Okay, now shifting to the southern part of the continent, I'd like to invite Dr. Johannes Enslin, who's from Cape Town, South Africa, and he's going to talk to us about individualizing surgery for patients with spasticity. Good morning. Thank you very much to the organizing committee for the invitation. It's a great privilege to be here with you. I'd like to talk to you a little bit about spasticity management, so changing the theme a little bit from neuromodulation and epilepsy to a topic that's dear to my heart. But specifically trying to show up some points where we need to move from a global perspective in managing spasticity from a recipe-based approach to really individualizing therapy for each patient. I've got no disclosures. We grow up, all of us grow up with some rules or dogma that is taught to us when we think about spasticity and management for it. And some of the examples is for spastic diplegia, you decide if the patient is able to stand up from sitting, then must be a good candidate for selective dorsal rhizotomy. If he's unable to do so, rather go for intrathecal baclofen therapy. And then definitely heavily dominated still by orthopedic colleagues in Africa in general and many places still around the world. Cerebral palsy, as an example of one of the spastic conditions, is still treated primarily by orthopedic surgeons. So tender lengthenings and derotation osteotomies, unfortunately, as I'll show you, is still done very early on in patients with spasticity before they are referred for treating the cause for the neurosurgical treatment. For patients with spastic quadriplegia, the options are very few. It's intrathecal baclofen therapy and then SEMILS, a single event multilevel surgery that's been proposed by the Australian orthopedic colleagues and then sort of took the world aflame from there, where they will do in one sitting, because the patient will of course need a derotation osteotomy and hamstring lengthenings and Achilles tendon lengthenings at some point in their life. So we'll just reduce it and do it all in one sitting and sort of a one-stop shop and then see what the outcome is. We're trying to change a bit of that dogma. So what are the problems with that? Well, it's very blunt tools that we have still today to treat spasticity. We do a selective dorsal rhizotomy. The selectivity doesn't really come into the function so much, however, as you know. And intrathecal baclofen therapy, where I can change the level of effect by the catheter placement to involve the upper limbs more or only the lower limbs, but it's still a blunt tool. We're only still treating the symptoms. It's as if we've given up hope with spasticity. We're not really thinking about the causes. We're not individualizing therapy to the causes of it even. We're only treating what we can see, the symptoms of it. And then an example of what I'm discussing is you did a dorsal rhizotomy for a patient. Patient's still functionally not as good. Still a little bit up on their toes, still some scissoring during the gait. But you've done a rhizotomy already. What do you do now? Traditional thought, those patients are then taken over back by the orthopedic surgeon and he tells everyone, I told you so, I should have lengthened the pendants rather than you sending the patient to the neurosurgeon. My favorite quote by Maslow, it's tempting if the only tool that you have in life is a hammer, that you'll start seeing everything that you're treating as a nail. We need to move away from that approach and really have multiple tools in our pockets. Now that quote by Maslow is not aimed overtly at orthopedic surgery, although if the shoe does fit them. The point I try to make with this slide is that if one really wants to be a dedicated center for managing spasticity, you need to be able to have a whole group of therapeutic interventions or tools in your pocket to treat it. So some few basic points that I'd like to illustrate and to remind us, why do we treat spasticity? Definitely not because it's present. One only should treat spasticity if it influences a patient's function. Then you need to decide, can my therapy improve the patient's function? And only if the answer to both of those questions is yes, I think the patient then is a surgical candidate. We can also treat spasticity if there's associated pain that's refractory to therapy or to prevent future morbidity as well. And I think it's very, very important, that last point, that we do not treat it because it is present. No center that manages spasticity effectively can only be based around a surgical intervention. As with most functional disorders like we're discussing today, the evaluation, patient selection, not necessarily patient selection in terms of, oh, my rhizotomy I do won't work, so therefore I can't help the patient. We really need to look at ways of helping each individual patient. Now, you know that I say every patient with spasticity can be treated. Not every patient will require an operation, however. And definitely not everyone that requires an operation can or should have a rhizotomy. There's many other options that can be done. And then, as from our French colleagues in Lyon, I'm always amazed by the setup that Professor Sindhu and Martens have in Lyon, where they refuse to do any of these surgical interventions for patients if the whole family doesn't book into a rehabilitation facility for a few weeks after the surgery. We don't have that luxury in Africa, definitely, but I think we can always aim to focus on the rehabilitation much more than we do in general for all functional patients. So when you evaluate spasticity, you need to always look at, is it more a focal, global effect of spasticity, or is there more focal areas that you can aim at during your treatment? And then to categorize the patient as well as that. Because all of this will play into what our best surgical therapeutic options are. One really needs to be an astute clinician. So I think spasticity management takes us back to our roots of really doing proper neurological examinations. You have to understand basic biomechanics, mechanics of gait. And also remember that the body is a continuum. What we've learned from selective dorsal rhizotomy procedures in the past 30 years that we've been doing them in our unit, is that we know we have this super marginal or overflow effect that you have from doing a dorsal rhizotomy that's mainly aimed at treating the lower limbs. But you also get an overflow beneficial effect on the upper limbs. But I think the important part that we should take from there is the whole body is a continuum. And that plays into my topic. One does not need to treat the whole limb that is spastic to have a functional improvement. Taking away key muscle areas or key spasticity patterns can have a beneficial functional result in a patient. And this is just to illustrate again to fit in with my theme of the blunt tools that we have of evaluating this. Those of you that are familiar with the GMFCS score will definitely agree with me that there probably needs to be about 10 subclassifications underneath each of these levels to really evaluate or to show what the beneficial effect of therapy is as well. We've got state-of-the-art facilities worldwide where we're relying on 3D gait analysis, which is very nice tools, but as I'll show in these videos, one really needs to pay special attention to each individual patient and look at what in this little boy should I do to make his gait better? How can I make him better? Just doing a rhizotomy, because that's what I do, is not necessarily the best answer. Same, just some examples of the 3D gait analysis. Same, just some examples of the 3D gait analysis. But what I'd rather want to show you is that and remind everyone, not one patient with spasticity, whether it's cerebral palsy or after a stroke or after a head injury, is the same. Therefore, it's ludicrous to use one tool for everyone and expect beneficial outcomes. From the gait analysis, one gets beautiful tables like this, which then should make it easy to decide or to tease out what you should do to treat the patient. What we need to remember however, is that human movement does not happen in two planes. Human movement is diagonal based. Human movement has nuances of rotation, elevation, depression. You really need to use your eyes and clinical acumen a lot in evaluating this. When we look at the grading of muscle power in patients with spasticity, what tool do you use? Does muscle power or grading system of muscle power really have a role? I'd like to make a point that I don't think muscle power in general is really important when you're evaluating or at least deciding whether surgery is possible or not. It's as to focus around function. So evaluating the patient, seeing little boy that we're teeing up for selective dorsal rhizotomy, but forgive me for moving away from the podium, we all know the little boy with spastic diaplegia has this gait pattern like this. Yes, he can walk and he can get up from a chair when he sits. So therefore, dorsal rhizotomy must be a very good option for him. Because the criteria says the patient must be able to stand up from sitting. But we also know, and all of us have examples of that, where you do a selective dorsal rhizotomy, take away that adductor spasticity that the child has, and suddenly he can't stand anymore. Or he cannot walk. Or now suddenly the little boy that could walk without the frame is Skywalker dependent now. So my talk is about how do I tease that out? How do I decide which therapy to use in each patient? Also remember that the dystonic component to spasticity is present in about 30% of all patients with cerebral palsy, as an example. And dystonia is contraindication for a lot of these techniques that we traditionally use. So these are the tools that we have in managing spasticity. We know absolutely orthopedic surgery does still play a role. But I think we should wait with orthopedic interventions until the tone has been improved by the neurosurgical treatment. And then the biomechanics can be taken on later. It's beautiful work done by Professor Sindhu and his colleagues on how to decide whether general spasticity, then these are the options that we have. If you want a reversible technique, then intrafecal baclofen is an option. If you want more permanent results, then lesioning, for instance, multiple rhizotomies is a way of treating the patient. If you have more focal spasticity, then definitely reversible. Butulinum toxin as a therapy for the patient. And you can mimic a permanent Botox effect by doing selective peripheral neurotomies. The importance is then as well, how do you evaluate your outcomes in these patients? And again, we have blunt tools of evaluation as well. Yes, I can make a beautiful publication in any journal by showing that I have a child with the Ashworth grade 1 spasticity that suddenly can now sit with his legs straight upright in the picture that I sent into the journal as well. But that doesn't tell me whether the child can walk easier or not. So we need to focus on the outcome of a patient. Small improvements for a patient with spasticity often is great for the patient in himself. We know the examples of a patient that is wheelchair bound, but they cannot sit upright in their own wheelchair because their hamstring spasticity literally pulls them off the wheelchair on a daily basis. That child cannot focus in school. So doing a procedure where you don't change his GMFCS score, he's still wheelchair bound, but he can now sit unsupported in his own wheelchair with his head upright, makes a big difference for that individual patient. And as an example, these two top pictures. So what do I mean with the more selective therapy to improve function? Well, we know that the limb, for instance, a post-stroke patient with upper limb spasticity was a professional golf player before, was then involved in a car accident or had a stroke, and is now spastic, cannot play golf anymore. How do I get him back to the Paralympic team that can take part in his favorite hobby again? Well, we need to remember that the whole limb, or the whole body for that matter, is a functional unit. Therefore, I do not need to treat spasticity in every single muscle in the limb for him to have functional improvements. But that's easy to say, but how do you then work up what to do? As an example, if I do a selective peripheral neurotomy and I follow general rules, I need to involve the median nerve and the ulnar nerve to make an improvement in the patient's arms or forearm hand so that he can hold his golf club again. I might end up causing hand deformities because of this delicate balance between the flexor digitorum superficialis and flexor digitorum profundus group as well. So now he still can't hold his golf club while he has a much better looking arm, though. I need to evaluate function for each individual patient. We spoke about human movement being in diagonals and not one or two dimensions even. And then we know that there's a delicate balance between the agonist as well as the antagonist muscle in each effect. So how do we decide? I think a detailed examination is still very important and understanding the biomechanics of movement. We know that doing a specific thing, or one-on-one, does not equal two when we manage spasticity. We really need to find a way to see what will my hypothesis or specific small intervention do to this patient's function. And we know we have a few tools to do that. We can do a peripheral neurotomy with a bupivacaine to test what the selective peripheral neurotomy effect is. But I really like the next one. To use Botox, but not because I think it should be a lone-standing therapeutic option. You have to repeat it every few months, as you know. After a while, many patients, especially children, do become resistant against some of the effects. But using selective injection of Botox, ultrasound guidance so that I know it's in the muscle that I think causes the problem, and then using that as a three to six month test to see, can the patient now improve functionally? So was my hypothesis correct? Can the little boy that has adductor spasticity that I want to do a rhizotomy for, can he still stand if I take away the adductor hypotonicity that he had before? Can the patient, my golf player example, can he now really putt better? Can he hold a golf club again? And I can test that by selectively injecting muscles with Botox. If my hypothesis was incorrect and he can't hold his golf club, it's not a problem, it's not a permanent solution. I can tailor it with the next set of Botox injections. Once I have the functional recipe for this patient, I can make it permanent with a peripheral neurotomy for that patient. And then one can then decide, do you want to use any of the tools that we have available? Selective dorsal rhizotomy, dresotomy, vresotomy, so ventral root entry zone lesion for patients where there's a dystonic component as well, works very effectively. Selective peripheral neurotomy. So what are some of the take-home messages? Really spend a lot of time. I think one evaluation and making a decision on a patient with spasticity is futile. One really needs to get to know the patient. Family videos, evaluating patients in their home surroundings is of the utmost importance. And we need to test function. We need to, more importantly, test how will my intervention improve or hinder the patient's function. Therefore, this guided or selective injection with botulinum toxin I think plays a very good, important role. And then one should never manage spasticity alone. Same as any other functional disorder, the rehabilitation afterward, as we said in the beginning, forms great, of very good importance. Thank you so much. We have time for one question if we have one. So I'll ask. So, you know, we see a, we have a referral center for pediatrics in the, sort of in the center of the country. And we see patients who have global secondary, excuse me, secondary dystonia. So they're CP children who 10, 15 years after the fact develop bad dystonia. The rehab doctors, you know, sort of your comment about if all you have is a hammer, everything looks like a nail, the rehab doctors will inject botulinum toxin. That doesn't work well for global distribution dystonia. And so we get involved to consider implantation of DBS after they failed other management. Do you work with someone who does that? Do you do that yourself? Do you see any role for it? I do. I do it myself. And I think there is definitely a role. There's definitely a big scope in developing the current ways of neuromodulation in that. And I think it ties in with my comment in the beginning. We've given up hope with regards to spasticity. We're focusing on the symptoms. And we need to find ways to get to the main organ. It's not called cerebral palsy for nothing. The problem is up in the brain. So we need to look at ways of doing that. And we're busy with experiments on that, definitely. But I do think that currently multimodal therapy in these patients absolutely play a big role. You're right in saying that Botox, and I think Botox doesn't work in these global children. But because there's a dose limit, you just literally cannot just give Botox to everything. So combining certain strategies and doing drosotomies and the ventral root entry zone lesions in patients, in larger limbs where there's a bigger dystonic component, so that you leave the Botox for maybe tinkering the smaller, the hand, for instance, and limbs that does not respond to the bigger intervention that you have done. I think that's where we are at the moment in really combining different strategies. One hammer doesn't fix every nail, absolutely. Thank you.

individualization of surgery

patients with spasticity

tailoring therapy

treatment options for spasticity

underlying causes

personalized and multi-modal approach