Good morning. For the sake of time, we have a lot of speakers today, so I'm going to try to get started right on time and try to keep on my time schedule of 15 minutes, so we'll see how we do. But I am Dr. Kelly Crawford. I come from Carolinas Rehabilitation in Charlotte, North Carolina, where I'm the Medical Director of the Brain Injury Program and the Residency Program Director for the PM&R Residency Program as well. So we're going to go through the various topics for secondary dystonia. I'm going to start off with the medication or the pharmacological management, and then we'll move on through the progression of different type of treatments. So first, I have no financial disclosure. So dystonia, I was actually very excited to speak about pharmacological management regarding dystonia because I don't actually do a lot medication-wise. I do a lot of botulinum toxin injections. Most of my medication regimen revolves around spasticity. So to specifically do dystonia, I was quite interested in doing a lot of the research. However, as you can see with my emoji up there, I didn't get a lot of wonderful concrete results from my literature research. So you'll find as we go through this, that's basically at the end, you'll be like, well, it could be anything. But to know what dystonia is, it is a heterogeneous disorder with many etiologies. We are going to focus on secondary factors today. So those folks with brain injury, stroke-type injuries. We could have varied clinical presentation, which also feeds into your treatment options as well. You could have focal dystonia or generalized dystonia, which you would treat very differently. And diverse treatment responses and treatment options. But the one thing I did gather from this is that there is a huge notable gap in well-designed controlled trials. So most of the research or studies you will see will be very small, with very limited data production. So there's room for opportunity. Treatments must be individualized and tailored. So as I said, they come in various shapes and sizes. You can have generalized whole body or focal cervical dystonia, which you would treat very differently in different patient populations. There are mechanism-based treatments that are aimed to modify disease course and improve outcomes. But those are only available in small heterogeneous group of rare inherited neurological disorders primarily found in children. So much of the treatments that we are using are not going to be focused in that category. We are going to be focused, or specifically I will say myself, being a brain injury doctor, and we will be at symptomatic treatments, or with the medication and therapy regimens that we provide for our patients. So pharmacological treatments in general, medication was the cornerstone of treatment options years ago, for years. However, over the past two decades botulinum toxin has come to the forefront and has really kind of taken over, especially with focal dystonia. That's not to say there's not a role for pharmacology or pharmacological treatments in this case. You can still have folks with generalized dystonia that respond well to certain medications. And those who do not, who don't respond well to botulinum toxin can also benefit from additional medication therapy as well. But as I've mentioned a couple times already, most of this data, or most of the medications we use are based upon empirical experience and little scientific rationale. You will also find that most patients will require a combination of oral medications or other additional treatments in order to help with symptom control. And you will also find there's an actual very high failure rate with these medications. Either patients don't have a benefit from the response, or due to the low tolerability of some of these medications and their side effect profile. So I'll first start with the dopamine agents. So dopamine is thought to act, the dopaminergic agents are thought to act by potentiating the dopamine neurotransmission through coactivation of the D1 and D2 receptors. And much of the literature in small case studies and small trials have shown levodopa to be beneficial. More importantly in the acquired forms, which is what we're talking about today, but also in the myoclonus dystonia and the rapid onset dystonia parkinsonism, which you can imagine the case with levodopa. There have also been small trials done on first generation dopamine agonists, specifically apomorphine and bromocryptine, which have shown small positive benefits. And I have aripiprazole, I apologize, that's supposed to be luriseride, and I accidentally put aripiprazole, which is the next one, but luriseride is no longer available in the United States, so I accidentally left that one off. But then there's also partial dopamine agonists, aripiprazole, which has been shown in case studies to be beneficial in tardive dystonia, and a few case reports have shown that to be beneficial. So that might be an agent you might want to consider using. On the opposite side, the exact opposite side of the sword, there's the antidopaminergic medication. And actually antidopaminergic agents back in the day were used extensively for dystonia treatment. However, over the recent course of years, they're actually frowned upon and discouraged from use, mostly because the literature has not shown a very positive efficacy or uncertain efficacy and extensive side effect profile, most importantly pertaining to the development of potential tardive syndromes from these medications. The only exception, or one of the exceptions that have shown positive response is actually clozapine, and the reason for that is thought because it's mostly a D4 receptor blocker with a sparing of the D2 receptors. And this has been shown to have benefit in tardive dystonia as well, compared to all the other antidopaminergic agents. The only drawback, or one of the drawbacks to this medication is that you have to do frequent blood draws because of the possible development of agranulocytosis. Other agents that you may not be familiar with or may not be using are the vesicular monoamine transporter 2 inhibitors. These have mostly shown through observational studies and small trial studies that they are beneficial for the treatment of tardive dystonia specifically. One of the most well-known ones is the tetrabenazine, which actually dates back to the 1970s in its use. However, it's only been approved here in the United States since 2008. But it is rarely used as a first-line agent, except in the tardive cases. However, if you do use this medication, it is actually only FDA approved for Huntington disease-related chorea. So if you are going to be using it for the treatment of tardive dystonia, it will be used off-label. So of course, all the insurance issues that may come with that, just keep that in mind. And then another medication within this category is reserpine, which has shown some in some small trials, some benefit in tardive cases as well. However, it's high limitation due to its hypotension and actually high risk of depression. And it is also no longer available in the United States at this time. Some two more recent, and I say more recent, past six years, I guess that's recent, are two novel VMA2 inhibitors, the dutetrabenazine and the valbenazine, were FDA approved for the treatment of tardive dyskinesia in 2017, and actually had shown very strong benefit in the tardive dystonia cases through a randomized controlled trial, and little side effects associated with these compared to the placebos that were a placebo effect that was involved as well. These were two studies. These two drugs together are actually involved in some of the most highest level patient involvement for hyperkinetic movement disorders. So there's actually very high literature behind these two medications. However, the one medication group considered to be among the most effective pharmacological agents for dystonia, and I think this is probably the one that I use the most, are the anticholinergic agents. They block the action of acetylcholine on central muscarinic receptors, and their efficacy is thought to be related to effects on the hyperactivity of the striatal cholinergic interneurons. And specifically, the medications that have been stated in the literature are the trihexylphenidyl, which I think most of us are familiar with, benztropine, ethopropazine, procycladine, and bipyridine. Anticholinergic medication, again, the trihexylphenidyl is the most well-known. It's been used since the early 1950s, been very well studied as well. One of the most heavily used, especially in generalized and acquired dystonia, the best for dystonia, are the side effects. And as I said, working in neurorehab with brain injury stroke patients, these are kind of the most limiting factors for me. I already have patients coming in with blurred vision, constipation, urinary retention, specifically also sedation, confusion, and mental fogginess, especially in my brain injury population. So then to add a medication on top of this that can make some of these issues worse, it's usually not the best option. But if the dystonia is bad enough or has developed to a significant degree, these are medications that would be worth looking at. And obviously, you want to make sure you start low and go slow in your titration. The other thing I found through literature as well is that children actually tolerate much higher doses than adults. I don't work with the pediatric population, but if you do do, you know, a transition clinic of some sort, just remember that children do tolerate higher doses. You would obviously have to monitor any side effects or any effects that they may have in their schoolwork as you start to titrate medication with these children. And of course, baclofen, tried and true baclofen, GABA-B receptor agonist that decreases the monosynaptic and polysynaptic reflex response in afferent terminal nerves and induces muscle relaxation. There have been open-label trials and small trials done in the 80s and 90s, both showing benefit within children, dystonia symptoms in children and adults, and actually sustains relief up to 21 to 24 months. So there's been good literature behind this as well. Again, the limiting factor is usually the side effects. So again, the nausea, the drowsiness, specifically dizziness. And the other thing I warn patients about anytime I start baclofen for any reason is the excessive reduction in muscle tone. So you can imagine this is probably a better medication used for generalized dystonia as opposed to maybe a focal dystonia of some sort. And always key for baclofen is make sure, start low, go slow, and make sure that patients are compliant. Because any abrupt disruption of baclofen medication can obviously have serious consequences with withdrawal. Those that are refractory to oral baclofen, it is recommended that an intrathecal baclofen pump for patients who have refractory combined dystonia and spasticity, obviously predominantly in the trunk and the lower limbs. And those who are refractory to dystonia and spasticity through the ITB or pump can also consider the interventricular baclofen. Another medication in the literature, which is not one of my favorites, being a brain injury doctor, are the benzodiazepines. These can be considered second and third line agents. They work by binding the GABA-A receptors and increasing the open frequency of chloride channels facilitating inhibitory signals. The ones we tend to lean towards are the clonazepam and the diazepam, mostly because of their longer half-lives. They're usually more well-tolerated. There have been open trial studies on clonazepam specifically, which has shown benefit in dystonia symptoms mostly in adults. However, in that same study when they compared them to the anticholinergic medications, there are actually more benefit with the anticholinergic medications. But this medication can be considered as noted as a second or third line agent. Again taking into consideration the side effects, mostly somnolence and dizziness and antaxia, all the things that most of our patients coming in have already. So you have to be aware of that. And with this medication, the same as baclofen, you have to make sure you have medication compliance because any abrupt stopping of this medication can have serious withdrawal effects as well. Other medications, and I just threw these on there, there's a couple case reports, case studies specifically on muscle relaxants, again more for generalized dystonia. And that's your cyclobenzaprine, tizanidine are included in this group as well. A few case studies again for generalized dystonia. And then one of the most interesting ones of recent has been the study, open-label trials two more recently of zolpidem, which actually has a high affinity for GABA benzodiazepine subtype receptors present in the basal ganglia. There have been two studies that have shown really good results and benefits up to two years again and comparable to the anticholinergic medications. However, as you can imagine, the limiting factor, dose-related factor for this medication is obviously sedation. So you have to be careful with that as well. But there were some promising results. And the one medication or what I should say that I get asked about most in my entire clinic for anything is the cannabinoids. I will say any results have been anecdotal. But anecdotal evidence for positive results with cervical dystonia, focal hand dystonia and generalized dystonia have been cited. However, actual controlled trials have shown no benefit or no positive results with cannabinoids. However, I do have one patient in my clinic with focal hand dystonia that says cannabinoids help with his golf game. So there's one story for you. But no actual controlled trials have shown benefit. So with moving on in conclusion, pharmacological treatment is based largely on empirical experience rather than actual scientific rationale. And that's due mostly because of the limited study of use in dystonia. Many patients require a combination of the oral medications or other treatments or the combination of other treatments with oral medications to help symptom control. And there are a high number of patients who fail due to lack of benefit or poor tolerability of these medications. And so I'm slightly over time. But I will move on and let the next presenter, there you go. Okay. And can I get a show of hands for everyone in the room? Who is residents? Okay, so a good number of residents. You might be called upon. So be at the ready. So my name is Dr. Mary Russell. I am an assistant professor with the University of Texas at Houston. And I work with Tier Memorial Hermann. I have a spasticity clinic that's down at Tier in Texas Medical Center. And then I do inpatient consults and medical director for the inpatient rehab unit that's up in the woodlands. And so what I'm talking about today is the treatment with injectables for treatment for dystonia. And so to the residents in the room, how would you define spasticity? Okay, yes, yeah. So spasticity is a velocity-dependent resistance to passive stretch. How about dystonia? So dystonia is kind of an overflow of motor activity. And secondary dystonia can often be caused after voluntary contraction when you're doing a specific activity and then you get an overflow of additional muscles. And so kind of what we'll be talking about today is the chemo denervation with botulinum toxins first, along with chemoneurolysis with phenol and alcohol, trigger point injections with or without steroids and lidocaine. And briefly, Dr. Lee is one of the on the forefront of cryoneurolysis, but also just kind of introduce you to that as a treatment as well. And so the botulinum toxins, they work by cleaving the snare protein that prevents acetylcholine release at the neuromuscular junction. And so if you look at the, whoopsie, okay, so if you look on the left side of the photo, you can see that the snare protein goes in, connects with the acetylcholine, this helps facilitate the release into the neuromuscular junction. And the action of the botulinum toxins, they work by cleaving that protein, which then doesn't allow the acetylcholine to be released. And there's three commercially available botulinum toxin type A's in the US. One is onobotulinum toxin, which is Botox, incobotulinum toxin, which is Xeomin, abobotulinum toxin, which is Dysport. And then there's a new one that's going to be released early 2024, which is Daxify, or by Rebans. And there's one botulinum toxin type B, which is Rheumabotulinum toxin, and that's myoblock, and all of those work by similar mechanisms. Okay, and so a lot of this part of the topic is going to be on which muscle to choose. So I loved this photo because I feel like that's, you know, someone that maybe doesn't have their, doesn't have full motion, maybe they have kind of a hemiplegic pattern, and now they can raise their arms. So yes, and so big thing in which muscles to choose for dystonia specifically is to get a very good history and physical. So with the history, you want to find out what is the pattern of abnormal contraction at the onset of symptoms. So what are they complaining about? Is it, you know, that they're a musician and it's a focal dystonia, and they're, you know, trying to play piano and they're having trouble with certain musical combinations? Or is it that they're, you know, when they're walking they're catching their elbow on something? Is it, you know, some other activity that that is eliciting it? The location of the tension. So where are they, where are they noting it? Maybe the, you know, they're catching their, they're catching their finger in their pants pocket. They can't get that out, but it's, you know, something stemming from the elbow. At patient perception, how much is it affecting their life? And the physical exam, you want to examine them at rest. You know, that's where you'd really kind of be able to see the hypertonia and the spasticity, but then also examine them with an activity. So if you can distract them, if you're walking, if you're having them be distracted doing something else, trying to walk, do the activity. If they play an instrument or something like that, have them bring that in so that you can actually see what's going on. And use your functional anatomy so that you can help determine what are the motions that are going to be most, most problematic to help identify muscles. And try to elicit the dystonia. So if they're having a problem with supination, you know, you want to try and pronate so, or supinate so that you can get a feel for how much of the, how much involvement there is. And upper limb dystonia. So the muscles that are involved. So this is going to be, anything with a star is going to be your primary muscle groups. And so elbow flexion, you have your biceps, brachialis, and brachioradialis. To the residents in the room, how would you differentiate between finding out if something's more biceps or brachialis? Yes. Yep. So supination with elbow flexion is going to be biceps. With the pronation is going to be brachialis. How about brachioradialis? It's going to usually be more of your thumb neutral. But then you can also have your pronator teres that's involved in that as well as ECR and FCR. And Dr. Alter and her group did a great article for focal limb dystonia in 2018. And I really like this. Let me see if this is the pointer. Oh, it is. Okay. So I really like this little graphic here that I got from this article over here to the right that's talking about upper limb and hand patters and cerebral palsy. And I really liked it for the postures that you can get, but then it also talks about the muscles that are involved. So as you can see, you know, in children with the cerebral palsy, but also in adults, you can get kind of a variety of involvement. Extension overwhelmingly going to be your triceps at the elbow. Pronation, pronator teres and pronator quadratus. Pronator teres, I would say, is probably going to be about 75 or 80 percent of your pronation predominantly. And then supination is going to be more of your supinator. At your wrist, your wrist flexion is going to be more of your flexor carpi radialis, your flexor carpi ulnaris. Extension is going to be kind of the extensor carpi radialis and ulnaris. And then you have your radial and your ulnar deviation. That's also going to play a part. And for fingers, you know, it's a very complex movement, so there's a lot of muscles that can be involved. And especially for someone that has like a focal hand dystonia, this is going to be, you know, a lot of fine motor movements, and so it's important to get the correct muscles. And the thumb, of course, there's a ton of movement involved with the thumb. And like, so you can see with this guy here in the picture that's up in the top left, you know, he's trying to write, but he's kind of getting that arm that shoulder elevation, abduction, that's making it difficult. And for lower limb dystonia, the muscles that are involved, hip flexion is going to be overwhelmingly iliopsoas, extension glute max, abduction. We always learned it in medical school as the agape muscles, so adductor longus magnus brevis, pectineus and gracilis, and the abduction is overwhelmingly going to be your gluteus gluteus maximus again. And for lower limb, knees, knee flexion is overwhelmingly going to be your hamstrings, extension the quads, dorsiflexion to the anterior, plantar flexion, gastroc and soleus, and inversion to the posterior. Eversion is going to be your combination of your perineal muscles. And so now we can move on to chemoneurolysis with phenol and alcohol. So they work by non-selectively denaturing the proteins perineurally or as a motor point block, and it interferes with the nerve conduction. And so it's generally used in a concentration of 5 to 7 percent. Less than 5 percent is not going to create that axonal degeneration or the Wallerian degeneration, and above 7 you're going to get a lot more side effects. Ethyl alcohol was something that we used for a short period of time when we had some issues getting phenol, and that worked well. Use it in similar volumes that you do to the phenol and in concentrations of 45 to 100 percent. Less than 45, again you're going to get similar issues, and close to 100 you're going to get a little more pain and side effects with the injections. And so side effects of those injections is going to be trauma to the injection site, muscle necrosis and fibrosis, risk of dysesthesias if you do a mixed nerve, and you want to have some caution in hempatic impairment for patients. With phenol, the anesthetic effect is usually very immediate. Above 5 percent causes axonal degeneration, and that usually takes about 7 to 9 days after injection. So the really nice thing about using phenol in clinic is you get to see pretty immediate effects because of that anesthetic effect, but they will continue to get improvement after about 7 to 9 days, and it can last up to 9 months. And then this is an article from Dr. Koropula that I really like the table because it just shows everything that you can do and which nerves you can block and which muscles you can affect with phenol. Alcohol, again it's a mixture of the with water or saline to about 50% would be most common. The intermuscular use of it has shown necrosis and fibrosis, specifically at the high concentrations. And one of the unique side effects is inebriation, so that's just something kind of to warn patients about if you go ahead and use alcohol. So now we'll come across to trigger points. And so pain arising from a trigger point was hypothesized to be the result of this excessive acetylcholine release from the neuromuscular junction after chronic muscle contraction. And so this can be in local myofascial tissues, it can be from CNS involvement or biomechanical factors. And Kamanali et al demonstrated that dry needling reduced pain scores and tenderness to palpation, that's my typo there, as well as botulinum toxin type A and lidocaine injection. So also the fact that you're putting a needle into those muscles helps with the pain. And now we'll go on to cryoneurolysis. So Dr. Lee would be able to attest to this much more than me, but it's an emerging technique for severe spasticity and dystonia. It has a cryoprobe that creates an ice ball that's 3.5 to 9.4 millimeters, that's at negative 60 degrees Celsius. And this causes axonal and myelin disruption and eventual Wollerian degeneration. It's proposed to be safer than alcohol and phenol due to decreased risk of damage to surrounding structures. And another thing that's really great about this is that effects can last one year or longer. Okay and I will now pass it on to my colleague Dr. Ibenhoe. It's like when I was a medical student in surgery, right, and I needed a step to step onto. Discriminating. Okay let me let me set my, all right you just tell me when I'm running out of time. So I sort of figured that any talk that deals with spasticity and dystonia was going to have a slide that none of us have, which is the distinction between what is the upper motor neuron syndrome. Because there is a lot of overlap when we talk about patients who are spastic or dystonic. We invariably, no matter who's in the room, will use those terms somewhat interchangeably. So I'm going to give you that little caveat because more often than not the patients you're going to see in my talk have mixed presentations of dystonia and spasticity. And the patients, in the interest of time because I have a fair number of videos, and should I stand on my toes? Videos and photographs. I may skip through a lot of slides so I'm very happy to answer questions afterwards. So I wanted to discuss reasons to intervene because it's not enough about I saw this elbow twist when the patient got up so I'm going to inject it. You have to really understand what it is you're trying to accomplish, particularly as insurance companies more and more limit what we are able to do. So I'm going to go over a little bit about neuromodulation and neuroplasticity because what we're trying to do generally is allow our patients to access more potential. Sometimes our goals are going to be more like let's just keep them comfortable and at home and sometimes our goals are going to be more like they're still gaining motion or their pain is different or they're able to work if they get injected or they can't work if they're not. So things like that to consider. So as physiatrists we're going to be considering function. Discuss coordination of services. It is never just what I inject. There are a lot of other things that will go into how your patients respond to treatments. And then we'll talk a little bit about patient consideration. So neuromodulation, I just thought that would be easy, right? Google, right? I should have used chat GPT. But Google, how would I define neuromodulation? And invariably first what came up was devices. And then I had to go a little bit deeper to get more to the definition I liked, which is positively modifying pathological activity. So think about it that way as we go through this. And then under treatments, neuromodulation, particularly devices, are often used for the minimally conscious state somewhat in conjunction with other things. Parkinson's disease obviously we'll be talking a little bit about deep brain stimulation, etc. Neuroplasticity, back in the day when I was a resident, this was a question. It's not a question anymore. We can have an impact on how patients recover or progress. I try to stay away from using recover, though I will, but I come from a brain injury perspective. And if you're taking care of a DOC patient and you say recover to a family member, they think that person's going to be jogging next week. Sometimes they are, if you were at the DOC presentation earlier today. But the ability of the nervous system to change its activity in response to intrinsic and extrinsic stimuli by reorganizing structure and functions. So garbaging, garbage out, and hopefully we can help modify what goes in and what we get out, our patients get out. So adaptive structural and functional changes to the brain or central nervous system, because there are changes in the cord. Capacity of neurons and neural networks in the brain to change their connections and behavior in response to information, sensory stimulation, etc. So we are trying to harness neuroplasticity. And there's no one single device, one single medication that's going to work. And there's a lot of art to how we manage patients considering social determinants of health. We're considering what their insurance will or will not cover, for example. Where they are in their whatever medical process is, where they are and what sorts of interventions they have had at different times in their lives. So combinations of interventions will depend on the goals and their access. So invariably one of the questions I ask patients in the first few minutes, usually one of my first five questions, is what's your insurance? And is it an HMO or is it a PPO? And how sick is that? That that's what we have to do. But you have to do that to have patients access what they can. Manipulating different aspects of the nervous system will affect other body systems. So like when we hear spasticity, particularly residents or medical students in the room, and you see that somebody's spasticity is worse, the board question is usually, what do you do? You look for a medical reason. But I would argue that spasticity and dystonia actually cause some of those medical reasons. And we need to be cognizant of that. So very little is really understood about what we're doing, bottom line. So moving right along, just for completeness sake, these are some of the devices that are used for neuromodulation. DBS most effective in the genetic dystonias. There are more and more identified all the time. ITB pumps obviously are spasticity and dystonia. And sometimes people will talk about dystonia theoretically would be off-label, except that being part of those FDA trials, I know that those patients were mixed hypertonias. So we will see changes in that as well. Transcranial direct current stimulation is being experimented with. Something that I think is really interesting, but I'll probably be retired by the time we know for sure, is the effect of spinal cord stimulation on motor return. Particularly now it's being looked at in the spinal cord population, but stay tuned. So challenges to management. The F word, as I like to call it, which is funding. So we kind of have to start there unfortunately. Expectations and biases, hours, the families, treating therapy teams, insurance companies. Those are just the realities and it's very hard to control for that. Coordination of services. When we first started injecting botulinum toxin, there was one in this country. It was Botox. We only could inject 200 units because we were afraid we were going to kill people. And we used to be able to do things like, well if you get your injections here, we can start your therapy on this date. Can we do that now? There are just way too many cooks in that kitchen. So the need for physical and cognitive assistance. Keep in mind that many of the studies that you're going to read, they control for cognitive deficits, language deficits, hemineglect. Is that our patients? I don't know. Maybe it is for you. They are not my patients as you'll see. Overwhelming amount of information for us to manage and even more importantly, an overwhelming amount of information that we give to patients and their families. And then shorter periods of intervention. You know, if a patient has two weeks length of stay in an inpatient setting and then they go out and they get thrown to the wind and they may or may not know where to go for follow-up or they may not be able to access it. So some of the clinical considerations when you look at patients are going to include pain, deformity, deformity you're trying to prevent, deformity that you're trying to manage, approaches to therapy, carryover considerations, what's realistic in terms of what we ask of patients and families, what other medications are they on, what other medical things might be affecting and their presentation as well as timing. So the most important thing in every lecture I give on spasticity or dystonia is how do you define the goals for your particular intervention. So depend again on the timing and the expectations. How are you going to facilitate other therapies? There's a hand you'll see toward the end of this, it's like this. So my goal for treating him is to be able to get him into weight-bearing, being able to get patients to cross midline in terms of how they approach their therapies. Shorter and longer term considerations for your intervention, prior interventions, responses, and the potential versus prevention. And I think that comes down to our own biases as well. This has been somewhat removed, reviewed. Daxify is currently available and now FDA approved for cosmetic, they always start there for some reason, and cervical dystonia. So the patient on the left has bad cervical dystonia. He came to see me right after getting out of prison where he had been beaten up and put on neuroleptics for multiple years on and off and that's where his cervical dystonia likely comes from. He got injected, he paid out-of-pocket for botulinum toxin injections. He came twice, he could not get into any insurance plan that would cover it, and he was lost to follow-up. The difference is, like this, with horrible pain, he was disabled. Okay. When he got injected, he was able to drive and go back to work as a truck driver. So how do you measure the cost-benefit analysis in a case like that? That's something to consider. And then Sarah, let's see, is this gonna work? Watch her tongue. Hey Sarah, can you move your head a little? Try and, I don't know. I want you to think about what are the potential goals here. Anybody wanna throw out a goal? Oh, did we get messed up? I hope I didn't lose the slide. We had quite the time yesterday with videos. So Sarah's spastic quadriplegic dystonic cerebral palsy. She was attending high school. She had a back with a pump place. She did really well. She got improved movement in all four extremities and then went for scoliosis surgery. Does anybody besides me see that as an issue or a consideration? Went to scoliosis surgery, had a horrible infection, hardware removal, months in the hospital, and before I got her as a patient, people just kept replacing her pump. So when I got her, she's on 1,000 micrograms a day of intrathecal baclofen. That should already be a red flag to people, and if it's not, it should be next time, okay? She's on tizanidine, chloral hydrate, valium, and she has a startle reflex when you walk in the room. So something isn't working, and neither are the chloral hydrate, the valium, the tizanidine. She gets botulinum toxin injections. That's her spine now. Isn't that painful? But I want you to hear her mom. I hope that you hear this. Okay, normally I can't hold her. You can tell she's balancing, and I'm not really holding her. Can you hear her? Before the injections last week, I couldn't have done this because she throws herself into extension and she can't get out of it. And so is it partly because her head's forward, you think, or she has a little more tongue control? It's because all the muscles are relaxed that normally are hypertonic, that take complete control of her body, and the Botox kills all that extension and all that flexion and all that hypertonic. And all I injected was around her neck. Yeah. Yeah, that's what she said, around her neck. Yeah. This too. I had it a big time around her neck. Where do you want to inject her? So when somebody has cervical dystonia, and you get their head into midline, and she's spastic and dystonic, right? You get their head into midline, you get their head into flexion, you can very often break up some of that tone, right? So my goals for her injection, injections, I should say, is always to get her out of that hyperextension, and I inject her tongue, okay? So we can decrease her tongue. The first time I said that in a room, people were like, but now I see heads nodding, so thank you for that. And same thing with David. David had multiple combined interventions. He had flipped in and out of tears several times. Every time he got a different physiatrist, I'll go through why. So initially, by the way, he always kept his eyes shut, and people thought, oh, DOC patient, and he was also encased in the cement of his own body, because he couldn't move anything. It really turned out, if you looked under the eyelids, that he had horrible keratitis, and he needed his eyes treated, and that's why he kept his eyes shut. You can see, he got progressing injections. It is not just about, I injected you once, and you didn't get better, right? And then he had, I'm not gonna tell you everything he had, but I will tell you this. He had eventually got an intrathecal baclofen pump after bouncing in and out, and all these other things done to him. And when he first came to see me in my office, I thought that he wasn't gonna be able to move, because for those of you who are comfortable with ITB therapy, usually you have to titrate that dose a bit. So this is when he first shows up, and his dose has barely been titrated. David, can you move your hands? Wow. Can you straighten out your arms? Nice. How about the right one? Can you bend the right one? How's the right one? That is pretty amazing. Let's look at your legs now. I don't know if you're gonna need a head start. Can you wiggle your feet at all? So I thought myself that that was an extensor reflex, but watch. You don't get isolated movement like that. So after his dose got titrated a little bit, he had orthopedic surgeries and readmitted to rehab. Can you tap your foot? At least your left, well, that one won't tap. Let's look at the left foot. Can you wiggle your heel, your foot up and down? Nice, really nice. So what did it take? Three shunt surgeries, a series of toxin injections, intrathecal baclofen, orthopedic surgeries, three different levels of rehabilitation, continuous therapy, continuous therapy for two plus years. I'm gonna talk about that. An advocating wife. That's why they kept getting different physiatrists. She's smart. She had three policies for him. She put money away. She works for a financial company. And whenever his insurance would go from one to the next to the next, she would pay independently for therapy if he ran out of therapy benefits. And so ultimately, that's him at home, okay? So again, think about what's worth it. How long do we generally follow patients in the majority of studies? How long does it really take? Because their improvements are not linear. And unfortunately, they're also impacted somewhat by extraneous influences. So we'll move on quickly. This is Brent. He came to see me after having, he has cerebral palsy. And he came, he's an engineer, he's employed. And he had had injections as a kid, a botulinum toxin A. And then he didn't think it was worth it anymore as he became independent. Now he's in his 30s and he comes to see me for the first time and he's like, prove it to me. Listen up. If you talk about something, my arm gets more tense. Like, that's the thing. When I wake up in the morning and I'm relaxed, then my arm's pretty, you know, loose. Okay. And you have to look at that hand. I won't get your face. Can you straighten out your arm? Can you straighten it out and bring your palm up? Not without a... Do you know what it's like to try to get my hand in there when I have to inject his fingers? All the way back. Okay, we'll move on. Okay, that's what he looks like on, I guess, your left. That's what he looks like without injections and that's what he looks like with injections. How many units do you guys wanna guess? He gets onobotulinum toxin A, he gets Botox specifically. Take a guess. 500, going once, going twice. Anybody wanna go higher? 600? Anybody wanna go higher? If you could, if you weren't concerned about medical costs, if you weren't concerned about Medicare, Medicaid, or an insurance policy first, not your patient, but that first, how much would you wanna give him? Mary Beth, you're cheating. He gets 1,000 units. We used to do that all the time until the company previously known as Allergan got their first FDA approval for asbestos. It took like 25 years or so, right? Now, we are letting other things that are not necessarily patient-directed tell us what we should or shouldn't do, but which arm looks more functional? Which arm looks more comfortable? Which arm can go to work and not get, display how nervous they are because when he gets nervous, his arm does this, right? So, a lot to consider in terms of that arm. What do you want me to do with my arm? What would you like to have relax in that arm? So, on the first slide, I was asking what he wants me to address because even with 1,000 units, I can't get it all, right? So, here we go. Sad but true, sometimes it amazes me that we have to do studies to show this. An interprofessional team approach involving neurologists, physiatrists, therapists, nurses, and other health professionals involved in patients receiving rehabilitation after neurological injury will provide the best outcome for patients. However, literature is limited in evaluating this care approach. Really? So, we need to prove that. I love this slide. Some of you may have seen it if you've ever heard me speak before. It says offhand, I'd say you're suffering from an arrow through your head, but just to play it safe, I'm going to order a bunch of tests. Because sometimes, and this is true also when you do your peer-to-peers, just be practical about why you wanna do something. And they will throw literature and FDA approvals at you because the toxins cost a lot, all right? But if you realize why you are injecting, and I'm gonna get more range of motion is really not gonna make sense to, I joke about this, but it's true, the retired gynecologist on the other end of the phone. They don't understand that. They may understand pressure sores, the risk of pressure sores. They may understand carpal tunnel surgery is longer term because of the twisting. In a lot of adults with cerebral palsy, you'll get a lot of cervical myelopathy over time. You have to watch for that. And along with neurogenic bladder and bowel. And dystonia, just like spasticity, and often they overlap again, will get worse with other medical conditions. And that's also something that is worth talking about. And with that, I'm going to self-promote. I'm on the board of the Neurotoxin Association. Our meeting is in Germany. We'd love to see you guys there. Let me know if you're interested. And then finally, we are finally getting our spasticity fellowship. It's here through the University of Texas. Dr. Lee over there and I are co-directors of the program. And you can see we have quite the faculty, including Dr. Russell, pediatrics, therapy, et cetera. So if anyone is interested, you can see Kathy Brown's number, or you can speak to Dr. Lee or myself. All right, thank you. Next. Thank you, Cindy. Thank you. So we're gonna go over more videos as well, so keep you guys interested. Thank you for all your time and attention. So what I'm gonna focus on today is we're gonna talk about how to utilize their sensory tricks and also bracing, which might actually utilize some sensory tricks as well to help these patients manage their dystonia and posturing. Dystonia, I think the two key things to keep in mind with dystonia is a patient who has sustained or intermittent muscle contractions causing abnormal, often repetitive movements, postures, or both. And you can see a lot of your patients probably have this, yet we continue to just focus on calling it spasticity. However, the reason why I call it the evil cousin is that they can often coexist, but they're very different from one another. It can occur anywhere, as Cindy was showing you, that the tongue, you don't ever get tongue spasticity, but you can get tongue dystonia. Now, I'm sure what Cindy will tell you, too, is when she injects it, you go through the bottom of the mouth. You're not trying to grab their tongue and stab it. You know? Because you have a lot of blood drooling out of their mouth and all that, so. So the parents might not be so happy about that. But anyways, what is a sensory trick? It can be a gentle touch or complicated multisensory input, tactile, proprioceptive, visual, auditory, thermal, imaginary, often it's self-developed, serendipitous discoveries. It's not me that's coming up with these sensory tricks. Oftentimes, if I take the time to listen to them, they'll actually tell me what they found. By the time, I'm seeing mainly adults, by the time they see me, some of these people have been suffering with this condition for 10, I had this one lady who first saw me, she had it for 17 years, a primary dystonia, but she kept going to ERs and they thought she was crazy. But we have to acknowledge that these other things are occurring, and this is considered additional sign of dystonia, others being mirror and overflow. Now, this was first described by this Frenchman, in 1893, in seven torticalis, and again, they emphasize how this is psychogenic, then, simple mannerism, childish behavior, a pathological fake. 1902, Maeg and Fendall termed this, and forgive my French, and again, they reinforced that psychogenic. However, later on, we were able to reintroduce the organicity of this disorder, and Patel, in 2014, suggested we call it an alleviating maneuver, because this sort of makes it less sound like some sort of trick or something that's in our heads. Unfortunately, this is less common than secondary dystonia, but what I'll try to show you is it does exist. Now, this is a lady, it's hard to say, is this a primary or secondary? She started to have cervical dystonia after she had a car accident, and ended up with a plate in her shoulder from a humerus fracture. So, in the first video, you can see, she's trying to turn her head to the right. Turning her head to the right. Sorry. Oop, what did I do? Relax. And then, here, in the next video, you can see, you know, just your typical trick, she uses to turn it, you know, puts a little bit of pressure there. Now, how do you know it's just not her pushing her head over forcefully? You know, I wanted to collect some data on her, so I did a dynamic surface EMG study on her, and you can see, let's see if this pointer works. You see, oh, sorry, I didn't. Oh, there it is, there's a very faint red dot there, but you can see on the right, with her attempted right turn, you can see, just to focus on the right SCM, you see how active that muscle is right there? But then, when you see when she uses that sensory trick, you can see how that activity just sort of changes, and then, all of a sudden, her left SCM is being incorporated as well. So, it's fascinating. This is another lady, this is another primary. She has a condition called captachormia. By the time I saw her, I think she's been suffering from this for over 20 years. She was seeing a lot of neurologists in the area, and you can see that this is sort of a, you know, a dystonia of her hip flexors, and also abdominal muscles. And here, what I did was, I did give her some injections to the iliopsoas, as well as the iliacus, and her obliques on the left side, primarily. She's slightly better. It's not completely resolved, but you also see she has some alleviating maneuvers she does. She'll put her hands on her thighs to try to walk. She'll also use a walker and walking sticks as well. But she did tell me one thing. She says she also has a tendency to clench her jaw, and what she found was, when she opened her mouth wide, like she was yawning the whole time, it actually got better. So, what did I do? I actually gave her some injections to the masseters for her, just a small amount. And you can see, you know, at first, I was like, is this really happening? You know, yeah, I know she's using walking sticks here, but she also told me herself, once her jaw relaxed, she felt less of that pulling on her core, on her hips. And you can see, when she walks without it, it's a lot better. Okay, so, these are both cases of primary. Now, can we apply this to a secondary? So, this is a young lady who has cerebral palsy. You can see, she sort of has, you know, all four limbs are affected by it, but the main thing, you know, I was treating her for is those ankles, her foot and ankle are very inverted, toes are curling. And I gave her, and she also had some clenching of her jaw, so I gave her treatment to the typical offenders, but, you know, first time I did it, it did wear off, but I tried it again and gave her a little bit to her masseters and temporalis, and I'll play this video again for you. And when she came back for her re-treatment at three months, she was actually still better, you know? In most cases, you would see her go back at three months for her next visit. So, you know, there are these things out there that I, you know, honestly, I can't really explain, but all that matters to me is that they're better. Now, I think Mary talked about trigger point injections, and they're helpful in relieving pain, because I think pain is also one of the main complaints of these patients. And here I have a patient, this is a very interesting case. I could talk about this guy for hours, but I won't. This guy had multiple strokes affecting a lot of different areas of his brain, and he has a lot of things going on with him, but, you know, what you'll see is he has these, you know, he has a hemidystonia on his right side. It affects primarily his hand, his wrist, and his ankle is very rigid. And what you'll notice is it's also causing him pain, so when you stretch him, you'll see a reaction on the left side. He actually, it looks like ballistic movements. Later, what I realized, this is called a cortical myoclonus on the left side. And what did I try to do? Obviously, I went with, you know, what I usually do is I injected him, and, you know, and did it work? You know, I injected his tibia anterior, EHL, and you see, not really. But what's interesting was he came back to see me again for a follow-up appointment to get repeat injections, and I examined him again, and it was gone, and I wish I had a video. I thought I recorded him after this, but I didn't. He also has a history of drug abuse, but due to his pain, his PCP, of all people, put him on Suboxone, and that seemed to help with this response. He still had some rigidity of that ankle, and we repeated injections because he felt like it helped actually improve his range of motion, and he felt more movement there, and he liked that. However, it did help, you know, that pain response got reduced, and therefore, he was mobilizing, you know, he was walking around better, and things like that. Now, bracing. Bracing these patients is very challenging, because you can imagine, if they're going into constant equinovirus, they're putting a lot of pressure on the outside of their foot, and they end up developing calluses here, lesions, just a lot of pain on the side, skin breakdown, and they often, you know, they'll come to me and tell me they had a carbon fiber brace, or they had this big plastic brace, or metal uprights, and they hated it, and they just would rather walk on the side of their feet rather than use this brace. Now, what I'm finding is sometimes, if you try to overcompensate for their movement, you know, you can end up in more trouble, so just giving them a little bit of support sometimes does a lot more than just trying to do your tried-and-true, you know, plastic molded articulating foot orthosis. Also, what I find is, if they are able to accept the brace, and you can just fix one thing, such as a sort of the equinus that they trip over, then they're less likely to have falls, they're less likely to have secondary injury from just overuse, and you can, you know, you can redirect the force as a joint with just cables, uprights, or struts, and I'll show you a case where a functional electrical stem may even work, but usually I wouldn't say, you know, they don't like to use double uprights. So this is a lady, she has this hemidystonia, you can see from childhood TBI. She was jumping on the bed and fell off, which is why you tell your children not to jump on the bed, and you can see how she inverts that ankle and walks on the side. We happen to have, and I wish I took a picture of what we did, but we happen to have a UCBL orthotic, which is pretty much, if you take your, if you take your standard MAFO, your molded articulating foot orthosis, you just cut it off right, right at the ankle. That's pretty much what UCBL is, and it fit her, and you can see here how much improved her foot is in that brace. We tried a double upright with her, I tried a MAFO with her, and she would still invert, and she hated it, and with this she was satisfied. I prescribed it for her, and she never came back to see me. So if you don't believe me, you know, we did some gait mat, and you can see with the shoes, I didn't show you shoes in UCBL, but, and with the shoes and her foot orthotic, you can see how her foot position is so much more symmetric, and she's walking less on the edge of her foot. Again, this is another lady with a dystonic equinovarious posture. She also had a MAFO and a carbon fiber brace, which she did not like, and therefore does not use, but she's also still tripping over her feet and falling from time to time, and, you know, if one thing I can't, I just can't stand these people when they come to me and tell me they're falling all over the place. So all I did was I gave her this over-the-counter brace that you can buy online for about $160, and you can see how she walks a lot more safely. I mean, I still give her injections, but injections are mainly to help control these spasms causing her pain. This is a really interesting case. This guy had a, he has a secondary dystonia from a childhood brain tumor, and right now he has a functional electrical stim device on, on his leg, and you can see, you know, he's walking fairly well with that, and then in a moment, he's actually going to turn it off for you, and you can see how it reverts. So, yeah, now it's off just to be, yeah, it's not causing, so. I'll give you a disclaimer. He is, you know, like Cindy said, the F-word, the funding issue. He paid for this out-of-pocket, and this, in addition to that, there's actually monthly fees for all the supplies to replenish the electrode pads, things like that, you know, and it's just, now I want to, you know, we're almost at the end, and with this, there is, you want to, you know, have, practice some caution, you know, especially when patients are coming to you from surgeons for your, for your opinion, as a lot of these patients have agonist and antagonist muscle activity. This lady that there's a picture of here, she is a cerebral palsy. She has a hemidystonia from that, and she used to have a very eye-ducted shoulder, and at the age of 11, she actually had a pectoralis major release done, and you can see her arm is now held out in abduction at a time, and this drives her crazy, and you can see in these recordings, these are another set of dynamic surface EMG. You can see that deltoid, and the traps, not recorded, but the upper traps are also constantly firing. Her sensory trick is to put her hand on her side, and that seems to relieve the muscle pulling, or she'll put her hand in her shirt, like this, and walk around, but, but I think in the end, what she said, what she tells me, she regrets ever having that surgery done, because she'd rather have her arm abducted in her side, rather than out, sticking out like that, so you just want to, you know, have some caution whenever these people are going to see a surgeon. So again, thank you for your attention. I think my wonderful collaborators, I'm glad we can reunite every year and talk about movement disorders, and you know, in summary, spastic dystonia are not the same, but they often coexist on our patients, and I feel this is constantly underdiagnosed, under-recognized in our patients, and it's very heterogeneous, as you saw, like all these different cases that can affect any limb, the mouth, the eyes, and it's hard to, like, gain evidence on our treatments for this, and it's truly an art at this point. We're all seeing these patients and treating them individually. You also be on, be on the lookout for leaving maneuvers, because they do exist, even in our patients, not just your cervical dystonia patients, and you may be able to use bracing, toxin injections, trigger point injections to help. In terms of pharmacologic, if they're having pain, you may want to address the pain, too. You know, is there a role for buprenorphine and naloxone for these patients, as well? You know, some of these have anoxic brain injuries from drug overdose, so, you know, they may be a candidate for that, and when you're prescribing braces, you don't want to just give them that solid MAFO just to restrict it. You want to just guide it, redirect it, and caution with muscle tendon lengthening surgery. Thank you guys for your attention, and if you have any questions, we're happy to answer any questions you may have. Thank you for your lecture. I have a few questions, but someone gets behind me, I'll stop it, too. With the phenol denervation, you said it lasts for nine months, but the phenol, you said, also causes axonal damage. Why is it not permanent? Why does the, you know, why is there re-enervation or whatever? Yeah, so that's a great question. So, the phenol, it can last up to nine months. It can be variable, but it works by degrading the myelin sheath on the axon, and so the body works to repair that myelin, and so that's why it will kind of regenerate and come back. So it's a demyelination procedure? Okay. The dry needling, it seems like, I don't know, you substitute one pain for another. Is the mechanism of action why it works, maybe through a gate theory of pain with a different stimulus, or are you disrupting maybe a mini contraction of the muscles there? I mean, if somebody has a mechanism as to why dry needling works, is it disrupting a mini contraction, or is it more like a gate theory of pain where you're substituting one stimulus, really one pain for another? I think it's disrupting the muscle contraction, because what, I know this might work, yeah, what I find is, even after I give toxin injections, people feel better right away. So, what I attribute to is, I tell them, I'm like, you're experiencing the acupuncture effect. This may go away tomorrow, but the effects of the toxin itself will take about a week to take effect and be on the lookout for that. So, I think that happens. Also, with some of my trigger point injections, I use bupivacaine as well, and even though bupivacaine only lasts four to six hours, I have patients who tell me they got like two to four weeks of relief of these painful spasms they're having from that. So, you're actually also doing the stretching. It's like the old spray and stretch. Yes, a little bit of that, too. Also, a lot of people do not feel that much pain with dry needling, and they'll feel almost instant relief with dry needling. Thank you to the group for the presentation as well. I had a question about compression garments and like movement kind of orthoses or suits, and I know we struggle with using that in secondary dystonia. I'm just curious about your experience with those. You know, it's sort of that when you've seen one patient with dystonia, you've seen one patient with dystonia thing, and you have to trial different things, and we go through, I've been at TIER a long time, and I've seen different groups of therapists go through times where they're going to do like cervical dystonia splints, which invariably tend to cause a lot of breakdown, at least in our place, and make people's necks hurt more, and then if your neck hurts more, your dystonia can get worse, too. So, but there are certain patients where it is helpful, and an example, it's sort of a mild example, is I have had a patient, he outgrew me, but where he had dystonic upper extremity, mostly wrist and fingers after traumatic brain injury, and he would wear like a golf glove, and his hand would go from that just to open it up, and he could use it functionally. So, it's sort of the same thing. You know, you're giving that feedback, sensory feedback, but you have to try them, but there are some patients where the garments are actually very helpful. Good question. We should add that if we do the course again. Hi again. Hi. Okay, way back in residency, and you don't want to know when, when a patient would come in with a post-stroke gait, I remember it being called hemispastic dystonia. Was my chairman incorrect, or it's just a hemispastic gait? Did he mix terms together inappropriately? The classic triple flexion and circumductive gait with a stiff leg. There are so many reasons for that gait, and we weren't there, so I don't know what your chairman was calling it. I mean, you know, we, we do a lot of modified ASHRAW scores. Some people do TARDU more than others to measure spasticity, and you're not, when you do an MAS with the exception of that one second thing, you're really not measuring a velocity-dependent increased resistance to stretch, and there are increasing variations in the definition. So, you know, that's one of the reasons I wanted to emphasize the upper motor neuron syndrome, because you'll see a host of the positive signs, the things we treat, the spasticity, the dystonia, we don't see apoptosis as much, myoclonus, all that would be the positive. The negatives would be the things that were, whether they've lost, they've lost coordination, they've lost isolated movement, they've lost strength, motor control, essentially. So, I don't know. I think, I think it depends which generation you're describing. Anybody? Yeah, I think everyone, it sounds like everyone has their own recipe. With the cerebral palsy engineer, just out of interest, do you know the etiology of his cerebral palsy? I mean, I'm suspecting maybe an intraventricular bleed in the basal ganglia, but do you have that history by any chance? Oh, yeah, and some of these patients, I will ask, you know, what the mechanism of injury was, and a lot of times, some, they'll have had a noxic injury, and that could also be a reason, you know, it could have had a cord wrapped around their neck at the time. Yeah, another point I think that we should make is, if you see a patient later in life who has new onset dystonia, or early in life as well, you really need to give them dopamine and make sure it's not a form of dopa, dopa-responsive dystonia. Thanks for a great discussion. Sometimes it can be very tricky teasing out spasticity versus dystonia for patients that have kind of a mixed presentation, and especially trying to figure out what is causing the most functional impact on their ambulation. How often are you sending those patients for formal gait analysis in a gait lab? I don't have the option. Yeah, unfortunately, not a lot of centers have the option of sending people to a gait laboratory. I think a lot of times people do, they may do diagnostic blocks. It'd be nice if dynamic EMG was more common, and then, because do you need this formal multi-million dollar laboratory to like measure the kinematics, the kinetics, when really all you're interested in is what the muscles underneath the surface, how are they responding? I think that's really where I think more of our intention should be focused on. So if the treating physician is having some questions, you know, we can always take a look at them. I think video is a good way to assert that, because a lot of times these will manifest with movement, and that's how, that's the main thing, you know, versus just a passive maneuver. Because a lot of the patients I demonstrated to you guys had Ashworth's of zero. I posted one time after a course I taught somewhere about when you're looking functionally, whether we call it spasticity or dystonia, does it really matter? And I asked that question, nobody wanted to answer me, which I found interesting, but you know, you kind of have to look at what you've got. Most of us don't have dynamic movement labs. Great, thank you. So in pediatrics, in our young patients with cerebral palsy, we use a lot of clonidine and gabapentin to treat dystonia, and I know adults have a lot more difficulty tolerating clonidine, but I wonder if gabapentin would be a good adjunct in the adult population too, if there maybe is a neuropathic pink component. It's very variable with everybody, but sometimes doing either clonidine and baclofen or gabapentin and baclofen, you can get some nice results in our pediatric patients. That is absolutely true, and I will tell you in my spasticity patients, there is literature behind gabapentin as being a second-line agent. I just didn't include it because there wasn't any specifically with the dystonia, but absolutely it has been used as a second-line agent. With the patient where you touch the right foot and the left foot would extend in myoclonus, but the suboxone helped, any possibility of some psychogenic components with all this? Because it seems a little unusual, but you tell me. I think if you looked at his MRI and saw he had lesions in his cerebellum and other places, I would say less likely psychogenic. But the dystonia would not come from the cerebellum. It should come from either basal ganglia or connections therein. Usually, but sometimes the pathology that you see on the MRI doesn't correlate with what you see, and that makes you wonder as well. I'm going to have to make a comment about the increasing use of the term functional or psychogenic in our patient populations in general because, and maybe I err, maybe that's my bias a little bit too much on giving patients the benefit of the doubt, but I had a conversation with a friend of mine earlier this morning actually about, you know, there are things like, for example, when I was in medical school there was no such thing as AIDS. We just like gay men got weird infections initially, right? And when I started in this field, I would hear attorneys say things like, or physicians say about a patient they were seeing for an attorney, well they can run backwards, but they can't run forward, so it must be psychogenic. And the truth is now that's runner's dystonia. So my point being, I think that we should keep open minds that we sure don't know everything there is to know in medicine, and things are evolving and changing environmentally, nutritionally, socially. So as I said, I would err more. You can see mirror dystonia, though, in patients in general, and basically the brain is rewiring incorrectly, so who knows. And you mentioned UCBL orthotic. What is the use, what's the UCBL stand for? University of California Biomechanic Laboratory. As it were. Thank you. Thank you very much for taking the questions. Anybody? I want to thank Dan and my co-speakers for putting this together, and the invite. Yeah, and thank you guys for all your questions. I've never seen a, you know, a session with so many questions. Thank you.

Dr. Kelly Crawford

Dr. Mary Russell

pharmacological treatments

injection treatments

secondary dystonia

individualized care

medication management

botulinum toxin injections

neuromodulation

deep brain stimulation

spastic quadriplegic dystonic cerebral palsy