Good afternoon. My name is Mark Ferrante and I'm a professor at the University of Tennessee Health Science Center. And this afternoon, I'll be speaking about how we localize and characterize lesions using electrodiagnostic testing. My only disclosures, really, are that some of the figures in this talk are taken from textbooks that I either authored or co-authored. The two major goals of the electrodiagnostic encounter are lesion localization and lesion characterization. The audience is mixed with EMG technicians and residents and fellows, as well as staff neurologists. And so I'm going to go through the important material that allows us to accomplish these two goals. And then I'll follow that with seven cases that show how this information is applied. I may only get through five of the cases, depending on time. But hopefully we'll get through five or six and maybe seven. So although nerves can be injured in a large number of ways, their pathologic and pathophysiologic responses are limited. Pathologically, we either have demyelination or axon loss. And then pathophysiologically, we have demyelinated conduction slowing, demyelinated conduction block, and conduction failure. The important point is that in order to see a lesion, you must run current through it. So on the left side of this slide, we have a demyelinating lesion at the elbow involving the ulnar nerve. That lesion is initially focal, and it remains focal until eventually remyelination occurs. And then it may or may not fully disappear. When we stimulate below the lesion, say at the wrist, we're not running current through the lesion, and so the response is normal. But when we stimulate above the elbow, we are running current through the nerve. I'm sorry. We are running current through the lesion, and so the response will be abnormal. And this is just an illustration of a demyelinating lesion involving half of the nerve. Stimulating below the lesion, no problem. Stimulating above the lesion is a problem for these three axons. When we disrupt the axon, we initially have a focal lesion. But once valerian degeneration occurs, that lesion expands in size and involves the rest of the nerve. The entire distal segment undergoes valerian degeneration. And so we go from this to this. And now it doesn't matter where we stimulate, below the lesion, at the lesion, or above the lesion. We are going to see the nerve because we're going to run current through it. If we stimulate the wrist, we run current through it. If we stimulate above, we initially start off good, but then we run current through it. With regard to pathophysiology and demyelination, when the amount of demyelination is mild, the axon potentials get through the lesion. But when the amount of demyelination is more significant, then the axon potentials don't get through and they're blocked. With slowing, when the axon potentials do get through the lesion, but they're delayed, the axon potentials may be uniformly delayed, where all the axon potentials are delayed to an equal degree. Or they may be non-uniformly delayed, so that some are delayed a lot, some are delayed a little, and some may not be delayed at all. A common example of uniform demyelination is early carpal tunnel syndrome. In that case, when we stimulated the wrist, we are running current through the lesion, and so we see that delay. There's an increase in the latency. When we stimulate above the lesion at the elbow, further up, we still run current through, and so we again see that delay. So both of these sites send current through the lesion, and therefore you have an effect. In this case, slowing. And again, because the slowing is uniform, the waveform morphology is preserved. Here's an example of non-uniform slowing. In this case, I put the lesion at the elbow, because we commonly see these with ulnar neuropathies. About a third of ulnar neuropathies are pure demyelination, one-third axon loss, and one-third mixed, roughly. When we stimulate the wrist, we're not running current through the lesion, and so we don't see it. But when we stimulate above the elbow, we are running current through, and we do see it. And in this case, we have dispersion of the response, because the slowing is non-uniform. Now, this same ulnar neuropathy, if it was a block, then those axon potentials would not be able to get through the lesion, and they would be removed. So here, we're not running current through the lesion. It's normal. But up above, we are, and we're losing signal, because the axon potentials are blocked by the lesion. And so we have a drop in amplitude and negative area under the curve. So here's an example of someone with a radial neuropathy at the spiral groove. And this shows the advantage of motor nerve conduction studies. They're able to assess long segments of nerve. And so we can stimulate quite a ways away from the recording electrodes. So here, when we perform a radial motor nerve conduction study, recording from the extensor indices, stimulating forearm, we see a normal response. Stimulating elbow, the same response. Stimulating below the spiral groove, another good response. And then above the spiral groove, we see a loss of signal. And so we know this is a demyelinating lesion, and it's located between the two stimulation sites. So this would be a radial neuropathy within the spiral groove. Now, malaria degeneration does not occur instantaneously. And so initially, if the median nerve is transfected partially, when we stimulate below the lesion, we don't see it. We have a normal proximal response. But when we stimulate above the lesion, current traverses that disruption, and we do see it. But once malaria degeneration occurs, the response drops down. And when malaria degeneration is complete, the responses become uniform. And we don't see that pseudo-demyelinating conduction block pattern, where the distal response is larger than the proximal. Now, I said malaria degeneration takes time. How much time? Well, it's important to realize that the neuromuscular junction degenerates before the nerve fibers do. And because the motor nerve conduction studies send current through the neuromuscular junction, the motor nerve conduction studies recognize the malaria degeneration sooner than the sensory nerve conduction studies. And in general, the motor responses start to decay around day two and bottom out around day six, whereas the sensory responses start to decay around day six and bottom out around day 10. And so in general, we want to perform nerve conduction studies after day 10. So the take-home point is that we have stimulating and recording electrodes. And when we perform a sensory or a motor nerve conduction study, we're looking for focal demyelination between the stimulation and recording sites, as well as early axon loss. But we're also looking for evidence of axon loss above the work site through malaria degeneration. And for that reason, it's extremely important to know where the axons that you're studying come from. So which anterior horn cells give rise to the motor axons under study? And which dorsal ganglion cells give rise to the sensory axons under study? I've been a little bit hoarse, so hopefully it won't interfere. Now, we talked about malaria degeneration. It occurs distal to the lesion and away from the cell body. So if we have an interspinal canal lesion, say that severs the dorsal and ventral roots, there's going to be malaria degeneration from the break point down, down to where we're studying the motor nerve conduction studies. And there'll also be a malaria degeneration of the sensory axons. But because the cell bodies are not in the interspinal canal, they're in the intervertebral foramen. Remember, the sensory neuron gives off two axons, one directed distally that we study with sensory nerve conduction studies, and one directed centrally. The central one is the affected one, and so the malaria degeneration will occur from that point away from the cell body and into the spinal cord. So the patient will have the symptoms of numbness, but we won't see that when we do sensory nerve conduction studies. Now, for example, if we put a needle in the biceps muscle, or if we perform a muscular cutaneous motor nerve conduction study recording biceps, we need to know the anterior horn cell innervation and the nerve innervation. And so we can just look on a myotomal chart like this one, and we see the biceps is innervated by the muscular cutaneous nerve and via the C5 and C6 anterior horn cells. And so we know when we perform a muscular cutaneous nerve conduction study that we're assessing not only the muscular cutaneous nerve from the biceps proximally, but also the lateral cord and the upper plexus. Now, with regard to brachial plexus terminology, the supraclavicular plexus is divided into three other plexuses. The upper plexus, which is the upper trunk and everything above it. The middle plexus, which is the middle trunk and everything above it. And the lower plexus, which is the lower trunk and everything above it. And so I'll use that terminology in this lecture. Now, for the sensory nerve conduction studies, when we perform a study, and I've included the ones we performed for the upper extremity, we want to know what dorsal ganglia they come from. So the LAPC, those sensory axons that we study are from C6, as is the median recording from the thumb. When we perform a median sensory nerve conduction study recording index finger, we're looking at C6 and even more so C7. And then from the median D3, it's not very helpful because it's all over the place. Superficial radial is a C6-7. Ulnar is a C8. And the MABC medial antebrachial cutaneous study, those axons come from T1. And knowing that allows us to know the pathways through the brachial plexus that we're studying. And I've included those in this talk. So, for example, when we perform a lateral antebrachial cutaneous study, we're not just looking at the lateral antebrachial cutaneous nerve. We're also looking at the muscular cutaneous nerve, the lateral cord, and the C6 elements of the upper plexus. And then I've included the pathways for the median D1, the superficial radial, the D2, the D3, which I said isn't too helpful except with lateral cord lesions, the ulnar D5, and the MABC pathways. If you think about it, this makes sense. The LABC we record here, and it's all C6. And if you follow this upper semi around, we come to the thumb, and it's all C6. And then we come to the superficial radial recording site, and it's all C6. And then we come to the radial recording site, and it's 6 and 7, but more times 6. And then we come to the index finger, and it's C7 more than 6. The middle finger, mostly C7. The pinky finger, C8. Dorsal antebrachial cutaneous, C8. MABC T1. So there's a pattern here that matches the brachial plexus. Whenever a patient is referred to us for an upper extremity assessment, we screen using the superficial radial median D2 and ulnar D5 sensory responses. And I've shown that in red, what we cover. And in blue, the routine motor responses, the median motor and the ulnar motor. And notice that the upper plexus isn't very well assessed. So anytime someone is referred for an upper plexus lesion, or we suspect that, we have to add studies. Now, I've included the studies that assess the upper plexus, the middle plexus, the lower plexus, the lateral cord, the posterior cord, and the medial cord, but I won't read through them all for time's sake. The order of performance doesn't matter a lot but in our case this is our order of performance. We perform the sensory nerve conduction studies first and we attempt to localize the lesion and defiance pathology. They are very helpful for localizing axon loss lesions. Then we do the motor nerve conduction studies to confirm that localization of pathology to better screen for demyelination and to assess severity. And then finally we do the needle EMG to confirm the nerve conduction study findings and then to get a better feel for the temporal acute, subacute, chronic features of the lesion. So whenever a person is referred to the lab, we need to decide which sensory nerve conduction studies to do first. So we always include our screening studies and then we also add studies based on the referral diagnosis. So if the referring physician suspects an ulnar neuropathy, we add ulnar nerve conduction studies. And then I also talk to the patients, take my own focus history, perform a focus exam and based on that I may add more studies to the story. And then the most important thing of today's talk is this next paragraph. Any time one of the two sensory nerve conduction studies that assesses the C6 or C7 segments is abnormal. So that would be the median D2 or the superficial radial. Whenever one of those two is abnormal, we add the LABC and the median D1 to better localize the lesion. And whenever the ulnar sensory response is abnormal, we add the MABC. And now I'm going to demonstrate all of this through case studies. So again, we want to localize and characterize the lesion. We want to localize it, we want to identify the pathophysiology, pathology, are the sensory motors involved, the motor, both, how bad is it and what's the timing. And so for the rest of the talk, I'm going to go through cases showing how we apply what I've already discussed to an actual case step-by-step. So the first case is a 67-year-old male who is referred for episodic hand numbness and tingling, right worse than left, and it's been going on for five years. So whenever someone is sent to me with episodic hand numbness, I usually ask about features of corporal tunnel syndrome. And so I asked them, is it present upon awakening? He said yes. Is it precipitated by driving? Do you have to change your hands when you're driving? He said yes. Does it occur when you're doing nothing, just sitting watching TV, for example? Yes. So those are features that suggest corporal tunnel syndrome. And then I asked about neck pain, which he denied. And that is important to me, as you'll see, with regard to the needle exam, which I'll get to. And his examination was normal. And so his clinical features suggest corporal tunnel syndrome, right worse than left. And we're just going to start on the right side with the sensory screening test, median ulnar superficial radial. We suspect corporal tunnel syndrome, and so the median D2 may be abnormal. But if it's not, we'll add the palmers, because they're more sensitive to corporal tunnel syndrome. And so this is the directions I give the technician at this point. And then I go away unless they have trouble, and then they call me back. But they had no trouble, and they called me back. And now we see, and since you don't have my normal values, I've highlighted the abnormalities in red. And so this is the first case. And the studies were performed on the right side first, since it was more symptomatic. The latency is shown, and the amplitude. And the studies are in the far left column, and where they emanate from. And so here we have an abnormal latency. So that means we have demyelination. It's somewhere between the stimulating and recording site. So we already know that we have a demyelinating lesion. There is somewhere between the risk stimulation site and the middle, I'm sorry, and the proximal phalanx of the second digit. Also, the amplitude is low. It should be greater than 10 for his age. And typically, we see a 2 to 1 ratio here, between the median sensor response and the ulnar after the age of 60. And so we have axon loss as well. Now we're ready to check the left side. And again, we'll start with the median detail. We don't need the screening studies. And if it's normal, we'll add the palmers. So now, the median sensor response was normal. For his age group, less than 3.8 is normal, and the amplitude should be greater than 10, and it is. So we add the palmers, and the median palmer response was delayed. And the difference is 0.5 milliseconds, so that's also abnormal, anything over 0.3. And so at the conclusion of the sensory nerve conduction studies, we know that we have bilateral median nerve lesions, distal to the wrist. On the right side, we have demyelinating and axon loss. And on the left side, demyelinating only. The amplitudes were normal. Severity is best determined by the motor nerve conduction studies and the temporal features by the needle. So now we're ready to move into the motor nerve conduction studies. And we'll just do our routine motors because they include the median. And then we'll also check the median on the other side. And when we do that, we have a delay in onset latency from the distal motor response, and we have a drop in amplitude. It should be greater than 6, and it's not. And so now we can say we have two median nerve lesions distal to the wrist and proximal to the senior eminence, which is where we're recording the motor response. On the right, there's demyelination and axon loss. It involves the sensory and motor fibers. On the left, there's demyelination of sensory fibers only. And this lesion has to be at least moderate in degree, moderate to severe, because we do have motor axon loss. And on the left side, it's mild. Now, for the needle exam, a lot of labs choose not to do a needle exam, but I always do. But I do a limited one. When someone has motor axon loss, when that lesion progresses slowly, collateral sprouting occurs. And that spares the motor response. So when reinnervation keeps pace with denervation, the motor response doesn't decrease. And so I want to look and see if there's any motor axon loss by needle exam, since it's more sensitive. And I do a limited one, but I do a limited one. And I start with the FDI, and it was normal. And now I want to compare the motor units in the APB to that muscle. And there was an obvious difference in some of the motor units. They were long in duration. And we typically look at the duration more so than the amplitude. We look at both. But the amplitude isn't as sensitive, whereas the duration is significantly more sensitive, because it reflects the majority of the muscle fibers contributing to the motor unit. And then I also compare those motor units to the other side. And in this case, the other side, the motor units look like the FDI. And so there was really no evidence of motor axon loss on the other side. There was an obvious asymmetry of the two sides. And then there was an ipsilateral difference as well. And so the report is done. All the information has been identified. And then I just characterize the lesions. A lot of our physicians want severity graded. And so that's why I put that in the report. They want to know how bad I think it is. But that's really a clinical decision, and circumstances may dictate the management better than the severity. But either way, I include it in the report. And then we usually suggest that when motor axon loss is present, that surgical intervention be considered. But then if they choose to treat conservatively, we restudy the nerve in a year, because it may progress asymptomatically. And I'll show a case of that in a moment. Right now, this is still case one. I just want to make another point about carpal tunnel syndrome. And so this is a different case, but the same story. This time, there's some examination abnormalities. We did the routine centuries, and the D2 was absent, and so was the palmer. We added the palmer, hoping that it would still be there and that it would be delayed, because that way we would be able to localize the lesion. But at this point, it can't be localized. There's a differential. This is a C6-7 study. So the lesion that could do this could be anywhere along the median nerve, the lateral cord, the upper plexus. And so normally, I have that rule I mentioned. If the median D2 is abnormal, add the LABC and the median D1. But this will be an exception, because we really think we're dealing with carpal tunnel syndrome. So we're going to wait and do the motors, and then see if that helps us localize. And so when we do the motor nerve conduction studies, we have a delay. And so now we know that the lesion is somewhere between the risk stimulation site and the senior eminence. There's demyelinating and axon loss, and then it's at least moderate to severe in degree. So we didn't have to do those two sensory add-ons. And now one more point. So here's someone that I know. They had come to see me for an EMG five years earlier, and they had the typical findings. And they were back. They saw me five years ago. I recommended surgical release on the right side, but they treated this gentleman concerningly. And according to him, his symptoms went away. But on exam, even though his symptoms went away, he had significantly decreased sensation in the median nerve distribution on both sides, decreased strength, and obvious senior eminence wasting, which you can see. The whole eminence is now gone. But his symptoms got better. Really what got better was he went from episodic tingling to constant numbness, which is often less symptomatic. So in his case, we start, and the sensories are absent. But again, because we know this is carpal tunnel, let's just wait and look at the motors. But the motor response is also absent. Now what to do? We could go back and do those other sensories, but it's good to know that the median recording second lumbar call is often less symptomatic. Recording the second lumbar call is often the last motor response to go. So before I give up, I add that one. Right now, we can only localize to the median nerve at or distal to the axilla. It can't be above that because the only sensory and only motor normal. So it can't be medial cord or lower plexus. But let's hopefully get lucky. We'll add the median L2. And when we do that, there's a big delay. And so now we can go ahead and localize the lesion to at or distal to the wrist. And so those were the points I wanted to make about case 1 and variations. By the time we get to case 4, we'll be able to pick up the speed considerably. But 2 and 3 will go a little bit slower. So case 2, a 70-year-old male with right hand numbness and weakness. It started after a stent was placed six weeks ago and an axillary approach was used. So if this really happened immediately after the procedure and the procedure was done in the axilla, that's a clue to where the problem might be. On exam, he had sensory loss in the median nerve distribution, including the skin over the center eminence. So that suggests median nerve damage above the wrist. And then he has weakness in the median hand muscles and the anterior interosseous nerve muscles. So the lesion has to be above the takeoff site of the anterior interosseous nerve from the median nerve. So this sounds like an antigenic median neuropathy. And in our lab, the policy is when one of our docs might have done something, we try and do an extensive study. Because this is the only chance we'll ever have to defend him. After this study is done, if this goes to court, an outside EMG will be involved or a neurologist or someone. And they may interpret things differently or do extra studies and find things that they interpret as abnormal that might not be. So we usually do an extensive study and define the abnormalities as best we can, identify any pre-existing abnormalities as well. So we're going to start with our routine studies, but again, because it's the antigenic, we'll add the median D1 and D3. We're pretty sure this is a median neuropathy. Again, above the wrist, the pulmonary cutaneous branch comes off above the wrist and enters the hand to a separate tunnel. So when it's involved, you know the median nerve is involved above the wrist. And then we had abnormalities, weakness in the hand intrinsics and the anterior osseous nerve and the beta-muscle stenoposites along with FTP, but not inflected herpes radialis and so we know we're at or above the anterior osseous nerve take-off site, so somewhere here. And when we do the sensory nerve endosynthesis, the epitopes are absent. So the three sensory sponsors are absent, and so our differential diagnosis is median nerve, lateral cord, and maybe even upper plasmas, but unlikely. Number one, the D2 only goes through the upper plasmas 20% of the time, so there's only a 1 in 5 chance, and the D3 only 10%, so that's a 1 in 10. So 1 in 5 times 1 in 10 is 1 in 50, so there's less than a 1 in 50 chance this is upper plasmas, but we want the EMG to speak for itself, it's an independent study. Because the responses are absent, we know this is an axon loss lesion, and because the median D2 is abnormal, we'll add the LABC and the median D1, but since we already did the median D1, we won't need to add it. And it's normal, so that argues against lateral cord and upper trunk, although it could still be a very distal lateral cord, beyond where the musculocutaneous nerve leaves the cord. So now, for the motors, we're going to do our routine studies and the L2, for the deoxygenic, and we want to compare that to the other side. And when we do that, we have a delay, but it's pretty small, but we have a big drop in amplitude, it's 50% down from our lower limit of normal of 6. But comparing to the other side, it's about 75% down, you know, it's only one fourth of that, roughly. And that's a little better than that if you compare the negative area under the curve. And then, the median L2 also shows a little bit of a delay with a large drop in amplitude. And when the drops are this big, we usually ignore small delays. And so this is a median nerve lesion, axon loss in nature. And it's 75% down, so it's severe. And we expect to see neurogenic recruitment on needle exam, once it's more than 50% down. And on the needle exam, the abnormalities involve the muscles that were weak on exam. But then in addition, there's also evidence of abnormalities in the pulmonary arteries and the flexural corporeal radialis. The needle exam is just a lot more sensitive than the clinical, but those muscles were less affected. We don't see any chronic changes, so there hasn't been enough time for collateral spreading, so this is acute to subacute. And the fibrillations, which I can't show in my table, were high in amplitude, indicating that the muscle fibers hadn't begun to atrophy yet. And again, this is a recent lesion, consistent with the six weeks stated by the patient. So we have an axon loss median neuropathy that involves roughly 75% of the motor axons to the senior eminence and to the second lumbar column. And then I usually educate, where appropriate, the referring provider, letting him know that I can only localize a lesion to above the elbow, because there aren't any motor branches given off by the median nerve in the arm above the elbow. And then we don't need to read every word for time reasons. Now let's move into case three. So this is a 70-year-old male who awoke 25 days ago. He had left hand tingling and was unable to extend his wrist or fingers. An examiner had sensory loss in a superficial radial nerve distribution and weakness of wrist extension. There was no radial deviation of the wrist, arguing against posterior interosseous nerve involvement. And his forearm extension strength was normal, so no evidence of triceps involvement. And so we'll do our sensory nerve conduction studies, but we're going to add, we're going to add the superficial radial sensory on the other side. And then this diagram just shows the triceps muscle was spared. And you know, both extension of the carpi muscles were probably involved, because there was no radial deviation with wrist extension. When you have a posterior interosseous nerve lesion down here, you only involve one hand. In that case, the extension of the carpi radialis is spared. But the brevis and the ulnaris are affected. And so when the patient attempts to extend the wrist, the extension of the carpi radialis causes deviation towards the thumb. Now when we look at our sensory nerve conduction studies, everything's normal. And when we look at the contralateral side, it's normal. There isn't asymmetry, but it's not enough to call on the sensory nerve conduction studies. We require the value to be below normal, or more than 50% below the contralateral side. And so everything's normal. However, this person has profound weakness. And we think he has a radial mononeuropathy. And in general, whenever you have an axon loss process affecting a PNS element, like the radial nerve, the sensory responses are affected at a proportion to the motor. So that makes me think maybe this is not axon loss. Another possibility would be that I'm doing it too soon. But we already know that's not the case from the history. We are 25 days out. Another possibility could be that it's not a radial, it's a C7. That would spare the sensory. And of course, another possibility is this is a block. And so knowing that, when we do the motor, radial motor responses, we're going to want to stimulate proximally and try and identify the block. So for the motors, we'll do our routine motors. And we'll add the contralateral radial motor responses as well. Now, with the distal radial, when we stimulate and we record extension indices, we have a response with an amplitude of 4 millivolts when we stimulate at the mid-forearm. About the same at the elbow and below spiral groove. And we can see that's true for the negative area under the curve as well. But when we stimulate above the elbow, there's a big drop for both values. And that's also what we see when we do the proximal radial response, recording extension in the digitorum. And so at this point, we know the lesions in the spiral groove. It's a demonic conduction block lesion. There might be a tad of axon loss given the sensory asymmetry, but we don't know yet. We'll wait for the near exam. The lesion is severe for the block. And then we'll wait for timing. And so at this point, we're ready to move into the near exam. And when we do that, we have abnormalities in the radial nerve distribution, but sparing the triceps and the ankinas. So again, confirming our original thoughts that this is a spiral groove lesion, which is actually verified by the block. The demonic conduction blocks are localizing. And we have severe neurogenic recruitment, so one unit down firing rapid, or maybe two, one to two motor units firing at a rapid rate. There's no chronic changes consistent with 25 days. The fibs were all high amplitude. But because there are fibrillations, there is axon loss. And so we know this is a mixed lesion, but the axon loss component is small, because we really didn't see it on the sensories. And so we just say this is severe, but we can be a lot more specific. So I'm going to just do a little bit of math and show you how to calculate the percentages of axon loss and block. Because sometimes this is important. So that table, whenever there's demyelination, I like to use the negative area under the curve values for my calculations. Because that way, I don't get tripped by any dispersion. Because there likely might be some demyelinating conduction because there likely might be some demyelinating conduction slowing. Anyway, so to calculate axon loss, we're going to compare the distal motor responses of the two sides. So on the good side, the output was 32.9 versus 28.9, so almost the same. And if you put that in fraction form, that's 88%. And so we know that the axon loss is the difference. So if 88% is normal, then 12% is axon loss. So we have the axon loss. So that's probably why the sensory responses were asymmetric. There is axon loss. There's not much of it. About 12%. How about the block? Well, then we're going to use the distal response versus the proximal. The proximal response drops off. So there's block here. Only 3.8 gets through. That's what gets through. So if you arrange it in fraction form, 14% gets through. That means 86% does not. So 86% of these fibers are blocked. But remember, this doesn't reflect the axon loss. So it's really 86% of 88%. The fibers that are not affected by axon loss are blocked. And so you just multiply those fractions, and you have 76% blocked. And that adds up to 88. So 100% minus 88% tells you the normal. And you can do the same thing for the other muscle. But we won't go through it again. And then there's the impression. I don't need to read it. It's what we've discussed. And now we're moving to case form. So a 52-year-old female is referred for left upper semi numbness and weakness. This started two months ago after a pacemaker was placed. She has weakness of forearm flesh, and so that makes me think biceps. And the pronations are pronataries. So that's musculotendous nerve, median nerve, or C5-6, C6-7. And then numbness along the lateral aspect of the forearm and hand. So let's just start with our routine sensories. When we do that, the amplitude of the median D2 is down. So here's our differential. Median nerve, lateral cord, upper plexus, middle plexus. Any lesion in any of these areas could make the median D2 low in amplitude. So we have an axon loss process somewhere in here. We're going to add the LABC and the median D1, because that's what we do when we are faced with an abnormality of either the D2 or the superficial radial. And we're going to do those bilaterally. Plus, I'm going to add the median D2, because I want to compare it to my 8.6. And when I do that, there's a real big difference side to side for all of them. And so now we know this can't be a median neuropathy, because the LABC is involved. So it could be a lateral cord or an upper plexus. But again, the D2 is only going through the upper plexus 20% of the time, so it's less likely. More likely, lateral cord. And the pacemaker placement was infravicular, and so that's a clue. But either way, the EMG is independent, and we need to rule out upper plexus. So with this differential, we'll add the musculoskeletal and axillary motor responses on both sides. With the upper plexus lesion, to a severe degree, we would expect them both to be involved. But with a lateral cord lesion, the axillary will be spared. And when we do that, the axillary motors are symmetric and spared on the ipsilateral side. And so we just have a low amplitude musculotaneous motor response. So now we know localization, lateral cord. Pathophysiology, as on loss. Severity, moderate to severe. And we can use a little formula, comparing the two sides distally, to estimate the axon loss. And then we do the needle, and the abnormalities are in the lateral cord muscle domain. The fibrillations were high amplitude, some medium, but either way, relatively young. It's severe and it's rare because we have neurogenic recruitment. Even though the neurogenic recruitment is mild, or any time you see neurogenic, it's a severe lesion. And then there's been no time for chronic changes. So that's consistent with the two-month history reported. And here's our impression, blah, blah, blah. All right. We're okay on time. Let's do case five. This will be important. So a 41-year-old female fell about a month ago. So we don't expect any chronic changes. Any chronic changes are pre-existing. She has numbness along the medial hand and forearm. So that's ulnar end MABC, or it's C8NT1, for root-level lesions, or anything in between. Weakness of grip, ulnar C8T1. Her exam shows numbness in that distribution. And weakness in the C8 median and ulnar, but also the extensor indices. That's such an important muscle to be aware of because it's C8 radial innervated. And you'll see how important that is in a minute. But for now, let's just start with our routine studies. And in this case, the ulnar sensory response is absent. So this is as a loss somewhere, either in the ulnar nerve, medial cord, or lower plasmas. Whenever the C8, whenever the ulnar is abnormal, we add the MABC. Now, if the MABC is also normal, then that means we can't localize it to the plasmas at that time. So we'll add the DUC. But first, let's just add the MABC and see if this is plasmas level. And when we add it, and I did it on the other side as well because we want to show that this isn't technical. We did not get it because we don't know what we're doing. Because we did get it on the other side. You don't want a lawyer asking, if you're the trained doctor, would that not be technical, doctor? Anyway, so now we know this is either a medial cord lesion or a lower plasmas lesion, and it's as a loss. On the motors, we're going to want to add the ulnar FDI because it'll help us rate severity. And the radial EI because it can save the day. And the motor response is on the other side for severity assessment. And this is how it saves the day. So we know we have two sensory responses that are abnormal, the ulnar and the MABC. And this is our differential. But the eccentric indices muscle is innervated through C8 and the radial nerve. So if we drew a line, it would be from So if we drew a line, it would be from the spinal cord segment here down this way. The point is, if the C8 is involved, the lesion has to be above the cord level. So it would be super convictuous. So if the EI is involved, then we deal with a lower plasmas lesion. And it is involved. And roughly, it's about two-thirds down. This one's about a half down. And this one about two-thirds. So this is a lower plasopathy as a loss in nature, severe degree. And that's confirmed on needle. And also, this is an acute to subacute lesion, and it's severe in degree. Case six, a 26-year-old female with right arm pain and numbness. She has aching pain along the medial aspect of the arm and forearm. It's episodic and has been present for at least 10 years. She has intermittent numbness in a similar distribution, but not the arm. It's been present for several years, especially when she lies on her back. And then her friend noticed her hand left body. So she has seen her MNs wasting. And then I'm going to go through the exam for time constraints. We don't need it. EMG is an exam. And we'll just skip it. We'll start with the routine. But it was done in real life. So the routine centuries are normal. But the owner D5 is suspicious. Why is that? And this is why I like digital antidromic. I don't do orthodromic D2 and D5. Because the amplitudes are really big with antidromic, and you can compare them. So when we look at the median D2 in her age group, it should be greater than 20. So the lower limit of normal is 20. And hers is 51. 50 is two and a half times as big as 20. When we look at the radial, the normal is 18. We'll just say 20. So she's about three times the lower limit of normal. So median D2, two and a half times, radial three times. Owner, normal is 12. She's only 1.25 times the lower limit of normal. So that's suspicious. So I'd like to see what the other side has to say. And the other side is three times normal. And so now we can say this is abnormal. It's not an absolute abnormal, it's a relative abnormal, but it is an abnormal. So we're going to add the MABC. If that's normal, the DEC. When we add the MABC, it's absent. We do it on the other side. You know, we're not technically inept. It's absent because it's absent, not for technical reasons. And so now we know we're dealing with a medial cord or lower plexus lesion. It's axon loss. But what you have to pick up on is the owner D5 is a C8. And it wasn't even absolutely abnormal. But the MABC, a T1, is absent. So whenever I see T1 affected out of proportion to C8, I think about the anterior primary ramus level because remember the C8 and T1 roots join to form the lower trunk. You could also see this if you had a lesion of the inferior lower trunk, because the C8 fibers are a little bit more, the T1 fibers are more inferior than the C8. Anyway, when I see this pattern, I think true neurogenic thoracic outlet syndrome. And it's the same story. We're going to add the FDI and the radial EI because we're dealing with medial cord or lower plexus. And when we do that, the EI is abnormal. So now we know this is a lower plexopathy. And again, the median APB, which is very heavily innervated by T1 is one-sixth roughly of the normal side. Whereas the owner is normal, but there's an asymmetry not enough to solve. Again, we need a 50% difference and there's not. But the asymmetry is suspicious. It's present at both onomotor responses. And then the radial EI is about 50% down and it's a C8. So it looks like the T1 fibers are much more affected than the C8 and T1. Again, that makes me think about true neurogenic thoracic outlet syndrome, but I don't know yet. And then when we do the EMG, all of the abnormalities are in the lower plexus distribution. There's chronic changes, severe in degree. So we know this has been going on for a while. The fibrillations were plentiful in the APB, but almost all of them were very low amplitude. But notice the APB had the most fibs, had the worst recruitment, the most severe chronic changes. And that's because this lesion affects T1 more than C8. And that's been present on the sensory, the motors and the needle. So with true neurogenic thoracic outlet syndrome, there's a fibrocortilaginous band that extends inferiorly from the first rib upward to the C7 vertebral body, either to a to the C7 vertebral body, either to a cervical rib or an elongated transverse process. And that band pushes the brachial plexus upward as well. And the contact site is usually at the anterior primary ramus level. And it hits T1 harder than C8. And even interoperatively, if you go in and look, you'll see that the T1 anterior primary ramus is stretched more, and it's more erythematous to the eye. The other hit site is the proximal lower trunk. And again, you can still have that T1 greater than C8 pattern. But sometimes it's just really bad and you don't see that pattern. And all you can say is it's a lower plaxoplasty. But in this case, we added that it's suspicious for trunogenic plastiality syndrome. She went to surgery through a supraclavicular approach, and there was a band that was resected. Her pain immediately went away. Her surgery symptoms improved. Her motor features did not. Because remember, with this disease, it's very slowly progressive, and so you're already massively collaterally sprouted. And so she didn't really notice a difference in her strength when, assuming she had further recovery, it wasn't significant. And then this is the more important case, because I've seen a couple of these with lawsuits. So, case seven. 71-year-old male referred for suspended post-op ulnar neuropathy. He had open heart surgery 26 days ago, and he's complaining of grip weakness and numbness on the medial aspect of the left hand, not the forearm. So it sounds like an ulnar. His emanation is top secret. So let's just start with the sensory nerve conduction studies. The ulnar sensory response is absent. So we add the MAPC. If it's normal, we'll add the DUC. And it is normal. So we added the DUC, which is absent. So what does that mean? Well, this could be an ulnar nerve lesion. It could still be a medial forward or lower plexus lesion, but that's likely given that the MAPC is normal. Of course, the MAPC goes through the T1 anterior primary ramus, and the ulnar and DUC go through the C8. So in the lower plexus, it could be a C8 anterior primary ramus. That would give both owners and spare the MAPC. Either way, it's absent or lost. It looks pretty bad, but we don't know yet. But again, it's the same story. We're going to add the radial EI and the FDI, and the contralateral motors. And when we do that, the EI is abnormal. It's about two-thirds down. So we know this is superficial vigor. It can't be an ulnar. And it's probably sparing the MAPC because it's not at the lower trunk. And so we move into the new exam. So we have a severe absent, lost, lower plexopathy. So we have a severe absent, lost, lower plexopathy. There's no chronic changes. The fibs are high amplitude. There's some insertion of positive sharp waves. So they're only 14 to 21 days old. Now, what is this? And this is something you just have to know. When someone has open heart surgery, when their sternum is split and spread, the first rib might injure the C8 anterior primary ramus. Most of the fibers in there are ulnar, ulnar sensory. And then there's ulnar motor, because that's in C8 and T1. And there's radial motor. And so we want to look, you know, that radial motor response might have been normal on this case. So we definitely want to look at it on the needle. And if the EI is normal, I then want to look at the extensive palsis brevis, another C8 radial. And if that's normal, then I'll relax. But until then, open heart surgery is a C8 anterior primary ramus lesion to improve it otherwise. Because what happens is, it sounds like an ulnar, you do routine studies, and you identify an ulnar, and you don't go after the C8 through the radial EI. And you say, yeah, it's an anthral loss ulnar neuropathy. And the surgeon operates. No big deal. But there's a bad outcome from the surgery. And then subsequently, say they botch it. And now the patient has a sore hand. You know, then they go back and they look. And someone says, you know, this isn't even an ulnar. The EMG made an error when he localized the lesion. This is a plexus lesion. That this patient should never have had surgery. If it weren't for that EMG mislocalization, my client would have a normal hand. So I've seen a couple of those. And so that's why EMG is an extension of the clinical exam. And you always want to try and surround your abnormal with normal. And so you need to know what elements are assessed when you're trying to things in and out. And at this point, we'll be able to take questions somewhat live, but in real time using the chat or the QA function. Thank you for your attention.

electrodiagnostic testing

lesion localization

lesion characterization

nerves

demyelination

axon loss

conduction slowing

conduction block

valerian degeneration

waveform morphology

stimulation sites