All right, thanks for coming to our session, we're going to get started. Some of the stuff is some housekeeping, we'll get that going right off the bat, but this is a really exciting session for us. I think we had a nice talk today for people who went to the neuromuscular group meeting about how important it is to have neuromuscular sessions at the meeting, how important it is to have electrodiagnostic talks at the meeting, talks that are relevant to our community but also bring in people from outside. I will give you just a couple heads-ups, there's some people listening online, so if you asked a question, please use the microphone so they can hear as well. We'll try to repeat them if we have to, but just let's try to use that. Mute your cell phones, the slides are going to be available online, so you shouldn't really need to take pictures or record anything, although we are a really photogenic group. As far as getting started here, the learning objectives today are really reflecting the three main talks. Lucky for you guys, I'm only doing a little bit of talking and mostly introducing. The first talk is going to be on electrodiagnostic approach to evaluations of patients who present with walking problems. And so you're going to define an approach in that case, and we're going to do it with a case-based discussion. We're going to also identify and differentiate various clinical conditions that mimic radiculopathy, and hopefully learning some of the knowledge and skills that you need in order to tackle those problems. They're not always bread-and-butter cases, so you need to be able to be an expert on all the possibilities, even if sometimes you have to expect the unexpected. And then understand the growing role for routine electrodiagnostics in cervical spinal cord injury patients, which is a really interesting topic, because it's very heterogeneous across the country right now with how we're using surgeries like tendon transfers or nerve transfers to manage these patients. And it raises a lot of interesting questions for the electrodiagnosticians working at these centers of how to think about these patients and how to help the surgeons and the spinal cord medicine physiatrists take good care of them. So for our first talk, I'm going to introduce Dr. Hearn. Sandra Hearn is an associate professor at Michigan Medicine in the Department of Physical Medicine and Rehab. She earned her undergrad and medical degrees from Harvard University and completed her PM&R residency at Case Western Reserves University's Metro Health Rehabilitation Institute. Dr. Hearn is board certified in physical medicine and rehabilitation, electrodiagnostic medicine. Her research focuses on electrodiagnostic strategies for peripheral nerve conditions, and she's actively involved in teaching and educational leadership. I'm sure you've probably, there's a good chance if you've been in this meeting before, you've probably heard her speak before. In recognition of her contributions, she's received the Sinyoung Lectureship Award and Scientific Impact Award from the AANEM. In fact, that was one of the first talks I heard her give, and I was blown away because she did such an excellent job there a few years ago. And then Dr. Hearn is really committed to medical education and served as the PM&R residency program director and interim associate chair of education and professional development at Michigan. She's honored with the Silver Crutch Teaching Award in 2016 and the Program Director Excellence Award in 2020, and she'll be presenting on electrodiagnostic correlations for patients who present with difficulty walking. Please welcome Dr. Hearn. Thank you for the very, very kind intro, Dr. Frantz. One second here, we'll get a little A.B. help. That's why I write everything out on a piece of paper. Never let me down with this. Should we let another speaker go and then troubleshoot? Sure. Let's see if another, the other slides will go up. Okay. So we, we're a pretty nimble organization here and so we'll, we'll come back to Dr. Earn in a moment. We'll introduce our second speaker, Dr. Rad, whose slides are pulling up. There's some silly issues, so we'll get that fixed in a second. Don't worry, we're going to get through all the talks today. Dr. Rad is someone I look up to. We work, we actually trained together, but she's kind of like a big sister to me too. She is younger than me, but she's well explained. She's between her clinical trial work, the sheer number of national presentations that she gives at conferences like AAPM and our AAM annual meetings. She's, I think, becoming the face of neuromuscular medicine and physiatry. She's a small group of us who have done fellowships, but I, I, I lagged behind her by a year, so she showed me the way and she's opening up new opportunities, I think, for other physiatrists to consider. It's not the only way to do electrodiagnostics, but it is a way to do it and there's pros and cons, so it's a conversation we can have offline. She's an assistant professor in the Department of Rehabilitation Medicine at the University of Washington. Her clinical roles include being the director of the electrodiagnostics lab, co-director of the Muscular Dystrophy Association Care Center at UW. She earned her bachelor's degree from the University of Southern California, her medical degree from Boston University School of Medicine, and she completed her PM&R residency at some place in Chicago. I was trying to look it up, but I, I, I Googled rehabilitation institute of Chicago. I couldn't find anything about it, so I guess it's, you can, maybe someone can fill me in on it later. And her clinical work includes electromyography as well and care for, caring for patients with ALS, spinal muscular atrophy, muscular dystrophies, and other general neuromuscular problems. Today, she'll be presenting on clinical mimics of radiculopathy. Thank you for that very kind introduction, and I'd like to say younger sister, but we'll stick. Well, you look older though. Thank you, thank you. And on that note, I'm going to transition, apologies, transition into the focus of my talk, which is clinical mimics of radiculopathy with no disclosures here. So why is it that we chose clinical mimics of radiculopathy to incorporate on a talk about EMG and patient care and treatment options? And the reason is, is because radiculopathy, whether you're a neuromuscular specialist, a sports medicine specialist, a general specialist, you will see patients with radiculopathies. In fact, studies have shown that radiculopathies are one of the most common referring question for electrodiagnostic referrals. This follows behind carpal tunnel syndrome, polyneuropathy, and followed by general mononeuropathy, so ulnar mononeuropathies, perineal and tibial mononeuropathies. Just like many, or should be all of our electrodiagnostic referral questions, the question of a radiculopathy should be an extension of your exam and your history taking. Typically you're looking for reports of pain, paresthesias radiating along a nerve root distribution with associated sensory loss and or muscle weakness. And based on that description, you can kind of understand why there would certainly be many mimics of radiculopathy. Taking a step back a little bit. So typically when we talk about the electrodiagnosis of radiculopathies, we teach our residents to evaluate at least one motor study, at least one sensory study, and to make sure you have a sufficient EMG screen looking at various muscles. And from those findings you would expect that the motor nerve conduction studies would either be normal or have a decreased amplitude. You would expect all your sensory nerve conduction studies to be normal. And you would expect to find needle abnormalities in two or more muscles innervated by the same nerve root and different peripheral nerves. Now this is just a framework for your study, especially when I talk about one motor and one sensory study. In reality, with our contending mimics, you're probably going to want to look at two motors, two sensories in the arm, and multiple available ones in the legs to rule out things like mononeuropathies, carpal tunnel, ulnar neuropathies, sciatic mononeuropathies. But this is just the basic framework for a radiculopathy. So now I'm going to dive into this case-based approach because I really don't think there's a better approach when you're talking about electrodiagnostics. These are all patients that were pulled from individuals that I saw. This EMG referral stated bilateral lower extremity symptoms concerning for peripheral polyneuropathy versus lumbar radiculopathy in a 70-year-old female. So I'm going to highlight the big information in the chart and then we'll dive into the history and exam findings. So off the bat, a patient with chronic low back pain, I just realized these might not be the most updated slides, but I can make do with that, left an L1 compression fracture status post in T11 to L3 PSIF in 2019, and then adjacent level disease that ended up resulting in L4-L5 bilateral partial hemilaminectomy and foramonomy. So she has ongoing low back pain and was sent to us for a surgical consultation so that they could determine if they needed to go back in for surgery. Now diving into her history and exam, she had, so recall that her initial surgery was in 2019 for a compression fracture. In 2021 she developed a left foot drop, and that's really what prompted her next surgery. But her left foot drop did not resolve after surgery. Following that, she then went on to develop a right foot drop, and today she says she doesn't have any back pain, but back pain has been an ongoing issue for several years. She reports generalized weakness throughout the lower extremities, which limits her ability to ambulate. She has numbness and tingling from calves to her feet bilaterally, and she denies any sensory changes or weakness in hands, no diffuse symptoms, no neck pain, bowel or bladder incontinence, no shortness of breath, no difficulty breathing, swallowing, cognitive changes, or weight loss. And when you examine her, her exam is kind of consistent with her history. She has some atrophy in her EDBs. She has weakness in both dorsiflexion, left plantar flexion, so a little worse on the left, EHLs. And she has sensation that's kind of lost in a stocking distribution with some asymmetric reflexes here. So on the right, 2 plus patella, absent on the left, absent Achilles. And her seated slump test and straight leg raise are negative. As many institutions, I'm sure you see a lot of, you're doing a lot of repeat EMGs, so I'm going to highlight that she had an EMG in 2021, and it was notable for bilateral L5-S1 radiculopathies. So Dillingham did a wonderful paper that was published in 2020 where evaluating different approaches to radiculopathies and put together this algorithm based on an extension of the history and physical exam findings. So if we walk through this, and you'll have this slide as a reference. But if we walk through this, so pain, weakness, gait, sensory, paresthesias, our patient certainly fits this category. And then we did see sensory loss on the exam. And we saw it pretty generalized. So in this algorithm, we have, with reduced reflexes, we have polyneuropathy, and then we're dealing with the lumbar, so lumbosacral radicota equina. So certainly radiculopathy is on the differential as well as polyneuropathy. Now let's see how well this differential in general works. So I'm going to pull up nerve conduction studies. I apologize, the numbers are really small. So highlighted in red are some abnormalities on this study. What we can see is on the left EDB, or both EDBs are absent responses. Moving up to the deep branch of the tibialis anterior on the left, we have low amplitude. We have significantly low amplitude tibial response on the left and non-attainable on the right. Moving on to the sensory studies, we have no serral responses. And so we moved up to the arm to compare to some sensory studies in the hand. And we have a prolonged latency and low amplitude in the median sensory and normal ulnar sensory So again, the most striking thing here is the fact that we have abnormal sensory studies in the leg. And at this point, are we dealing with a polyneuropathy? Are we dealing with a radiculopathy with these other motor low amplitudes and dealing with a concomitant polyneuropathy? So needle exam is key for radiculopathy. We started, so you see everything on this needle finding. And I apologize. What I thought I had edited out in the updated slides was getting rid of the squiggly red marks that my Word document doesn't love. So some of those are abnormal and some of them are just not the right spelling for them. So when you look here, I'd like us just to focus on the left leg because that's where we started. And we thought, okay, she already had an EMG that said radic. Things, for the most part, fit with a radic. So we started in the left. After going through four different muscles, the tibialis anterior, gastroc, vastus, and TFL, all with neurogenic findings, we realized, yes, polyradic could still be in this differential. She's had extensive surgical history. She has no weakness in her arms, no other symptoms. But before we keep needling this leg that has multiple nerve root and peripheral nerve distributions, let's just move into the hand to see an area that's uninvolved and should be normal. Looking into the FDI, unfortunately, we also see neurogenic changes. Looking into the triceps and deltoids, so now shifting this approach to more widespread in the arm, we see no active de-innervation, but we do see chronic de-innervation. We move to the other side to look at another arm muscle. And again, we see neurogenic changes. So now we're seeing this pretty widespread. Rather than doing a lumbar paraspinal or cervical paraspinal, we decided to elect something that would rule out radix. And that would be our thoracic paraspinals. Wonderful when we're looking for things like motor neuron disease or myopathy, remembering that they are the most proximal muscles that we have to study. And unfortunately, we are also seeing neurogenic changes. Is radiculopathy still on our differential? So normal low amplitude motor studies, yes. Normal SURLs, no. Needle abnormalities found in two or more muscles innervated by the same nerve root and different peripheral nerves, no, unless we're going to say that there are multiple peripheral nerves. And so the key takeaway points of this study is to make sure that you surround abnormal with normal. So I don't know what our patient presented with in 2021 and what her EMG may have looked like back then. But I do know that the arms weren't looked at. And so if we stop at the abnormalities of the legs, we certainly could have said this might have been a polyradiculopathy with her history and exam and ignored other normal areas. The other thing I want to point out as we're thinking about how do we interpret this study is sometimes a unifying diagnosis isn't going to fit. And common things are still common. Carpal tunnel is still common. Neuropathies are still common. And you can have multiple things going on, especially as patients age. So in this particular case, what we wrote was that there was electrodiagnostic evidence of active and chronic de-innervation in multiple spinal segments, which was concerning for a diffuse lower motor neuron process. There, given the absent serral responses, which of note in 2021 were normal on that last EMG, was suggestive that there may be a concomitant large fiber polyneuropathy going on. And then let's not forget the carpal tunnel finding that we just saw on the EMG with right demyelinating and axonal median sensory mononeuropathy. Now, how does this EMG help guide our treatment? So what now? So I brought this individual back into my neuromuscular clinic. Her copper level was 36, low, low zinc. And then the rest of the lab workup for a neuropathy workup as listed here, SPEP, ANA, B12, TSH, ANCA, all normal. We sent her to HEMOC because she had neutropenia and macrocytosis. And they said this is probably from her copper deficiency. Based on the conversations that we were having with her and our thought process, which I'll share on the next page, she said, I am going to Mayo because I do not want what you're telling me. So Mayo did another EMG. Unfortunately, it was unchanged. They did cervical spine imaging, a bone marrow biopsy, all unrevealing. And the only thing they added, which was still key, was send her to GI to see if she has something to explain the copper. So let's take a step back a little bit as we talk about bringing this back into clinical mimics. Severe copper, so now we're trying to decide, do you have a severe copper deficiency, peripheral polyneuropathy versus progressive muscular atrophy? So the kind of descriptions of these, typically when we see somebody with a severe copper deficiency neuropathy, it's associated with a myelopathy. So we would have seen upper motor neuron signs, although there is very few case reports where you don't have to have a myelopathy. It is also typically a sensory neuropathy, although I could identify like three case reports where it was not a sensory neuropathy and it presented similar to ALS with weakness, atrophy, and EMG changes. And then looking at the risk factors for copper deficiency, which our patient didn't have, history of gastric surgery, high levels of zinc, malabsorption, and unfortunately, no cause identified in 20%. Progressive muscular atrophy, for those that are not familiar with it, is a form of lower motor neuron predominant ALS. Accounts for about 15% of our sporadic motor neuron disease with distal muscle weakness, fasciculation, and cramps, although you can have proximal involvement. No sensory symptoms, no upper motor neuron symptoms. Thankfully, a slower progression, bulbar involvement is rare. And then when you're concerned about this, important to rule out mimics like multifocal motor neuropathy, in which you would be looking for conduction blocks. I don't have the time to delve into that for this particular case, but we didn't see any conduction blocks on her exam. And so our ultimate thought was that she didn't fit well for copper deficiency. She didn't respond to treatment, and that unfortunately, she had a diagnosis of PMA with a concomitant peripheral neuropathy. So electrodiagnostics were key here. We prevented unnecessary surgery, and we were able to identify involvement not obvious on her physical exam, so areas of the arm that were completely normal, and ultimately aid in accurate diagnosis, treatment, and management. I have another case, but for time. Maybe I can... What do you think? Well, we have time for a little discussion, and maybe we could save a bonus case. Okay, perfect. I was going to say, we can, or I can... Do we have any questions right now about the first case? Do we have questions about the first case? I have a few minutes for a second case, unless anyone has questions about that one. Then I'll answer questions and not do this case. Let's push forward, but do this one quick. I will speak faster. Okay. So in this referral, again, both referrals came from my wonderful sports colleagues who identified, like, okay, these need additional workup. So right greater than left shoulder pain and weakness. In a gentleman who had a lot of football injuries. I'm gonna summarize this to essentially say he was convinced he had rotator cuff tears in the past and he was now experiencing more pain in those areas and difficulty with shoulder abduction. And sports was like, yes, you have rotator cuff injuries, but what you're presenting with doesn't exactly fit what we would expect. Physical exam, the key highlights. He had bilateral pec atrophy and pec folds and some scapular winging with limited shoulder abduction. Again, because we tend to get a lot of second referrals, he had a prior EMG not long ago without any evidence they wrote of cervical RIDDIC, plexopathy, large fiber neuropathy, or myopathy. So on this algorithm, I'm gonna highlight the fact that MSK disorders is in this. This updated slide or slide set removed a slide that I had on here. So Muscle & Nerve recently published a monogram on MSK RIDDICs, mimics of RIDDICs. So I encourage you to look over that. It is 42% of cervical RIDDIC questions end up having an MSK diagnosis and sometimes they're concomitant. His motor and sensory exam findings look great. And then when we look at the EMG, I'm gonna highlight that he has some early recruitment, some small units in one muscle. And so we ended up calling this a non-irritative myopathic process. And looking at his particular physical exam, so when it comes to myopathies, a lot of times you are basing it based on your history and physical exam findings. And so based on the constellation of his symptoms, we sent off genetic testing for FSHD1, which came back positive. So the things I wanna highlight in this case is, again, EMG is driven by your physical exam, right? And his diagnosis was driven by his physical exam. That's how we knew how to target what genetic testing to test for, because FSHD is not on a panel testing. Also recognize that subtle myopathic findings are sometimes just early recruitment. So it can be very easy to miss. And a lot of times we do get EMG reports that say no myopathic-looking units in our patients that we end up diagnosing with myopathies. And ultimately, the goal of EMGs is to aid accurate diagnosis, treatment, and management. So thank you for bearing with me through those two cases. Thank you, Dr. Ratt. We already introduced Dr. Hearn, so we'll just jump onto the next talk and keep moving ahead. And then we'll watch time. If there's a couple minutes here, we'll aim to take a few questions and then do the third talk, okay? So take it away. Thanks, Dr. Frantz. All right, everyone, let's get going. Let's talk about electrodiagnosis in the setting of gait difficulty. So how do we localize a lesion? Where does that localize when someone comes in and says, hey, doctor, I have trouble walking? Well, it's kind of a trick question, isn't it? There's not just one spot. There's not just one part of the central or peripheral nervous system that's responsible for difficulty walking. So that means we need to move through a process of localization. As we pull up, I'm gonna take us through some of the areas of the central and peripheral nervous system to which some of these lesions could localize and share a few tips on thinking about, okay, about thinking about where these lesions could be. Quick question for you. If I pull up on my own laptop, can we just switch those two computers out? Is that equivalent? One thing that I like to keep in mind as an electrodiagnostician is, I think we learn pretty early in training that electrodiagnostics doesn't help us too much with the central nervous system, right? We don't really see the details of the brain or the spinal cord or the psyche, the mind, those elements. We also don't see most musculoskeletal disorders. If someone's really having trouble walking because of gluteus medius tendon-related pain, that's gonna be a normal electrodiagnostic study. But one of the things I enjoy working through with our trainees in the lab is that we don't wanna throw out our clinical radar for those things. My first slide says, beware the ghost of electrodiagnosis when it comes to walking and walking trouble. Even though our nerve conduction studies and our EMG needle won't show us that it's the brain or it's the gluteus medius tendon, thank you, or any of those things, it could still be those things. Because electrodiagnosis is an extension of the physical exam, when those things are the culprit and we can tease those things out, it helps us with our interpretation of our normal study or a normal study with decreased activation. And that in and of itself can guide patient care immensely. So that's something I would want to keep in mind. Okay, here's our localization slide. There's the ghost. I know we're a little bit past Halloween, a little late for Halloween, but know that the ghost of electrodiagnosis, can you still hear me? Yes, is the mind or the psyche, the central nervous system, meaning brain or spinal cord, and the joints, muscles, and bones, the biomechanical stuff that we do so well as physiatrists. What else? Well, gait is a multifactorial thing, right? Impairment stack. So if you think about those eight boxes that I had on the previous slide that had both central and peripheral nervous system components and muscles, and you throw them all together, well, the reality is if you've got multiple dysfunctions in those systems, impairment stack. And sometimes the patient with a gait abnormality that we're evaluating actually has several of these different things going on. Now let's consider a way of localizing things through three lenses. So one is the pathophysiologic process. Number two is the sensory involvement, both clinically and electrophysiologically, how those things can create a clue for us. And then the third is the pattern of involvement, body region. And then what we'll do is apply these to cases. I'll take you through a few interesting cases of patients I've seen who have come in with a problem of trouble walking. So pathophysiologic process, here are eight localizations again. You all in the room probably are familiar with which one of these are neurogenic, right? This probably feels pretty good for you all, that disorders of the peripheral nervous system, the plexus, the nerves, the nerve roots, and the anterior horn cells of the spinal cord. Disorders there will show up as neurogenic findings. Here are positive sharp waves, fibrillations, decreased recruitment of motor unit potentials that might have re-innervation changes. Neuromuscular junction disease and muscle function, those things will manifest differently. We'll see repetitive nerve stimulation abnormalities. I shouldn't just put decrement, it could be increment depending on what the disorder is. And muscle disorders will present as a myopathy, as Dr. Rad has already shown. And then we have our ghosts, right? And these will just show maybe varying degrees of decreased activation, right? So important to learn to distinguish the difference between decreased recruitment and decreased activation so that we can see where that weakness localizes. Okay, so that's localization by pathophysiology. The sensory involvement. Out of all eight of these boxes here, there's only one box where both clinically and electrophysiologically we have an abnormality, right? Which one is it? This one, right? Peripheral nerve, peripheral nerve processes, people will have sensory nerve abnormalities on the electrophysiologic study, and clinically they'll have some level of dysesthesia, numbness, sensory loss. You know, the exception of this would be if you really have involvement of an effectively motor-only nerve that does not supply cutaneous innervation. Everything else is a little different, right? If you look at the disorders here in gray, these are our motor-only disorders, right? Motor neuronopathy, neuromuscular junction disease, disorders of the muscle. These things will not have a sensory symptom set. They will not have sensory nerve conduction study abnormalities. And then the other things are a little bit variable. They will not have sensory nerve conduction study abnormalities, right? But they may have, well, I should point out this particular box, the nerve root lesions will have electrophysiologic abnormalities seen in the motor system. Okay, so that's that box there. And then the other three, that one, that one in the bottom, those are our ghosts again, right? Those are completely normal studies. So now when we overlay thinking about the sensory system with thinking about the pathophysiologic process, we can really see, all right, are we seeing this pattern of sensory and motor and electrophysiologic abnormalities here? Are we seeing the sensory looks fine, but the patient doesn't feel fine? And then the peripheral nervous system from a motor standpoint is hit, that's this box. Are we seeing our motor-only disorders? Lastly, we can think about localization by body region. What area of the patient's body is most affected? We can think about processes that are primarily distal, like a neuropathy. I was thinking through Dr. Rad's thought process as she was presenting that case, and I was thinking, is there length dependence? Is there length dependence? You can think about a proximal, predominant proximal pattern. That's our classic myopathy pattern for many but not all myopathies. What about the disorders of the brain and the mind or when someone's hip hurts and so they can't walk? How might that present from a regional standpoint? I think those often present as a regional type of complaint. People may say, hey, I don't feel right around here, my hip, or I'm numb from the knee on down, regional. Then we can have myotomal, or dermatomal or myotomal findings, right? Root-related by root level. So that's thinking about localization by body region involvement. All right, let's apply things and take a look at some cases now. Case one is a 67-year-old gentleman with rapidly progressive weakness. He was admitted to the hospital five days ago with no pain, but so weak that he can't walk and can't take care of himself at home. There's some vague paresthesias in the hands and feet. Looking back a little further through his history, four months ago, he was treated with chemotherapy and radiation for cancer, and shortly thereafter, he began to notice forelimb weakness. He progressed from ambulating independently to needing a walker, having frequent falls at home even with the walker, and ultimately started physical therapy. Weakness continued to progress and started to involve his hands, losing fine motor function in his hands. Yeah, that was about two months ago, and with this gradual progression and decline in function, he was ultimately admitted to the hospital. On examination, we see a flicker of movement for toe extension, ankle dorsiflexion, and knee extension. Three out of five strength for ankle plantar flexion and finger abduction. Okay, so we're in both the lowers and the uppers, there's weakness. Four out of five for thumb opposition, wrist extension, hip flexion. Five out of five for biceps, triceps, deltoid, proximal uppers. The right upper limb is slightly weaker than the left within these grades. Sensory exam has diminished to vibration and in all four limbs distally and preserved at the face and shoulder. And reflexes are absent in the lower limbs. Triceps and biceps and brachioradialis are all one plus bilaterally. So thinking about this picture as a whole, we're seeing some pattern that could reflect some length dependence. We're seeing some signs of sensory involvement. Let's take a look at his study. So this is someone where I might start with a nice, simple, distal lower limb study. Let's take that SERL. On the right, we have a latency of 4.3, amplitude 4.1, conduction velocity 41.2. Let's see what the motors look like. Here's his deep perineal motor. Latency, 8.6 milliseconds. Amplitude, 0.7 millivolts. No conduction block that's clear across the leg, but we have a very slow conduction velocity at 23.6 meters per second. Better get another nerve. Here's the tibial. Latency, 8.9 milliseconds. Amplitude, 0.5 millivolts. I'm curious about a nerve segment that'd be slightly more proximal, where there may be still some better axonal preservation to see whether there's still significant slowing. So let's take a recording over anterior tibialis, so another deep fibular study. And this one shows also a low amplitude and a conduction velocity of 15.4 meters per second. Granted, this is across the fibular head, this is across the knee, but we have to interpret in conjunction with the total pattern that we're seeing. We can go to the other side, see if there's some symmetry to this process, and there is. We can move to the upper limb. Here's an ulnar motor study. Very long latency, five milliseconds. Amplitudes are low, and conduction velocities are slow, not only across the elbow, but also across the forearm. And because this amplitude is so well-preserved, it's not normal, but it's relatively well-preserved and clearly recordable, we go ahead and grab an F-wave, and we're at 45.2 milliseconds. All right, that's about 150% of the upper limit of normal. That's very slow. We can take a little bit more sensory data, see if there's any signs of sensory abnormalities, and yeah, it's not great, there might be. The other note here is that the distal compound muscle action potential, or CMAP, durations were all very long, all greater than 10 milliseconds in duration. So we take a look at the EMG for this patient. Anterior tibialis shows positive sharp waves and fibrillations, decreased recruitment of motor unit potentials with normal morphologies. This is someone whose weakness has progressed on the order of months, so he may well be in a phase where we're not seeing re-innervation by collateral sprouting yet. This is an early process, and this is a quick process. We take some muscles innervated by other peripheral nerves and other myotomes, and we also see abnormalities in the gastrocnemius. We can move up to tensor fascia lata. We see significantly decreased recruitment, still fibrillations, relative sparing of vastus medialis. We can check the lumbar paraspinals, and they're fibrillating. We can move up to the hand. Are we seeing a length-dependent process? Well, distally in the upper limb, it's also abnormal. And when we move a little further approximately up through the upper limb, there's deltoid, things are much closer to normal. So putting together the puzzle, electrophysiologically and clinically, what is the process? And we said, let's look at process, let's think about sensory, let's think about region. The process here is a demyelinating disorder. We're seeing fairly widespread demyelinating findings. From a sensory standpoint, there are clinical signs and symptoms, and there's probably electrophysiologic abnormality, even though it's not as pronounced as the motor. And then regionally, the patient complains largely of distal abnormalities. There's some evidence of proximal involvement as well. We have the lumbar paraspinals, the tensor fascia lata. So I'd say we have a neurogenic demyelinating process. There's sensory involvement both clinically and electrophysiologically. It's largely distal, but there's some root involvement. Remember the P for CIDP is a polyradiculoneuropathy. CIDP affects the nerves and the nerve roots. And so we have this set of findings. A subacute or early, because there's no reinnervation yet, chronic, early chronic, motor predominant polyradiculoneuropathy that is predominantly demyelinating with evidence of secondary axonal loss compatible with CIDP. Motor nerve conduction criteria for CIDP were updated in 2021. Would encourage you to use the newer guideline set if you have not seen these yet. Note that point G refers to this distal C-map duration. So the duration of the distal C-map, and I'll show this on the next slide so people can see what this looks like. In A, it's normal. And B and C are both patients with CIDP. This is from a paper by Isos et al in 2009. And you can see in example C, it happens to be a complex C-map with multiple negative peaks. And so in taking the duration, you start from the onset of the deflection to the return of the last negative peak to baseline. Okay, that's how you measure distal C-map duration for someone with a complex distal C-map. And that is called dispersion when it's long like that. And it's relatively specific for the demyelinating neuropathies. So teaching highlights from here. What atypical features do we see? Demyelination, motor predominance, non-length dependence, right, all the way up to tensor fascia latae on the paraspinals. A subacute time course with a normal motor unit morphologies. Role of the F-wave. The F-wave checks our proximal nerve segments and it checks that we have a normal motor unit morphology. And it checks the nerve segment along a long path. So if there's patchy segmental demyelination, the F-wave study is more likely to find it. And then we saw some hallmarks of acquired demyelination. The non-uniform slowing of conduction velocity. Some velocities were normal, some were 15 meters per second. Conduction blocks this patient did not have so much. And then that distal C-map dispersion I showed you from a paper. Next one. 69-year-old lady with chronic left foot drop presents with three to eight months of new gait difficulty. She has a complex past medical history. She had a left thalamic hemorrhage four years ago, resulting in right hemiparesis that improved to the point that she was ambulatory. Then she has a chronic left foot drop, and when I ask her, she says none of her doctors have really ever figured it out or told her why she has this foot drop, but it's old. It's been more than four years, and at the time of her stroke, she already had it. She also had a right total hip arthroplasty. This was the most recent piece. This happened eight months ago, and it's around that time that things started to get worse to the point that she's falling weakly. These falls, I ask her, what's going on? Are you tripping? Are you losing your balance? She says she has a sense of lower limb fatigue, like her legs aren't going to hold her up anymore, and she knows she has to sit down. If she's able to sit down, everything's fine, but if she doesn't sit down, she may fall. She's only symptomatic when standing and walking. If she's sitting in a chair, lying down, it's just like before. There's not any sense of heaviness or numbness or tingling. A little bit of episodic back pain. It does radiate a little to the right thigh, but it's not temporally aligned with her falls, and there are no paresthesia, sensory loss, upper limb weakness, dysphagia, or dysarthria. On exam, she's quite weak for left ankle dorsiflexion, less than two out of five. Other muscle groups are largely grossly full. I thought she was a little bit on the weaker end overall for age, but not to the point where I could feel that one particular set of regional muscles were weaker than the others. She has a steppage gait bilaterally, wide base of support, increased lumbar lordosis, and if I have her get down on the floor, she had a lot of trouble getting up off the floor. She can't do a heel walk, but she can get up on her tiptoes. Sensory exam's normal. Reflexes are traced at the knees and absent at the ankles. Well, here's her set of nerve conduction studies. We won't go through the table, the animation this time, but what you'll see for her is, just like her clinical history, her sensory nerve conduction studies that are relevant are normal. Her motor nerve conduction studies are also almost normal. These are some pretty good CMAP amplitudes overall. The anterior tibialis are maybe a little bit low relative to the tibial and the deep perineal motor. It's a little strange to see those potentially being a little low at 2.6 when the deep perineal motor are so good at the EDB, but that's subtle, that's a soft call. That's something that gets my eyebrows up, but I wouldn't pin a diagnosis on that. So, here's what we see in her anterior tibialis. Sorry, this is voluntary activity, I should say analysis of voluntary activity. I ask her to dorsiflex her foot. We see early or rapid recruitment of motor unit potentials with low amplitude, short duration, and polyphasia. What's that? It's a myopathic process. So this is her overall spread of findings. What you can appreciate is a little bit of increase in social activity, brief myotonic-like discharges, and then myopathic findings in some muscles, especially the anterior compartment of the leg, anterior tibialis, and it's bilateral. Okay, so overall putting things together, the process is myopathic, the sensory involvement is none, and the region is largely distal, which is weird, which is weird for myopathy. Okay, so we went ahead and called that, and further workup yielded a mildly elevated CK and a biopsy with some mild myopathic changes, and ultimately genetic testing revealed a type of facial scapulohumeral muscular dystrophy type 1. Last case, I'm going to go really fast, Dr. Franz, I promise, and we'll save questions to the end. Last case is a 69-year-old gentleman with several years of progressively impaired balance, presenting with five months of new plantar foot numbness and perceived lower limb weakness. He has difficulty maintaining balance when playing golf and when rising from the floor. Occasional finger paresthesias, no changes to his usual chronic axial low back pain. His strength testing is completely normal. His muscle bulk is normal. Vibration is diminished to light touch in a stocking distribution. Vibration is markedly diminished, not palpable at the knee or ankle. Reflexes are 2-plus in the upper limbs, brisk at the patellae, absent at Achilles, Hoffman's is negative, and plantar response withdraws. There's some slowed coordination in the hands and feet, Romberg is positive, and his gait shows decreased ankle movement, increased lumbar lordosis. Here's his study set. Here we see sensory nerve conduction studies that are, again, normal, relatively normal. We have motor nerve conduction studies. The left deep perineal motor study doesn't look great. Looks like it could be axonal loss pattern. The other studies look okay. And here's the EMG. Little bit of increased insertional activity in two leg muscles on different sides. Little bit of larger units in the anterior tibialis. What are we looking at? This person's having all this trouble, decreased sensation. That's his EMG. It's way too good, right? That's way, way too good for that clinical presentation. So this process is either nothing or something central. Sensory, it's clinically involved, not electrodiagnostically involved, and the region that he's complaining of is distal. Okay, so this is one of the three ghosts. Communicate, right? So here's an email. Thanks for referring to this study. He seems to be experiencing progressive decline with a relatively normal EDX of peripheral function. I wonder about myelopathy versus something central. Further workup. MRI showed a Chiari malformation with tonsillar herniation and a large cervical syrinx extending down to C4-5. He ended up getting a suboccipital craniectomy, decompression, and that was underlying his problem. So take-home points for this section, electrophysiology as it pertains to gait. Number one, don't lose sight of the invisible, the ghost that electrodiagnosis doesn't see, the mind, the CNS, the musculoskeletal disorders. We saw that in case three. Number two, gait is a complex process, multiple impairments stack, and sometimes someone with a mild, slow-grade myopathy or muscular dystrophy, something else happens, the hips, the stroke, it tips them over the edge functionally. And then number three, this process of thinking, the pathophysiology, the sensory involvement for clinical versus electrophysiologic, and then the pattern of body region involvement. And I'll stop there. Thank you. All right. Well, we're off to a great start, and I'm going to introduce our last speaker, and then we'll have some time for discussion at the end. Dr. Attaway, I don't think I did you any favors here after following those two talks. But believe it or not, I want to introduce Dr. Attaway to you as a rising star in our specialty. She is a physiatrist, a scientist, and also someone who's recently completed a neuromuscular medicine fellowship. She's trained in biomedical engineering during her undergraduate at Harvard, followed by many, many, many years at Northwestern for MSTP, MD, PhD. She actually worked with a well-known physiatrist named Todd Kiken for her PhD, residency in physical medicine, and then was in the neurology department at Northwestern for her neuromuscular fellowship. Her research interests include the neurocontrol of movement, biological signal processing, neurophysiology. And more recently, we kind of dumbed her down so she could do some projects with us on motor units, and particularly like motor unit health after spinal cord injury. She's been supported by the Foundation for PMNR, who's awarded her the Richard Matterson New Investigator Research Award just actually at last year's meeting, and her project was on motor unit number estimation in spinal cord injury. And I think you'll see that with the clinical and research pedigree, it makes her a perfect person to present on this interesting topic about nerve transfer surgery for cervical spinal cord injury, the importance of electrodiagnostics for assessing lower motor neuron health. Thank you. Thank you for that introduction. I'll try to make my predecessors proud. All right. First let's make sure this works. Is there a pointer? Click once on the screen. I wasn't, I was just using the slide. Oh, okay. No pointer. That's okay. All right. Let's begin. So excited to be here with you guys today. I have no disclosures. So for my talk, this really isn't designed as a step-by-step approach to electrodiagnostics in people who have spinal cord injury and are potential candidates for nerve transfer. But I just want to leave you guys with some key points to consider. And so let's just delve right in. So let's say there's a 22-year-old male, 10 weeks after a traumatic injury. He's a C5 Asia A and presents to your EMG lab after your colleague notices that he's got some asymmetric weakness on his admission Asia exam and is wondering, is there something else going on? Because he doesn't typically see that. And so you notice that on his left side, he's notably much stronger distally compared to his right side. And so how do you approach this? What diagnosis do you think could be going on? And so given that you are a great physiatrist, given his mechanism of injury, you think, hey, maybe there's some nerve root avulsion going on on that side that could be causing his asymmetric weakness. Maybe he has a traumatic plexopathy on that side. Perhaps there is some other asymmetric neuropathy going on. But could this also just be part of his injury? Could this be lower motor neuron involvement of his spinal cord injury? And so classically, when we think about spinal cord injury, here we've got this image of a C6-C7 dislocation. At that level, you have a mixed injury presentation, right? Injury to both the descending cortical spinal tracts as well as the cell bodies, so the lower motor neurons. Above that level of the injury, presumably these are normal segments. And below the level of that injury, there is no descending information from the upper motor neurons. But the cell body should be intact. And so lower motor neurons should be intact. And then just to demonstrate that a little bit more on that right image here, so at that point of injury, if that lower motor neuron there is intact, right, that remains attached to your muscle and you don't get atrophy. But with an injury, let's say there's damage to that, you lose that motor neuron. And over time, you get denervation atrophy, which is distinct from disuse atrophy, in that over time, denervation atrophy after about 12 or 18 months is irreversible. And that's an important point that I'll get to later. So some work by Christine Grumbles, sort of pivotal work in this field, where she looked at what happens in the spinal cord post-mortem in individuals with chronic spinal cord injury. And so just to walk you through this, if you look at the images on the right, and so here in A, okay, excellent, you can see that, is what a normal section looks like, right? You can see your white matter tracts and your gray matter. B, C, and D, which are sections from the epicenter of the lesion at the lumbar, thoracic, and cervical segments, respectively. You can see, obviously, just the decimation of the architecture of the white matter and the gray matter, not surprisingly. And now if you look at E, this is a stain for the large, for malignant fibers within the spinal cord. And here, just for those of you who are not used to seeing these images, is what a normal section should look like. You can see those large malignant fibers, right, your alpha mononeurons. In E, you can see that, oh, you can't see these fibers anymore, right? And this is a section from the epicenter of the lesion, not surprising. What's interesting here in F, this is a section taken from L1 in an individual who has a T9 injury, right, so four segments below. You see some malignant fibers. They're mostly small, right, not large. But it's not normal. It doesn't look like what normal is. And so you're not just seeing these lower motor neuron damage at the level, we're seeing it multiple segments below the level of the injury. And so she went forward to quantify that, right? And so here in this figure, where your y-axis is the percent of uninjured mononeurons, and E just stands for the epicenter of the lesion, you can see that not only do you have loss of those motor neurons at the epicenter, but also further away from that epicenter. And so now obviously we can't look at post-mortem sections in our individuals with spinal cord injury. What can we do? Well, as you guessed, electrodiagnostics, right? So some work by Michael Berger out in Vancouver, where he looked at people with chronic spinal cord injury, so similar population, right, but looking at a hierarchical approach to abnormal motor neuron, lower motor neurons, where he looked at both C-MAP abnormalities, so it was, is the C-MAP there? Is it not there? And if it is there, is it normal or abnormal? And also looked at evidence of abnormalities using EMG, specifically looking at spontaneous activity, right, because you can't look at voluntary activity for these muscles below the level of the injury. And found evidence of abnormality in 87% of the muscles that he looked at. And this was done in 10 subjects. And so some of the work that I did, similarly, but looking at sub-acute, people who are, you know, earlier on after the injury, and if you look at the table on the left, we even had some individuals who were just a, you know, four weeks out to eight weeks out of their injury. And despite that they were so sub-acute, we still saw evidence of lower motor abnormality in this population. And so we saw that in 90% of subjects, 47% of them had abnormal C-MAPs. And, you know, of the people who had abnormal EMG, 90%, 14 of those individuals of the 19 had abnormal spontaneous activity. So we're seeing these changes. We've seen them post-mortem. We're seeing them in people with chronic spinal cord injury. And now we're also seeing it sub-acutely after a spinal cord injury. And then we went on to do a retrospective study looking at 37 individuals over 60 limbs, kind of similar to what, you know, Christine Thomas did looking at what does that look like at the epicenter and also downstream from that epicenter. You would think that you wouldn't see changes far from that. What you see in this figure on the right where this red there is the neurologic level of the injury, we see abnormalities not just at that level but one, two, three, four, five segments below in a significant percentage of individuals. And so this drives home the fact that it's important. One cannot assume that you won't have low motor abnormalities below that neurologic level of the injury. And why is this important? Why should we care about this, right? Because, you know, clinically when we do that ASIA exam and you have your strengths, we don't distinguish clinically if that weakness is from upper or lower motor neuron damage. And why is that important? It has several implications, but I want to focus today on nerve transfer surgery because this has implications for that. And for those who are not familiar with that, I'll just go through it briefly. So this is a procedure that's been described as early as 1948. Initially was developed for managing brachial plexopathies, right? And so the idea is that if you have an injury, let's say we take a brachial plexus injury to a peripheral nerve, which results in denervation of the muscle. What you can do is borrow from an intact low motor neuron, ideally something that's redundant, right? And so you don't lose strength from the donor. And then moving it to that paralyzed muscle, right? And so that allows you to sort of recover the strength and reinnervate those muscles. And so similarly, in a spinal cord injury, it's a similar idea, except now that injury is within the spinal cord, but you're still bypassing that injury. So now you've got information above the level of the injury and are able to voluntarily activate muscles below the level of the injury. That's something that's sort of just beginning to be done in different institutions across the U.S. And so putting that together, right? So why is that idea of that lower motor neuron important? And in this figure here, you can see that at the lesion, you have that mixed upper and lower motor neuron damage, which causes denervation and denervation atrophy. Below the level of the injury, if it is intact, if that lower motor neuron is intact, there isn't this idea of a time sensitivity to doing this procedure. If you imagine if it is not intact, right? Which means that it will eventually denervate and get atrophy. Now there is some time sensitivity to having that patient be evaluated by surgery and given and have surgery. And so to talk about a little bit more about what's commonly done with that surgery and what improvements one can get. So if you have a patient say with a C5, C6 level and you want to restore elbow extension, a common donor is the axillary branch to the posterior deltoid. And then you can transfer that to one of the heads of the triceps, remaining with the other triceps, with the other heads of the deltoids intact, right? So you're not losing shoulder abduction. If you want to restore wrist and finger extension, one can take the axillary branch to teres minor or the radial branch of the supinator to attach it to the posterior interosseous nerve, which as we know, allows us to do our wrist extension and our finger extension. And if you want to do wrist, finger and thumb flexion, common donor sites are the musculocutaneous branch that would normally go to brachialis or the radial branch that goes to your extensor carpi radialis brevis. And then reattach it to the anterior interosseous nerve, right, to give us that thumb flexion back and finger flexion back. And so the idea of that time sensitivity is important in terms of what this graphic demonstrates. With a purely upper motor neuron lesion, right, there isn't that time constraint. With low motor neuron lesion, so let's say in a brachial plixopathy where there's no upper motor neuron component, there is a time sensitivity. And where it's mixed, right, we still have that. This is what we know. We currently think that, you know, six to nine months is a good time. After 12 months, you are getting that denervation atrophy and, you know, time is running out. And so when you're doing your electrodiagnostics, what do you do, right? Typically we'll do our five nerve study with our three sensories, median, radial, ulnar, and our median and ulnar motor studies. And so what we found, what we found is that for the axillary to radial transfer option, right, it's important to look at your median snaps or your sensory potentials, right, because you want to make sure there is no other, nothing else going on, like a concurrent brachial plixopathy, right, or other lesion, to confirm that this is a pure low motor neuron involvement. For the supinator to pin transfer, it's good to avoid doing the ulnar snap at D5 because this can be abnormal in an ulnar neuropathy, right? And so you, it's, and so we avoid that. Oh, no, we avoid that because you will, again, you want to make sure that this is a low motor neuron. And so it's a, we think it's, you know, it's better to do your, your median endocubital cutaneous nerve, right? Because that's not commonly injured. And similarly, you'd want to evaluate that with a brachioradialis ECRB transfer option. And so just put that all together. Let's look at a case together. So again, same 20-year-old, 10 weeks from his injury. He's a C5 AJA coming to you for a nerve transfer. And for him, and so here, pretty good proximal strength, not much distal strength. Left side is a little bit worse than the right with two out of five strength in his wrist flexors. And so for him, what's important to restore, right? This is important when you're planning the study because each study should be designed for what the patient needs, right? And there is no sort of cookbook. So for him, finger flexion is important, right? Finger extension is important for him to be able to grab. And so when you're doing your electrodiagnostics, you want to focus on that. You want to focus on the muscles for that and also focus on the donor sites, right? And so you're working with this surgeon to figure out what muscles you want to do. And so let's take a look at his study. I think that's big enough to see. So as you can all see here, if you look at his motor studies for his bilateral distal C8 T1 muscles, so his APB and his ADM, no responses, right? Completely no responses. And this again is an individual at the C5 level, right? And we're seeing no responses at C8 T1 muscles. We look at his sensory studies and those are relatively intact, right? They're pretty normal. And so we have this picture where again, motor is affected, sensory is not affected, right? And so that's painting sort of this lower motor neuron problem picture. And so let's look at his EMG study. And from the get-go, you notice that this isn't your typical radiculopathy five muscle screen, right? This is designed for what we're looking for. We want to look at his potential donors. So I highlight that there. His brachioradialis, remember I said, the musculocutaneous branch to brachialis is a potential donor site. So you want to make sure to needle that, right? Because you want a healthy donor. And so here highlighted in green, we see that's pretty normal, right? On the right side and on the left side. We also look at his supinator because that's a potential donor site to reinnervate the pin, whereas brachialis is a potential site to reinnervate the AIM. And so those are important to look at when you're doing, in this particular study. And as I mentioned, again, important to look at your recipient. Because, and look at, is there evidence of lower motor abnormality? Are you seeing fibrillations? Are you seeing positive sharp waves? Now obviously, when you don't have the actual motor units because you can't voluntarily activate, you can't really look at the motor units there. And so here, the fibrillation and the positive sharp waves and increased insertions do give us evidence of lower motor neuron abnormalities. And so we see, we focus here on, again, those finger flexors and his extensors. So he's EPL, FDS, FTP on both sides. Interestingly enough, his extensive digitorum communist doesn't have much in terms of spontaneous activity. It looks pretty good with his, it looks pretty normal. And so here we see a mixed picture, right, where some muscles have lower motor neuron damage and some are pretty normal. We have a mixed upper and lower motor neuron picture. And so for this individual, he ended up getting a bilateral brachialis to AIN, an FDS, right, to restore his finger flexion. When he came for, when we came for surgery, he actually had recovery of his right finger extensors. And so they did not do that surgery and focused on that left side. And he got that supinator to pin transfer on his left side. And so this case will illustrate that, you know, doing electrodiagnostic is important for distinguishing that upper motor and lower motor neuron patterns of injury. And so I hope that I've convinced you that, you know, lower motor neuron degeneration is important in spinal cord injury. It's an important problem. Implications for prognosis, for potential reconstruction, and designing the best treatment options for your patients. And with that, I'll end and take questions. All right, I guess the panel can take questions and we have some microphones there so you can have a seat. And if there's any questions out in the audience, I don't see any online. I'll start off with a question though. So, Dr. Attaway, you have a study on motor unit number estimation. You didn't talk at all about that technique, but it's, tell me why would you, how would you use that in a spinal cord injury patient? And we'll take that. That's a great question. Is this on? I think it is, okay. And so, I don't know if you guys recall. So, I mentioned that below the level of the injury, you can't really assess the units themselves, right? Does that make sense? Because you can't voluntarily activate it. How do we assess the units? And so, some of the things I'm working on is can we actually electrodiagnostically assess the units? And so, Dr. Franz brought up this idea of motor unit number estimation, which is the idea that using conduction studies at the surface, so this is not needle EMG, right? We can elicit single motor units at the surface, look at the CMAP, right? So, look at the total compound muscle axon potential. If we are able to get a sample of 10 to 20 individual units, right, by stimulating across the nerve, right, proximally and distally, right? And remember, with an axon potential, it's all or nothing, right? And so, you stimulate at very tiny, low potentials. And that first response is that one unit, right? If you get it and it's repeatable, it's that one unit. Remember, the all or nothing. And you stimulate somewhere else, you find another response that's a different morphology, right, that's repeatable, it's a different unit. And so, if we get a sample of 10 to 20 individual units, we have, and you have the compound muscle axon potential, we can actually estimate how many motor units there are, right, simple division. And so, that gives us an idea, right, of how healthy that nerve is, right, in a muscle that we couldn't activate because that patient has a spinal cord injury. Great, and we have a question here, so let's. I have a few, but cut me off at the second if somebody else comes. For the last lecture, sorry, I can't get your name. Oh, that's okay. Back when I was in training many, many, many years ago, they spoke more of tendon transfers. And I guess the trophic, neurotrophic influence of an intact nerve versus a spinal cord injured nerve is helpful. What are the outcome studies in terms of this nerve transplant versus a previous tendon transplant? Do they do better with the nerve transplants? That's a great question. So, there are different indications for nerve versus tendon transfers. Now, with a tendon transfer, you know, they're in a cast afterwards. It's a prolonged rehabilitation, whereas with nerve transfers, not as prolonged. They don't need to be in a cast. And interestingly enough, you know, I brought up the idea of this lower motor neuron injury. What if they do have significant lower motor neuron injury, right? And so what that means is if you do the transfer, it's not gonna work, right? The cable's cut. There's no signal that's going through. And so in those scenarios, then a tendon transfer might be more appropriate. And that's something we're actually looking into, right, is how do we electrodiagnostically now set up a framework to assess people who do better served by nerve transfer and people who do better served by tendon transfer. It sounds like tendon transfer, I'm sorry, nerve transfer would be better because you're having neurotrophic influence on the muscle unless it can't be done. Yeah, unless- That may be what seems to be going. Thank you. We don't wanna start any fistfights here, so we'll just say that, you know, nerve versus tendon transfers, it's a hot topic. It's hard to compare them head to head. And we work for someone who's been involved with tendon transfer work for a very long time. So there's definitely situations where tendon transfers have some advantages. We're not endorsing one over the other here, just to be clear. For a copper deficiency, you mentioned bariatric surgery. Is it more a danger with, let's say, a Roux-en-Y bypass or a gastric sleeve, or both? That's a great question. To be honest, I actually don't know the answer to that. Both have been listed as risk factors in the studies, so I'm not sure if one versus the other. And so the other influence on gastric bypass surgeries is, so the primary reason is the malnutrition, and the compliance with supplementation. So most of those individuals are given copper supplementation. They just have a high number of supplementation and vitamins they have to take. So the real leading factor is not supplementing. How much copper per day? When we follow a protocol where we supplement with like five, three, one, so like milligrams per day. I don't know for bariatric patients what they would do. When you have copper deficiencies, there's a few protocols. And if you don't respond to that, then it's intravenous copper. No one else? All right, I got two more, if that's okay. All right, just in one. The patient who had FSHD1, I mean, obviously that was made from blood tests and also the electrodiagnostic studies, but from clinical presentation, why couldn't he have been scapulohumeral dystrophy? I think we both have FSHD1, so scapulohumeral, so it's the same thing as fascial scapulohumeral dystrophy. It's kind of a subset, though. So this particular patient had the genetic mutation for FSHD1, I'm presuming like the scapular dystrophy of just like a myopathic picture without genetics. Is that the question, just so I better understand? I guess there's a variant of. It's not FSH, but maybe a variant which is scapulohumeral without the face being involved particularly. And I'm just wondering, maybe this is a genetic variant where it just didn't show the face yet. Right, and within FSHD1, you can have patients not have facial symptoms, and they would still be categorized as FSHD. Oh, sorry, I apologize. I thought you meant without a genetic mutation. Yes, and I think Dr. Hearn's case also brings up another unique presentation where eventually, the most common presentation for FSHD that we see is most patients come in complaining of shoulder weakness, and then you'll find subtle facial. And then later on in their progression, the anterior compartment of their leg, which is Dr. Hearn's patient had the foot drop presentation but all of those subsets would still test positive for FSHD1. So it's kind of a variant but has a gene. Right, they all fall in the same gene. There is an FSHD type two, which has a different genetic mutation. And here's the dumb question. I've never heard of progressive muscular atrophy. Is this a so-called benign form of ALS or is it a rendition? No, PMA is a form of ALS. So unfortunately, these individuals do continue to progress. We think of ALS as a spectrum. And so on the more lower motor neuron predominant is PMA. And then on the only upper motor neuron predominant is PLS. And I think PLS probably gets more attention. And then when we initially diagnosed somebody with PMA or PLS, we pay close attention over the next five years because they may develop either, so for the PMA patients, they may go on to develop upper motor neuron signs and convert to a true ALS and vice versa for PLS, they may go on to develop motor neuron signs. Unfortunately, for all of those spectrums though, the disease will continue to progress. Thank you very much. Absolutely. All right, well, I'm getting the sign. We're gonna have to give up the room. This was a great session, wonderful talks and thanks everyone for coming out. And please fill out the survey. We appreciate any feedback you have on our session. Thank you.

electrodiagnostic approach

evaluating patients

walking problems

neuromuscular sessions

learning objectives

mimic radiculopathy

case-based discussion

clinical mimics

EMG

lesion localization

peripheral neuropathy

cervical spinal cord injury