Good afternoon. Can you hear me OK from the back? OK, great. Thank you for coming to our session on gait disorders. And this is later in the afternoon. There's a competing session on the other side. And thank you for coming. And gait disorders after spastic hemiplegic is very common, yet it's very complicated. So three of us today will address this issue from a different perspective from our own clinical and research experience. And each of us will speak about 20 minutes and save about 10, 15 minutes for the question at the end. So my talk is from a perspective on the neuromechanical consequences of the post-stroke hemiplegia. I have no disclosure related to this talk. And before we jump to the post-stroke hemiplegia gait, I would like to remind you the normal walking. This is a simulated skeleton walking. Well, this is a little too early for Halloween. But this gives us some idea of how we understand the gait issue. So this simulated skeleton walking reminds us what's so-called six kinematic determinants of the gait with all the three pelvic factors with the knee and ankle, all these factors together to make a smooth line or the move of the center of the gravity of our body. However, this does not address the common observation that we observe on the treadmill walking. And as shown here, on this treadmill walking, the tip of the toe is only about 1 to 2 centimeters above the treadmill with less than 4 millimeter step to step variation. And this cannot be explained by all these kinematic determination. And this is actually a result of all these muscles in the leg and the trunk, even the upper limb, that controls the movement or the control of the tip of the toe. Now, as we can see here, they simulated the muscle activities from instrumented gait lab in the literature. As we can see here, every single step, there's spatial and temporal coordination and activation of the muscles in two legs. So let's take a snapshot. Let's see what's the focus on the left leg mid-swing phase. On the left, we have all these, the iliopsoas, quads, tibiaris, anterior for the left leg mid-swing phase. But at the same time, there's a muscle activation on the right leg in the mid-stance phase. There's activation of hamstring, quads, tibiaris, anterior, and the glute max. Now, let's take a look at the temporal sequence and the activation of this muscle. Now, starting with the left leg early mid-stance phase, there's activation of quads, tibiaris, and the glute max. And at the push-off, there's kicking the glute max and calf muscle. And at the very early swing of the left leg muscle, and there's iliopsoas, quads, and calf muscle activation. And at the mid-swing phase, there's increased activation of the tibiaris, the anteriors kicks in. And at the later swing, and all quiet down. And at the terminal swing, the hamstring is activated to decelerate the left leg, prepare for landing. So from this serious event and to the previous slides of SNAPstrap of the bilateral leg muscle activation coordination, and then lead it to the idea of the muscle synergy, or modules of the muscle synergies for gait control. So the idea is that different muscles are grouped together to activate at a certain time point during the gait cycle to control the tip of the toe, or where the leg, different joints in space. So normally, in normal healthy subjects, like what we do in normal street level walking, we have about five or six motor modules. And these modules have a very complicated neural network control. And this is a very busy and colorful slide. Let me break it down. So there's all the network involved in red is involved in the autonomic process that involves brainstem, cerebellum, spinal cord. All these are for the automatic ground walking. And there's a volitional process. This is the cerebral cortex. And we know when we want to start and when we want to stop. And there's a green one, the emotional process. When we are hungry or we want to go to the bathroom, for example, and we want to speed up or slow down. And there's modulations with the visual, pre-perceptive, and these kind of inputs that will lead to modulate how we walk. And for example, when we see the traffic light is red, we want to stop. This is how this is a normal gait is controlled with a very complicated neural network. So what happened after the stroke in terms of this neural control and the muscles? So we know here from this slide. And we know for hemiparesis, there's a few things. One is the weakness. The other is the spasticity, is positive sign, and also the spastic synergistic elevation. I want to highlight that these are mediated by different mechanisms. And muscle weakness is on the left side. Basically, it's a result of interrupted corticospinal tract damage, while on the right side is the due to this motor cortex or the corticospinal tract damage lead to the unmasking of the brainstem descending pathways become hyper excitable. That is including reticular formation and the rubrospinal tract or other brainstem descending pathways. And these pathways become hyper excitable and mediate the spasticity and synergistic activation. So more importantly related to the gait is all these unmasked hyper excitable brainstem pathways will merge, simplify all these motor synergies. So to make isolated voluntary control of a single muscle is more complicated. So as shown here in one of the earlier studies, from the left to right, from the right to left, as we can see the original EMG signals. And this is with the higher motor synergies. And we have more isolated EMG activities in the leg muscles. And when the stroke, when the patients get more severely impaired and they get less motor synergies, I would say it's detectable motor synergies. And as reflected on EMG, when there's a very severely impaired on the left side, there's only two motor modules. And EMG is almost sustained involuntary EMG activity throughout with a sparked burst of voluntary activation. So based on all these pathophysiology occurred in post-stroke hemiparesis, we propose that this neuromechanics of a post-stroke gait. On the left side, we say there's a weakness as a result of corticospinal tract damage. And on the right side, as a result of unmasking and resultant hyper excitable brainstem descending pathways and simplified motor synergies. And they interact with each other since abnormal synergies will lead it to the abnormal joint position and lead it to the abnormal kinematic change in the joints in the leg. So there's abnormal grantor reaction force. So the final resultant gait pattern is a result of these three factors. It depends on how weak the leg is, and how severe the spasticity is, and how abnormal is the joint alignment is what determine of this. So based on these pathophysiologists and the pathomechanics, and I would say there's a hierarchy of post-stroke gait impairment. There's, to me, and there's no stereotypical post-stroke hemiplegic gait as often described in the literature or in the textbook. Here, I will demonstrate to you from very early mild weakness with almost no spasticity. And this patient with a mild weakness in the calf muscle with a lack of the ankle plantar flexion push off. So this patient, he's, this gentleman able to walk relatively faster. So when this gentleman has a little ball weakness in the quads, and not able to hold knee into full extension during stance phase, and he's walk more slower. And as the severe progresses, and now the quads, knee extensor become much weaker, and the glute max has to kick in, and to pull the femur backwards. And that's what we call a stereotypical hemiplegic gait, a circumductor gait. This is one of the categories. Now, when the glute max is continue to become weaker, and not able to hold the femur come backwards, and all the hip into flexion, knee into flexion, ankle and foot into flexion. And as shown in this video, this gentleman is very able to making a few steps. So there's approaches to understand the post-structural gait. Now, in the literature, there's, I find that there's the pelvic girdle muscles is not emphasized, but which in clinical practice, I find that they're very important, because that is the, well, just to remind you, there's three out of six kinematic determinants related to the pelvis. And the pelvic muscle is weak, and the spastic will lead to the abnormal pelvic girdle position, will lead to the abnormal gait. So here, on the left, this patient is about two years out of stroke, with a left hemi, and came to the clinic for intervention for botulinum toxin injection. However, she had, after one round of injections, she said, there's too much needle sticks. I only want to stick one needle, only one muscle. And I said, OK, what's your main goal? How can I help you? And she said, well, I want to make my walk better. So among all the muscles in the body, I selected one muscle, and this is about a six or eight weeks follow-up. And her trunk is less leaning on the left side, and the walking is better. And we can see, during the right stance phase there's less hip hiking, and they make walking a little easier. So the muscle I injected in the left, because as we can see, this is one of the largest muscles in the body, very powerful. And this leads to the shoulder adduction, internal rotation, as well as trunk lateral leaning. So this is a part of the muscles I think we need to pay more attention to if we select to inject. So another muscle it's often forgotten to inject, to intervene, is the glute meds. And this is the gentleman showed in the first video who walks relatively fast. So after I injected to glute meds with 75 units of Arterium toxin, and at eight weeks follow-up, he's able to squat down. So this squat down, that means it's less limiting for the left leg or impaired leg advancing during the swings phase. So he's able to swing to a greater step length. So there's neuromechanics and spastic kinematic chain issue. So here is another patient. I want to show you the 25 years left hand me on assessment with a relatively good quadri-strength, but mainly calf muscle spasticity, no cloneness. So for this, we can see here when patients are standing during the left leg middle stance phase, we can see ankle into the plantar flexion, which pulls the knee back. So the ground to reaction force at this position is actually anterior to the knee joint. And to compensate this, and also in order to maintain the center of gravity within the base of support, and he has to pull back the knee in the knee hyperextension to maintain the stability. That's what this happens. To prove this clinical hypothesis, I did a lidocaine block to tibial nerve, block at the pulmonary level. And we can see the knee position is much improved during the left leg middle stance phase. And as we're showing here, the left leg is much straighter. And because of this clinical evidence after diagnostic test, so we continued with phenol injection to the motor branches from tibial nerve to both gastric and soleus. And at four weeks follow up, his leg is still dragging, but this is related to the left leg cause weakness and hip flexor weakness. But during the left leg stance phase, it's much better. So here is another similar case with a stroke five years out with a left spastic hemi. In addition to the calf muscle spasticity, this patient has both hamstring spasticity and quads spasticity. So she's walking with ankle plantar flexed and a knee flexed as well. At this time, because the involuntary activation of the hamstrings due to spasticity and put the knee into a flexion phase, because of the knee flex and ankle plantar flex, the resultant ground reaction force is actually going through the knee joint axis of rotation. So that's why she's not in hyperextension. Now, we also did a diagnostic test to the tibial nerve. The diagnostic test was successful as evidenced by the disappearance of ankle cloneness. However, her walking pattern does not seem to change. Relatively speaking, there's the same from the clinical perspective. So the main cause of this change is from the hamstring. And then next week, I'm going to do the diagnostic of the block to the hamstring of to the sciatic nerve to hamstring to see whether this is going to improve further. So here's another interesting case. I just want to bring this up. On the left, this is the two years after right MCA stroke. He walks at a moderate speed. But on the right side of seven years later, he walks much slower. And it seems that the gait pattern has changed. So the question to the audience will be, what is the primary cause of worsening gait? OK, here's this. Well, we can discuss that later after we are finished. So there's a wide range of hierarchy of post-stroke hemiplegic gait. And this abnormal gait is a refraction of interaction among weakness, spasticity, and synergistic activation and a grander reaction force. So identification of key contributors is important. And we can use a different diagnostic tool to figure it out. And I want to highlight this, pay attention to pelvis stabilizer controller. And the key to my perspective is understanding the normal gait and the functional anatomy. And we can put all these into perspective. And thank you. And I will hand over to our distinguished speaker, Dr. Muening. Thank you. There we go. All right. Can everyone hear me okay in the back? Good. Excellent. So, I think this is a really great, and I'm so glad everybody's here joining us, because you're going to hear different approaches to the management of spastic gate, and it's okay that you're going to hear different ideas, different ways of doing things, and maybe in the discussion section at the end, you can ask us questions and give us feedback and input, and we can see how we can learn collaboratively together. So I'm going to be talking more about today, ultrasound guidance to improve, and guidance and neurolytic injections to improve spastic gate. I have some disclosures, research support and consulting, but I believe there are no conflicts with this talk. So just to highlight from what Shen was talking about, you know, there are these supraspinal mechanisms for abnormal tone with gate. This is a nice slide from Ganguly in the Journal of Toxins from last year, looking at, you know, let me go back here, excuse me, where's the, oh, here it is here. The motor cortex and premotor cortex, there are facilitary and inhibitory influences that underlie the stretch reflex circuitry. Remember, the stretch reflex has the 1A and 2 afferents from the nuclear bag, nuclear chain fibers. They influence the gamma efferents and the alpha motor efferents, but essentially what's happening in our patients is that the inhibitory pathways are being disordered, and even the facilitary pathways are not normal. Remember, if the facilitary pathway is abnormal, that leads to paresis or weakness. So what are the common spastic patterns of gate that we will typically see? Some of this is basic, but just so we're all talking at a common viewpoint. So at the hip, what I see more often is adduction, adduction, scissoring gate, narrow basal support reduces balance. At the knee joint, as Shen showed in his videos, extension, oftentimes due to a stiff knee, and this contributes to insufficient foot clearance during swing phase of gate. At the ankle, you can see either plantar flexion, which is also termed equinus, or plantar flexion and inversion, which is termed equinoveris. And this gives you instability of heel strike, difficulty clearing the toe during swing phase, and often we'll see the combined knee and ankle dynamic extensor tone. What's important about this is that when you range them at rest, the modified ASHRAE scores at rest can be very unimpressive, but dynamically the extensor synergy, that kicks in and often affects both the knee and the ankle joint. So we want to use our tools and the things that we're trained to do to improve patient's spastic gate. So we're going to use chemo denervation in this regard. So our overarching goals are to improve functional gate pattern and or transfer technique, improve knee flexion, mid stance, and ankle clearance and stability. These are the typical muscles that at least I find useful in this regard. For knee extension, we're looking at the rectus femoris, the vastus lateralis and medialis for plantar flexion, gastroc soleus, of course, but remember FDL is also a weak plantar flexor. For inversion, tibialis posterior, inversion, which is inward portion of the ankle with a little bit of dorsiflexion or upward ankle motion is termed supination. And that often is caused by the spastic tibialis anterior and the extensor hallucis longus, the astridal gate, astridal toe, can also bring the foot into supination. For toe flexion, you're thinking about the flexor digitorum longus and the brevis, which is the bottom part of the foot. And as a pearl, I believe to get patients with spastic toe flexion that impedes gate, you have to inject both the FDL and the FDB muscles. And lastly, the flexor hallucis longus. Oh, and to the hip, I should have mentioned, adductor longus and brevis. That's going to minimize the adducted gate pattern we talked about. So like anything, there are benefits and risks to chemodenervation. This is not an exclusive list, but just some basics that I think are worth discussing. That the botulinum toxins or even phenol injections are focal, specific, and they're non-sedating. Remember that our oral antispasticity agents often come with a price, cognitive sedation, tiredness, which could be limiting in terms of overall functionality. So we obviate the need with injection therapy. We also can combine chemodenervation with gate training, strengthening range of motion or orthotics to maximize function. And overall, this lessens the energy cost of ambulation. What are the risks? Stance phase instability at the knee and ankle. So if you overdo it, we know that tone can be useful for stability. If we take too much of that away, we can lead to instability, increased falls. From our procedural technique, there's also issues, local bleeding, edema, dysesthesias, when we talk about some of the neurolytics. And e-atrogenic injury to nerve and blood vessels, but we'll show you how not to do that here, hopefully. So I want to just throw a couple of basic slides on the basic pharmacology of these injectables. Many of you in the audience know this. I'm sure it's review, but for those who don't, this might be some helpful background information. Phenol neuralysis, it impairs nerve transmission by protein denaturation and malaria degeneration when injected near neural structures. Chemistry-wise, you have a benzene ring and a hydroxyl group. This leads to nerve destruction and myonecrosis, occlusion, and fibrosis of nerve microcirculation. But it also can fibrose muscle as well, the nerve. You see a reference there from Dr. Safant and myself in 2001. Can you believe it? He's shaking his head. Okay, neither can I. All right. There's also issues or things with phenol we should talk about that you want to target easily localized motor nerves with limited sensory component for the most part. We're typically using 6% sterile aqueous phenol. It has an immediate onset. From Dr. Lee's work, we know that the peak effect is in seven days. To do this procedure, you need some kind of instrumented guidance. You can use a nerve stimulation. You can use ultrasound guidance or perhaps even combined guidance, which could be very useful. I'm going to show you here in this video here, this is an obturator nerve block for hip abduction tone. You'll see the stimulator hitting the muscle. That's the injector coming in right there. It'll loop around here. We'll play it again here. These are the two branches of the anterior branch. Here's the anterior branch here, and it splits into two branches there. Notice also as the injector comes in, the stimulation will go away. That's a really nice block right there on top of those nerves, and the stimulation stops as we do that. It's a nice phenol obturator nerve block. For knee extensor tone, motor point blocks to the rectus femoris can be utilized. For plantar flexor tone, motor point blocks to the gastrocnemius and tibialis posterior. Realizing that neural isis to the tibial nerve and or even its branches can run the risk of distal seizures. Don't forget about elbow flexor tone. You saw this after Dr. Lee's videos, some of those patients with severe elbow, I always call it a boxer posture. That will tilt the center of gravity away from the plesic side, affects stride length, and so you want to treat the flexed elbow to improve gait. Not just for upper extremity, but to improve gait. This is an example of a phenol block to the muscutaneous nerve. This is a long axis. The other example was a short axis injection. There is the nerve right there. We'll turn it on right there. Once we get our impulse, we turn the stimulator off, and you'll see 0.25 cc's of phenol being instilled. Here it comes. There it is. I want to show you something that I think is fascinating that I learned when I started doing this with ultrasound. Look at the nerve is right in here, and you'll see that the phenol kind of goes a little bit off the nerve at the very end. So you have to actually layer or hydro-dissect the phenol at 0.25 cc aliquots to really get the full nerve covered, and it's going to be looping here. We published this in a paper, Molly Matsumoto, my resident at the time, a large study of muscutaneous nerve blocks. We showed less dose was needed when we used combined ultrasound and e-stim guidance for the muscutaneous nerve here. All right. Let's transition quickly to botulinum toxin. Again, I know many of you are very much familiar, but just some basics to review for everyone. We have type A and type D neurotoxins that are improved. The way the toxin works, it binds to the synaptic vesicle protein, 2 or SV2, here. It's internalized. It comes in a heavy chain and a light chain, and there's a disulfide bond that breaks out, and then the light chain is really the chain that does the pharmacological effect, and it cleaves either the SNAP25 protein docking complex or synaptobrevin, which is on the acetylcholine vesicles themselves. There is possible up-regulation of inflammatory and fibrotic pathways, which we'll talk about in a moment. That is interesting. When we inject these drugs, there could be some changes to the muscle, and acetylcholine release returns from neural sprouts and recovery at the original neuromuscular junction. So don't forget that many of us will do single-event, multilevel chemoneuralysis, and this is treating spasticity at multiple levels with more than one chemoneuralytic agent. So for example, you can use phenol to target the larger muscle groups. For example, you saw the obturator nerve block for the hippoductors. You could use botulinum toxin for the smaller muscles that have mixed motor and sensory innervation, such as the toe flexors and ankle inverters. Toxin can be spared if you use less dose, because phenol allows other muscles to be covered adequately and quite well. And overall, there's a cost savings, because phenol is much less expensive than neurotoxin. So how do we optimize our localization for chemoneuralization? Well, certainly those that know me, I'm a huge proponent for ultrasound guidance, along with Catherine Alter in the back there and others. And I think there are so many benefits. Real briefly, ultrasound identifies the anatomical variation of nerve muscles. If you just use surface anatomy only, it's less effective. Ultrasound allows for direct visualization of spastic musculature, and it allows tracking of the injectant to make sure you're keeping that injectant within the fascial planes of the muscle. These fascial planes are not watertight, and you can leak toxin outside of where you want it to be. So here's a really good paper. I really enjoy showing this. This is 2012 in France. Schnitzler and his group, mostly physiatrists from France, and they were told to inject the gastrocnemius in the cadavers, and then they looked at the India ink, and then they saw where it was. And amazingly enough, only 43% of the injections were successful. Two-thirds went too deep, and as injectors, we have this urge to want to keep driving the needle. Go, go, go. And we go right through the superficial muscles, and that's what they found here. Two-thirds were too deep into the soleus. One-third was too superficial and was injected into the fat. So it really tells you, even in a big lower limb muscle group that you'd want to use for gait treatment, you can miss the targeted muscle with surface-only guidance. So the other thing ultrasound allows you to do is to make some determination of the modified Heckman scale. So this is a paper that we published. Marissa Moretta is our lead author there. Also with Rajiv Rewi from the University of British Columbia and colleagues. And what we did is we took the original Heckman scale, which was used for grading muscle echo texture in myopathies, and then applied it for spasticity, because myopathies, the muscles are uniformly changed. But in spasticity, we are finding that there's pockets of change until you get to a more severe stage. This is modified Heckman 1, 2, a little bit of change there, 3, most of the muscle is getting to the echo texture of bone, and 4 is very hyper-echoic, very much looking like bone. And so with your ultrasound, you can look at these muscles, make this grade on real time. And in this paper, we compared this to quantitative ultrasound with ImageJ software and found that the modified Heckman grades were in proportion to the quantitative scale, showing this was a very valid way to assess these muscle changes. So think about that. We're going to come back to why you're learning about that in a moment with Gates. So I have two quick cases I would like to present. The first is a 27-year-old male, TBI, right spastic hemiparousis. He has increased tone at the right knee and ankle, but when he stands, his ankle goes into such inversion, it's like cringeworthy. It's almost like, you know, sit back down, you know, it is uncomfortably inverted. He always wears AFO because of this, but he's starting to develop a periodic skin ulceration within the orophosis. He has difficulty clearing his toe with excessive wear on the right shoe. He does have knee tone at rest, however. So we have a lot of possible targets we'd want to treat. So as we went through in this case, we kind of thought that we were going to target the plantar flexor tone and the severe ankle inversion. And I just want to mention real quickly, in these two cases, we didn't do diagnostic nerve blocks. Not everyone has the time or the ability to do that. And so this is going to, these two cases will show an approach where we just use our clinical judgment at the time and made some game time decisions to then do our injections. And we could talk about whether that we should or shouldn't do it that way. That could be a nice discussion point afterwards. So our rationale, getting back to this case, significant ankle instability and equinovarus results in unstable foot contact, making ambulation without the AFO just totally unsafe. And we decided not to treat his knee extensors due to the risk of stance phase instability, because his ankle was so unstable, we just didn't want to risk both knee and ankle becoming potentially unstable. So we just did the ankle. We used 1,000 units, in this case, of abibotulinum toxin A, divided between the soleus and tibialis posterior. Now, you might be asking yourself, why the soleus? Why not the medial gastrocnemius? I have ultrasound. I can find the muscle. Well, here's why. This is the case. Look at the modified Heckmuth score of the medial gastrocnemius. It's essentially all white. It's the same, it's a modified Heckmuth 4, the same color of bone. This muscle has very little of any electrical activity, and if you put your toxin there, you're not going to get any positive effects. So instead, we injected the large soleus. Here you see an out-of-plane injection, one site there, and then one site here. And so we injected the soleus, rather than the very hyper-echoic, abnormal modified Heckmuth 4 medial gastrocnemius, and the latter looked just the same, by the way. So what were our outcomes in this case? Improved ability to wear the right AFO comfortably, reduced ankle clonus, decreased right ankle pain, and improved balance. Case 2, this is a 61-year-old female with a pontine stroke, right spastic hemiparesis, increased tone in the right knee and ankle, MAS of 2. She has a very nice recovery, though. She's a community ambulator, walks slowly in the community without an assistive device, no bracing needed. But what she's complaining about to us is that she has right genia recrivotum during stance phase, and she's getting some knee soreness, it's uncomfortable for her. She has minimal ankle tone at rest, but she's also a little bothered by inversion during swing phase, which is an annoyance. And she wants to be able to do more and be more functional. Again, she has a great stroke recovery, but our patients want us to challenge us to do more, you know, and let's make it even better. And so these were some of the questions that she raised to us. So we had similar targets as in case 1, including the knee extensors, plantar flexors, and inverters. Again, I told you this patient is very independent, high level of stroke recovery, has adequate volitional active strength at the hip and knee, and no ankle instability at heel strike. So again, no nerve blocks, we decided to treat her, and we decided to treat both tone at the knee and at the ankle. Here we targeted the knee extensors with the rectus femoris to address the knee hyperextension moment. Remembering that the rectus is a two-way acting muscle that crosses over the hip and knee joint. It extends the knee and assists the iliopsoas and hip flexion, but when it's spastic, it really locks the knee in extension. We also targeted the medial and lateral crashtachnemius, as well as the tibialis posterior to treat her dynamic equinovarus, which was most prominent during gait, not as prominent at rest. And we used 400 total units of onobotulinum toxin A in this case. So this is the injection of her rectus femoris. This is her subcutaneous fat, almost the same size as the rectus femoris. If you know this is rectus femoris, you see the tendon of the rectus there. Here we're coming out of plane. You see a little perturbation. You'll then see the fluid inject underneath there, right there. It'll stay within the rectus femoris fascia here. Underneath here is the vastus intermedius, and this is the femur here, and here comes the injection. Notice how the blush stays within the fascia of the rectus femoris, and we get a very good isolated block, and we're not wasting our drug within the superficial fat layer. So our outcomes in this case, again, were excellent. Less knee hyperextension during stance phase, improved right ankle positioning during stance phase, and improved ambulation distance. Okay, so I'll just summarize here, and these are some of the key points I'd like to leave you with. That chemodenervation is certainly helpful to address spastic gait. The evaluation should address the hip, knee, and ankle tone. In my opinion, if spasticity affects the ankle predominantly, treat this pattern first. Address both knee and ankle tone if sufficient stance phase stability is seen in your patient. Address hip adduction when there's a narrow base of support or scissoring. And I would argue that you should use ultrasound to optimize your localization and assess muscle echo texture. Thank you so much. Thank you. Thank you, Michael. Very enjoyable. I'm Abe Alfaro. Nice to see many of you that I've seen in the past. I'm going to introduce you to a slightly different approach to treating spasticity and in some cases dystonia. Disclosure, I have AbbVie stock. A lot of the information that you've dealt with here I'm going to bypass and let's get right to the meat of it. This is a 50-year-old woman, had a stroke, was in level 1 rehabilitation. I'm not quite sure what they did for her in level 1. They sent her to level 2 rehab where the therapist asked me for a CAFO, K-A-F-O, knee ankle foot orthosis to control her ankle and the genu recruvotum. I did a physical examination and found she had sustained ankle clonus, significant weakness with 1 plus, at most 2 minus for ankle, knee, and hip muscles. Question, what should we do? Number one, should we give the therapist a K-A-F-O to trial with the patient? We're going to have to order that. That's a couple of thousand dollars, I think. How many people opt for a CAFO? Good. We're on the right track. Number two, how many people will aim for an AFO of some type? I'm not specifying molded or articulating. How many people would like to bring her into the office and inject a chemodenovate with a toxin? There's a problem with the toxin because she's in the nursing home less than 30 days and the toxin is going to take 1 or 2 weeks to work. How about phenol or alcohol or cryoablation, cryoneurolysis? Where am I coming from? I need to treat this patient quickly to capitalize on the therapy and prevent her from going home. She's got an ankle instability and a genu record bottom. Not there, but now. Whoa. When I look at weakness, I usually say, is the weakness for muscles above or below the knee? Is the spasticity above or below the knee? It's oftentimes in both cases. In terms of what I'm going to give her a trial of right here, we definitely decided no CAFO. Swedish knee cage, that'll control maybe the knee, but definitely not the ankle. I'm going to go with an AFO and I'm going to try some heel lifts. In so doing, what I want to do is get my ground reaction force. She strikes the ground there, so the ground reaction force comes up way anterior to the knee. I'm going to try to get it closer to the knee. I can do that by giving her, number one, a MAFO, M-A-F-O, solid. By the way, I have a lot of MAFOs in my office. Why? Because all these people were coming to me with spasticity, with ankle clonus, and I would give them injections. They'd get up off the table and they started walking. Not the AFO. Do you mind if I have your AFO? Sure, I don't want it. I accumulated all these MAFOs and a few AFOs. I would just take one and I gave it to her, but that alone was not enough. I put a heel lift on inside the shoe, but under the MAFO. That's going to increase the heel strike, and you can see here with this. Let's see what happens. Here she is with the MAFO and the heel lift. Inside the shoe, and I think I put one on the bottom of the shoe. Much better. Someone needs support from someone. Now she's still got ankle clonus, and if I was to give her this MAFO, which I did to use until I prescribed something permanent for her, I would look at the heel. Inside the heel, is there debris? If there's debris inside the heel of the MAFO, that means her heel is not touching the MAFO, and the debris just accumulates. And then I know that the heel is not touching, I've got to get rid of the ankle plantar flexor spasticity. So I'm going to bring her into my office for that. Here she is six months later. Notice no longer a hemi walker. She's got a stabilizer cane. She has her AFO with a dorsiflexion assist, and she's independent ambulating. When I prescribe an AFO, I want to make sure that it's hinged and I use these polyurethane hinges that are curved so that when you're holding the AFO proximally, this is in dorsiflexion. And if you put it down on the table, this is flexed. Make sure that if you write for the prescription that they have the Tamarack, or that's a brand name, the polyurethane hinges and your orthotist knows how to make them. I've seen too often they make it the wrong way. I have a collection of these in the office. I tend not to use them. It's primarily for people who have significant weakness. But moving on. So I injected that woman with phenol. And I inject at the popliteal crease. So for this patient with the left spastic hemiparesis, she's lying on her right side. Put a pillow between the knees and a little support under the ankle. So I can watch as I stimulate the tibial nerve at the popliteal crease that the ankle is plantar flexing very strongly. You must have strong contraction. And I'm going to inject, when I'm at a stimulus less than 0.5 milliamps, I'm going to inject less than 0.5 ml phenol, 5 or 6%. With this, studies in Belgium and France have shown that the soleus muscle accounts for the spasticity 75% of the time. The gastrocnemius 13% of the time. Her clonus was gone. My study downstairs, and you have it somehow in your computer there, shows also that for 51 patients with this injection, 70% of my patients had clonus obliterated. So that means that there's another 30%, and they probably require a block of the gastrocnemius motor branches. But if I had ultrasound with the HECMAT scale, I could identify whether or not I should inject them via the branches there. Or I also can go by the study by Deltoum in 2004 in the archives for the soleus. It's 13 millimeters, correction, 17 millimeters lateral to the midline and for the tibialis posterior. Let's look at a few more cases. Traumatic brain injury. You already know what I'm going to do. It's going to be a phenol block to the tibial nerve at the popliteal fossa. Very interesting case. This is a 30-year-old woman, had a stroke. She saw me four years later. When she came to me, her major complaint was that she was walking on the lateral aspect of the foot. So I injected the tibialis anterior because the ankle was in some dorsiflexion. Tibialis anterior, you'll come back, I'll chemo-denovate the tibialis anterior. She has a dystonia. Dystonias often change. When she came back, her ankle was more in plantar flexion, but still inverted. I blocked the tibial nerve at the popliteal fossa. Ankle clonus was gone, and her dystonia was gone. These injections, for me, at the tib-pop will last well over a year. All of my patients have an exercise program. So with the exercise program for the soleus type I muscle fiber, repetitive exercise for endurance. Range of motion, stretching. Be careful about the stretching, especially there's cases where they have phenol blocks. They stretch the muscle while they were on the step. As a result, the heel, instead of being on the ground, was off the step. That means that the soleus and the gastroc were eccentrically contracting. They're contracting, but you want to stretch the muscle. So make sure, use a two by four. Heel is on the ground, and they can lean forward to stretch. Just a couple of quick examples, obturator nerve blocks, spasticity Ashworth IV. Post-injection, she can lift her leg. There's no spasticity. For this patient with MS, this was all about hygiene. But for some of my other patients, this one had Lyme's disease in the CSF, adducting, ankles inverted, post-injection to the obturator, and the tibialis posterior. She's walking with a stiff knee gait. Because it's bilateral and there was spasticity for other muscles, I recommended I consider an ITB. She was moving to Columbia, South America, and didn't want any part of that, because we couldn't find anybody down there who she felt comfortable with. So in conclusion, I've been doing this for close to 30 years. I feel we're making a lot of progress, but we're going at a snail's pace in terms of treating spasticity. I see people who are doing injections without adequate training. And my question is, are they practicing best practices? They have the standard of care in the community. But in my opinion, it is a sub-standard of care. We really need to focus on optimal best practices. My daughter, when graduating from law school, I said to her, listen, maybe you'd go into malpractice. I could send a lot of patients to you who I think really weren't properly treated or were simply neglected, like that first patient that I showed in the nursing home who was not treated, even in level one, by a physiatrist. What do they say? We'll wait until you get out, and then you'll come back to my office, and I'll inject you with a toxin. So bottom line is, I think we're not going to see significant change until you see on TV or the billboard, do you have spasticity, difficulty walking after a stroke? If so, call the law offices of. Amen. We are happy now to take any questions, if you have. So if not, I'm going to ask Abe a question. Is that microphone on there? No, it's not working, but I can talk. It's on now. Hello? There we go. So you talked about, in some of those cases, doing tibial phenol nerve blocks at the... hated me for that time, they were happy about four or five months later because they got a really good response that was long-lasting in many cases, but how do you balance the dysesthesia risk versus what you showed us some nice outcomes in that case? I'm glad you're asking that question. So a few things. Number one, if the toes are flexing when I'm stimulating the tibial nerve, don't inject. Why? The work in Belgium and France has shown that the flexor digitorum longest adjacent to it are the sensory fibers. So one thing is don't inject if it's the FDL, the toes are flexing. Number two, I'm not sure that we need to hydro dissect the nerve. I think that the small volume of phenol that I'm putting on the nerve, 0.2, 0.3, 0.4, 0.5 ml is probably not hydro dissecting the nerve. What is it that we want to do? We don't want to destroy alpha motor neurons. We want to inactivate muscle spindles. And that's done by blocking 1A afferents and or gamma efferents. Research for this is documented or suggested by the H max, M max ratio, which decreases, indicating that we're blocking the monosynaptic reflex. So it's a very good question that Michael asks, and I'm concerned that if other people, a lot of people are blocking the tibial nerve at that spot, that we might get more dyshestiasis. For my 51 patients, I only had one patient with healed dyshestiasis. If you put too much in, I think it's going to spread to the sensory fibers. So that's my response. I certainly welcome other responses and what people are concerned about. Marilyn Pacheco. My question is, so what would you do with the tibial nerve block versus the motor point block? Like, do you have, like, because it's like, there's motor point block points and there's, and then there's, for phenol, and then there's toxin. So... I'm going to let Dr. Shang and Munin comment, but very quickly, the tibial block at the popliteal crease is below the gastroc-motor branches. So I'm probably going to get 70 to 75 percent of the patients with clonus obliterated for the soleus. If I don't succeed and they still have clonus, then I go to a couple of other sites, including the gastrocnemius motor branches. I'm always concerned, and I share this with you, about causing weakness. So I know that the phenol molecule has a component that's similar to lidocaine. So immediately after the injection, there will be some weakness. But after about an hour or two, that weakness goes away. So with a small amount, we should not be seeing significant weakness. Shang? Okay. All right. In the tomicory, I think there's a structure between the nerve trunk and the motor point. There's a structure called the motor branch. This is a place where I... I would personally avoid doing that, since it's very difficult to control where it flows. In the case with the current advanced guidance with the ultrasound and the e-STEM, I'm very confident that I can find motor branches without involving the sensory component. If I can do that, why would I risk injecting the component, the area that mixes the sensory and motor area? So my approach is to avoid the sensory-motor-mixed area and target the motor branches as much as possible. And I'll just chime in as a third approach. I like chemo-denervation with botulinum toxins for the gastroc soleus. What I would say is you saw an example with the modified hecumen for the immunogastroc. If you see a lot of that, that might be a muscle that needs an orthopedic surgery referral, and maybe we're not doing chemo-denervation to that particular case. As an aside, the clinical, the pivotal trials for botulinum toxin for lower limb, the effect size is really small, and the p-values were just barely positive. And so even in our randomized trials where we're using chemo-denervation, and I think some of that might be is these muscles change a lot over time. So again, if you have a healthy muscle that's going to respond well to botulinum toxin, phenol certainly could be used. Yeah. Thank you for the very interesting perspectives. I just wanted to ask, Dr. Noonan, you stated that you have proximal and distal issues. You typically treat the distal issues first, right? In the lower limb, yes. For gait, we're talking about, yes. Right, for gait. For the ankle, to be more specific, yes. Do you treat the ankle instability first with toxin, you know, treating the distal bone? Many of these patients are already wearing an AFO, as Dr. Alfaro showed, right? So if they're wearing an AFO for normal ambulation, and they come to you, you know, you're examining them without the AFO, you see some distal instability, you see their proximal problems, would you still treat the ankle first? Because they're going back into the AFO. but I have a relationship. Okay, I will follow on that. So, thank you, Dr. Regevay. I think it's a great point. For me, if the patient has an For the arm it's different, but for the leg, the severity of spasticity is not correlated with gait speed, which means it does not intervene function. So if it does not intervene function, then why would I just do the injection and intervene the spasticity? However, in your situation, what you just described with the AFO, if there's a fitting issue, like Dr. Muehling just said, because of the abnormal ankle joint position, difficult to fit in, of course I will inject. But if there's no fitting issue... You had some results injecting the latissimus dorsi to balance out the pelvis. Are there other muscles that you think are pretty important in getting pelvic stability in some of these people? So there's I think that all the big muscles around the pelvis needs some attention. So in the last video show the patient five years later is walking slower. The primary contributor is hip flexor. So the patient is now, the primary evidence for that patient is he's no longer able to step through his impaired leg. Put the unimpaired, the unimpaired leg in front of the impaired leg because if they want to do, put the healthy leg in front of the impaired, that means that the parietic side hip joint being stretched. And because of the hip flexor is kicking and there's not, that limits the hip, the healthy leg advancement. So I inject the hip flexors for that patient and reportedly his gait improved a lot. And for the other patients I have shown the hip extensors, lats, and all these are the big muscles around the pelvis and patient specific. So that's the last point I highlight. We needed to know the functional anatomy and the normal gait and how they play a role in their gait. And for any specific patients and we just to determine all these three factors, weakness, spasticity, and the chronic reaction. Okay, I'm glad I get my own private microphone. For those of us who don't use the modified HECMAT scale or aren't familiar with it, can you clarify, is a modified IV automatically electrically silent? Repeat the question, Mike. The question is, with the modified HECMAT scale, is a modified HECMAT IV, does it equal electrical silence? It is a phenomenal question. We're doing the research study right now, so we're doing a study now where we're doing five upper limb, three lower limb muscles. We're doing modified HECMAT grading on all of these muscles. We're seeing how much toxin or phenol are being delivered, and we're doing EMG to each of those muscles individually. So I'll be able to answer that question, hopefully, maybe next year's session. Because otherwise, then the question arises, as we heard yesterday in Dr. Winston's talk, is the toxin not effective on those muscles because, is it something else, like they're just too spastic? No, there's fiber, fatty infiltration, and there's not a whole lot of muscle tissue remaining. But there's something else that's going on with it, I guess, to... Yes, the muscle has changed its architecture, and not responsive to the internalization I showed you on the pathophysiology side. Thank you. Yeah, there's a study from Europe, and they look at the HECMAT scale and the response to botulinum toxin injection. And for those who are on the HECMAT scale three and four respond less as compared to HECMAT scale one and two. What's causing those histological changes in the muscle with the HECMAT scale? Another great question, which we're going to hopefully look at. There's two competing hypotheses. The first is a denervation change. There's some interesting pediatric literature where they've done, during heel lengthening, they biopsied kids who had multiple botulinum toxin sessions, and have seen a change to greater percentages of type two fiber, which were unexpected. Or it could just be the disease process itself. Remembering that we talked about the dysregulation of the inhibitory and facilitory pathways. I think there's also a change in the muscle architecture as well, perhaps due to these conditions. Which we haven't appreciated. So hopefully more work will be able to tease those hypotheses out. So if the muscle on that HECMAT scale showed this atrophy or disuse, is that muscle likely to contribute to the stiffness, the decreased joint range of motion? That's a great question. Yes. I believe the answer would probably be stiffness, but not from a spasticity mechanism. Any other questions? I know you have the questions, and you're going to come up here at the very end and ask us. So don't be embarrassed. There are no stupid questions. Here we go. Hi. My name is Natasha Mehta. I'm a recent TBI fellow graduate, and so I do spasticity management. I have a question about lidocaine blocks, and just sort of how you integrate that into the flow of a practice in terms of insurance approval. Do you need insurance approval? Can you do that on the first day? How would you do this? Go ahead. I'm not sure that I heard the whole question, but it was about insurance? Diagnostic blocks. Oh, diagnostic blocks. Interesting. So when I first started doing these injections 30, 25, 30 years ago, I learned on my own. I wasn't really sure what to do. So I did primarily, at that time, diagnostic blocks. I had been doing toxins, so I had an appreciation with the EMG. Then I advanced to stimulating the muscles, putting the toxin in. It just wasn't lasting long enough. Is there insurance issues? Is that your question? How do you work it into your practice and into the flow of treatment? If I wasn't sure, do your lidocaine or bupivacaine injections? Yeah, I think I will follow on that. In most cases, you know there's a patient with spasticity. But for those who don't know, and you are very busy, you don't want to inject into the wrong muscle, or unnecessarily you inject this muscle group. So then in that case, I will just do lidocaine block to prove that the patient is going to benefit from your intervention. But for the most cases, if I know, I will directly go to toxin or phenol. So if you have any doubts whether a patient is going to get benefited from your intervention, you will do this. You accumulate more clinical experience, and you will know when and whether you need to do it. I would concur with that. Just a little bit of a comment about the blocks, like the patient that you had, the tibant tightness. So we have a patient often that has an equinoverous deformity. It's really pointed down. And you do a tibial block, and they stand up and they walk completely everted. Because what you didn't appreciate in that severe equinoverous is actually the tibant is in a sustained contracture, but because you're so plantarflexed, you actually didn't notice the tibant. So when you do the first block, you say, aha, this is all equinoverous tibial, but now we have the peroneal division for that. So for me, the blocks, when it's quite a contracted arm, we do one muscle, you do the brachialis, the arm lengthens, and you say, aha, the biceps is still shortened. So the advantage of doing blocks in a tight arm, not one that's fully reducible, is you see which muscles are shortened and how many of those you need to inject. It might just be that often it's just the brachialis, but you get to the end of the brachialis to 120 degrees, and you see that biceps tendon now, which you didn't see before. So that's really one good advantage of the blocks, is to tell you how many of the muscles are contributing to the shortening. Good point, Paul. Thank you, Paul. Great point. And for the sake of time, thank you for coming, and we'll stop here now, and we will have a next session in the coming time. Thank you.

gait disorders

spastic hemiplegia

orthotics

AFO

ankle foot orthosis

phenol nerve blocks

spasticity

botulinum toxin injections

chemodenervation

post-stroke hemiplegia

neuromechanical consequences