve innervates the flexor pollicis longus the flexor digitorum profundus to digits two and three specifically and the pronator quadratus. So pure motor branch off the median nerve that innervates just those four muscles. And there it is right there. So moving more distally just proximal to the wrist we have the palmar cutaneous sensory branch that provides sensation to the thenar eminence. Why does that matter? So there it is right there in blue that should be spared in clinical carpal tunnel syndrome because it actually comes off proximal to the carpal tunnel. Then through the carpal tunnel the motor division goes to the first and second lumbricals. And then we have the recurrent thenar motor branch that supplies the muscles that are median innervated in the thenar eminence, including the opponents the abductor pollicis brevis which we will talk about quite a bit and the superficial head of the flexor pollicis brevis. Now the sensory branch that then goes through the carpal tunnel supplies the medial thumb index finger, middle finger and lateral half of the ring finger. And you see that right here in this sort of pinkish rose color. There you go. And so now we're going to start jumping into the nerve connection studies. And so for each nerve, we'll go over the anatomy followed by the setup for the nerve connection studies. I am going to show you the antedromic setup for the sensories, but you of course can reverse and use a similar technique but backwards for the orthodromic setup if you'd like. Also what you'll notice when we go through each of these nerve connection studies I've included at the bottom a table here where this is all of this data of the normal values is pulled from Preston and Shapiro. So you all likely have your own normal values for your lab or you've borrowed them from another lab but to keep things consistent I am borrowing from Preston and Shapiro. I will not be reading these out to you. It would put you to sleep. And so please reference my slides later. If you'd like to pull this information off of there. All right, so back to our median sensory nerve. So we're going to record this antedromic. As I said, we're going to record over digit two. And as Dr. Salajegi mentioned for this we're going to use our ring electrodes. We're going to separate it by three to four centimeters. G1 is over the metacarpal phalangeal joint. G2 is over the distal interphalangeal joint. And we're going to be stimulating at the wrist on the median nerve, right between the tendons. So the flexor carpi radialis and palmaris longus. And then the distance here is 13 centimeters, okay? And then as I said, you can reverse it for orthodromic. So as you know, the median nerve also supplies digits one, digits three and digits four. And so we can use that to our advantage and also do median sensory studies recording over those digits. And we will get to some of that in a little bit when we go over some of the carpal tunnel studies or median mononeuropathy at the wrist studies. So for the median motor study, this is the belly tendon montage that Dr. Sala-Jage was talking about. We're going to stick G1 right here over the abductor pollicis brevis. G2 is going to be over the first metacarpal phalangeal joint and we will be stimulating at the wrist at a similar location as we did for the median sensory antedromic study. And then that's the distal stimulation site. And when we stimulate more proximally, it's going to be at the antecubital fossa right over that brachial artery pulse. And then the distal distance for this is between six or seven centimeters. All right, and we'll shift gear. We'll come back to median nerve in just a little bit when we go over carpal tunnel studies. So shifting gears for now to ulnar nerve anatomy. As you all recall, the ulnar nerve is derived from the C8 and T1 nerve roots. These fibers travel through the lower trunk and then into the medial cord and then gives off the medial brachial and medial antebrachial cutaneous sensory nerves are also off that medial cord. And we will get to that again in a little bit as well. So then around the elbow, the ulnar nerve descends through the upper arm and passes through the arcade of strethers, which is made up of deep fascia muscle fibers from the medial head of the triceps. And then it enters the ulnar groove and then travels under that tendinous arch of the two heads of the flexor carpi ulnaris and it makes up that humeral ulnar aponeurosis or cubital tunnel. Then branches to the FCU, excuse me, and the FTP to digits four and five are then given off. And then there's our HUA. All right, now moving to more distally, the ulnar nerve gives off the dorsal ulnar cutaneous branch or the duck as we lovingly call it at the level of the ulnar styloid. The palmar cutaneous sensory branch supplies the sensation to the proximal medial palm. And then, sorry, there's our dorsal ulnar cutaneous sensory distribution. And then the nerve goes through Guyon's canal at the wrist. So that's at the medial wrist and it supplies sensation to the volar fifth and medial fourth digits, as well as a lot of muscular innervation to hand intrinsic muscles, right? Your hypothenar muscles, your palmar and dorsal interossei muscles, your third and fourth lumbar coles. And then don't forget, they're actually two muscles buried in the thenar eminence that are supplied by the ulnar nerve. And they are the adductor pollicis and the D pit of the flexor pollicis brevis. So similar to the median sensory study that I described for you, we're going to shift gears and look at the ulnar sensory study. This time we're gonna be recording over the fifth digit with those same ring electrodes, okay? Similar placement here. And we're going to stimulate at the wrist, the medial wrist adjacent to the flexor carpi ulnaris tendon, okay? And then the distance for this is 11 centimeters between the stimulation and G1. And then again, I have demonstrated to you the antedromic study. So the dorsal ulnar cutaneous study. So why would we be doing this? First, I'm gonna show you how we're gonna set it up. So you're going to record in the dorsal hand right here. G1 is over that web space between the little finger and the ring finger. And then G2, of course, three to four centimeters distally, ground in the middle. And then we're going to stimulate just proximal and inferior to the ulnar styloid. You can actually see the styloid here with the hand pronated. And then the distance here is somewhere between eight to 10 centimeters. So this should be normal in someone with an ulnar neuropathy at the wrist, okay? Because it comes off proximal to the wrist. Whereas an ulnar to digit five routine antedromic sensory nerve action potential, which you look for probably every day is going to be abnormal. So for me, I tend to use these dorsal ulnar cutaneous studies when I'm doing an ulnar neuropathy at the wrist workup. Okay, ulnar motor studies. So there are two main muscles that we record over for the ulnar motor studies. We record over the abductor digiti minimi ADM, which is probably the most commonly recorded muscle. And so we're going to put G1 right over the muscle belly. G2 is going to be distal over the fifth metacarpal phalangeal joint. And we have three different sites of stimulation. We're going to stimulate at the wrist, below the elbow and above the elbow. So at the wrist, again, it's going to be just adjacent to the FCU tendon. And then I like to, you have the patient positioned at 90 degrees of flexion. You go five centimeters distally and five centimeters above and stimulate at those three sites. And the reason that we set it up this way is as Dr. Salagiege nicely set up for me, we are looking for focal conduction block or focal slowing at the elbow segment and patients suspected to have an ulnar mononeuropathy that localizes to the elbow. So we're looking for conduction block between the above and below elbow sites, as well as slowing of conduction velocity across the elbow segment compared to the calculated conduction velocity in the forearm. So a drop of 10 meters per second across the elbow segment compared to the forearm, 10 meters per second or greater, I should say, compared to the forearm is consistent with an ulnar neuropathy at the elbow. And then a shameless plug, we are doing another session on Friday afternoon, looking at technical anomalies called when something doesn't look right. And we do a lot of troubleshooting of what to avoid doing when you do ulnar nerve studies and other types of nerve conduction studies if something doesn't look correct, how to troubleshoot and figure out where that's coming from. And then this is one of my favorites, the ulnar motor study recording over the first dorsal interosseus. And so if someone comes in and there's a high clinical suspicion that they have an ulnar mononeuropathy at the elbow and the ulnar recording over the ADM study is normal, I always reflex to this first dorsal interosseus study. And the reason is, and I think Dr. Salajege mentioned this as well, that potentially you could be compressing the fascicle that goes to the FDI and the fascicle to the ADM really is spared. And so you might miss it completely on the ADM study and find it on the FDI study. And so the way that I was always taught to do this is you give someone an okay sign, right? Have them do this. And you're gonna put G1 right over that muscle belly and the dorsal web space between the thumb and the index finger and G2 right over the metacarpophalangeal joint of the thumb. And then exactly the same set up in terms of where you're going to stimulate the positioning of the patient. Again, three stimulation sites. I'm not gonna read it out to you again, but we wanna keep them at 90 degrees of flexion. And so the distance is variable with the FDI study. You would really need calipers to measure correctly the distance. All right, we're gonna shift gear to radial nerve. Okay. So the radial nerve, as you guys recall, receives innervation from all three trunks of that brachial plexus. And so the posterior divisions of the three trunks come together to make that posterior cord. And from the posterior cord comes the radial nerve and the axillary nerve. And then the three sensory branches that come off first are the posterior cutaneous nerve of the arm, then lower lateral cutaneous nerve of the arm, and posterior cutaneous nerve of the forearm. We have muscular branches to the triceps and anconeus. And then it wraps around the posterior humerus of the spiral, in the spiral groove. And we'll get to that in a moment. And in the region of the elbow, it then gives off a branch to the brachioradialis and the long head of the extensor carpi radialis. And these are right here. And then three to four centimeters distal to the lateral epicondyle, the radial nerve really bifurcates into two nerves. We've got a sensory branch and a motor branch. So the sensory branch is a superficial radial sensory nerve, something we routinely study every day in the EMG lab. And it supplies the sensation to the lateral dorsum of the hand and dorsal proximal phalanges of digits two, three, and four in this distribution. Then the deep radial motor branch supplies extensor carpi radialis brevis and supinator. And then it enters the supinator muscle under the arcate of Frosch. Then it becomes the posterior interosseous nerve or the PIN, which you will recall, supplies most of the finger and wrist extensors. Okay, it's a pure motor branch, kind of akin to the AIN, but on the radial side. And so you see here listed the various extensors, extensor digitorum communis, carpi ulnaris, abductor pollicis longus, extensor indices, extensor indices pollicis longus, and brevis. And there it is right there. And so radiosensory study, like I already said, we study this all day, every day in our lab, looking at it in the context of generalized polyneuropathies. And so G1 is going to be right over the superficial radial nerve as it runs over the extensor tendons of the thumb. And then G2, of course, three, four centimeters distally. And then we're going to simulate right at that distal mid-radius up 10 centimeters, okay? And then radial motor studies are a little bit more challenging, I would say. So we're going to record for this one over the extensor indices, sorry, right here. So it's exactly where you would needle it in EMG. So G1 is two finger breadths proximal to the ulnar styloid. And then G2 is right on the ulnar styloid, got ground in the middle, and you're going to simulate here. And then you're going to simulate in the forearm for your distal stimulation site, as I show you here, four to six centimeters proximal to that active recording electrode. And then you're going to stimulate at several other locations, including the elbow between the biceps and brachioradialis, below the spiral groove and above the spiral groove, okay? So the idea here, again, is that we're stimulating at different locations to try and find focal conduction block or focal slowing of conduction velocity to localize that radial mononeuropathy most commonly to the spiral groove, as in a Saturday night palsy, right? You've heard of the people who fall asleep on the park bench with their arm draped over and they wake up and they have wrist and finger extensor weakness. So studies for medium mononeuropathies at the wrist or carpal tunnel syndrome. So this is one of my favorite topics. I could talk about this for a long time, but we're going to try and keep it very simple and very brief. So starting off with some comparison studies, okay? So if you think about it, if you're going to study the median nerves conduction transmission or conduction velocity through the carpal tunnel, you could do that and compare it to your lab normal values to see if it's abnormal, but it's significantly more sensitive to compare it to an internal control. So I'm first going to show you the median versus ulnar palmar or transcarpal mixed nerve studies. This comparison study. It's a short segment study. So just eight centimeters between the stimulation site and the recording site for the median and the ulnar nerve. What is the beauty of this? It controls for disease state, the size of the hand, temperature, age of patient, all of those things. So it's a much better to compare the median nerve transmission to the ulnar nerve or some other nerve or the radial nerve, which we'll show you in a minute, than to compare it to published normal values. So this is an orthodromic study. We're going to stimulate in the palm over the median nerve recording over the wrist and over the ulnar nerve recording over the wrist at eight centimeters difference. Okay, so an inter latency difference of 0.4 milliseconds or greater prolonged for the median compared to its ulnar counterpart and also having a median latency of prolonged of 2.2 milliseconds or greater supports a medium mononeuropathy at the wrist, okay? So very sensitive. You might miss it on your routine antidromic studies, but you might catch it on the Palmer comparison study. So I'm going to reveal to you how bad I am with PowerPoint right now. So this is my hand and this is how I was taught probably by Dr. Sala-Jage how to set this study up. And so here we have first a line drawn between our second and third digits down to the kind of middle portion of the wrist. This is where our median nerve is going to be. Our red line is between the fourth and fifth digits down to the rest kind of where the ulnar nerve is going to be you're going to draw an imaginary line between kind of the crease between your index finger and your thumb straight across your palm. And then where there's this intersection, this is where you're going to stimulate for the median and stimulate for the ulnar. You're going to take a ruler or measuring tape and measure eight centimeters approximately. And then that for the ulnar as well. And then you're going to record, put your G1 and G2, I use the surface electrodes for this at the wrist and you're going to stimulate here. So again, here we go. Stimulate here at the intersection, record over the wrist, G1, G2, ulnar same thing, G1, G2. Hopefully that helps. All right. So a different comparison study, which I very much adore as well. This is a motor comparison study. This is the medium versus ulnar lumbrical to interosseous study. Why do I like it? Because it's quick, it's easy. Anyone can do it in about two minutes and it has a really special role. So sometimes in patients who have very advanced carpal tunnel syndrome and you do a routine medium motor study, recording over the abductor pollicis brevis, you get no response, right? We've all seen those patients, abductor pollicis brevis is wasted. There's an unobtainable CMAP. And so the response of the median nerve recording over the lumbrical hangs around longer. So instead of taking that patient and saying they have a non-localizing median mononeuropathy, which you would have to say if you can't demonstrate focal slowing, you can use this study to bail you out and say it does actually localize to the wrist, okay, to the carpal tunnel. So our recording site is the same for both the median and the ulnar nerves. And what you'll see here is we've got recording sites, the second lumbrical and first palmar interosseous from the same site. G1 is slightly lateral to the midpoint of the third metacarpal right here. G2 is over the metacarpal phalangeal joint of digit two. And then we're gonna simulate the median and stimulate the ulnar here. And then the distance just needs to be consistent between the median and the ulnar nerves, right? You can't use eight centimeters for one and 10 for the other. Of course, the math doesn't work out. And what you're looking for is a significant inter-latency difference. So 0.5 milliseconds or greater would be concerning. If the median is that much slower or greater than the ulnar over that same distance, that would be abnormal. The other beautiful thing about this study is you can consider it in the opposite way for an ulnar mononeuropathy at the wrist at Guyon's canal. And you can look for a focal slowing of the ulnar nerve recording over the interosseous compared to the median. So just the opposite way described to you. Okay, more comparison studies. So we've got antidermic comparison studies too. So remember how we talked about the fourth digits innervated by both the median and the ulnar nerve, right? So we can set this up again, quick and easy. We can put the ring electrodes over the fourth digit and stimulate the median and stimulate the ulnar again at a standard distance between those two nerves. And a significant inter-latency difference for this is gonna also be 0.5 milliseconds or greater, okay? And then you can also do the same thing with the thumb. So the median and the radial nerves innervate the thumb, put your ring electrodes right there over the thumb, similar setup. You're gonna stimulate the median and the radial nerve at a set of distance, and then look at the latency difference of 0.5 milliseconds or greater. And then briefly, less commonly used upper extremity nerves. So we were talking a little bit in the last session about brachial plexopathies. This is really when we pull these nerve conduction studies out. So the medial antebrachial cutaneous sensory study, which is really helpful in if we're thinking lower trunk medial cord, and the way that we set this up is I like to think about where I'm gonna stimulate first for this one. So you're gonna stimulate at the midpoint between the biceps tendon and the medial epicondyle. And then you're gonna draw a line 12 centimeters down between the stimulation site and toward the ulnar wrist. So you'll draw that line, stick your ground in the middle, and 12 centimeters down G1 and G2. These are tiny little sensory responses, must be very delicate when you're looking for them, okay? And then similar, but the opposite, the lateral antebrachial cutaneous sensory study. Of course, we're using this upper trunk, lower core brachial plexopathy. And so, yeah, so for this one, again, similarly, I like to think about where I'm stimulating first. So you're gonna stimulate in the AC fossa just lateral to that biceps tendon, draw a line down toward the radial wrist now, 12 centimeters G1, then G2, three to four centimeters, distally ground in the middle, and there you go. All right, and then in the last seven and a half minutes, we'll try and get through our lower extremity nerve connection studies. So the fibular nerve, I apologize in advance if I accidentally call it the perineal nerve, that's still how it's programmed in my brain. The fibular nerve is derived from the L4 to S1 nerve roots and travels through that lumbosacral plexus and then through the sciatic nerve in a nice bundle that's separate from the tibial nerve fibers. And the posterior thigh, the fibular nerve innervates the short head of the biceps femoris. Remember that, that's on the right exam for any residents out there. The sciatic nerve then bifurcates in the popliteal fossa to the common fibular nerve that gives off that little lateral cutaneous nerve of the knee and then passes through the fibular tunnel. That's very important. It's another site of potential entrapment or compression. And the common fibular nerve divides into the deep and superficial branches. So here we go. The deep fibular nerve, remember it's a very motor predominant nerve. So it has a lot of innervation of muscles. So fibularis tertius, tibios anterior, that's a big one, right? So if this goes out, we have foot drop, extensor digitorum longus, hallucis longus and digitorum brevis. And then it's sensory innervation is tiny, this little bitty patch of skin between the first and second toes. And then in terms of the superficial fibular nerve, is called peroneal, it does have more of a sensory footprint. So we've got innervation of our foot everters, fibularis longus and brevis, and then our sensory distribution of the mid lower lateral calf here in green, and then it goes on to the top of the foot. All right. So how are we going to set up a common fibular motor study? So similar to the ulnar motor study that I just talked about, you can record over two different muscles. You can record over the extensor digitorum brevis and the tibios anterior, which I'll show you next. So for the extensor digitorum brevis, we're going to record right here, dorsolateral foot with G1 right over the muscle belly. Remember to have the patients wiggle their toes so it pops up and you can stick G1 right on there. And G2 is going to be over the metatarsophalangeal joint of the little toe. We're going to stimulate at three different sites because we're going to look for compression or focal demyelination at the fibular head. Okay. So we're going to stimulate first at the ankle, which I show you up here, just lateral to the tibios anterior tendon below the fibular head, and then also in the lateral popliteal fossa. Okay. So for when you're finding the site to stimulate at the fibular head, you want to go about one to two finger breadth just inferior to it. So you can palpate it and go distal to it. And then the lateral popliteal fossa, it's just adjacent to those external hamstring tendons. Okay. And you're going to do all of those measurements. I'll calculate out conduction velocities for both of those segments. And you can look to see if there's any focal slowing. Okay. So sometimes even more helpful, if someone has dense foot drop and your common fibular response recording over the EDB is unobtainable, then it can be very helpful to record over the tibia and as my mentors are always told me, it's not toe drop, it's foot drop. So let's record over the muscle that matters, right? So we record over the tibialis anterior. You just stick G1 right on that muscle belly, G2s over the anterior ankle. And then we're only stimulating, of course, just below fibular head and above the fibular head to look for focal conduction blocking and slowing. Okay. Superficial fibular sensory study. This is commonly used in our lab. We will use this sometimes in our sensory polyneuropathy studies. We will use it as well, of course, if someone has foot drop in our kind of fibular neuropathy studies as well. So we're going to record in the lateral ankle down here. So G1 is between the tibialis anterior tendon and lateral malleolus. You split the distance in half and go about a centimeter distally, ground in the middle, and then you're gonna stimulate 14 centimeters up. I like to draw a line up about 12 centimeters and down about two centimeters and that usually gets you in the right place. And then moving quickly on to distal tibial nerve anatomy. So occasionally we'll refer patients for a question of tarsal tunnel syndrome. And so as the tibial nerve descends distal to the medial malleolus through the tarsal tunnel. So remember the tarsal tunnel is a fibro-osseous tunnel made up of the medial malleolus and flexor retinaculum. So similar to the carpal tunnel in a way. The distal tibial nerve then divides into the medial and lateral calcaneal sensory nerves that go right here. And we really can't study those, but then onto the medial and lateral plantar nerves. Now these are mixed nerves. They have motor and sensory fibers in those nerves. So the medial plantar nerve innervates our abductor hallucis brevis, flexor hallucis brevis and flexor digitorum brevis. Lateral plantar nerve innervates digiti quintipedis. All right, so here we go. Our standard tibial motor study, which you guys likely do every day in your lab. So we are going to record over the abductor hallucis brevis right here. So G1 is one centimeter proximal and inferior to the navicular prominence. G2 is right over the metatarsal flangeal joint of the great toe. We're gonna stimulate right behind, right here in the medial ankle, just behind the medial malleolus and then also in the popliteal fossa. The nerve is very deep there. You need to have the patient relax and so that your stimulator can come in close contact with the nerve or closer to the nerve and ideally over the popliteal pulse. All right, medial and lateral plantar mixed nerve studies. So akin to our palmar or transcarpal studies that I described earlier, these two are mixed nerve studies. So we're gonna stimulate in the sole of the foot and record over the distal tibial nerve at the ankle. So starting here, again, recording site is gonna be here. You see how it's set up. G1 is proximal and posterior medial malleolus and then stimulation, the medial sole and the lateral sole for the medial and lateral plantar nerves. So just keeping an eye on the time. So for the medial sole, what I would recommend doing from the site of recording, you're gonna draw a line seven centimeters to the sole of the foot, right into the middle of the foot and then you're gonna draw a line up between the big toe and the second toe and then go seven centimeters up that way. That will be, which is right here, which is gonna be where you're gonna stimulate for the medial plantar. So you're gonna do the same thing for the lateral plantar. Seven centimeters into the sole of the foot, seven centimeters up a line between the fourth and fifth toes and that will be your stimulation site. These are very challenging to get in older individuals and even sometimes in younger individuals with the lateral plantar mixed nerve study. Okay, and then we do side to side comparisons definitely if tarsal tunnel syndrome is suspected. This carries a lot more weight if they're absent on one side and present on the other side, right? So you could see absent or diminished medial lateral plantar mixed nerve studies, mixed nerve responses in patients with a very distal sensory polyneuropathy. So you can do it in that context as well. All right, seronerve study. So we, this is again, maybe if we're gonna vote for a nerve that's studied most often, it's either this or the median sensory nerve, right? So we're gonna record over the posterior ankle right here. G1's place, posterior lateral malleolus. And then we're gonna stimulate 14 centimeters up and you're gonna kind of draw a line that is aligned with the Achilles tendon, ground in the middle. So we say this all day every day for anyone coming in with a question of polyneuropathy, but also can be helpful in the context of sciatic mononeuropathies because remember, it comes off of the fibular and tibial nerves. And so you could do side to side comparisons in that context. Femoral nerve anatomy briefly. So the femoral nerve is derived from the lumbar plexus L2, 3, and 4 nerve roots. And the muscular branches, as you know, give off, are given off to the psoas and iliacus. And then it runs under the inguinal ligament and then divides as a medial intermediate cutaneous nerves of the thigh. All right, the posterior division. This is extremely important from an anatomy standpoint. And in terms of setting up your nerve connection studies, the posterior division supplies the quadriceps femoris muscle and then continues to become the saphenous nerve, right? And so Dr. Salajegue mentioned the benefits and when we consider doing saphenous nerve studies in his talk. So the lateral femoral cutaneous nerve technically comes off the lumbar plexus and receives innervation from L2 and 3 nerve roots. All right, femoral motor study. Once in a blue moon, we do this. And so we're going to record right over the rectus femoris muscle, G1, right smack dab in the middle, G2 over the knee. And you're going to stimulate in the middle of that inguinal area, palpate the femoral pulse and go just lateral, okay? And below the inguinal ligament. The saphenous nerve study, super challenging to do, especially in elderly individuals, people with diabetes and the like. So this is kind of the opposite of the superficial fibular sensory nerve study in a way. So we are going to record here between the medial malleolus and tibias anterior tendon, cut the distance in half, go a centimeter distally, put your bar electrode there. And then you're going to stimulate up here in the medial calf, just between the groove, between the tibia and the medial gastrocnemius muscle, 14 centimeters up. And then helpful, of course, in femoral mononeuropathies and upper lumbar plexopathies, as Dr. Sala-Jaggi already mentioned. And we're doing great, we're catching up. So very quickly, the last one I'm going to cover is the phrenic motor nerve conduction study. So occasionally we're asked to do this. And so we're recording over the diaphragm. So we're going to record G1 is right here, five centimeters above the xiphoid process, with G2 16 centimeters away from G1 over the anterior costal margin. We'll stimulate in the lateral neck, just behind the sternocleidomastoid. You do need firm pressure, but be careful, because if you overstimulate, you could also get a response from the brachial plexus or the spinal accessory nerve. So again, very, very uncommonly we're asked to do these studies. And you would think we wouldn't get a response recording over the bone, but we do. So with that, I'm over time. I want to say thank you for your attention, and my references are here, and happy to take any questions with Dr. Sala-Jaggi, or if you want to have coffee. So thank you. Thank you. Thank you. Thank you very much. Yeah, please. Yes, sir. Correct, yeah. Oh, for the sensories? So, I mean, I guess starting with the motor studies, we have standard normal values for the distal motor latency because that is at a consistent distance, right? So if you're doing your median to APB, and you're measuring six or seven centimeters, you should have published normal values for the distal motor, and that's what we take. Yeah, so I mean, so that's calculated off of the onset latency of the motor response. The, for sensories, which I think is a little bit more debated, we tend to use the peak latency because it's more consistent from individual to individual. And so our lab really focuses more on the peak latencies for sensories than the onset latencies. Do you have any additional thoughts about that? So the problem with the peak latency, the onset latency is hard to find out where it is. Remember, you have to use the standard measurements, use the peak latency because it depends on the, so you have to have the exact, so if you can't, if someone has a big hand and you measure 13, for example, and it ends up here, then you can't shock the 15, then you can't use the peak latency anymore because it's not standard distance. Then you use the velocity, which is calculated using the onset latency. So we don't usually use the onset latency, but we can use it to calculate the velocity in certain circumstances. It is actually more accurate to determine the speed of the nerve because that's the fastest fibers, but it's sometimes hard to place it, so it's not as reliable as the peak latency, I hope that answers your question. Some people actually say you should technically, for the Palmar studies, not use the peak, but use the onset. It's actually, I don't know if they published, but they were doing a study, we're discussing whether which one is more sensitive. Again, the problem always is it's correct in terms of representing the fastest fibers, but it's hard to make sure it's not reproducible as well. Other questions? That's good. Thank you. just before the normal CMAP or if it's like yeah is it before or after yeah so so i mean first of all remember it depends on where you're putting your g1 g2 so if you change a little bit it's going to change now uh usually i mean i think most labs do baseline to the peak to determine the amplitude now if you do the whole area under the curve then that should not be different it doesn't matter where you put it but we don't really use the positive deflection afterwards for anything in particular i just have to be careful that you know you're putting the your electrodes correctly i'm not sure if that answers your question if you want to calculate the area under the curve as a total then yes you can use that because once you put the cursor beginning at the end it's going to calculate the whole area then yes you can use it you know but i'm actually i'm actually have to go back i don't know if your machine will use the uh the positive sign uh and add it to or does it occur the current activity uh yeah i i know i just use the amplitude as the first negative so i just go back and repeat the study if detected it i'm not sure i go and change things around to make sure we uh we do that yeah sometimes an absinthe is a small amplitude because it's really hard to place the some of the attributes for muscle and that's just hard to do but uh but that's how we use it i'm not sure other people have other

nerve conduction studies

ncs

electromyography

EMG

neuromuscular disorders

nerve function

diagnosis

upper extremity

lower extremity

nerve anatomy

side-to-side comparisons

plexopathies

mononeuropathies

ALS

amyotrophic lateral sclerosis

nerve injuries