Good afternoon. Hey. Thanks for joining us. I'm going to take off my thing here. So thanks for joining us on a late Saturday afternoon. If you guys haven't seen me before, my name is Debra Venicey, and as of like two hours ago, I was the president. So it's been fun. This has been a great day. I'm going to go back one. I am I think one of the most fun things that I've had with the academy, if you guys haven't figured out, is this volunteering and networking. And my esteemed colleagues here, Dr. Farron Williams, Bill Pease, Eric Wood, are people that I have met over the years. A long time. And I'm honestly honored that they keep asking me, and I wasn't quite sure why I wanted to do it after all the things I've been doing today, but here I am. But I just wanted to tell you, this is the reason to do it. I wouldn't have a chance to have met with and worked with these folks, so just a little plug there. I'm going to go first, and then I think Bill, Bill Pease, and then Dr. Ensrud, and then Dr. Williams. Is that correct? And then what we'll do is we'll open up for questions thereafter, so Farron asked if we could just hold the questions after that, and we'll take it from there. We also are going to be live-streamed, so we're hoping for some of that interaction. And over the past two years, we've done these presentations via the Zoom, and that's really one of the things that we really missed was seeing people and having that chance to interact. I work at the Cleveland Clinic, and I don't have any financial disclosures. I told Farron that my talk today is going to be just a slight bit different in regards to electrodiagnostic. There is some electrodiagnosis, but one of my passions has certainly been listening to the patient and things that I've changed in my own clinical practice, so this is one of my favorite Brene Brown quotes. Empathy has no script. There is no right way or wrong way to do it. It's simply listening, holding space, withholding judgment, emotionally connecting, and communicating that incredible healing message of you're not alone. So let me share with you this case that I met a very nice lady on October 5th. She's an 81-year-old right-hand dominant woman. She was referred to neurology, and I know Dr. Ensrud is a neurologist, but I am not, for upper arm pain and an abnormal EMG. So at the clinic, we're like medical spine or your surgical spine, so she was referred to me. So my mindset at that time was I was kind of pissed off, because I had looked at her EMG, and I knew what was wrong, and I'm like, why is she here? So that was my mindset. So I tried to call on my inner, what I've been talking about, like, okay, go in there. So when you scheduled this visit with me, what were your main concerns? Honestly, I was like, deep breath, and so let me tell you about that. So as I said, she was referred for that. Her main concern was really whoop, sorry about that. She had pressure. She had pain in her upper arms, right more than left, and that was her main concern. She had no weakness. She had pain in her arms when she was lying on her side, brushing her hair, lifting her arm, vacuuming. She did have this EMG a couple months earlier, as I looked at, on May 12th, 2022, which diagnosed severe carpal tunnel or median neuropathy, and she had surgery for her right median neuropathy on August 8th. So she was referred to neurology by her orthopedic surgeon for upper arm pain. Let me share with you her nerve conductions that were done. If you look at them clearly, no responses, median sensory on both sides. Ulners, great. She was referred for right over left, so they did the right side. Median responses, pretty slow. We have 8.1 on the right and 8.59 on the left. Teensy amplitudes, ulners were pretty good. I'd say very good, 2.45. This is her needle electrode exam. Can you guys see that? Not real well. Bottom line, it was essentially normal. It looked like in the right tricep there was a little bit of some chronic motor unit changes, so no irritability, nothing else going on, just like it didn't sound exactly right. And then in the APB, also similar types of things. I'm sorry, I tried to do a screenshot and do that. So that's why she was referred. So their interpretation from the neurologist that did this study was that she had a right more than left median neuropathy, severe, based on absence sensory responses, et cetera. And then he indicated that there was this chronic motor axon loss and only limited to the right tricep. Finding is uncertain, clinical, significant, insufficient, reliable, electrodiagnostic evidence of a C7. Didn't really talk about the ulnar, which was normal. So that was really the primary care physician kind of focused on that. And then even though she had the surgery, the orthopedic surgeon then again just said to go to neurology. So let me go back to her findings. So really, as I said, 81-year-old lady, bright with it, normal gait, rounded shoulders, forward head. I'm sure that's what I have right now. Range of motion not so great with her neck, but really within normal. Her hand, her scar was like beautiful. She had no pain, no paresthesias, nothing on the left. Muscle stretch reflexes, nothing. No upper motor neuron signs. So pretty much a normal exam aside for the fact that she couldn't move her shoulders. So I said, gosh, I think we need to take some x-rays of your shoulders and maybe have you go see orthopedics, maybe some different orthopedic person. I mean, she has significant shoulder arthropathy. And so I guess maybe just listening to the patient as to why are you here. So in regards, I did review her electrodiagnostics. She had really pretty bad or pretty severe median neuropathy. And just that one non-diagnostic finding on the needle exam, it always makes me cautious about what we write to our referring providers. And my conclusions at that time was I think that it's your shoulder and I think that we can help you. So let's get you into some therapy and try not to step on someone's toes and get you into the right ortho person that might do a little shoulder injection. I just got a message on Epic and she has seen one of our super nice ortho PAs and she's doing much better. But I just, I guess it made me think about my own reaction to her, why she was there, kind of chilling about that and saying, okay. Deep breath. Why are you here? And I just wanted to put a little shout out to the AAPMNR Board of Governors and some of the staff on the picture. And this is a shout out to my new Guardians team that were actually in the series when I did this study. So it's me wearing an Indian shirt and a Guardians bridge. Hence the name Guardians. Thank you. I'm going to turn it over to I think Bill. Thank you. That was very much an EMG case, Deb. Looks good. Okay. We'll get up my slides. And I've got a case that runs at 12 year course of time. Oh, maybe I could have. Alright. And I think it brings up some interesting points about taking care of a diabetic because it's not your typical diabetic patient in the EMG lab. We have no conflicts of interest for me either. So the value of the electronic health record is rapid access to patient's entire history since we went on to the system and fortunately we adopted EPIC in 2008 2009. So this 34 year old woman at that time with uncontrolled type 1 diabetes for three years at the time had a one year history of severe pain in the right leg described as neuropathic by the referring physician. Muscle bulk was good. Right ankle jerk reflex is absent. Left is normal. This morning she said her blood glucose was 200, fasting and her hemoglobin A1c is twice what we would hope it would be. So we proceeded with an EMG and starting with sensory nerve conductions. This was not me. This was another board certified electromyographer in Ohio. The sensory nerve conduction findings in the lower limb are normal. The motor nerve conduction studies both perineal nerves normal, symmetrical, as much alike as you would want. You could argue that conduction velocities are in the lower range of normal but always ascribed to normal as normal. The right perineal F wave response is 5 centimeters different than the left I would take as asymmetric. 5 milliseconds slower than the other side and the right H reflex is significantly delayed compared to the left. Needle EMG findings are of large amplitude motor units in the extensor dige brevis but many motor units are reported. That's what the many in that column means. So there's a good number of motor units activated although decreased recruitment and motor units that are described as 8 to 10 millivolts. So not outrageously large especially for a foot intrinsic muscle. Just a little bit larger than what you'd expect for an adult in their 30s. And the rest of the EMG including the paraspinals and including the left sided extensor dige brevis are normal. So it doesn't look like we have symmetrical distal neuropathy. We have something only affecting the right leg based on all of our nerve conduction tests and the needle EMG. So the findings reported with that report and I'm just going to skip to the impression that it looks like a right S1 radiculopathy and then it says the findings could also represent a right sciatic neuropathy but this is less likely due to the presence of symmetric sensory responses. Personally I don't see what compelled this electromyographer to make that second comment. With the normal sensory response from both in both the sural nerve and the tibial medial planter sensory response I wouldn't have commented about a possible right sciatic neuropathy which should have knocked out those two sensory responses. The only reason I can think why he reported it this way is that the paraspinals were normal and he thought that for a radiculopathy we should have abnormalities in the paraspinals. I'm here to tell you that in an S1 radiculopathy you do not usually have abnormalities in the paraspinals. There's not very much S1 innervation of the paraspinals and the anatomically is obvious with a little thought. The S1 root exits after the from the fused sacrum and does not exit into the area where the paraspinal muscles exist. Of course the next step was to get an MRI of the spine and see about this radiculopathy and I see five well hydrated, healthy discs and no ruptures. You'll have to trust me that all the other images from this MRI were pretty much as normal as this one. Not surprisingly, skipping to the bottom of this list, neurosurgery didn't see anything to operate on. Follow up was planned with the neuromuscular medicine specialist who had done the EMG and a consult that preceded the EMG but that never happened. This happened to be as I read the records a period of a couple of hospitalizations for control of blood sugar and the patient got reasonably comfortable from what I could tell in the notes. Mostly primary care that gabapentin and amitriptyline were controlling the neuropathic pain. Beyond that, we left well enough alone until she again came to another EMG lab for an upper limb study because now she had some numbness in her hands. There's bilateral mild carpal tunnel not surprising for a violinist who's diabetic. That didn't surprise anybody. Then I finally got to meet her this year. Still complaining of pain but now there's bilateral cramping and numbness in both legs. Her hemoglobin A1c is reasonable for a type 1 diabetic at this point. She's learned a lot about diabetes management. The pain's been getting progressively worse over the last year. It goes up to her mid-thighs. She believes she has some weakness in the right leg that causes her walking and stair climbing. She still has numbness in her hands. Just conservative treatment for her carpal tunnel syndrome. She's adopted using a cane sometimes but didn't talk about falls or any injuries. Lower limb strength was okay to manual muscle testing. There was some decrease in sensation in the right leg. Reflexes were the same as 12 years before. Teller's absent right ankle. A decent response from the left ankle. Her gait did seem notably wide-based. Now when we did the EMG we still had responses in both legs although they're asymmetric at this point. The right serral seems smaller than the left. Both are smaller than the responses reported in 2010. The right peroneal motor from the EDB is now half the size of the one on the left although compared to the previous study that peroneal response is the same and the left is larger. There's some variations in technique even though we both, even though motor techniques are the same everywhere. I will say that these sensories are done antidromically and the first set were done orthodromically. F-wave responses were similar if not faster than the F-wave latencies recorded in 2010. So Dr. Camero would be glad that the F-wave improved with 12 years of good glucose control. But certainly those don't point to a peripheral neuropathy problem nor do the sensory responses. Just as a caveat on the small size of the right serral sensory, we had a noise problem in the lab that day and I'm not sure I trust the amplitude measurement that we got. The left, somehow the noise went away for long enough for us to record that one. But you can see the two peroneal motor responses being quite different on the same amplification scale. And the right peroneal F-wave looks pretty good. You have varying sizes of F-wave responses. You don't have 100% persistence but you don't expect that in the peroneal nerve. Needle EMG abnormalities were limited to L5 and S1 muscles. Increased amplitude and reduced numbers of motor units activated. I did not do the paraspinal muscles on this study. In part because finding no fibrillations or positive waves in the limb, the absence of positive waves in the paraspinals wouldn't have bothered me or changed my diagnosis. So my impression is still with L5-S1 radiculopathy, chronic without any acute changes and no clear evidence of diabetic polyneuropathy. In fact, the EMG evidence still speaks against it, which is nice to see in a patient who we all know as a type 1 diabetic with sugar control problems. It's very fortunate not to have polyneuropathy because she's at very high risk. No more lumbar imaging has been done up until as recently as last week when I checked again to see if anybody following up on this case had ordered it again based on the radiculopathy. So I present this patient as a case of diabetic neuropathy. Does that bother anybody? No. Now, she's not a case of symmetrical distal diabetic polyneuropathy, but she is a case of diabetic neuropathy. Her entire course of pain, weakness, and balance difficulty is caused by diabetes. According to the San Antonio Convention on Diabetic Neurologic Syndromes, there are three big categories. Patients have subclinical neuropathy that only shows up on EMG testing and other testing. There are the diffuse clinical neuropathy syndromes, especially symmetric sensory motor neuropathy and autonomic syndromes, and then there are the focal syndromes. And the focal syndromes we see most often is carpal tunnel syndrome, but they also include radiculopathy. Thoracic radiculopathy, cervical radiculopathy, and lumbar radiculopathy can all happen. And I've always broken these down and this is a Dr. Johnson system, or I think that's where I learned it, into one and two being the two systemic generalized problems, and then four different types of focal pathology. Most of us have seen the lumbar plexopathy, femoral amyotrophy type cases, which can spread to bilateral, but usually improve over the course of several months. Polyradiculopathies, which also present as sudden severe pain, just like the plexopathies, and sometimes these are lumped together as radiculoplexopathy. The mononeuropathy multiplexes are the vascular component from small vessel disease of diabetes. And the other focal neuropathies from entrapments, but they also include cranial nerve involvement. One and two are progressive and we don't have any good treatments for them other than symptomatic control. Three to six are important to recognize because they can improve over time, and you can give the patient a more positive prognosis. So the distal polyneuropathy, the mild slowing and axon loss with occasional conduction blocks of myelin disruption, some asymptomatic slowing at entrapment sites often occurs, focal findings, and it's important to note that neuropathic signs and symptoms and EMG findings can precede the diagnosis of diabetes by hyperglycemia. So thinking back to the asymmetry I saw, the peroneal motor response, what does that mean? Well, it means there's a chronic neuropathy with distal sprouting re-intervation that always happens when a nerve is injured, and that now the sprouting re-intervation cannot keep up with the axon loss to maintain a normal amplitude compound muscle action potential. And if we take the usual three to four-fold increase in intervation ratio that axons can usually provide, that means that her surviving number of axons in that nerve are in the 10% range, if she can get a 50% CMAP amplitude activation of the muscle fibers in that. So you should always recognize that when you're actually recording a small compound muscle action potential, whether it's in carpal tunnel syndrome or in peripheral neuropathy, it means that there's been a huge loss of axons. It's not proportional to the number of axons because the motor units have grown by distal sprouting and each have a larger number of motor axons that we're stimulating. And that's the end of my presentation, and we'll have questions later, I believe, and if you think of things later, here's my email address. »» Thank you, Bill. And now we have Dr. Eric Ensrud who's a professor at University of Missouri, at least the last time we talked to him that's where he was. And so he's going to talk to us about an upper extremity case again. »» No, that's not Iowa, that's Illinois, with these people from Ohio I just had. Top one, sir? Thanks. Okay. So thanks for coming. I'm glad we've got people here for what is one of the last, besides the talks tomorrow morning, one of the last sessions. So this talk is, I've entitled, Accents Don't Have to be Verbal. It's one of the unusual things that I learned from this situation. So this is a 70-year-old male who's here, was sent to me for a third opinion on the left hand. And this patient is hearing impaired, has been hearing impaired his entire life and communicates with American Sign Language as does his spouse. And he came in and had been getting really frustrated having difficulty communicating with ASL because secondary to weakness in his left hand. So he can't move the fingers on the left hand normally. And it's been present for a few years at the time that I saw him. And he just said that he's quite frustrated. So he's able to communicate with his wife via ASL, as they do, with the left hand weakness. And they kind of feel like he has almost an ASL accent in that he's difficult to understand with some of the signs unless you're familiar with him. And the ASL interpreter who I'm communicating through, I do have one of my sisters who's quite a bit older and retired, is a speech pathologist who this was her area. And she worked for many years as a teacher in the Madison Public Schools with autistic hearing impaired kids. But she never taught me ASL. She just, I think, used it to throw expletives at me or things like that. So she relates that she's worked with this couple many times. And over time, she can understand his left hand signing better. So it's something that she's learned to understand. Oops. There we go. So this patient, this left arm, has a very complex extremity. And the patient has a chronic extremity history. He was having chronic neck pain about 15 years ago. And at that time, he had a cervical MRI. And it showed what was said to be severe central canal stenosis at C5-6. The patient himself reports that at that time, he wasn't having any pain radiating from his neck into the arms. But the localized neck pain, he had a three-level decompression infusion about 12 years ago. And he'd also had some difficulties with numbness in the opposite arm, had a right carpal tunnel release and ulnar nerve release with good results. But for things, for an indication that looking back through the records, and somebody mentioned Epic. Does anyone here use Epic? Is anyone here frustrated with Epic? Let me tell you, I was frustrated with Epic. And I use Cerner now. And you don't know how good you have it. So trust me. It could be worse. So for unclear reasons, about four years ago, he had revision and repeat of the C4-6 posterior decompression infusion with plate revision. And he really doesn't feel like he had any symptoms in the arm prior to the second surgery, you know, other than the right-sided symptoms that resolved. But after the second surgery is when he really started noticing the left-hand weakness. So more history, he had a follow-up ortho appointment after that successful right carpal tunnel release. And the chronic left-hand weakness was noted at that appointment. And there really wasn't much exam documented. And he was sent for a left arm EMG. So he again notes that he had no numbness in the left arm and hand, just weakness. And so that first EMG was done last September. And it showed there was an exam done. And they checked shoulder abduction, elbow flexion, elbow extension, wrist extension, wrist flexion, and finger abduction. And everything was normal except the left finger abduction. The right was normal at 5. So no other muscles were examined. And they did nerve conduction studies, including the left median motor. And the distal latency was 4.8 milliseconds. And the amplitude was 1 millivolt. And conduction velocity was 27 meters per second. And then they did the left ulnar motor study to ADM. And the distal latency was 3.7. All the amplitudes were 0.7 millivolts. And the conduction velocities were 21 in the distal segment and 10 in the proximal segment. So needle EMG was notable for 2-plus fibrillations in the left triceps and pronator teres with fasciculations, decreased insertional activity without fibrillations or positive sharp waves in the left FDI and APB. And no units were recruited in the FDI and APB, excuse me. So one question that I had here looking at this is, does a median distal latency to most of you, if you're doing the median motor study and you see a distal latency of 4.8, which is prolonged, does that explain an amplitude of 1.0 and why or why not? Yeah, yeah. So it doesn't really make sense that just a mildly prolonged distal latency would cause such a dramatic decrease in amplitude. That sounds a little fishy to me. And should we even care? Why or why not? Well, we'll keep looking at this and see if there's a reason that we should care about it. And so ortho comes back. And the patient returned to orthopedics after that EMG last September. And he had a left ulnar nerve decompression surgery with anterior submuscular transposition and a left carpal tunnel release. And the patient then reported when I saw him that he had no improvement whatsoever in the left hand function or sensation after the left ulnar and median nerve releases. Remember he didn't have problems with sensation. So those surgeries were done and nothing changed. And so his exam when I saw him, right on the top there and left on the bottom row, so the deltoid elbow flexion, elbow extension, pronator teres, they were all 5 on both sides. The FDI was mildly decreased on the right and profoundly, I could just feel it contract on the left. The APB was 0 on the left and 5 on the right. The FPL was 5 on the right and 3 on the left. The EIP was 5 on the right and 3- on the affected left side. And the EDC was 5 on the right or normal and 3-plus out of 5 on the affected left side. Of note, the patient had flexion contractures of the left, second, third, fourth and fifth digits. That's what's causing the problem with signing. Any thoughts about this? So I just wanted to use this to point out how helpful the EIP can be. It's radial nerve, so it's very rarely involved in a compressive neuropathy unless you have a Saturday night type of palsy. And one thing I love about it is you can check it side to side very easily. So I just have the patients grab their knees with all the fingers, because if they don't activate all the flexors, some of the other fingers may come up. And it's just a very slight force muscle. I mean, it doesn't generate a lot of force normally. It's just to spread the weight of the fingers against gravity. And of course, the finger flexors are much stronger. That's why we can have trigger fingers, because we can pull the ligament through a loop with the swelling and then not being able to extend it. And it's got this great advantage, as I mentioned, of not being involved in ulnar neuropathy or CTS. When I see people miss things on it, they're hitting it too hard. And I always say, like, if we had marshmallows, if we were going to make s'mores, we had two bags and we opened one bag a week before the campfire and we put one marshmallow from each bag out and you slammed on them like that, you wouldn't really be able to tell the difference. So if you just lightly touch them and lightly increase the force, you're going to find that you can really discover things with this muscle, the EIP. But if you push too hard to start your examination, you'll miss it, because they're just mild decreases in force. So I decided to look at the recent cervical MRI images. And here's the sagittal images. Does anybody see this? This was kind of explained as maybe an artifact. And you can see this very long fusion here. And then so whenever something looks like an artifact, I always look at the images, the T2 sagittal versus the T2 axial. And so here's what we're looking at there. That is definitely not normal. And then here's the axial images. And remember what's towards the top of the screen is on the anterior side. And then here we've got, if you look at that increased T2 signal, that is right where the anterior horn cells are. So this is at a level that roughly corresponds with this fused and refused spine to about left C6. But what about the level of the injury of the spinal cord? You know, it's not C8, and we're looking on exam, and it's a C8 problem. Well, just to kind of point out that anterior horn levels are very different than root levels in both the cervical and the lumbosacral segments. And motor neurons in those spinal cord levels are always superior above their nerve root level by one to two levels in the mid and lower cervical cord, and one to four levels in the LS cord or the conus medullaris. So for example, that C6 spinal cord level is actually where the anterior horn cells are for the C8 nerve root. And that's why ASIA levels, sometimes I'll see people use ASIA levels for radiculopathy, and they're not intended for that at all. And in the cervical, they really don't correlate well because they're not nerve root levels. So I'm always asking people, please don't use them for nerve root levels because of this phenomenon. So it's also true for conus medullaris lesions. This is an interesting paper for a few years back on conus medullaris stroke, and they were looking at F waves to see if those will predict ambulation. But if you look at that picture in the bottom right there, you can see the increased T2 signal or myelomalacia or ischemia. So this patient is going to have weakness in proximal and distal L5 and S1 muscles because it's non-length dependent. It's affecting the motor neurons right where they originate, where their nuclei are. So these spinal cord and anterior horn cell lesions usually don't cause numbness. And why, of course, because the anterior horn cells are at a different level. I'm just having trouble with this pointer here. But the sensory neurons, of course, are in the dorsal root ganglia there, and they're outside the spinal cord in a different vascular supply. So when you have this problem, usually you're not going to have numbness when you have ischemia of the anterior horn cells. So this decreased muscle force from left C8 anterior horn cell injury caused paresis of the left C8 muscles without numbness and caused problems with signing, so what we could consider an ASL accent. And so in the EMG room, pulled up those images, looked at them, showed them to the patient and his spouse, and explained the situation. They were actually very relieved to be informed. And he still does have functional communication in the left hand. It's more difficult with people who don't know him, but people who know him are able to eventually understand him, like anyone who has a verbal or audio accent. And he's actually getting really tired of having all these surgeries, so he was actually very glad that no further surgery or appointments for this were indicated. And so the learning points is that everything that's axonal on EMG doesn't necessarily represent peripheral axon loss, that motor abnormalities without sensory changes can localize to the spinal cord. To question low motor amplitudes in the APB if the distal latency isn't markedly prolonged, and my kind of rule of thumb just by experience is not to expect the amplitude of the APB to be decreased just due to a distal latency unless it's greater than 8. And consider checking the EIP for an EZC8 muscle that's not ulnar or median. And I did learn that this is the side for DUND. So that case is DUND. Thanks. »» Thank you, Eric. And if you can think about any questions you might have, we'll save those for the end. So getting back to the lower extremity, I work at a level one trauma center, now UMass Chan. If you donate enough millions, you can have your name on the medical school as many have around the country. So I'm going to talk now about some lower extremity problems that can be diagnosed with electrodiagnostics, but also how that will help you. And I work directly with the orthopedist with your orthotic scripts for the patient based on what you're finding. I do not have any financial disclosures. So the first one, it's kind of timely because unfortunately, this accident happened last Halloween. A very nice young man, 23 years old, who had a little too much to drink and then got in the car after that, was unrestrained driver. Last Halloween ejected from the vehicle. He had significant injuries, some more minor. But as you can see, he also had bilateral transverse posterior wall acetabular fractures with the left treated surgically and the right conservatively. He had a left-sided sacroiliac screw joint fixation. He developed, I saw him for the first time about three months later, and he still was having a draining incisional wound. He had a left fibular fracture and the entire left leg had some altered sensation and hyperpathia over the foot. Just to show you the extent of these injuries, this was his initial pelvic fracture on the left with the transverse posterior wall fracture. This is his surgical fixation, which may have also contributed to his problems. And if you're an orthopedist, you might notice more about that. But when I saw him a few months out, at this time, he was quite debilitated because number one, he had all these injuries. He had bilateral lower extremity problems and had been non-weight-bearing through the entire left leg. But even what he could do through the right leg had, until recently, not been very much. So when I first saw him, he could hardly stand. And his left leg, though, was significantly weaker, even approximately. He had 2 minus over 5 strength, not that much more, you know, in the 2 plus to 3 minus range even on the right leg. But the left leg was definitely weaker. And he had no distal strength, maybe a trace of dorsiflexion. But everything else at the ankle was zero. He did have some altered sensation in that entire left leg, and it was more sensitive to touch in the foot dorsum and the sole, and to the extent that, you know, even having a sheet over the leg was a little bit irritating to him. As I said, it was three months out, so both legs had significant atrophy. But the left quads did measure 2 centimeters less than the right. And, you know, atrophy can be a little misleading. So you all should have a tape measure in the EMG lab to get it out and measure it at the same distance bilaterally, and you can get an accurate measurement of how much there really is in terms of atrophy. He had decreased reflexes on the entire left leg. He did have down-going toes. As an aside, he also had spinal fusion because of a problem at T11 to L1, but was not felt to have any spinal cord injury. He was fairly intact cognitively, I mean, really quite intact cognitively. Came actually with his mother, but only because he needed her to drive him, and he had been staying at their place because he actually did own a condo, but it was on the second floor and he couldn't do all the stairs, and even to get into his parents' house, he had to do about six stairs, which at this time, they'd been pretty much carrying him in and out as he really couldn't transfer or hardly come from sit to stand on his own. So here's what I found with nerve conductions. Left perineal motor amplitude was significantly decreased, 0.2 microvolts. And again, this is a 23-year-old male with, and in his case, significant bilateral lower extremity trauma. But the importance of studying the contralateral limb, especially in these younger individuals whose baseline nerve amplitudes could be significantly more than what you might see in a 40, 50-year-old patient. And as you can see on the right, perineal motor, despite being debilitated, was significantly better, 5.9 millivolts. Similarly for the left. Now that one, maybe for some people, could be getting to be not exactly normal, but closer to normal, 3.5 on the left side. But again, compared to the right, it was 12 on the right side, so it's only a quarter, which suggests, with both of those together, that there's been a significant degree of axonal loss. And then the same with the sural sensory and the superficial perineal. Both of those are significantly decreased by about more so for the superficial perineal, but three-fold less for the sural, and almost 10 times less for the superficial perineal on the right side. So this gets back to what Dr. Pease was alluding to, that you have in this case both motor and sensory changes. So it leads you to think that this most likely is not a root-level problem, and again, he had more pelvic injuries. He also had spontaneous activity in all of the distal muscles, but also some in the biceps, both short and long hips, biceps femoris. He had no motor units in the EHL, posterior tibialis peroneus longus, or short head of the biceps femoris. And he did have some motor units in tibialis anterior, just reduced in the medial gastrocs and long head of biceps femoris, with the more proximal muscles, including vastus medialis and tensor fasciae latae, and I didn't do the gluteal ones because of the draining wound and also he still had problems with positioning, but those were relatively normal. So in this case, this represents a left sciatic nerve palsy involving the peroneal greater than the tibial portions involving both motor and sensory, as you remember from the diagram we just saw of the motor units and where the sensory ganglion sits in relationship to the anterior horn cell and the nerve root. There was already some slight reinnervation, though, in the more proximal innervated muscles proximal to the sciatic nerve that I had studied, like tensor fasciae latae were spared. So that combined with the patient's age suggested a fairly good prognosis or a fair prognosis at least for further reinnervation. And he didn't have any other comorbidities because he'd recovered from many of the other injuries. So in terms of talking about prognosis, obviously the improving distal strength or some distal muscles like in the TA having reinnervations was encouraging. Patient also was very slightly built and other problems were related to this non-healing wound which caused him to be more sedentary and we talked about environmental obstacles such as the stairs and he also did have significant weight bearing pain, though, through the left leg which further limited his ability. And when you tried to look at him walk, he couldn't do much, had a very steppage gait, but he couldn't really at that time even stabilize the left leg much to do very much. And he did have a few months later the ability to walk short distances with a walker and a mild knee flexion contracture because he was just weak in general. So I also point this out to show you how the elective diagnostics can help with the general rehabilitation program. We actually got him at three months out after that initial EMG into an acute rehab setting that he hadn't had before because initially he was too ill and he couldn't do enough to meet rehab goals. And as I said, when I first met him he couldn't even transfer. So that in a short time, even less than a week, he made a lot of progress just having somebody work with him on what he had to do to learn to transfer and progress to standing, et cetera. But then later we re-evaluated him together with an orthotist and looked at what was happening with the nerves and looked at some different bracing options. And for him, you want to give him enough support, but you don't want to over brace him. You want something that gives him a little bit more of a ground reaction force, but a little bit more stability because he did have that knee that wanted to buckle. So we finally decided on this one type of brace for him that was a custom-fitted AFO that didn't have as much of the medial lateral stability, but did allow him to advance the leg further without the foot drop and allowed him to work on the progression of his strength in the contralateral limb as well. So after a few months, he slowly started to progress, and I'm pleased to say he also started to get more clinical improvement in his foot-ankle musculature as well, both dorsiflexion and plantarflexion. Unfortunately, he still has a long way to go. And the other thing about him is I also was concerned about the fact that he still seemed to have a disproportionate amount of pelvic or hip pain on that left side with weight bearing to the extent, and sometimes you have to be willing to do this, I sent him for an opinion from a different orthopedic surgeon. And that's when they discovered that there were truly in fact some problems with the hardware, that this was not a normal situation, that unfortunately for him it's going to have to be taken, he's already had a spacer put in, there's a whole lot of other orthopedic stuff that needs to happen to him. So you know, you have to kind of be willing sometimes to think about what else might be going on when a young man who really didn't complain that much for the extent of problems that he had still had so much pain that it was limiting how much more he could do, and then he still had this wound, which is another problem in his case, and even in terms of orthopedic issues, seeing what was going on with that and dealing with that was a big part of what they could do when. Okay. And then I have just one other quick case I think we can do and then we'll have time for questions, which is similar, but slightly different, and a different age, a 65-year-old male with a dropped foot. This gentleman, who was probably about twice the weight of the other person who only weighed about 100 pounds, and this patient was more of an average size 200, maybe a little bit more, but he had fallen off a ladder at work seven months before with a femur fracture, had a right total hip arthroplasty, also had some other medical issues, but over time he developed this foot drop, which usually tells you there's been some nerve degeneration. If it had happened more immediately, it might be a more proximal problem or something, you know, related to like the motor neuron or the spinal root, but anyway, he, when I first saw him, he was kind of walking with a cane, but he couldn't really pick up his foot. Here's his fracture and his arthroplasty. And six months out, which is the first time I believe I met him, he also had significant weakness proximally, but he also did not have any strength in the ankle at the dorsiflexion, plantar flexion, inversion, eversion, extensor hallucis, or any of the toe inverters or flexors, and also had decreased reflexes on that side. And the reflexes should tell you that you have a problem, either a lower motor neuron problem or a problem distal to that. Because if it's a more proximal problem or a problem from a higher level at the spinal cord, after this length of time you may see hyperreflexia and it may not be so asymmetrical. But he had no movement in the right toe, but that was because he had no strength on that side and he also had decreased sensation in the deep greater than superficial perineal nerves more than the tibial. He did have intact pulses and he could walk, but he really wasn't picking up the foot. He did a lot of hip hiking to clear the right toe. And at that point he had an over-the-counter, a pretty flimsy AFO that wasn't very appropriate for his size or his body weight. And so he couldn't get any real push off or any ability to really control the knee. And then on his electrodiagnostic test at six months, he had no perineal response recording. And again, if you don't find these from the EDB, go to the tibialis anterior to make sure there really isn't anything there. And even more fundamental than that, if you don't find the lower extremity motor or upper for that matter at your usual settings, you have to change the gain on the machine to make sure it's just not that you can't see it on a five microvolt gain or whatever your default setting is to. You really have to go down to 200 microvolts or whatever so you can find these very slow amplitude responses. So he had left perineal motor, just to show you, was relatively normal for amplitudes from the EDB. And right tibial motor, also no response with the pretty normal left tibial motor. He had no serral sensory, only did serral in his case. And a little low amplitude for the left serral sensory. But this patient again was 65 years old and could have some other things in his history or background. Sorry, I went past the needle. The needle showed spontaneous activity in most of the distal muscles and no motor units, including the short head of the biceps, but also none in the tensor fasciae latae. And he had in the gluteus maximus, in the long head of the biceps femoris, some motor units, decreased recruitment, really discrete recruitment, and some polyphasic motor units. And no spontaneous activity in the paraspinals. Such that his interpretation, as Dr. Pease eloquently pointed out, you could consider, is this a lumbar sacral plexopathy versus a lumbar sacral radiculopathy, with that one being less likely, because you have different nerves involved and you have the asymmetry of the sensory. And in this case, his prognosis with those findings is much more guarded, because it's now been six months with no motor units in many of those studies. Perhaps another study in three to four months might be helpful. Imaging of the lower back, everyone, especially many of my colleagues, like to always image the back, even if people don't have much in the way of back pain, and you find mild to moderate degenerative changes, but no canal stenosis, some neuroforamenal narrowing. And at nine months out, just clinically, he had no improvement. He kind of did his own thing. So he drove using the left foot. And he did manage to live in a third floor walk-up apartment, because he just drove himself up there, but he could not return to work as a carpenter. And he really didn't have much support with this over-the-counter AFO that he had. So in re-evaluating his orthotic needs, he needed something with more medial lateral support to prevent that ankle inversion, and we went to a carbon fiber for durability and stiffness, and to actually get a more normal gait pattern for this gentleman, so he could function a little more normally and use this. This is one possibility, the step flex, but went to this vector one, because it has more built-in medial lateral support, which he was also not willing to use anything that was a little too cumbersome, but this was a good compromise for him. And I would say thank you. And the other thing I've started to do with some of those kinds of patients, which has been really helpful, and I've gotten referrals to now from some of the local orthotists, is doing a telehealth visit with them at the time that they're at the orthotist's office. And that way, they have more equipment, like parallel bars or whatever, and we can kind of assess the patient together. And now they're even saying, well, what did you find on the electrodiagnostic testing? I'm educating them about how they can use some of this information to help figure out, do we need this orthotic for a longer term, or do we need something lesser, because the patient is continuing to improve like the first case. So thank you. I guess we'll all come back up front so we can take questions, and we have a moderator for questions. Okay. Yes. In regards to the first case, with the triceps, the pancreas improvement, I'm sorry, testing. There we go. So in regards to the first case with the decreased recruitment in the triceps, I believe it was, I just wanted to hear all your perspectives on this. Whenever I see a case, if anybody's had a prior EMG, I always try to get that to compare to mine. And what I've found in my region is people are pretty quick to call things based on decreased recruitment or even polyphasicity. And I have a little bit of a problem with that just because, you know, positive sharp waves, fibs, don't question that. But when you get into the motor unit action potentials and the recruitment, that can be very subjective. So if you're not doing quantitative, I kind of question diagnosing things based on that. And then especially based on the muscle that you're looking at, I find that triceps often looks decreased when it really isn't, especially if your needle's not deep enough. And so I just wanted to hear your comments on that. »» Is this on? It is. Yeah. I was thinking the same. I didn't do the study. It's an 81-year-old lady. I would agree. I'd actually welcome your input. I guess that was the point, like, gosh, we made a lot out of nothing. But maybe it was okay that she came to see me because she clearly didn't have a spine issue. Or maybe she had an issue and I could help get her to the right place. Yeah. What do you guys think? »» I always try to make sure that every resident rotating with me on EMG understands that the motor units in the triceps do not look like the motor units in the biceps. They're larger in amplitude and more likely to show a few more polyphasics. And the larger amplitude can make it appear that there's decreased number too if you don't carefully look in more than one area of the muscle. I think some EMGers short circuit the test by looking at recruitment real quick in one place and making a call. And that's fine if everything you see is normal. But, you know, I frequently see the residents getting ready to stop and I say, no, we need to look at another area. Because that area didn't sound quite right to my ear in terms of recruitment. So let's look again. »» Yeah. I think your comments on the firing in the triceps are very observant. Many of the radial innervated muscles fire at a really fast rate, faster than muscles innervated by the median or ulnar nerves, for example. So they do tend to get kind of over called as decreased recruitment when that's actually their native firing rate. Yeah. »» Thanks for the question. All right. Thank you. »» Thank you. So this is about the last case with regards to that 65-year-old man with the severe lumbosacral plexopathy after that hip fracture. Given the really poor recovery after six months, did you consider neurosurgical evaluation for nerve reconstruction options? »» Yeah, I guess first of all, what do you mean by nerve reconstruction? Because there's only so much one can do. »» Right. Well, they would have to borrow from another limb somewhere else and it would take a long time to regrow. But the sural nerve, let's say on the other side, presumably if that's intact, it's pretty long and big. At least one could use it to recover some function in that leg. »» I don't know how much experience some of the other people have. We've done certainly some peripheral nerve even transfers more in the upper extremities. And I think, you know, even at that, like they're often not very successful and sometimes we don't know how they work long-term because the patients get somewhat lost to follow-up. But I think it's even more challenging with a big nerve in the lower extremity. And in his case, you know, he had both proximal weakness as well as the distal weakness. If he had more working in the distal leg than something like a tendon transfer to assist with dorsiflexion, you know, could be more helpful. But I don't have enough unless somebody else does with the peripheral nerve. I mean, I will tell you that a lot of the surgeons go to a few conferences and get very excited about now all these things they can do with peripheral nerve. And I went to a lecture where the implication was actually that so many of these people, and this was lesser problems, more upper extremity, did better if they had peripheral nerve surgeries earlier. But I had a medical student that did a pretty thorough review of some of our peripheral nerve trauma a few years ago. And it wasn't blind. It was all retrospective. But there were some good cases that we had even some follow-up and serial EMGs. And she had enough, like at least a dozen cases where there was some surgical intervention and a similar number where there was not. And over the longer term, when you looked at the patients about a year later, she didn't really find much statistical difference with the ones who had surgery versus the ones who didn't. So some of what the surgeons are saying is an improvement, is just normal physiological regeneration of the nerves. It may have had nothing to do with the actual surgical intervention, if that makes sense. But because we know from following these patients electrodiagnostically that many of them do make significant recoveries over a year or two years or whatever. I mean, it's really an interesting point that you bring up. And there are definitely different centers in the country that are doing a lot of it and doing more of it. And these patients are really affected. So I hope that it's successful. I do think what Farn mentioned about intervening in something that has a natural history of getting better makes it difficult. There are people who do interventions that then attribute all the improvement to their intervention rather than the natural history. So I think that makes it kind of, it is difficult. And I think it's going to be more likely to be helpful with a smaller muscle, something more distal, like your hand muscles as opposed to your deltoid. Because I can think of a patient with a total axillary nerve problem and a concomitant vascular problem. He did have a little reinnervation after a year or a couple of years. But it was never enough to give him enough strength to lift that arm up. And then he subsequently found a surgeon. And he was very hopeful that this was going to be the answer. And they showed a few motor units spiring after the surgery. But if they looked back at the study I did before that, they had already been there before. But it didn't improve to the extent he had any more arm function. So that's always the question. How much is it really going to improve the function down the road? And if it's a bigger muscle that you need more strength, it's not as likely it's going to help functionally. Thank you. Just a couple of quick comments about nerve regeneration and nerve grafting. There's a length limit to how far axons can regenerate that's 12 to 16 inches. Because the neural tube starts fibrosing before the axons can grow much farther than that. And a grafting or transfer really has to be done within four to six months after injury. Because after that, that neural fibrosis is taken over. And the effects of the surgery really aren't going to be of benefit. Which makes EMG very important to evaluate patients at three to four months. So that selection of an appropriate surgical technique can be done. I recently came across a paper that looks kind of promising. Patients with an isolated perineal nerve injury can take a transfer from their healthy tibial nerve, a branch of the tibial nerve out of the gastroc and connect it to the deep perineal, and we're able to regain some dorsiflexion function. And those kind of transfers, and there's an ulnar to median connection in the hand that's being done on some people with severe carpal tunnel syndrome. Those kind of transfers where you can take a distal axon from another healthy nerve in the same limb and transfer them to the damaged are a way to get distal function. But otherwise, if you've got a shoulder or hip level injury, getting axons functional into the intrinsics of the hand or foot just doesn't happen. Oh, okay. We've got a few minutes, and I'm going to get to the online questions as well, too. Oh, I didn't realize there were still online questions. Yeah, yeah. Am I allowed to ask more than one question? Sure. Like an EMG report question and then like a treatment type question. Thank you again for your talk, by the way. My EMG report was for the diabetic neuropathy. Kind of like in the early stage with these relatively normal EMGs, I've gotten in the habit of commenting on how nerve conduction studies are unable to detect small fiber neuropathies. And I guess that wasn't really in your report. And do you feel like that tends to lead people down a rabbit hole and you leave it out, or do you actually do that in your report sometimes just to remind the primary care doctors that there's limits to this test and that could explain some of the symptoms? I am selective in putting those comments in. It depends on whether I think the patient might well have small fiber painful neuropathy. I'll put it in, but if I think the patient's concerns are mostly muscular pain, fibromyalgia or something else, or other musculoskeletal causes of pain, I will leave it out so that I'm not dragging them down the rabbit hole, as you just said, by telling them that the EMG really didn't identify the problem. Okay, fair enough. My second question is regarding the sciatic neuropathy case. So did they ever really try to find the cause, or did they just say blunt force trauma? Was it due to being sedentary and sitting on the sciatic nerve? Was it a surgical issue? Did it lead to any imaging? No, I think in his case, the trauma was definitely a factor. That combined with the hardware. Did they do any actual imaging of the sciatic nerve to look for continuity or any? Well, his nerve has to have continuity, or we wouldn't have been getting some of the signals through there that we got, and some of the evidence for the re-innervation and the needle EMG. So the only reason why I ask is because unlike blunt force trauma, I tend to get gunshot wounds just because of where I am, and it's usually a EMG referral, I diagnose sciatic neuropathy, they then image the area to see, oh, did the bullet trajectory actually go through? Fortunately, it never does, and I could have told them that, it's not transected, just on the EMG, but anyways, they get the EMG, or they get the MRI, and it's just shockwave. And part of why I ask is, do you feel as though the mechanism matters in recovery, like would shockwave heal prognosis be any better than blunt force than trauma? I think it has more to do with the distance that you have to re-innervate, but also the length of time you had compression on the nerves, be it from some potential hematoma, he still had a wound in this case that had fluid and drainage, and in his case, there were issues with the hardware, and he actually has been taken over by a different trauma surgeon now at a different location, and I actually know that person, and he indicated that he's himself not that keen about the approach that was used with the initial surgery, because there's a little more risk of causing more problems with the sciatic nerve the way it was done initially, not transecting it, but just more stretch or more problems with it down the road. So I don't know how you can say it's one thing versus another, because in his case, there's so many multiple factors, including just the trauma itself. »» Fair enough. Thank you. »» We'll get to you in just a second. We've got a number of online questions, and I don't want the Zoom contingent to feel left out. The first one is per Preston and Shapiro text, ulnar neuropathy at the elbow can sometimes present with just low CMAP amplitude in the absence of slowing or partial conduction block across the elbow. Ulnar nerve compression at the elbow present with just diffused slow conduction velocity, so both across the elbow and across the forearm on NCS is the only abnormality. I'll address that one. I mean, it's possible, but I think it's very dangerous to assume that. And for a number of reasons, if you get that finding that you've got low amplitudes and low conduction velocities throughout the ulnar nerve, I really think there's three things that need to be tested. The first is the EIP to assess could this be a C8 radiculopathy. And then the other thing to be very careful about not forgetting to think about is a lower plexopathy. I've had a number of patients who have had breast cancer, for example, and had recurrent breast cancer and got diagnosed with ulnar neuropathy due to the invasion. Remember cancer invades from the lower plexus upwards. So two things I always check in those patients is the medial forearm. I call this the danger zone because that's, you know, the T1 fibers, the lowest part of the plexus. So I check that side to side, light touch, and you can certainly do the, you know, the medial anabrachial cutaneous side to side. And then in those patients, I always needle the APB because there's T1 motor fibers in the APB. And even in the, you know, with the normal amplitude, if you don't look at it, you can miss that there's been involvement of the T1 fibers. So those are the three things that I would, two of them you can do on exam and then you need to do needle EMG of the APB. Also things like I've had patients who've had, you know, non-localizing ulnar neuropathy who've ended up having neuromas or, you know, tumors of the nerve. Patients who've had compression proximally by a tricep slip and so on. So I think that's something that you always have to be careful of. Also, if the patient is diabetic, there's a good paper, kind of a landmark paper on diabetic ulnar neuropathy of the forearm that patients get a non-localizing ulnar neuropathy in the forearm. It's by Seward-Rutkove, R-U-T-K-O-V-E. So just, that would be kind of a diagnosis of exclusion. I wouldn't jump on that. The next question is, what caused hyperintensity of the T2 signal at the C6 level? He had two prior spine surgeries but weakness developed after the second surgery. Was this the result of prior stenosis or surgical complication? I don't know. But when you get ischemia from stenosis, you get usually ischemia in the watershed area between the anterior spinal artery and the two posterior spinal arteries. So usually it goes right through the corticospinal tracts. That's the watershed area. This was different. It was anterior. So I assume that it's more likely to be a surgical complication. But I don't know. But it also occurred. And then we've got a question for Dr. Pease. Apologize if I missed, but did the patient have PT? If so, was it focused on spine rehabilitation given suspicion for the S1 radiculopathy? With this type of peripheral neuropathy presentation, would PT be expected to help if focused on the leg or peripheral nerve? So the original diagnosis of radiculopathy in 2010 was followed by lack of follow-up with anybody except a visit with a spine surgeon who agreed that the MRI didn't indicate surgery. And I don't know anything else was done at that time. When I saw the patient, I certainly agree that physical therapy would be indicated. She had adopted a cane on her own, and everybody does better if they get some instruction on how to use the cane and proper balance to climb stairs and for other activities around the home. And every new onset diabetic neuropathy patient that I see, I think, can benefit from physical therapy just to get some coaching on how their body works in its new way to prevent falls. Thanks for your patience. We have one more online question. At what elderly age would you consider absence of serosensory responses as possibly doing related to advanced age as opposed to being definitively reflective of pathology? This is a quick answer, because there's a nice paper by Ginny Taveed, J-I-N-N-Y, Taveed, sorry, the last name is T-A-V-E-E, looking at seroresponses in normal elderly. And you definitely can't tell anything after age 75 that the absence of sensorial responses means anything. And it starts to be a factor around age 70. So unfortunately, there are a lot of elderly people getting diagnosed with peripheral neuropathy for osteoarthritic changes and for foot pain, getting put on gabapentin, which increases their risk of falls and hip fracture and so on. So it's a great question, because that's a problem. Yeah. But you also will see 90-year-olds with cerebral nerves as normal as a 20-year-old. Yeah. So it has a very poor negative predictive value. One of my friends in former residence refers to a normal seroresponse in an 80-year-old as a sign of longevity and tells them they're going to live to 100. Speedy nerves. Go ahead. Hi, everybody. My name is Nick. I'm a fourth-year medical student from Michigan State. Thank you all for your presentations. As someone who's particularly interested in EMG studies, I was curious as to your perspectives as for as long as you've been involved in the field, how have you seen EMGs grow in its utilization in the clinical field? And is there any particular advancements in EMG studies that you're excited about in the coming future? You're going to stick it on the old guy? No. What's that? Stick it on the past president of AANEM, Dr. Bill Pease. EMG has evolved in several ways, although a lot of what we do, you know, everything I talked about in the ulnar nerve workshop earlier today could have been done on equipment that we had 40 years ago when I started. The basic techniques haven't changed, but getting the results and the accuracy and the reproducibility of what we've done has improved tremendously as a result of increased technology and better knowledge of how the nerves work and what to expect after injury. Having a deep knowledge of what happens to a nerve after an injury, and Larry Robinson has written extensively on this now, and as he studied trauma when he was still at the University of Washington, but he's still writing on the topic, he gives a very good understanding of what we've known for a long time happens to nerves. The use of EMG has changed dramatically, and I, you know, the ratio of lower limb cases to upper limb cases has flipped in my lifetime from two-thirds lower limb to now two-thirds upper limb, but we do much more with the hand center on upper limb nerve injuries and in studies of patients who may benefit from some kind of reconstructive procedure, either for upper motor neuron problems or lower motor neuron problems, because they're operating in new ways on those patients all the time, and EMG helps them evaluate them. I think we all wonder where, in what ways, imaging will substitute for what we find on EMG, just like the MRI took away a lot of the lumbar spine work that was part of my daily mantra when I was a resident, and, you know, we don't take care, we don't see those patients now because the patients are taken care of based on their imaging results. We get the EMGs that are more interesting because they're the ones that can't be figured out easily by the routine testing, and we can be more sophisticated in our evaluation, but it's still important to know what makes the muscles move and the body do the mechanical work that we need it to do for our activities of daily living. Well, I was just going to add, it's your expertise and interpretation, though, not what the machine automatically generates just based on the broad data that's going to drive how meaningful the report is and how much the referring doctors or whoever sends you the patients find it's helpful for them, whether it's in surgical decision-making, orthotic prescriptions, as I mentioned, or any other ways in which it might be helpful, even whether the person would benefit from therapy or whatever. It's really your expertise that no one else has that makes it meaningful for the referring providers, and I would just emphasize that there's no substitute for the learning that you've done over the last few years to, you know, to compensate, that can take the place of that, and the people you work with will kind of appreciate that if you work with them closely enough. Yeah, there are definitely some technical advances. I just got a new couple of EMG machines with a brand new software that has just some remarkable motor unit evaluation programs in it that I've never used before that are new. You know, there hasn't been a lot of change in the needles. I'm always learning better ways to do nerve conduction studies, and I've been doing it 20 years, and I'm still learning better ways to be more accurate. It's so easy to make for things to be abnormal and not necessarily get the best response, so I think as long as you're open to it, you'll learn. It's not going to be a static field for you, yeah, and there are definitely lots of publications still coming out in EMG and lots of publications on understanding of EMG and so on, so I wouldn't I certainly don't see it as static at all. Maybe I'm just a slow learner, but after 20 years, I'm still learning a lot, yeah. Thank you. Thanks. We have one more. Concerning surgical care of nerve injuries, please comment on possibility of a post-traumatic neuroma in continuity giving potentially surgical treatable lesion. I'm not... Isn't the answer to that just yes? Okay. I'll say the answer is yes. Yeah, that is a possibility. I'd say that's a possibility, and that's when combining ultrasound and EMG in the same patient is especially valuable. Yes, I had another question, and again, yeah, thank you all for your presentations, and Dr. Pease, with your presentation, thank you for reminding us that there's... Things are not as easy as they seem. That book probably shouldn't have been called Easy EMG because it's not easy, but anyway, on that case in particular, though, where there was a series of tests, and the diagnosis kind of changed over time there, but when the sural nerve became involved, I was just wondering why you still called it radiculopathy. Oh, so in my EMG where one sural nerve had a small amplitude, but that's the importance of having the pictures, the images from the nerve conduction data available to you. So the amplitude measurement was technically obstructed by the shock artifact that was interfering with the response, or maybe that was 60-cycle noise, and that, you know... Yeah, it was a downward slope. Later, I don't remember which it was, okay, but I tried to mention in the presentation that I didn't think that two or three millivolts sural amplitude was accurate. Oh, okay. Yeah, sorry, I missed that. Yeah, okay. I'm glad you clarified it because somebody else probably had the same question. Certainly you can have that much asymmetry caused by diabetic neuropathy. The left sural sensory response was smaller than the one recorded before, and so there may have been some mild progressive polyneuropathy that affected both sural nerves and reduced them, say, by half, but they were both... But the left one was still greater than five microvolts, which is my limit of normal, so you know... But that doesn't mean it wasn't smaller than it used to be and that there hadn't been some sensory loss underlying the problem. It just wasn't enough to make it the primary diagnosis for this patient. Maybe it was contributing to the wide base gait in the use of the cane, however. I can't say it wasn't, and I know I recently saw a case where, you know, we all agreed, looking back, that a normal amplitude motor response had fooled some people on a real diagnosis when, you know, the diagnosis of, like, a perineal nerve of three millivolts was said, well, that's normal, so there's nothing wrong with the perineal nerve. But it turns out there was some axon loss in that muscle already. It just wasn't enough to show up on the normal values table yet. I would really discourage people. There is kind of a trend to say, cannot rule out small fiber neuropathy, and there really is an industry that has arisen in doing skin biopsies for small fiber, and there are real problems with overdiagnosis. Several of the commercial labs call basically just about everything small fiber neuropathy, so unless at the EMG there's an exam with pinprick that shows a loss, you know, like distally to pinprick that wasn't there on light touch, I would really be cautious about doing that. I think that's going to be one of the next big scandals that comes up in our field is the overuse of skin biopsies for small fiber neuropathy. I just heard yesterday about one of the major labs in the country was shut down. You know, and it's kind of like everything small fiber neuropathy, long COVID is small fiber neuropathy. You can find Parkinson's with small fiber neuropathy. Don't leave out fibromyalgia. Fibromyalgia. Oh, yeah, I forgot about that. Yeah, so. I'm sorry. I'm just full of questions. Yeah. That brings up another question. So I get a lot of referrals for confirming a peripheral neuropathy. I kind of question, like, couldn't that often be made based on clinical grounds? Do you really think we should be using EMG as much to confirm all these peripheral neuropathies? Because like you said in the other day, everyone, or I think, or maybe it was the other lecturers, everyone in America is entitled to have a neuropathy or something. I mean, I think one problem is that, I mean, let's face it, there's a real almost crisis in providers, health care providers in this country. I wouldn't limit it at all to physicians. It's there for nurses, nurse practitioners, PAs. There's a lot of financial pressures. There's not enough time. You know, like, one of the most meaningful things I learned this year is that, should we really be referring to physician burnout when the physician, the problem is systematic failure, but everything's being placed on the physicians. You know, the physicians are the ones that are burning out. Actually, the failure is the system, for example. And I think in the time that I've been doing EMG, I see less and less and less exam being done. And I think rather than even checking for a peripheral neuropathy on exam, it's easier just to check the box in the EMR for an EMG. You know, so I think a lot of the referrals, do you need an EMG to determine that there's a length-dependent sensory neuropathy? No, not at all. But that probably takes more time than checking, you know, depending on the EMR, checking the box for an EMG. Yeah. I agree with that. I prefer not to do EMGs on, you know, a diabetic with paresthesias in both feet and diminished reflexes at the ankle, unless there's some reason to do it. Like, now they have pain in their thigh, and they may have amyotrophy, or they have back pain and may have stenosis. And then I focus my exam not on the diagnosis of the neuropathy, but on the second, the other problem that may be there, whose symptoms may be confusing because of the neuropathy. You know, they're not going to have typical pain in their leg of a radiculopathy if they have peripheral neuropathy, because their sensation is going to be altered. I want to thank everybody for your time. I know it's late on Saturday, and we've run over time with the questions. We'll be available for a few more minutes if anyone has something else they want to talk to us about. But I'd also echo the same, as you've already heard, that the clinical is still critical in helping you with the diagnosis. And as you saw with myelo-extremity cases, you really can't even begin to know how to design the electrodiagnostic study if you haven't done a good clinical exam to begin with. So I thank you. See everybody in New Orleans, if not tomorrow morning. Not tomorrow, next year. Thank you.

neurological conditions

lower extremity trauma

left peroneal motor amplitude

hand weakness

American Sign Language

left C8 anterior horn cells

upper arm pain

shoulder arthropathy

carpal tunnel syndrome

peripheral neuropathy

orthotic options

foot drop

clinical evaluation