All right, thanks for coming out. Welcome to the session. There's a few announcements. I'll go through the first few, this is too long. I can't read all this. Cell phones and audio or video recordings remind participants to silence your cell phones except for workshops. There's evaluation forms. Please complete them at the end of the course. It's really helpful so we can do a better job with our sessions. This year, I'll just point out, we are also part of the neuromuscular EDX community, and last year there wasn't so much. And we made an effort as our group to kind of get a little bit more into the meeting this year. And there seems to be a lot between the ultrasound of peripheral nerves, EDX, and some of the neuromuscular sessions. So your feedback does make a difference, and I think it influences what's in the program for future years. And I guess what we're gonna do, we're gonna really do this in a case-based format today. So we'll hold the questions and the discussions of the cases, at least at kind of a broader level to the end. But if there's immediate questions, for example, if there's a question about the localization and someone wants to wave or yell out, we'll repeat whatever we hear, and if there's a pause and there's no response, we'll just keep going. Cuz it is hard to do the cases in such a big audience, big format, and really expect a consistent participation. Our focus today is gonna be on neuromuscular complications on the neurorehab unit. And we're gonna really highlight EMG, electrodiagnostics, and ultrasound as it can help navigate our way through some of these complex presentations. I'm Colin Franz. I'm at Shirley Ryan Ability Lab in Northwestern Chicago. My partner here, Dr. Attaway, is also at Shirley Ryan. We were able to kind of put this together when asked with sort of short notice. So we usually try to get people from all over the country to join us on these panels, but we made it work together. And both of us have one thing in common anyways, in addition to being in Chicago, we're both neuromuscular fellowship trained physiatrists, which is something that's still in need of support from our colleagues, because what I see out there in the community is, although we are allowing physiatrists to do these fellowships, I see consistently now the last few years, zero job postings that are asking for anyone at the neuromuscular fellowship training at any of our physiatry hospitals, including our own. So a lot of us are coming out of fellowship and doing a lot of leg work. You'll see a few examples of maybe why we're kind of helpful to have around your hospitals, okay? We're gonna go through some background on some of the complications. Keep it sort of brief, because we wanna get through some cases, which I think will be the fun part of the session. And of course, the question and answer, there should be some time to hear from you guys at the end of the session. Peripheral nerve injuries and trauma in general is how I thought I'd start with. So we know from a few key studies that peripheral nerve injuries are diagnosed about 1% to 3% of people with trauma that present to the emergency room. People who are undergoing TBI rehab are at more risk than just the typical trauma patients. So when you do studies, including pediatric studies, there's about 7% to 34% of patients have been diagnosed with peripheral nerve injuries in addition to the traumatic brain injury. So it's something, I joke with some of my partners at the hospital, is I haven't had a referral for an inpatient EMG from a TBI patient that hasn't been massively abnormal. And if everyone is abnormal, I'm assuming that means that we're not referring enough patients for electrodiagnostic evaluation. It's super complicated sometimes to sort these presentations out, so the electrodiagnostics can be really useful. Spinal cord injury, not just acute, but in the chronic setting, is notorious for entrapment mononeuropathies. Carpal tunnel syndrome is very prevalent, cubital tunnel syndrome, particularly in our tetraplegic patients who are resting their elbows and often lack protective sensation. When you, we see them in the context of nerve transfer surgeries, which I'll mention in a second. So when we do electrodiagnostic studies from then, they're usually predominantly preganglionic, except it's hard to get ulners if they had their spinal cord injury for more than a few months because of the tendency to have compression of the ulner at the elbow, if you're not looking out for that. And it's often asymptomatic in those patients. And you can see that this is, these are much greater rates than the general population. On that point about nerve transfer surgery, first of all, let me point out before I get into this, that Dr. Attaway already did like a very nice session on this at our neuromuscular update presentation earlier this week. So if you guys access the recording, you can hear a little bit more about it. But what we basically are emphasizing here is more and more for tetraplegia when we're looking at restoring arm functions. We have options to use nerve transfer surgeries that were developed for brachial plexus injury to help restore functions, give levels of functions essentially below the neurological level of injury. For example, a C5 patient converting to having a C6 or C7 functions with some of these surgeries. Also, tendon transfers, of course. The reason we emphasize the nerve transfer option is because that one tends to be exquisitely time sensitive in a subset, not a small subset, of spinal cord patients who actually lose motor neurons near and adjacent to the epicenter of their lesion. And this diagram here, darn it, shows a lesion epicenter here with just a modest amount of motor unit lost in the adjacent area here, relatively intact muscle bulk. And a pretty ideal candidate here for receiving a nerve transfer, and that can even wait sometimes over a year to be done with some efficacy. In contrast, the patient here with the epicenter actually engulfing those lower motor neurons that are below the neurological level of injury. Hard to examine on physical exam. Often associated with more muscle atrophy, but it's hard to hang your hat on that alone. And these patients, if we don't get to see them early on for assessments, can easily time out. Just like a brachial plexus patient, if they don't get referred, usually within six months, these patients can time out from that window of time where we're able to offer that procedure. They still may benefit from a tendon transfer later. But more and more with the programs that are advertising this possibility, you'll find yourself having to answer questions like, why didn't anyone tell me about this when I was an inpatient getting rehabilitation here? And it turns out that the surgeon's now telling me I'm not a candidate for this surgery that some places are promoting heavily. We do a bit of both, but it's good to think about these things early. And then a little project that sort of came out of just the serendipity or the misfortune of being at the front end of the COVID pandemic, where Chicago was hit fairly early and severely. Is that we noticed that there's a lot of mononeuropathies and multiple mononeuropathies in single COVID patients who are admitted. And some of the early studies, including from our institution, showed anywhere from 10 to 16% of patients were presenting and being diagnosed during inpatient stays, one in the acute setting, a couple in the rehab setting with mononeuropathies, particularly affecting the upper limb. There's a heat map over here of some of the hotspots that we noticed. And often we saw parallels here is the medial elbow here. So for showing where like an ulnar nerve entrapment in here is around the fibular head. So bony compression sites that we know where nerves are susceptible to injury. And when patients were ventilated and often on muscle relaxers, were very vulnerable. And you could see the mechanisms are sort of implied of external compression. And sometimes traction injuries in these patients. In comparison, when we look back at some of our data that we published at the same interval of time or the preceding years of COVID. We actually didn't diagnose entrapment neuropathies very often in other inpatient populations. So it was an order of a magnitude greater. There's a potential for some bias there, but it was still a pretty stunning number. And with that, sort of highlighting some of the things that we're always thinking about and very heavily in this case, I guess some of the, from the nerve side, more so than the muscle side of what we see. But these are the ones that we tend to get recruited in on to consult. We're getting you just a flavor for some of the potential complications before we get into our cases. But there's still a lot more that I didn't cover here. So let's start with the case. And I'll do the first couple and then I'll invite Dr. Attaway up to do a few more. So the first case, Mr. R is a 66-year-old male. He had a PUS, prediabetes, and he was admitted for COVID complicated by a very, actually a very complicated course. Including a pneumothorax, it's gonna be relevant to this case, with an emergent right chest tube. He also had tracheostomy, gastric tube, the COVID pneumonia, the always necrotizing pneumonia, pulmonary embolism. And was managed for a period of time in prone positioning, times three days. He spent 48 days in the ICU on mechanical ventilation, and it took over 200 days for him to arrive to inpatient rehab. Okay, so just relevant to what we're gonna get into. I wanted to show you some films here. So usually you don't get a chest x-ray when there's a pneumothorax. But in this particular case, one was done. And you can see, here's the day, I think a day or two before. This is lung field, this is the diaphragm, this is the abdomen. And this is the diaphragm on the other side, lung field. You can see here, obviously, it's not a mystery of what we're showing here, but that large pneumothorax with shifting the midline structures. And then a couple days later, they did another scan on him, and this is what we're seeing, an elevated right hemidiaphragm. So ipsilateral to where the pneumothorax was. So I was consultant when he was admitted, because even though he was off mechanical ventilation at this point, he was having a lot of shortness of breath that was limiting his rehab progress. So I actually have been doing a lot of diaphragm ultrasound for a while. I got into it during fellowship and thought it was gonna be really important for taking care of ALS patients. We do use it in neuromuscular clinics, but as it turns out, it's really had a lot of uses in the inpatient side of the rehab hospital. And both for ventilator weaning, which we're not gonna talk about today, but also just the often overlooked elevated diaphragm from phrenic neuropathies. So in this technique here, apologies, let me see if I can go back. Can I get my picture back? Can you help me there? I think I hit the button with the tape on it that was like tape, so I didn't do it. I couldn't help it, it was just like, I know it's the wrong one, but it seemed like the right one at the time. Can you give me one more back? There we go, yeah, yeah, cuz I wanted to talk about layer cake. That's the way I describe it, so when you, that's me, that's me. That was not the laser pointer. They're both green though, it's in my defense. There we, all right, thank you. So here's the technique, Andrea Boone I have to give a lot of credit, both for writing such clear papers that was pretty easy to follow along with her recommendation for doing this B mode technique with the ultrasound through these lower rib spaces. But also for like after I read her papers, being willing to talk to me and help me figure out the ins and outs of doing it. But here's the ultrasound probe placed here. You can actually see cuz the diaphragm's hard to picture, but there's like a three dimensional dome here. And at these lower ribs, it's actually sitting right up against the rib. You can image it nicely. And you can do other techniques as well, like looking at M mode and excursions. But this is our workhorse technique. And at this level, when you look between the ribs, the diaphragm's, I can't always compare to this layer cake. Cuz you have a central tendinous slip. You get a bright plural line and a line here for the peritoneum that sandwiched the pink diaphragm muscle here in between. And above it there you have intercostal. So now I'll show you a video. There's rib 8, so this is the 8th intercostal window. You can see the diaphragm muscle right there. Can we loop it one more time on the video? I don't trust my buttons. Go back one more time and make that go. Thanks. And there it goes. And that's the lung coming down, peeling it off the chest wall. So then you're not, no doubt about your anatomy, that's just a normal diaphragm, but it contracts, it's got a certain thickness, and when it contracts you can see the change in thickness. So breathe in, gets thicker, breathe out, gets thinner. For people watching from home, you didn't see me, but breathing in it's like I'm flexing my biceps. It gets a little bigger, not much for me, but for some of the people in the audience it would be impressive. And then out it gets thinner when you relax, and that's what the diaphragm does. So now we saw the results for this case, and you can see the left side here, which is intact, nice thick, meaty diaphragm, and with the breath in the bottom line drops, that's the peritoneum, the pleura, and there's some thickening. And then on the other side, let me look at this screen here, it's actually even hard to see, let me advance. It is this thin sheet of paper here, let me show you on the next slide. Right there, marked by that little hash mark, this is what I call like a paper thin diaphragm, but it's usually associated when we do a conduction, which we did in him, you can't evoke a response, you put a needle in it, you get fibs and positives, and you're lucky if you get any units. This is an axonal injury to the phrenic nerve causing severe diaphragm atrophy, and this is the intact side. And you can appreciate what I mean by thickening ratio, breathe in it gets thicker, breathe out it gets thinner. Usually it goes up by about 50 to 70 percent, but just 20 percent thickening is acceptable. And Dr. Boone has one of her best studies, she's got many, but this one was really key, is that they look back in a retrospective fashion at some of the cases that came to the lab at Mayo, and when they compared patients who had ultrasound to patients with just plain films or with sniff tests and nerve conduction studies in needle EMGs, they found that out of all those things, the diaphragm ultrasound was, had the most impressive profile of both being highly sensitive and highly specific. And so as a single best test for looking at diaphragm paralysis, especially in the case of like a unilateral phrenic, you can't beat this. And it's actually kind of neat, she hasn't described this in a paper, but you know we've talked about this a lot, and here's an example from this case. You can actually use it over time, and you can imagine if you were proposing to do phrenic nerve conduction studies or needle EMG of the diaphragm over time, people might not always want to play ball with you, but this is a pretty quick and painless procedure. And look at this data here, so we look at our initial study where the diaphragm is, the thickening ratio here, so this is the index of contractility, this is time. You can see that initially it's paralyzed, it's not getting thicker, in fact it got a little thinner. And then you can see here with the breath in, and you can see here it's still below normal, and then eventually, and look at that time, it's like 200 days, so a little bit more than half a year, and then it starts to kick back in. And remember, he saw us on delay, because it took so long to even come to us, so there was that time interval too before we actually did our initial assessment. And so just a couple of examples, so here's the diaphragm, I think this is the, the diaphragm's looking a little thicker here, but it's still not contracting, it's on a weird view, so I kind of tilted this, but that was what we could get that day. And then here's an example of it, and here's an example of it, the recovered diaphragm, where it's got nice thickness. You can see that little bit of opening there, the lung's not coming down as a bright thing, but you can see that peeling of the, of the pleura there off the chest wall, and again, really dissects the anatomy for you, so you're not debating, is it the diaphragm, is it the intercostal? And this is his recovery. And we actually recently put out a paper looking at, like, recoveries, like the one advantage of Chicago is we see a lot of the same people over and over again, whereas, you know, we, and we do see a fairly high volume, surprisingly, of these neuropathies in our outpatient clinic, and so when you break them down, cardiothoracic, post-ICU, idiopathic, neurologic chemotherapy, trauma, or tumors and masses, and look at, like, whether or not they recover, you know, the percentage of patients that, that make an improvement, which is the blue bar versus the red, you can actually see that the overall take-home is that most patients, even in all these different ways of acquiring a phrenic neuropathy, make some improvement. And this is by far, you know, except for, like, I think less than 10% of our cases where there's been interventions, like a diaphragm placation, or nerve surgery usually done somewhere else on the phrenic nerve, but most of these are just spontaneous recoveries. So if you give them time, and time is the key, they can recover, so, but the recovery's slow. So when we looked at our data, the median is about a year and a half, just under. And when you look at it, actually, the ultrasound's the first thing that picks up recovery, even sooner than people are subjectively reporting improvements, or we can measure it with, like, a pulmonary function test. And overall, about 70% of patients with a phrenic neuropathy, if you give them time, will improve. So we usually recommend, if you're going to do interventions, that you consider waiting. There's some examples where you know the nerve is lacerated. For example, if there's, like, a tumor that's resected, and you know the nerve is sacrificed, that's different. You might want to graft that. But a lot of the cases, we think that you get pretty good outcomes when you give them time, and then, you know, talk to them about pulmonary rehabilitation, including things like passive range of motion, breath stacking, which we do in neuromuscular patients, as well as, like, diaphragm muscle, sort of focused respiratory muscle training. So we'll move on to our next case. So now we're on a different diagnosis, TBI, polytrauma. So the 29-year-old male fell off a 20-foot roof onto concrete while working at a construction site. He sustained a TBI, multiple fractures. Most notably, I think we'll focus on this right humeral fracture with an open reduction in internal fixation, and also a closed reduction of a distal radius fracture. That happened a couple weeks after his fall. It took him about four weeks to be admitted to inpatient rehab. And when you look at his examination, you can see that on the examination for the right arm, there's four to five shoulder abduction, four to five elbow flexion, wrist flexion, and then all of a sudden this major drop off, so wrist extension and finger extension are zero out of five. So, and then also reduced the finger flexion. So what we also point out here is that the sensation was basically intact through the arm. This was documented by the inpatient team, and then as the admission went along, so two and a half weeks in, they noticed that he had this new complaint that his, sorry, can we go back? There we go. That he had now this new loss of sensation over the dorsal aspect of the forearm and his thumb. So they asked me to do an EMG at this point. So this is my first time meeting him. And what we noticed was when you look at his testing, a couple things. One is that he had no motor response at the, his radial motor. He also had no radial sensory, the superficial radial. Presumably based on that exam at admission, we would have been able to get a response here clinically, but this is what's changed. And you can see that not only is there no response here, but when you put a needle in, you can't get any motor units in EDC or brachioradialis. Notably, just for thinking about the anatomy of the triceps and the spiral groove, triceps is okay, which is, we see this a lot. So, you know, causing wrist drop. So localization, we're thinking radial nerve, spiral groove. But why is this person getting worse while they're admitted to rehab? This is what, we don't have an answer for this. So this was someone we were just a little bit skeptical about what it is exactly that's going on. So not trusting just to rely on the EDX, which you could just attribute to this, maybe to positioning or like an entrapment that happened. We went ahead and got an ultrasound. And the light's a little bright, but what we found, let's see if I can, I don't know if you guys can see this better than I can, just with the angle. Forgive me. So here's the, I can see it here on the screen. So this is the radial nerve here. I think there's markers there showing this little bit of hyper-echoic rim here and then some shadowing. And what, we actually had this one done by our MSK radiologist, but the read on this was that there was an area of hypertrophic ossification along the mid-humeral diathesis that was partially encasing the right radial nerve. And we went ahead and got a CT scan and did further imaging, but this was HO. And so the management and the outcomes and the prognosis here is way different than if we just attributed this to entrapment. So he quickly, rather than, you know, a lot of the times with the, especially with radial nerves, you'd like to give them time. They have actually a pretty good regenerative capacity overall. And so although we weren't seeing responses, we were going to typically follow this out for at least six months before deciding about going in and doing surgical exploration. But in this particular case, we immediately realized that that HO on the nerve wasn't going to get better. If anything, it was going to get worse. So we referred him to our interdisciplinary clinic partner, Dr. Kevin Swong. He's a peripheral nerve surgeon, neurosurgeon, who went in and did surgery to resect the HO from the radial nerve. And actually, the thing that really stunned me about this case, which sometimes happens to us, I think, when the nerve is very edematous, is that you would expect that recovery would be slow in a nerve injury with so much axonal loss. But he actually made improvements at the first postoperative visit that were really impressive, sort of defying the electrophysiology in this case. I see this every now and then. So the diagnosis of radial neuropathy at about the spiral groove, but the ultrasound combined with electrodiagnostics now gives us etiology. So generally, we would give these patients more time before we intervene, but we changed the management in this case. The red flag for why we pursued this one with imaging so early and more aggressively while he was currently in inpatient was that he did lose function, which didn't make any sense to us. He already had the motor deficits, but that loss of sensory was enough to sort of raise our suspicion. And HO, this case actually just was at the AAM meeting. I saw a similar case that Sarah Smith presented out from Seattle. So I guess this does happen from time to time, although I really can't quote an incidence of this involving a peripheral nerve like this. In fact, we're more likely to see maybe hardware from like a repair of a humeral fracture entrapping the nerve than we are to come across a case like this of HO. So those are my references for what we've done so far. There's some more cases we want to do. I'm going to switch this over to Dr. Attaway. Okay. Hold your applause. Please hold your applause. Okay, thank you. All right. Let's get started. It's closer to me so you can all hear. So thank you for the early introduction, everyone. I'm Dr. Attaway. I'm also at the Shirley Ryan Ability Lab. And so I'm just going to continue on with a couple of more cases for us to go through. I have no disclosures. Hitting the button and it's not. So I can go backwards but not forwards here on these slides. All right, okay, we're good, I got it. Backwards and forwards, excellent, it's working now. So I have nothing to disclose. So let's go right into it, case three. All right, so we have an 18-year-old male with a spinal cord injury, high level, C2-HSC, and he's currently inpatient at your inpatient rehab spinal cord injury unit, and is complaining of asymmetric weakness. So a little bit more about his history. He had several gunshot wounds, one to the spine with retained bullet in his fecal sac, one to his left upper extremity. His injuries include a C4 laminar and spinous process fractures. He did get surgery, C3 to 5 labonectomy, and removal of the foreign body. But at the outside hospital, they decided to manage his left comminuted diaphysal humeral fracture non-operatively. And so he's in rehab, he's noticing that he's getting better, but his right hand is getting better a lot faster than his left hand is, and he's noticing that his left hand is quite weaker. And so as a SCI attending physician, you decide you've got some neuromuscular specialists, let's get them on board and see what's going on, right? And so we got consulted at this time. So on exam, as you can see clearly, he's anti-gravity on his right side. On his left side, he's a lot weaker, but in certain muscles, right, in his elbow flexors, his elbow extensors, wrist extensors, and wrist flexors, and thumb abduction. But he's got some deep finger motion, right? So he can flex his deep fingers a little bit, deep finger flexors, as well as FDS, and he can abduct his fingers a little bit. And so you're like, oh, what's going on, right? You know, there isn't a clear pattern involved. And so as the title of this talk is, we decided to go and do some electrodiagnostic studies. So on his sensory studies, they look actually pretty good, except he has no radial sensory response, completely absent. And so we move on and we do his motor studies. So a lot of words, a lot of numbers over there. So I'm just gonna highlight what's important, which is that his radial motor on the left side is also completely absent. And I decided, you know, let me get another radial nerve, the motor nerve, but that's a little higher. That's not C8, that's C7, so I did the anconius, which is also absent on that left side. He also has a little bit of reduced amplitude of his median motor response at the abductor pollicis brevis. All right, so let's move on to the needle study. Long needle study that he loved. I'm just kidding, no. So again, a lot of numbers here. Let's highlight what's important, right? Which is that we can see active denervation in almost every muscle that we insert our needle in. So on the left side, active denervation throughout. On the right side, we don't see active denervation in his FDI or his EIP, right? So we don't see active denervation in his C8 muscles, but we do see it in his C5 to C7 muscles. And then in terms of his motor units, we don't see any units on the left side in his EIP, his EDC, his brachioradialis, his supinator. So hopefully you're seeing a pattern, right? Those seem all radially innervated. But also, we don't see units in his left brachialis and in his biceps, you can only really see one unit, right? But remember, he has a spinal cord injury, right? So as you can imagine, that sort of complicates the picture, right, how much of this is upper versus lower, right? How much of this is, you know, he just can't activate the units because he doesn't have that descending drive. So putting all this information together, if you're thinking, you know, his sensories were pretty good except that radial, so overall it looked pretty preganglionic, then you're right, right? So we decide he's got on the right side a preganglionic lesion, right, at the C5 to C7 levels. And so his C8 muscles looked pretty good, right, and both the nerve conduction and the needle studies on the left side, we say he also has a preganglionic lesion affecting the C5 to T1, right? But recall, we also saw some changes in those radially innervated muscles and say that he actually has a superimposed radial mononeuropathy localized proximal to the brachialis, right? And so as you can imagine, because of that spinal cord injury and involvement of his lower motor neurons, right, it can be hard to tease out what's going on, but putting the information from our nerve conductions and our EMGs really helps us tease that out. I don't have the image here, but we did a quick ultrasound, bedside ultrasound, and saw that his radial nerve was in discontinuity. Consulted with orthopedic surgery and plastic surgery with our own surgeons, and they thought that his fractured should be operated on and not be managed non-operatively. So he did end up getting an open reduction internal fixation of that left humeral fracture. And at the same time, he got a reconstruction of his radial nerve with cable nerve grafting. So this is quite recently. So he's currently in therapies. He's getting a little bit stronger, but it takes time for nerves to grow and recover, right? A millimeter a day if you're in Canada, an inch a month if you live in the US. So hopefully we are, we're gonna continue following him and we expect him to recover. And so some important take-home points, right? So he had asymmetric weakness, and that can be hard to tease out in a spinal cord injury, right? So how much of, when someone has asymmetric weakness, how much of that is that due to spinal cord injury? Like you can have involvement, asymmetric involvement of the cord itself, right? Or you can have symmetric involvement of your cord and a superimposed post-ganglionic issue like a mononeuropathy or a plexopathy. And so that's hard to tease out by just doing your exam or doing your Asia exam. Like everything is weak. And so the EDX was really important in this case, right? Because it changed his care, right? If we hadn't done the electrodiagnostics and if he hadn't gotten the care, right, he would have gone on, continued therapy, right? Recovered probably on his right side and not recovered on his left side, right? And then come back a year later and says, I'm still not getting better. And then at that point in time, probably had irreversible denervation atrophy, right? And not eligible for reconstruction, or not eligible, but would make it less successful. And so hopefully, I think that's a really great takeaway point. And on that, we'll move on to that next case, all right? All righty. So our next case, case four, is a 75 year old woman. She has a history of Parkinson's disease and she was admitted to inpatient rehab after she had several syncopal episodes in assistant living. She has some other medical history, hypertension, hypolipidemia, hypothyroidism, B12 deficiency, for which she's on supplement. But then while you do her admission exam, you notice she's weak, right? And then it's not just a difficulty with movement and related to her Parkinson's. She's been having, this actually has been going on for 10 months, and she's been to other rehab centers and has continued to get better, I'm sorry, has continued to get worse, even with therapy. And it's not just weakness, it's sensation changes as well. So numbness, some paresthesias and sensations. Before she got to you, she saw a neurologist, they did her some labs, and saw that her B6 was high, right? And so they know that B6 toxicity can cause neuropathy. And so they said, this is all due to your B6, stop your B6 supplement and things will get better, right? But being the great physiatrist that we are, we know that B6 toxicity typically presents with sensory loss and does not have motor loss, right? And so you think, well, that doesn't really make sense. And also you repeat her B6 and it's normal, why is she getting worse, right? Why is the pattern not making sense with B6? And then just some other prior workup for this syncopal episode she had had been negative. And so again, you realize, hey, you've got your neighborhood neuromuscular physiatrist in the building, and then you get them in for a consult to take a look at the patient. On exam, her general exam heart, lungs were otherwise normal or stable, higher intellectual function is intact, nothing prominent in her neck exam or her cranial nerve exam. And so you do her strength exam and she's pretty symmetric. She's weak throughout, but more weak distally, right? So she doesn't have any plantar flexion, any dorsiflexion, first direction inversion. She's got four to four minus at the hips and the knees. Fingers wise, she's threes to three minuses and more approximately in the upper extremities, she's four to four minuses, right? So already she looks like she's got some sort of length dependent symmetric process going on. So you continue her exam, right? She has no reflexes anywhere, biceps, triceps, brachioradialis, patellar, achilles, and no other pathologic reflexes like Clonus, Hoffman's, or Babinski. And then you do her sensory exam and you're like, wow, there's a lot going on, right? And so on proprioception, she has no proprioception at her toes, at her ankles, but she can sense it at her knees. When you look at her upper extremities, no proprioception at her distal and proximal to phalangeal joints. And at the wrist, she requires large excursions to be able to sense that proprioception. You test vibration, right? And the only place that she can sense your vibration with your 128 Hertz tuning fork is at her hip, at her ASIS, at her acromion, right? In the proximal arm and midline, chest, and the chin, right? So some really significant large fiber loss. Cold and temperature seem normal. Pimpric is also reduced in the upper thighs. Light touch is only really present at the neck and absent in the arms and the legs up until her sort of inguinal ligament. So you think, you know what? Let's get an EMG, right? And so we did her nerve conduction studies, right? Had no sensory response anywhere, bilaterally through typical median, ulnar, radial, as well as superficial fibular and sural responses. So I've highlighted that. And so we then do her motor responses. We can see that here. So again, I've highlighted the red, so hopefully we can see that here. Distally in her feet, she has no responses, right? For her fibular and her tibial motor nerves. In the hands, those are also significantly abnormal, right? You have both significantly reduced amplitude, prolonged latencies, right? And because that's so prolonged, the conduction velocities are quite low, right? We should be in the 40s, 50s, 60s. But even though she has both axonal loss, right, as well as some sort of demyelinating component, it seems like it's primarily demyelinating with an axonal component. And that's what, 16, yeah, 16.2 milliseconds in latency, right? Which is quite slow. And so based on this, we're, it's not her Parkinson's, in case you were wondering. We then continue and we do her EMG studies, which doesn't look that bad, right? Oh, go back. No, I showed you the answer. All right. So on her EMGs, you weren't really able to get her to activate her tiband and gastroc on the right and her gastroc on the left. And then also some reduced activation of the tiband on the left as well. But elsewhere in the upper extremities, proximally, even in the FDIs, those seem okay, right? And that kind of fits in with the nerve conduction studies where it seems sort of predominantly demyelinating with some axonal component, right? And we know that with demyelination, we expect there to be some sort of reduced recruitment, but not significant axonal component, which you can get when it gets severe enough, which in her case, it is quite severe. And so we were concerned for her about CIDP. And so just before, I think we've already talked about this, so this is a length-dependent sensory motor demyelinating an axonal polyneuropathy affecting both her uppers and lowers. But like I said, we were concerned about CIDP at this time. And so she was actually sent back to acute care for further workup. We were able to get some labs in before she went into acute care, which all seemed pretty good. The CBC was fine. BMP was fine. Repeated all her vitamin levels that were fine. Did some electrophoresis of her serum and her urine that was fine. And her autoimmune panel was fine. She went to acute care. They did an LP. The CSF was actually relatively bland. Her spine imaging seemed stable. But because of the findings on EMG and the concern for CIDP and her worsening weakness, she was given IVIG over five days and actually got better in both strength and in sensation and was ultimately discharged and didn't actually come back to acute inpatient rehab. So I think this was a very interesting case. I think that one of the major points to take away from this is to always question the diagnosis. Does it fit and does it explain my patient's symptoms? Does this B6 toxicity fit with her symptoms? No, it didn't, right? And pursue that even more. And obviously her EMG and her NCS were an important part of her diagnostic workup. All right, and so let's move on to our next case, case five. So here you've got a young 27-year-old man with a chronic C7 spinal cord injury who comes to you presenting of worsening thumb weakness, right, and so his injury was about five years ago. He's a C7 Asia B, and he's concerned he has left thumb flexion weakness, and remember, this is really important, right, because he's young, right, and so what does that mean? That means he can't scroll on his phone, right, or it makes it difficult to, if he's using that thumb, to control his powered wheelchair, right, so it might seem like a small thing, but we know that when you already have a prior injury, any worsening weakness can significantly affect your function, and so he tells you that two weeks ago, he thinks he had a whiplash injury where he was on his wheelchair, he stopped abruptly, and it caused him to bend forward, and he thinks that since then is when his symptoms started, and he tells you that, you know, I have to sort of hyperextend my neck to get my thumb to bend more, and you're like, well, interesting. You do a full review of systems, and everything seems okay, except that he's got some upper back pain. His sensation seems unchanged compared to his prior baseline. He doesn't have any new issues with autonomic dysreflexia that seem to have been resolved. He doesn't have any changes in his spasticity or in his spasms, so you go on to do a general exam. Heart, lung, skin, that seems okay and stable. Higher intellectual function is fine. Cranial nerves are intact. Neck is pretty strong, and you go on to do his physical exam. Can we see that here? And so, those things there. And so on exam, so again, he's strong, so he's a C7, he should be strong proximally. Distally, he's weak, but that's sort of baseline from his spinal cord injury. Wrist extension is also strong. Before he came to you, his strong side was his left side, and you look at your prior notes, and his thumb flexion was a four out of five before, and now it's a one out of five, but then you're doing his exam, and he then says, oh, but I can bend my neck back, and now he can go against gravity with thumb flexion. So you can see the exam. Lower extremity is, again, stable, zero out of five throughout from his spinal cord injury. His sensation also seemed to be stable and just impaired C7 and below. He's also hyperreflexive throughout, which is not surprising to you, given his prior spinal cord injury. So what are we thinking is going on right now? Anytime someone comes with weakness, it's important to just think about the big picture and what could be going on, right? So weakness can be caused by anything all the way from the brain to the muscle and everything in between, right? And as physiatrists and particularly neuromuscular specialists, in this case, we're thinking is something happening at the spinal cord level or the root level, the plexus level, peripheral nerve level, given his presentation. And so because of this weird neck thing that's going on, let's get an X-ray. We can get that in clinic pretty quickly. So we get an X-ray. We get C-spine images on the same day, which show essentially stable anterior fusion with a cryptectomy, right? So nothing has changed. Everything is stable compared to his prior X-rays. And so, well, you're like, let's get an EMG. Let's dig a little bit deeper. And we do the EMG. We get his sensory nerve conductions, which are all normal and look pretty good, right? So normal amplitudes, normal latencies. Then you look at his motor study. And I've highlighted there in red, his ADM and APB bilaterally, right, have either are absent or quite low in amplitude. Also did an FCR, which isn't commonly done, right, but it's a little more proximal, similar to the anchornius that we showed previously on. And you do get a response on both sides. Typically, the mean amplitude with the FCR is about a 10.2. The low end of normal is about a 2.3. So it's technically still in that normal range, though I'll be on the lower side of normal. So what could be going on? Well, let's do his needle study. And we go on and do his needle examination. And so let's break this down a little bit. Distally, right, in his FDI and his, okay, there we go. On the right side, FDI and FPL, you have no voluntary activation, right, because of the spinal cord injury. On his left side, his FDI, no voluntary activation. On his FPL, you initially don't really get any activation. Then he says, oh, but I can get a little bit more activation when I'm extending my neck. And you can see some more activation, though you do see some reduced recruitment and increased duration. So some neurogenic changes in his left FPL. In addition to that, there are some neurogenic changes in his left triceps, as well as his right triceps with some activation in his left triceps, right. And so you look at this and you're thinking, all right, what's going on? Well, you know, maybe this distal stuff going on is from his spinal cord injury, right, his lower motor neuron involvement. Maybe he has, you know, a C7 preganglionic issue going on, right, and maybe that's sort of affecting the FPL. And so when this was read, there we go, no clear active denervation in that FPL, but he did have neurogenic changes on that left FPL. Some concern that there was some motor unit remodeling, in that C7 myotome, let's go back, that C7 myotome, as well as these fibrillations and sharps and neurogenic changes that are seeing in the C8 T1, C8 T1 myotomes, right. So there's a lot going on here. What's our differential, right? A lot of things in our differential, right? Again, we wanna keep it broad for him, right? Anything trauma, neoplasm, infection, vascular autoimmune, structural, degenerative, endocrine, and all this, and nutritional. But again, his sensory studies were normal, right? So we're thinking maybe this is all preganglionic and there's something in the spine, he has a spinal cord injury. Let's, you know, maybe highlight a maybe post-traumatic syrinx or radiculopathy that could be going on, right? So that's our focus here. And so we decide to get an MRI of his C-spine. Hopefully you can see that all here. So he's certainly got a lesion here. He's got a essentially cavitary myelomyelitia and old hemorrhage, but he's had previous imaging, right? And that was there as well, and it's stable, right? There's no changes in that spine. It's consistent with his spinal cord injury. No syrinx on this image. And let's move on here. And I'm just showing the axial view. I can't really see it here, too. But to show that if you look at his, for Raymond, those are wide open, right? And no compression there as well. So we can see that pretty well there. Move on, all right. Okay, so what's going on, right? He was talking about all these positional nature of his symptoms that seemed pretty striking, right? But it didn't seem positional. His imaging looked fine. What else could we do, right? What else could cause the finding in his symptoms? Well, maybe it's some sort of peripheral neuritis or a compressive neuropathy and his mono or mono neuritis multiplex, right? And the story about him, the whiplash was just sort of a red herring, right? It just sort of, and he started to notice it then. And so what would you do next, right? You've already done EMG, you've done MRI, you've done an X-ray of his neck. How, what else would you do? Well, you probably know from the title of this talk. Well, let me, let's get an ultrasound, right? But what would you ultrasound? Where would you ultrasound? So we started with ultrasound of his form. And so this is a transverse ultrasound image of the mid-left forearm. And what it's showing, hopefully what that's supposed to be encircling there is an abnormally thickened anterior interosseous nerve next to, and I think the red there is just pointing an adjacent vessel. And the comparison on, there, so this was him. And on the right side is the unaffected side, right? And so you can, and so this is just showing the thickening that is asymmetric on this affected side compared to his unaffected side. And so, and it's formally read by radiology. They also noticed diffuse asymmetric fatty atrophy in his left forearm flexor muscles. His FPL tendon seems to be intact, but you do see fascicular enlargement and hypoecogenicity of that left anterior nerve. Let's move on. And we wanted to sort of take a closer look and did get an MRI as well of that forearm, which did show diffuse edema of his forearm flexors, but sparing his pronator teres, his pronator quadratus, right? Which is AIN innervated, had diffuse edema and atrophy. And also he had edema of his median nerve, I think median nerve distal to his pronator teres. Let me move on here. So all of this is pointing to an AIN neuropathy, right? And so if the anterior thoracic is a pure motor nerve, right, so it explains why all his, you know, the sensory studies are normal. And there are multiple sites where that can get compressed or you could have entrapments. Commonly, or the most common compression site or entrapment site is in the deep head of the pronator teres. It can also be entrapped by the flexor digitorum superficialis arch. It can be compressed by an accessory head of the FPL, Ganser's muscle or accessory muscles within the FDS or FTP or some sort of arterial thrombosis. If you recall from the image, it's pretty close to the artery that's running by it. So that could cause compression and in the past, the radial and or ulnar nerve have been implicated, right? And so we all know the AOK sign. Obviously in him, it's hard to do this test because he has a spinal cord injury, right? So he already has weakness of his distal muscles, right? But in someone without a spinal cord injury, when they have weakness, when you have an AIN neuropathy, right, that impacts the FTP of your second and third digits, right, your pointed quadratus and your FPL, when you ask someone to make an OK sign, they can't, right? And they end up using their ulnar innervated muscles to hold that piece of paper or to do the motion that you asked them to do. All right, so moving on there. No, come back. All right, go back to work. Also, I guess I should have warned you, we've got some surgical photos yet. So hopefully no one is crazy or just had lunch. We did refer him to our surgeons and get a surgical exploration and neurolysis of his anterior and serratius nerve. Interestingly enough, interoperatively, right, they noted that he had this intramuscular septum of his deep head of the pronator teres that seemed to be hypertrophied and compressing his nerve. But he also had a vascular leash crossing his anterior interosseous nerve and a fibrous band from his FDS. Multiple things there compressing his AIN. And so they completed the procedure, did the neurolysis of his AIN, and then four months postoperatively, his strength went from one to a four, four out of five. And they actually repeated an EMG, which I won't go through again, but I'll just say that he did, he had better activation this time of his left FPL muscle. And he was pretty happy with the outcomes. And so what do we take away from this? Honestly, that localization can be really tricky in someone with a prior spinal cord injury or a pre-existing injury. And in this case, imaging can be really helpful to help tease out the etiology of the presenting symptoms. In addition to that, in spinal cord injury, because you can have both lower motor neuron damage that you can see on EMG, as well as upper motor neuron damage that affects activation that can also complicate the picture. And also in this case, when you do have a loss of function with a prior injury, that can actually be quite impactful in quality of life. And so just to summarize all the cases that we've talked about so far today, hopefully we've convinced you that in complex cases that combining imaging and electrodiagnostics can be really useful, not just for localizing, but also for determining etiology of the symptoms. That patients can have undiagnosed neuromuscular issues when they come into inpatient rehab, right? They can come in for deconditioning for Parkinson's or for SCI and have something else neuromuscular going on that no one has really evaluated. And also that things can develop inpatient, new neuromuscular conditions can develop. So that being said, definitely do not hesitate to reach out to your local neuromuscular or EDX trained physiatrist to get their input and to provide your patients with better care. All right, and so with that, I'll say thank you and let's start our discussions and we'll take questions. Thank you. Oh, here it is, okay. You mentioned motor unit remodeling. What is that? What is motor unit remodeling? Correct. So, or I guess I'd call it neurogenic. So it's basically when you have injury to a peripheral nerve, right, you have injury to some of the motor neurons, or loss of those motor neurons, and neighboring motor neurons can reinnervate the denervated muscles. So it's sprouting, basically. Yeah, essentially. It's just sprouting right in, yeah. Second question was, in case number five, the patient had a whiplash injury, but it looks like there was a lot of local damage to the arm, which should not have occurred. What's the etiology of all these things that occurred in the arm? That's a great question. I mean, ultimately, we don't know, but he's had his injury for five years, and he's obviously using his manual wheelchair, so I feel a lot of that particular hypertrophy of those forearm muscles might be related to the forearm use with his transfers and with his wheelchair. So it's an overuse thing. Yeah. But... You know, the other thing that came up with him, I knew the case, was the surgeon told me that he admitted to being a big gamer. A big what? Video game player. Oh. And he was wondering if that may have contributed. Yeah. Thank you very much. That's a good question. I just think that was a red herring, right? So was it just... Was he just doing this? Could you repeat the question? Oh, sorry. The question was, why did he seem to be better when he was extending his neck, right? And so I just wonder, when he was extending his neck, was he also doing something else with his forearm? I don't know. Yeah. I see a question over here. Yeah. So I guess, like, a neurotension... Yeah. ...type of thing. Yeah. For both presenters, could you summarize one more time the treatment window for nerve transfer after spinal cord injury? Sure. So... That's Dr. Attaway's specialty. So after a spinal cord injury, right, so you are trying to re-innervate muscles below the level of the injury, right? If you want to re-innervate them, you cannot have irreversible muscle atrophy or irreversible denervation atrophy of your muscle. And so we think that denervation atrophy of the muscle occurs about, you know, in about 12 to 18 months, right? And so when you do the transfers, it takes time for the nerve to grow and get to the target. And so typically, we want to do the transfers by six months. So the remaining six months, the nerve is traveling and can get to the muscle, the target muscle, right? And so that sweet time to do the transfers are, you know, three to six months, right, such that you can re-innervate those muscles before you have denervation atrophy of those muscles. Does that answer your question? Any others? Any other questions? Yeah. How do you explain how some patients with SCI at a certain level, they have denervation many, many levels below? Oh, that's a great question. So yeah, and this is, I mean, this is an active area of interest of mine, right? And I would, first of all, the other talk that Dr. Franz promoted, we went through that in detail. And we definitely listened to that, but not just at the level of the injury or the NLI, neurologic level injury, but below the levels, we are seeing evidence of chronic, of denervation, of remodeling of units, if there are units, because it's hard to activate. Why is that? I think it's multifactorial, right? I think the answer is we don't know, right? Is it direct trauma from the injury, right? Or is it something about, is it a vascular issue in the perioperative period? Is it something about the loss of supraspinal input that causes that over time? We don't know, but what we do know is that up to five levels below, 50% of, when we did a study with about 68 individuals, 50% of muscles had evidence of denervation five segments below the neurologic level of injury. I'll add to that. There's a lot of work going on now on maintaining in the acute care, like mean arterial pressure above certain goals for the acute management of patients with spinal cord injury, between the possibility for neurogenic shock, so in other words, like low perfusion pressure, but also a mismatch, because it's raised to intrathecal pressure. So most centers aren't monitoring intrathecal pressures, although there's a few sites I know the team that we collaborate with on some of the EMG stuff, one of their surgeons there is big on intrathecal monitoring of spinal pressure, and then calculating a perfusion pressure between the mean arterial, the relationship between the two. So when you see such a big distribution, and it really defies what we would expect for the anatomy of the injury and just inflammatory injury, it does make you wonder if there could be hypoperfusion. It also doesn't extend rostrally. It's a caudal pattern that we see. So that's a hand-wavy thing. I mean, I would keep it to myself if I had a way of addressing that quickly and try to publish, you know, because we've been interested. But I mean, I would encourage anyone to think about that, too, if you're positioned to kind of define that. But I think that those guidelines, which may actually improve outcomes, they think about sparing white matter for their outcomes. We think that the gray matter, which tells us about the spinal tissue, is actually a pretty good surrogate that we have really good measurements for. So, you know, like doing acute monitoring of F waves at levels below the injury may actually be a pretty rational thing to do. Of course, it's not what the spinal cord field is thinking about white matter a lot. And so we do have to remind them that the gray matter might be useful both for deciding on these surgical decision-making pathways that Dr. Adewai is a specialist in. But I think that there's more that we can do with it. And we have great tools in the neuromuscular field that could help them, so. Why don't we wind down, get lunch? If anyone wants to come up, chat with us, we're here. And yeah, thank you very much for coming out on the last day to our session. It was a great turnout. Appreciate it. Thank you.

neuromuscular complications

electrodiagnostics

ultrasound imaging

rehabilitation

phrenic nerve issues

hypertrophic ossification

chronic inflammatory demyelinating polyneuropathy

nerve transfer surgeries

interdisciplinary collaboration

patient outcomes