Good afternoon. I realize that we might be the only thing standing between you and an adult beverage for the evening, so we are going to get started on time to hopefully end on time. My name is Mike Salino. I am Chair of Physical Medicine and Rehabilitation at Cooper University Health Care. Welcome to the horses and zebras in the Spasticity Zoo. The idea of this course would be to talk about two spasticity presentations, one that might have a common management or a common presentation, and one might have an uncommon or unusual presentation to compare and contrast. In the spirit of San Diego having a world-famous zoo, we thought this would be a terrific concept. All of the presenters are colleagues and dear friends of mine, so give them your great attention. First up, out of the box, is Dr. Kimberly Heckert, who is at Jefferson and runs a spasticity fellowship there that is a tremendous learning experience. Many of our other fellows are also here presenting also. Dr. Heckert, you are first on deck. Thank you very much for that introduction. In preparing, I happened to get on the left-hand side of the screen a zebra selfie just for today. In the middle, I don't have a horse and a zebra, but I managed to get a donkey and a zebra, so I guess that is what happens when you're in San Diego. These are my disclosures. And the first case I'm going to present is a case that involves spastic finger flexion. So in this particular case, there was a 60-year-old woman with a left brain infarct 10 years ago. So she has had these symptoms for a while. She's got spastic hemiparesis of her right side and aphasia, and she had several spastic muscle groups that were problematic with a modified Ashworth score of at least two, and those included her shoulder adductors, her elbow extensors, forearm pronators, and then her finger flexors were tight, and that was across the MCP joints, the PIP joints, and the DIP joints. She had full or near full passive range of motion in those areas, but there was spasticity there. So what I'm trying to get at here is she didn't have a contracture. On exam, she had some active wrist extension, and she could initiate a little bit of finger flexion, but she couldn't really overcome that finger flexion spasticity in order to have meaningful grasp. So that was her biggest goal, and I think it's very important when you meet a patient to talk about their goals so you understand what the two of you are trying to do together. So we decided on an initial plan to do some chemodenervation, and on the early rounds, I treated her. The first round, I treated her pectoralis to address the shoulder adduction, her triceps, her pronator teres, and I addressed her FDS, her FTP, and all four lumbricals. So I think if we were talking about a horse, I think we've all seen horses where we treat FDS or FTP. Maybe we treat the lumbricals too if they were involved, but this case presented a little bit as a zebra. At a follow-up visit, she reported she had a great response to treatment in her shoulder adductors and her elbow extensors and her forearm pronators, but not her fingers. And remember I said that was actually the biggest goal is she wanted functional reach. So yes, you need some of these other players to have a functional reach, but in order to grasp an object, you have to be able to open your hand to get it around the object. So why did she have such a great response in all these other muscle groups and not her finger flexors? Because I told you I got all the characters, right? I told you I went for extrinsic and intrinsic. So what was happening here? What are the possible reasons for the suboptimal response that I saw in her finger flexors? Who wants to participate today before I start picking on friends? Come on, somebody say something. Maybe it was the wrong dose. Great, what else? Thank you so much. Maybe I missed my target. That's great. What else? It was off. So it's dosing. Maybe I got to rob Peter for Paul and redistribute. Yeah, did you have something? Yes. Yeah, I mean, I will say it was a suboptimal response, it was. But right, expectations, okay. All right, so here's a list of the things that I thought about as possible reasons. So maybe she was a non-responder, although I told you she had a great response in all those other muscles. So that's probably not it. Maybe it was poor localization. Thank you so much to my resident and the crowd that can attest to the fact that I got the muscles I intended, right. So I'm using, I'm always using guidance, at least one, often two, occasionally three types of guidance. So I'm pretty confident I can get the muscles I want. Maybe though, I went to a part of the tissue where the tissue itself was non-responsive in those sarcomeres. Maybe there's too much atrophy, fibrosis, that area was not particularly responsive to chemodenervation. And maybe you don't think about this one, but I've had to think about this before, improper handling or reconstitution. So I reconstitute my own drug or my fellow or residents do it under my direct supervision every single time. So I was confident that at least that piece had not happened. But you know, has ever the fridge gone out at night and I don't know, I don't know. So it's something to think about if you're using, say, a toxin that has to be refrigerated, for instance. Maybe the problem wasn't spasticity in the first place. Maybe it was contracture or some other type of disordered motor control. Now I told you a little bit in the beginning that it wasn't, you know, her full passive range of motion was there. So it wasn't a contracture in this case. Maybe the dose was insufficient. Maybe I didn't address all of the correct muscles. Or maybe as somebody else said, the goals were not aligned or there was a problem with the expectation. So that's pretty much as many things as I could think of. Anybody think of anything else that I didn't think of? Okay. Yeah. Yeah. That was a very good question, friend. Very good question. Okay. A little spoiler alert. The doctor in the audience wants to know what her wrist extensors were doing. I'm not sure. How do I play this video? Okay. So when she fires her wrist extensors, her hand flexes more. So she's trying to fire her wrist and finger extensors to take this cup from me. I have the poor man's motor control lab at my clinic. I don't have the fancy dynamic EMG analysis here. But that's what's happening in this patient. When she fires her wrist extensors, as somebody very astutely said, something was happening in her finger flexors. So I believe what was happening here is she was getting a spastic tenodesis. And one muscle that I didn't tell you I treated in the early round or two was extensor carpi radialis longus. So on a subsequent cycle I included extensor carpi radialis longus. This is post-treatment of wrist extensors. And we're almost there after the very next cycle. She almost got her hand around that cylinder. And there I kind of helped her just to show that she could do it. And I sent her to OT. And on another round, I increased the dose to the wrist extensors. And now we have achieved her goal. Questions on the first case? Or maybe I'll save them for the end. Let's save them for the end. I'm going to go to a second case of a man with spastic diplegia who had an ITV pump. This is a 54-year-old man with history of spastic diplegia. He had an ITV pump placed long before I ever knew him. He came to me as a transfer of care from several hours away because no one can seem to get my pump right. The history that I gathered from him is that his pump was implanted about two years prior. He had two separate trials before going to implantation. Because in the first 50-microgram trial, which if any of you are not doing pump trials, that's typically the dose that we would try for somebody first would be a 50-microgram trial. And if it wasn't sufficient, we might think about going to 75. Or if it was in this case, it made him too weak. So he was retrialed at 25 micrograms. And he had a good result. So he proceeded to implantation. Predominantly lower limb spasticity with stiffness, scissoring, inability to elevate his legs at rest. But after ITV pump placement, he could bring his legs up. He could kind of flex his hip and bring his legs up, which he needed to do because he had a problem with chronic edema. But whenever that happened, he would have severe toe spasms. So he and his doctor tried a lot of different dosing regimens to try to get that right so that he would be able to elevate his legs and not have his toes go crazy. And they tried simple continuous. They tried increasing the dose. They tried bolus only. They tried flex dosing. But what he described to me, and again, I wasn't really there in fairness, was that whenever the dose would be increased, he would get spasticity relief proximally. And then he could move his legs proximally. But then his spasticity would worsen destily. And plus, the higher he got in the dosing, the harder it was for him to walk. And I think that we had a suggestion that that might be the case early on because he needed a trial at a lower dose because of weakness. So ultimately, he was so frustrated that he had them turn the pump to minimal flow. And that's when he decided to come to me to see if it was worthwhile to keep this thing. His other history, as I mentioned, chronic edema. He had had his ankles fused. And he did not report any problems related to his bowel or bladder, no skin problems, no current infections, anything like that. He had a scissoring gait. His knees were always extended throughout the entire gait cycle. He had a step-through pattern, but it was more like a swing-through pattern, foot flat. I told you his ankles were fused. And he had, in addition to hip adduction, he had the knee extension. He had spasticity in his ankle plantar flexors, but it did also look like he was depending on some of the spasticity to stand due to underlying weakness. Okay, he had cavus feet, valgus ankles, limited range of motion at both ankles because they are fused. When we were able to prop his feet up, we did see kind of a tenodesis in his toes where they were, you know, sometimes when you extend the knee, you see more plantar flexion. But his ankle was fused, so we just saw his toes get tighter. And he had less than anti-gravity hip flexion while seated. Very difficult to isolate various muscle groups for manual muscle testing. Just a lot of stiffness there. So I interrogated his pump. Minimal flow was confirmed. The logs showed nothing concerning. I got some x-rays. There's no catheter disruption. I did a catheter access port accession in the office, and I sent that for analysis of beta-2-transferrin. Beta-2-transferrin is a protein that we find typically in the CSF, and I wanted to make sure I was getting CSF back. And then I decided that because his trial went well at 25 micrograms, that I would start him on 25 micrograms a day, simple continuous, and see how he tolerated that. And then we made a plan that we were going to admit him to our inpatient rehab hospital nearby my office so that we could make some adjustments on a daily basis and have some feedback from the therapist and really get to the bottom of the issues. Because I think I mentioned early on that he came to me from a place about three hours from my office. So it had been very difficult for me to see him as often as I felt would be needed. But I decided before I bring him in for this expensive rehab stay, I better go ahead and make sure there's absolutely no problem with his pump. So I wanted to do a little more investigation with that first. And I also planned to do a little bit of chemo-denervation for his lower limbs about two weeks prior to bringing him in, because I was really trying to time this so that he would have the most bang for his buck out of an inpatient rehab admission. So I brought him to radiology for a CT myelogram. On the day he came for that procedure, and that procedure is basically the same procedure that I did in the office. So I'm withdrawing a little bit of fluid from the catheter access port of his pump and putting in an Omnipake dye and then having him go through the CT scanner to track the dye through his catheter. And on that day, it was significantly more challenging for me to access the catheter access port than it had been in the office just a week prior. Did the study actually look okay? There was dye the entire way around the cord. And we were able to clearly see his catheter tip. And there were no obvious disruptions of the catheter with this study. What did I find on the CT? Yeah, yeah, that's not a baby in there. That is this man's bladder. And let me tell you something. I wasn't born yesterday. I will promise you I asked him about his bladder. I promise you I asked him about all the big ones, bowels, infections, skin, okay? He denied it all. So he's got marked bladder distension and he's got, they called it grade 2 spondylolisthesis of L5 on S1. So I have these findings in real time because that's a CT myelogram. I'm standing there in the scanner with the patient. So I start to question him a little bit more. You having any trouble peeing today, sir? And he denied that he had any trouble except that he took three hours to get to Jefferson and he didn't take his Lasix. So he said he had no trauma. Well, he couldn't go in the CT suite. So he had to go to the ER where he was catheterized for 1600. Didn't disclose it to me, but to the ED physician, he had been in a different ER the night before and had received anesthesia for removal of a foreign body in his urethra. And if you really did a deep dive from there, that was all we needed to hear. But suffice to say, I did ask a lot of these questions beforehand, but if we're being honest, I never did ask him if he had inserted a foreign body into his urethra. That didn't come up. He was referred to urology. He subsequently started voiding again on sildenafil. He did come in for rehab. He did great. Once we timed everything, he left on a flex dose, total daily dose of 69 micrograms. That's all it took to control this man. And he was referred to neurosurgery for a spondylolisthesis. So what did I learn from this? I always ask about bladder, but what's normal bladder function? What I would consider normal would be urinating a couple times a day at least, and that might not be normal to somebody else. And I think the other thing I learned from this is that patients aren't always going to just volunteer their sexual problems to you. And if you think that it might be related to something that's going on, you definitely need to ask those questions. So there's my second zebra. And my last slide is showing, next to my own kids, the kids in this photo are my favorite people. These are the graduates of our spasticity fellowship. If you have questions for me, my email is here. If you happen to be interested in our fellowship program, the email for the program is there as well. And I guess I will save questions for the end. Okay. Thank you very much. Thank you. Hi, how are you guys? This room filled up so quickly. So I'm Shivani Gupta, Specialty Management, Physical Medicine and Rehab, currently working in Chicago, Illinois. Disclosures, I'm on the Bureau for Ibsen. So the case I chose today was a case that I encountered very early on in my career when I first ended fellowship and it was my first year as an attending. And this patient had already gone to a neurologist. They had already seen a very seasoned physiatrist at a well-known academic center and they were now coming to me for a third opinion. And you know, imposter syndrome is a real thing. When you first come out and you're just finishing fellowship or you're just finishing your training and you're seeing these patients, you know, you can kind of question what you can really offer to them. And that can play a role into your ability to treat them. Dr. Salina recently sent us a quote, smaller in number are we, but larger in mind. And so, you know, we really can help our patients if we just take a minute to be patient with them and to really talk to them about their goals. And so this case is a patient that I saw and it took multiple different attempts to treat them appropriately. And so anybody in this room might have treated this patient very differently. And so there's not one set way to treat your specificity patients and you really have to just do a trial and error. So this patient was a 60 year old female who came to our office for, can everyone hear me okay? Yeah, okay. Who came to our office for gait disturbances. Now I told you that this patient had already seen a neurologist, had already seen a physiatrist. They had ordered an MRI of her brain and of her lumbar spine. She had some arthritis, a little bit of lumbar spondylosis, but other than that she was, she was doing okay. So they had put her in physical therapy. They had tried a bunch of medications on her that made her lethargic and she was now coming to see us. So, you know, on physical examination she had non-focal weakness in her upper extremity. She had complained about difficulty holding objects. She did have a four out of five strength throughout and in her lower extremity on the right she had a three out of five, so just anti-gravity strength with her ability to dorsiflex. But what really stood out was those upper motor neuron signs that we saw. So she had a positive Hoffman. She was hyper-reflexic throughout. She had a catch and then a release in her elbow and her finger flexors and then she had that rapid, with dorsiflexion she had that sustained clonus. And so immediately, you know, with the gait imbalance and with the signs, especially in the upper extremity, the first thought was cervical myelopathy. So we ordered an MRI of her cervical spine and she did indeed have compression of her cord. She went for an immediate decompression infusion and after that she went for inpatient rehab and I didn't see her for another six months afterwards. So six months post she comes in, she says her neck pain is doing better, her upper extremities have gotten stronger, but she's still requiring to use a rolling walker. She said she had these Michael Jackson shakes, which I was like what? But when she would start walking she would all of a sudden start shaking and she felt she was like dancing while she was walking. She still had that clonus, she still had these toe curlings in her feet that were very painful for her. So she still had upper motor neuron syndrome in her lower extremities that was really affecting her quality of life even after the surgery. So again what we saw on physical examination now was still that weakness in her right lower, so still that three out of five with dorsiflexion. She had sustained clonus with rapid dorsiflexion. She had co-contraction of her knee flexors and extensors, which I find very hard to treat. Does anyone know what co- contraction is? Anyone want to say it out loud? Yeah, so the antagonist muscle is supposed to relax, right, while the agonist muscle is activating. But when you have both of them happening at the same time that's the co-contraction, exactly. So when you have injury to your brain near your spinal cord, not only do you have spasticity, but you have all these other signs of symptoms that you can see. So spastic co-contraction is one of them. I think it's very difficult to treat. In addition, she had the triple flexion reflex, which, what is that again? Yeah, yeah, exactly, yeah. So you know we all have, if we were to step on something sharp, our hip would flex, our knee would flex, our ankle would dorsiflex, but in this patient it was exaggerated and it was affecting her ability to sleep. And she also had that toe clawing of her toes when she was trying to walk. So what would you want to do? What would your treatment be for her? So we have a whole list of things that we can use to treat patients with these symptoms, right? So we tried them all. So the first thing is, does she have generalized or does she have focal? Is it affecting her upper or is it affecting her lower, right? Does she have more than spasticity? Yeah, she had the co-contraction, she had the flexor synergistic patterns, she had chronic activity, right? So she had tried pretty much all of the oral medications already with the neurologist and the physiatrist. The one that she hadn't tried was Dantrolene. It gave her some blurry vision, which I haven't seen very often. I probably have a couple of patients who have complained of that with that. So unfortunately, we had to stop the Dantrolene. We did a back-up-at-home trial. had the flexor synergistic Yeah, perfect. So that's what we did. So we tried chemoduration. So we used Tocline, we did her bilateral FHL and FTL, her gastrocnemius, soleus, medial and lateral, and then her tibialis posterior for that inversion. But when you think about that, that is actually quite a lot of muscle that you're trying to use. So even though we diluted it and we used our maximum dose, she still was having complaints even after that. So now we're really trying to think, what else can we do for this patient? We've tried oral medication, she's done therapy, she has a pump. So, perfect segue, I'm going to be talking about, you know, spastic toe curling. Okay, let's see. Okay, we're gonna be talking about some off-label muscle targets as well. And the reason why I bring this up is there are things before I prepare for this presentation I didn't realize I had some suspicion of and hopefully you guys will also, you know, have your eyes open and realize a lot of these other things that exist. So, here we go. So, spastic toe curling, flexed toe deformity due to overactivity of the toe flexors. Oftentimes, you have it with Aquinas, Varus, and Equinavirus deformities. And it's a big issue for our patients. You know, not only can they cause them discomfort in their bracing or when they're walking, but ingrown toenails, skin issues, and, you know, it can also further worsen the Aquinas and Varus deformity. As well as, if you imagine if your toes are curling when you're walking, how does it affect you in the gait cycle? You can imagine in, you know, Dr. Glockenflecken's favorite, you know, phase of stance, terminal stance, as you roll over your forefoot, this toe curling will inhibit your ability to roll over that forefoot. So, thank you, Dr. Glockenflecken. So, alright. So, here's a patient, you know, this is a patient with a brain injury. I'm going to show you a lot of pictures of feet. Hopefully, you guys are okay with that. You can see he got, he had ankle clonus, but then, you know, how many times do you stretch the toes and you get a little toe flexor clonus. So, now, a lot of times we've, you know, we treat the FDL and FHL, and there was actually a study done, a multicenter study done, where they looked at with, you know, they compared this treatment of the gastroc soleus and to posterior with the addition of the FDL and FHL, and I show these complicated graphs below, but in, you know, at the end, they just show that if you treat the FHL and FDL, you get a better ASHRAE score, you know, post injection, but they had to increase the dose significantly for that. So, here's a patient of mine. He's about, let's say, he's about four or five months post-stroke with a right hemi, and you can see him walking. So, I have a, I have a handful of patients I share with another, a partner of mine, who only treats the upper limb, so we sort of divvy up the dose, and, you know, I have 200 units of onabotulinum toxin to treat his leg. So, I guess my question to you guys would be, which... We treat the gastroc, the soleus. Yeah, it's something you just notice is his foot stiff, he has trouble walking. A lot of times they just come to me like yeah my leg is stiff and you take the shoes off and everything and they show you all these things. So you know if you look at him closely you'll notice which toes are crawling more, was it the big toe or the little toe? It's actually more the big toe. So we ended up treating his FHL. He also had a lot of clonus in his gastroc so we treated that as well. I don't know if you noticed when he was swinging through he also had a little bit of shaking. So we did that and you can see him walking now. This is one month post treatment. No? Yes? He felt better. I think that's really the most important thing and he was. If you, you know, you see a little inversion but if you slow it down and you look at him pre and post, what you'll notice is, you know, pre-injection you can see his hallux really curling down into the ground and then post you can see how the hallux is relaxed. The other thing you'll notice is not just his hallux, his second toe is also curled a little bit but post-injection you also notice a little bit more of the lesser toes flexing up. And why is that? His dorsiflexion improved. So as his dorsiflexion improved, I put a little bit more stretch on the FDL as well. So now the thing about the FDL and FHL that I sort of suspected but I didn't have a good explanation for is, why do people when you inject the FHL, like, why do people have these weird toe flexion patterns where they may just have the hallux and the second toe or the first three toes curled and the last two relaxed? Like, do you guys see this in clinic? No, nobody looks at the feet. Or vice versa. And I always suspected that there was some anatomical abnormality where the FHL had some, you know, tendons split off going into the second or third toe. And actually it's sort of true but it's not really that FHL has a tendon. There's actually a tendon slip that slips over. And there are these other prior docs who, you know, it's called the Master Knot of Henry right here. And this has been noticed by a lot of other anatomical studies. You can see there are a lot of varieties that we're not gonna really go into but it's there. You can look back at these slides or take a picture of this if you want to look at this later. And a lot more. And how you can test this is you can actually put your thumb or your finger underneath the big toe and have it curl against resistance. You can do it now and you can see, does a big toe curl by itself or does it involve the other toes together? And are we symmetric? I'll tell you, I did it to myself and on one side my first three toes curled and on my other side four of them curled. So I guess the answer is some of us maybe but not all of us. I'm definitely not. So here's another case. This is a lady. She's, she had a brain injury. I want to say she had it about ten years ago. And this is actually a video of her and she had gotten treatment to her gastroc soleus to posterior and FDL by another provider. But we have a video of her like one month post-treatment. And you know it's on the left side. It's a little different, right? You know, what's, what do you notice that's different about her foot deformity here? or flexed. Yeah. Yeah, so it looks like an intrinsic plastic deformity in the hand, but it's in the foot. So you can see her hallux is curled or flexed at the MTP joint, right? So she has great dorsiflexion. She's really a trooper. So what, you know, so here are my, sort of, my zebras here. You know, you also have these muscles in the foot. And then, you know, it's sort of the limitation of our education is, did any of you guys get to dissect a foot in anatomy class in med school? Did some of you guys? Raise your hands if you did. Because we didn't. They just sort of stopped right at the ankle and they didn't have any feet, you know. Yeah, we kept their shoes on, I guess. So, yeah, but if you look in the foot, you have like three different layers. It's a very rich area. You know, if you look at the bottom, you have your plantar fascia. Underneath that, you have your flexor digitorum brevis. And then, you go a little bit further, you have a quadratus plantae here and the flexor hallucis brevis, as well as you have a flexor digitorum minimi brevis as well. And your adductor muscles and lumbar cools and all sorts of, you know, fun stuff in there. So, so here are these muscles. And it's, it's interesting because, you know, we just think that they just flex at the MTP joint. However, some of these, you know, if you look at the flexor hallucis brevis, I thought it was just like an MTP flexor, but it's actually similar to the FDS in the hand. It actually does do a little curling at the IP joint, but the proximal IP joint. Whereas, the quadratus plantae does a little bit more, oh, yeah, it does, it acts, you know, acts similar to FDL. However, the flexor hallucis brevis just curls at the base, at the MTP joint itself, as well as the lumbar close and interossei muscles in the foot. So, you have just several rounds of treatment to our flexor hallucis brevis, included in all the other muscles. you can see her foot's now a lot more flatter right there. So here's a gentleman who's, this is a this is a gentleman who had a stroke, similar but he has a lot of Aquinas, actually a lot of varus deformity in addition. He usually wears a brace but I had him walk barefoot for me just to show you guys. And you know after several rounds of injections I wasn't quite happy with his response so I actually you know I sent him to surgery but I'll show you his post-op video in a second. But what are other things? I know we always talk about toxins but you also want to think about you know there's splints you can use at night to help stretch out the toes. One's a, it's called a Strasburg sock, you can find these online. You can look at your, the shoes and you can try to find a shoe that has a negative toe rocker to help offload the toe a little bit, as well as some of the bracing. With the bracing you can think about, let's say if they have a lot of dorsiflexion range, you can try to control the dorsiflexion so they don't curl as much. And then also surgical considerations, you know long toe flexor release but also you know we also have seen people undergo plantar fascia or FDB releases. So here's this gentleman post release of his plantar fascia as well as a lengthening of his to posterior FDL-FHL. Yeah, a lot better, a lot faster. This is surgery, yeah. No, this is not me. This is a very good, hmm? They might have done this, I think they did a splat. Yeah, sorry. So in this shot, I've only seen one case but there is actually a flexor determ accessory along this muscle. This was a patient who had some dystonic toe curling and they had an MRI that showed this. So there's some others. So some take-home points from this talk is just always inspect the feet, the insoles, the shoes. If you can, when it's safe, observe them walking barefoot and try to figure out is it the long toes, is it the short toes. And then be aware, like if it's the second and third toe curling along with the big toe, is that coming from the FHL, the FDL, or both? You know, because if you look at this this image here, you notice the second and third are curling more. The hallux is a little bit and the lesser toe is a little bit, but yeah could this lady have, you know, slips of the FHL going to the second and third toe. And then sometimes you want to treat the toes before you really aggressively treat the varus or the equinus deformity because if you treat those without treating the toes, then the toe curling will worsen. And then, you know, don't be afraid of sending a foot and ankle surgeon for releases as well. So thank you and after this talk what I realized is, you know, zebras are probably horses dressed in stripes. So thank you. All right, so I figured I'd have a little bit of fun with this if we have horses and zebras in the title, then me being a Florida resident, I figured I'd throw some alligators in there as well. So I used our friendly AI to generate an image with all three of them in a pen together. So yeah, so I'm one of the former fellows in the Jefferson Specialty Fellowship, which you guys have heard of a few times this hour. I was a class of 2022, which felt like yesterday, but now I'm like middle of the pack now, so I feel really, I'm feeling it now. Yeah, but I'm down in Sarasota, currently working with the group down there. Most of my practice is focused on neurorehab and tone management, so I've got just a few cases here for you guys. So first case, this is somebody who was referred to me by, I believe it was a neurosurgeon, a 48-year-old male with, he said, back pain and spasms, previously healthy. He was a dentist, had his own practice, doing very well. Back in about 2017, late 2017, early 2018, started to develop progressive truncal weakness, and it was really affecting him because, obviously, as a dentist, you're spending so much time bent over looking in people's mouths, and he was finding that he couldn't really maintain that posture anymore. He couldn't stay in that bent position. So it really was affecting his ability to actually do his job. So they did some imaging. It did confirm thoracolumbar stenosis with concern for myelopathy. So he underwent kind of a unique surgery, T9 subtraction osteotomy, T4 to L1 posterior fusion, so that was a pretty extensive fusion, as well as a T7 to T8 decompressive laminectomy in 2018. Post-operatively, he did develop what he said were painful muscle spasms. Three to four-month post-op visit with the surgeon, per his recollection of the interaction with the surgeon. He came in with these complaints and these issues. Per him, he said the surgeon told him nothing went wrong, the surgery was perfect, and basically said, you know, get out of my practice, because he was making a big deal of it. He was also evaluated by several pain physicians, orthopedic specialists, had undergone aggressive PT, modalities, TENS, underwent a few different medication trials, gabapentin, flexeril, some trigger point injections, thoracic lumbar radiofrequency ablation, nothing helped. He later underwent a repeat MRI in July of 2023, which at this point when I saw him was his most recent imaging, and really relatively unremarkable. I didn't quite, I didn't have the imaging available, it was done in some outside facility that we couldn't get a CD ever, but at least the results said post-operative hardware intact, nothing else acute. So at this point when he's coming to see me, he had basically stopped his whole professional career, sold his dental business, he was on disability insurance, and for the most part, about half the time, if not more than half the time, he was depending on a rolling walker for ambulation because of these spasms. So certainly quite a change of events for this gentleman over two, three years. So again, I'm coming to see him, and at this point, like I said, he's gone through the ringers, a lot of the conservative pain measures and treatments and everything like that, and I, you know, he points to the cervical thoracic region, describes it as tight, overall limits his neck and trunk range of motion when twisting. Key point here is that he says it completely seems to go away, he doesn't feel spasms when he lays down. He denies radiating pain, paresthesias, all the, you know, warning signs and symbols, no focal neurologic deficits, nothing else going on in the arms and legs, strength is totally fine, walking is fine, everything else kind of checks out, right, nothing else going on. So on exam, symmetric shoulder rise, mild forward flexed posturing, certainly, you know, I think a lot of that was kind of trying to alleviate spasms through kind of manipulating his posture kind of whenever he could, kind of felt like he was just on edge all the time, and so again, feeling that it was better when he's laying down, he spent most of his time in bed because it felt better when he's laying down. He did have some tenderness along the paraspinal musculature, particularly from lower cervical to mid-thoracic region, and again, everything else checked out, you know, his gait, strength, sensation, everything like that was completely fine, reflexes, everything like that. And then we take the shirt off. So, as you can understand and appreciate, this is static sitting, I'm not asking him to twist, I'm not asking him to do anything crazy, metaphorically, my jaw was on the floor at this point when I, when we did that, and this moment was pretty, again, I was just kind of flabbergasted because he had told me, you know, he'd been through four or five different physicians who had seen him, nobody had taken his shirt off to look at this, and if they did, I'm kind of postulating because I'm like, how did this, how did nobody come across this over a few years, right? And my guess would be that maybe he was laying down, right, when they came in to examine him or even for the radiofrequency ablations and stuff like that, because certainly when you do lay him down supine or prone, there's no contraction at all, it's the craziest thing. So anytime I, we'll get to the treatment here in a second, but anytime I treat him, I make sure that he's sitting up to see the activity before I go and do it. So, you know, obviously I see this, first thought goes to my head, obviously, you know, we have our treatments that we like to provide, but given that this was a very unique case, you know, obviously it's involuntary, it's sustained contractions. I did reach out to our movement disorder specialists, you know, some people who kind of delve a little bit more into the dystonia realm. I want to make sure I'm not like, you know, missing out on some other dyskinetic, dystonic kind of syndrome or something like that. They pretty much told me, kind of checked out, really there's nothing else from his history or anything else on exam that would lead them down a different path or anything like that, you know, nothing that they would give a medication trial of or anything like that. So we see this a decent amount, you know, for anybody that treats cervical dystonia, there's this kind of relationship of spinal fusions and relative dystonia. Now whether that is a primary dystonia that goes undiagnosed and then somebody treats it as, you know, oh, this is probably, you know, some cord compression, kind of like this gentleman, or, you know, is it a secondary dystonia that's kind of reactive to the procedure? It's hard to say. If you ask him, you know, again, he felt more weakness and never really had any feeling of tightness or spasm or pain or anything like that prior to the surgery. So again, once I kind of cleared it and I was like, okay, I got the blessing from the neurology folk, we started with the first cycle of Botox. So he had mentioned a little bit of tightness in his, what seemed like the upper traps, and so we put a little bit in there. And then I increased the dilution and put about 100 units. I think I had like texted our fellowship group and everybody's like, oh, that's low dose. Come on, man. You know, I think even Captain Conservative up here mentioned, she's like, I would do more than that. But yeah, no, I figured, you know, first cycle, let's just see how it goes. Diluted two to one, four separate sites. And it was really tricky because I basically would wait for that muscle to activate and then go in with the needle, hear the EMG fire, and then go. So very, very interesting procedurally too. I think my MA was about to pass out watching it. So this is one month later. Try to see if you can provoke it a little bit. You said you're kind of extending the back a little bit. That's me trying to do it. Seeing it kind of fires from the bottom or at least it feels like it does or lower. So, relatively speaking, before and after, pretty significant difference. And he came in just absolutely astonished at how things felt. If you guys could kind of see on that, there was a little bit of movement still on that right side. So what I ended up doing is we actually, I didn't want to do any more in the traps. I don't think it was really helping as much and so we ended up just deciding to double the dose on the right side. So I ended up putting 200 into those right thoracic paraspinal muscles. So we did 200 on the right side, 100 on the left side. Again, did the injections while he was seated and with EMG guidance, wait for the activity and then go in with the needle and get confirmation of that. Obviously in that area you have a lot of different paraspinal muscles, your spinalis, your longitimus, everything like that. So hard to classify exactly which paraspinal. So I kind of just, that's why I diluted as much as I can and kind of pepper it in different areas along that whole region. So follow-up wise, now I see him. He's very well controlled on Botox. That last addition of increasing that right side seemed to really take care of most of it. He takes a little bit of Robaxin here and there if he's having a rough day and he's feeling a little bit of refractory spasms. But he's back to honestly relative independence. He's getting around town. He's trying some work at home. He doesn't feel like he has to lay in bed all day or anything like that. So every time I see him, he makes sure to tell me thank you before he sees me, thank you after. And he's just like, Doc, I'm so, you know, and I'm like, I appreciate it. But it's amazing to hear the impact that you can have on patients' lives with interventions such as these. And again, crazy to think that it had gone that long without somebody doing anything about it. And that goes back to Dr. Moon's point of evaluate everything. Take off the clothes, take off the the shoes and the socks and everything like that, right? I mean you want to, you really want to get a good glimpse of this and do a very thorough physical exam if you're going to be treating this. So I put dystonia unspecified. Yeah. And so I used CPT codes for truncal muscles. And in Florida, you have to use Botox for dystonia other. Yeah, that's kind of the first-line treatment for that. So yeah, encounter with an alien, that's a good one too. Yeah, yeah. I mean, knowing ICDs, there's like explosion from jet skis and stuff like that. So there's all sorts of crazy ICDs out there. All right. My second case, these are, I call them unforeseen consequences. This is kind of a unique one that I just came across in the last few months. 50-year-old female from inland rural Florida. So not a lot of providers around her. History of a stroke back in 2015, right dominant spastic hemiparesis. Per the patient, you know, she came in classic, you know, new patient, no paperwork whatsoever. And she doesn't really know her history and so I'm trying to kind of glean what I can from her. You know, she had mentioned that she'd undergone multiple rounds of botulinum toxin injections and she says it was for her shoulders, elbow, wrist, fingers, and some in her calf muscles, which she said worked well. And then about three to four cycles into her treatment, she said she had side effects from the injections. And I asked what what type of side effects? She said what it did to my hand. And let me take a look at the hand. And I'm looking at this. Certainly that is a, that's a, that's a definite, you know, swan neck. If you could define a swan neck, right? At this point, again, her stroke was in 2015. I think her injections were in, you know, 2016, 2017 time frame. So I'm seeing seven, eight years of post, whether it's injection complication, post spasticity complication. So I'm looking at this hand and, you know, the the PIP definitely, the MCPs, you know, kind of stuck in that position. PIP stuck in that hyper extension position. I'm not able to really move anything at all. She was certainly not a fan of the idea of receiving any further injections. She didn't want to do anything else for it. And so really we kind of ended the appointment trying to kind of figure out to make like some sort of custom, you know, wrist hand orthosis, wrist hand finger orthosis if we can to kind of prevent anything further from happening. But it's just very, very confusing. So swan neck deformities, I just figured I'd kind of touch base on that just for a second. You know, certainly it's PIP hyper extension and DIP flexion. It's an imbalance of that extensor mechanism. Potential causes, right? You could have loss of extensor components at the distal phalanx. Or it could also be, you know, tightening or over pulling of the proximal phalanx. So just like anything in the body, right? It's the combination of vector forces on any joint that's going to pull it in a certain way and how that can change it. So, you know, commonly if you see a swan neck, you know, it could be some sort of laceration, some sort of avulsion injury. You know, folks with, you know, rheumatoid arthritis, inflammatory, post-inflammatory changes, certainly you have changes in the connective tissue fascia and ligaments to kind of, you know, put them more at risk for something like this. She, per her at least, did not have any history of autoimmune rheumatologic issues. She was very confident about that. And, you know, the other thing is an increased pull at the the central slip is probably, I would say, less common. But the idea here being, you know, you look at your lumbricals, you look at your interosseous muscles, you know, they do attach onto that extensor hood. And depending on how much activity there is in the intrinsics, you could potentially argue hyperactivity of that extensor component could lead to something like that. Again, I didn't see her back in 2017, 2018, you know, so I don't know all the variables that went into getting her to that point. She denied any trauma, no accidents, no cutting of her fingers, nothing like that, right? So she never, I prescribed the brace, she never followed up with me, she never, you know, she kind of canceled her appointments and stuff like that because I think to her it felt like we couldn't really do much more than that. But it was just something, you know, very unique. Again, a zebra that I think is, I'm still kind of wrapping my head around how that presentation came to be, but, you know, certainly I thought it was just interesting to kind of talk about it and just see, is this something that, you know, maybe you guys might see in the future. And then last, these are, I guess, not necessarily zebras, but this was some of the work I had the pleasure of going up to Victoria to work with Paul Winston. Mike Salino was with me during this time and, you know, a lot of these patients were patients that were zebras in the fact that, you know, they had tried toxin and toxin and toxin and didn't quite get the improvement that they wanted, and so these were patients before and after, patients that, thankfully, I had the chance to perform their cryo-neurolysis on various muscles and to kind of see the before and after. Dr. Winston's really great about, you know, taking before and after videos and really kind of that comparison, which I think is really groundbreaking. I think really shows a lot to people. So this was one gentleman. You can see very difficult, hard to move, and then no extension. So this, that's not so bad, but we did above the elbow to really get everything out. So this is what is a reducible deformity. There's another before and after. This, this, this female had a significant amount of co-contraction, especially with peronear teres and peronear quadratus that she couldn't really, you know, supinate the hand for self-cares or anything like that. This is before and after. This is the first time she could actually kind of see her palm without trying to kind of bend over completely. So it does release, so it is reducible, but there's a lot of tone. And the same with here, like look at the resistance. And finally, to the front. Good, and straighten your arm. The gentleman on the left, he couldn't really do anything without, again, bending all the way at 45 degrees in one way to use his shoulder, and then you see him open up with flexion and extension of the shoulder and all the things he could do there. You couldn't really get him above 45 degrees of shoulder abduction, and then here we have actually about almost near full range of the shoulder. So we always do it lying up, because when they lie down, they relax a little bit. Okay. So the fingers do open, but there's tenodesis, so as soon as you try to get it. If you get a chance to spend any time with Dr. Winston up in Victoria, highly recommended. Really, really, he's a fantastic clinic. You learn a lot from him, and really, Victoria is beautiful, too. So if nothing else, just go for the views. So, yep, again, Sarasota Memorial Hospital. We're in Sarasota here. We got a, this is our mobility garden for patients on the first floor. We do have a putting green, so patients can work on their putting. So they always love to tell me how they did that day. So, love what I do. That's my license plate to my car on the right. It's my favorite muscle. So, you know, do what you love, love what you do, and hopefully you guys learned something from today's presentation. Thank you. So, thanks to all my colleagues, and especially my junior colleagues for showing me up and doing such an awesome job. I get to bat in the fifth position in cleanup to talk a little bit about some of the things that I do. I'll be brief because I know we're running a little bit behind, and I want to leave a little bit of time for questions. So, these are my disclosures. Nothing really off-label here, per se. I only use brand names if absolutely necessary, and because I have a leadership position at Cooper, I have to disclose that these opinions do not represent the opinions of Cooper University Health Care. The cases that I'm going to describe are a little bit de-identified to protect the innocent and obscure the guilty. These are really the cases that I get. The zebras and the zebraic unicorns, things that no one else has seen before that I have to try to unpack a little bit. So, they start out very similar. So, as always, this happens at the witching hour of medicine. That is four o'clock on Friday afternoon. Receive a call from your hospitalist group that they are in need of urgent attention for those of us who manage intrathecal pumps. No one else in the medical universe knows anything about these systems, so only us can figure it out. A 35-year-old guy with multiple sclerosis presents with, from recent implant of an intrathecal pump two days ago, or a few days ago, was managed by an outside clinic by a physician who does not have privileges at your hospital. So, it is your obligation to begin to figure out. He was implanted at an ambulatory surgery center and then seen two days later in the office by his clinician. Has been growing increasingly somnolent over the last two days and presented to a local ER being minimally responsive. So, of course, it has to be the pump at all times, so they send to only those places that know how to deal with it. Again, the managing physician does not have clinical privileges. They send them to us and we have to figure it out. Again, the hospital internists completely throw up their hands saying that it must be the pump and please help us. So, first thing to do is to get more history and then the thing to do after that is to get more history again. So, you call up the managing clinician. Seemed like a relatively straightforward case. Pretty classic MS appearance, spastic paraparesis, neurogenic bowel and bladder, typically well-managed. Really didn't have much in the way of past medical history. The clinician had done a trial at 50 micrograms, had a good but not excessive response in any way. Implanted at an ambulatory surgery center, discharged on the same day in stable condition. The infusion was started at 100, not completely unreasonable if you had a good response at 50 to start the infusion at 100. He was very quickly weaned from oral spasticity medications. Seen three days after implant, increased from 100 to 125. Maybe a little bit aggressive but not, you know, completely crazy. The managing doc confided to me that the neuro exam was at his baseline. He was cogent, well-responsive and other than that, his spasticity was well controlled. So, we go to see him. Minimally arousable, adult male, had no tone on exam. His incisions look fine. His UA was positive but really didn't have anything in the way of peripheral white count. His telemetry and logs looked okay and he was at 125. So, when I was a young pup, this was the pneumonic that I was given for change in mental status called Move Stupid. The things that this could be is metabolic, oxygen deficiency, vascular, endocrine or electrolyte, seizures, trauma, uremia, psychiatric, infection or drug. So, I still use this anytime I'm confronted with someone who isn't behaving normally to just kind of do all the check marks. And we went through just about all of them and nothing was really turning up. His imaging looked okay. So, just out of an abundance of caution, I asked the primary to get a CT of the belly to make sure that there wasn't some kind of intra-abdominal abscess as a result of the impact. While we were working this up, again, if you're in a situation where you're concerned about either baclofen withdrawal or overdose, while you're doing the workup, initiate treatment. So, we began to do just sequential decreases. We went from 125 to 100 to 75 to 100. He was eventually found to have acute bacterial prostatitis. It was probably something that was brewing for a long time with neurogenic bladder. His PSA was 50, which is a pretty high number. He was treated with four weeks of antibiotics. As soon as he got a second dose of IV antibiotics, his level of arousal improved really nicely, transferred back to the managing physician without issue. So, teaching points with this. Do not let your brain fall out when you're taking care of patients. It is not always the pump. And teach our colleagues and the rest of medicine to use their good medical skills to work things up and continue to move forward. So, then my unicorn. So, pretty much the exact same presentation. Implanted in an ambulatory surgery center, managed by an outside physician who doesn't have privileges. So, again, they come to us and we have to figure out what's going on. Same presentation, minimally responsive, nothing really dramatic on exam that we could pick up. Nothing really different about this. This was not the same managing physician. Again, these cases are de-identified so that, you know, no one gets in trouble. But a very similar presentation. Hey, I trialed this guy. The guy did great on the trial. I referred him to the neurosurgeon who I always work with. He always does a good implant. Implant was fine. I saw him two days later in the office. Bumped him a little bit. Doing really fine in asbestos. He was obliterated. And again, shows up with a mildly positive white count, but nothing really dramatic. Went back to my move stupid analogy for change in mental status, but really nothing showing up. And, yeah, everyone's kind of looking at me like, you deal with this all the time. You fix it. I'm like, well, tell me what to do. Like, I have no idea. So, again, I just started walking things down and maybe he was getting a little bit improved. But really, the primary team was worried about this guy's gonna aspirate and he's gonna have lung problems. We're gonna have to intubate him. So, eventually, I just said, you know, let's take the whole thing out and see what, see what we did. So, I accessed the reservoir. The right volume was in there. Replaced it with normal saline. The solution looked absolutely fine. Did send it for analysis. Like, maybe it was a contaminant. The guy had meningitis. It was really normal. Didn't see anything. As we often do in these situations, access the catheter access port. Positive for beta-2 transference. So, he was in CSF. Essentially normal. So, just put him on saline. Reprogrammed him with a priming bolus after the catheter access port study and just left it at minimal flow rate. Very, very gradually, he started to get better. Maybe over the course of a week or so, but never really got any tone back. Was, you know, weak. Didn't want to go to rehab. Just wanted to go home and went back to the managing physician. So, something didn't smell right with all of this. There's something wrong. Luckily, I sent the fluid back for more quantitative analysis. The baclofen concentration was not 500 but 5,000. This was compounded baclofen made by a pharmacy tech at the ASC. So, when he was increased from 100 to 125, he was really increased from 1,000 to 1,200. And so, he went from 0 to 1,200 in the matter of five days. No wonder he overdosed. We did let his managing physician know that maybe he should use branded product, especially when starting someone off. And we did let risk management know, not that we had anything involved with it, but this was clearly a case of a medication error. So, sometimes it is the pump and you can't eliminate the possibility. As I've told all the, all the, my distinguished fellows, they know this. They all call me Yoda because I've trained 900 years of Jedi masters and now they're outstripping me with my ability. It's never the pump until it is. And that's a really important point to think about. Pretty unusual, but not to be overlooked to consider a medication error. And if you do take the medication out, send it for analysis. Most big hospitals have a way to do some quantitative analysis. It won't come back in a day or two, but this was a clear case of a medication interview. Remember, the pump is a robot. It only does what we tell it to do. And whoever put the material in clearly made a dilution error when they were making things up. And we had two minutes to spare during things, so we caught up a little bit. I'd like all our co-presenters to come up and maybe take some questions from the audience. I'm sure we'll stay around a little bit later knowing that we are coming down to the end of a long first day of the Academy. Any big questions for any of us? I think it probably had some contributing factor, but I suspect that he just had a chronically conylized bladder. Maybe he always had a degree of retention that seeded the prostate and the implant and maybe a little bit of colonization just tipped him over the edge. your block location for that? Alder? No, for the motor point branches. So, in the second case where it was really rapid, I actually was doing it every 12 hours because the primary team was getting increasingly nervous that this guy was going to lose an airway. So, I had no problem with it. Plus, we trial folks at 100, and nobody goes into withdrawal after a trial, so I felt reasonably confident. But here, I was really dropping him from 1,200 to 1,000 to 750 to 500 to 250, and there was just an overwhelming amount of baclofen and CSF that just needed to clear. Were you going in every 12? I was doing it—well, the first time I went in and just dropped him to 100, went back the same day, did it 12 hours later, but then afterwards was just doing a 12-hour bolus to bring him down. I'm going to call time out at this point and let everyone get off to some fun things for the evening. Thank you so much for attending. Enjoy the rest of the conference.

spasticity

physical medicine

rehabilitation

Cooper University

case study

treatment goals

spastic diplegia

intrathecal pump

chemodenervation

Botox

dystonia