Monday, April 24th, 2023
Last modified on December 21st, 2023
Hello everyone, welcome to another episode of the No Plateau podcast. I am your host, Henry Hoffman. I’m thrilled to be with you today. Today we’re going to talk about spasticity treatment following stroke. For many patients, spasticity rears its ugly head soon after a stroke, and it’s a tough nut to crack. Up to 40% of first-time stroke patients suffer from spasticity, so it is a big deal. To help me discuss this topic, I invited Dr. Samuel Milton to join me on the show, and he graciously accepted.
Samuel Milton (00:44.97):
Well, welcome. Thank you. And not to date myself, but over 30 years. I’ve been at Emory for 20 years.
Henry Hoffman (00:48.066):
Uh oh, okay, well, I tried to be, yeah, yeah, I was trying to be extra nice with you on that one. How you doing today? And thanks for joining, by the way.
Samuel Milton (00:53.95):
Thank you. I’m doing very well and I’m very excited to talk about this topic.
Henry Hoffman (00:58.806):
All right, well great. Well, let’s first just, if you don’t mind, just talk a little bit brief background about you so the audience, which is made up of both patients and clinicians, can learn a little bit more.
Samuel Milton (01:09.99):
Sure. So after I finished my residency training at National Rehab Hospital, I’ve always been involved in a teaching academic type of practice with inpatient and outpatient, but mostly running stroke rehab units, which has led me to my current position at Emory as an associate professor. I currently manage the inpatient stroke and brain injury unit for Emory, which is about a 20-bed unit. And I also have an outpatient practice where I manage patients who have stroke deficits as well. And spasticity is one of the areas that I find fascinating and interesting, and I see many patients who have issues because of spasticity.
Henry Hoffman (01:57.266):
Yeah, yeah. Well, again, it’s a pleasure having you. And you know, we’re going to talk a lot about spasticity now. And obviously with normal muscles, this is for the patients and the therapists, the brain inhibits most reflexes when we’re dealing with normal muscles. But following an upper neuron injury, like a stroke, the patients go through the classic, you know, Brunstrom recovery stages. Some people know it as Brunstrom, some people know it as recovery stages or healing stages.
Henry Hoffman (02:27.246):
Hopefully, if they don’t get stuck at that stage, to breaking out of synergy or breaking out of that spastic nature and performing some more isolated functional tasks. But the major problem, as you know, is the loss of supra-spinal control from these reflexes. And the spinal reflex activity is normally, you know, tightly regulated. And if inhibitory control is lost, the balance is tipped. Obviously, you’re gonna have this hyper-excitability of the spinal reflexes. So imagine constantly folks lifting up a 50-pound dumbbell.
And that’s not going to be fun, it’s not going to be comfortable. A buddy of mine in a purveyor of stroke recovery, the late Pete Levine, you know, he used to preach the muscles, the victim, and the brain’s the perpetrator. You know, from our perspective, it’s a brain issue, and it’s not a muscle problem. And you really just have to rewire. That’s what I want to dive into. But from your perspective, you’ve been doing this a long time. How do you describe spasticity to your patients? What’s the best way to describe it to a patient?
Samuel Milton (03:12.118):
Henry Hoffman (03:27.186):
Minutes just to get to the definition and then they end up saying and there’s still a lot that we just don’t know. So how do you typically describe spasticity of patients?
Samuel Milton (03:29.992):
Samuel Milton (03:36.73):
That’s correct. First of all, I have to make patients understand and their caregivers understand that we all have normal tone. We’re not floppy or we’re not flaccid, but all people have normal tone. What’s interesting about spasticity from a cerebral origin, like a stroke, it’s a little different than other types of spasticity that you may see with multiple sclerosis. And you described it pretty well with that synergistic movement pattern, meaning that both…
When we execute a movement, one muscle actually shortens the joint while the other muscle relaxes to allow that joint to be shortened. So the brain has an on-off mechanism that allows fluidity of our movements. So when we have a patient who’s had a stroke, we lose that fluidity where both muscles are on at the same time. So they’re both fighting each other. They’re both in synergy, meaning they’re both contracting at the same time.
Specific type of spasticity that is unique and obviously very challenging.
Henry Hoffman (04:42.506):
Why do you think when we see spasticity in patients come into the clinic, it’s typically in a flexor pattern? And I know mechanically the flexors are stronger than the extensors, and, you know, some argue that there’s spasticity in both the flexors and extensors, but the flexors are winning. Or they’ll say it’s an overexcitation of a certain descending pathway. Why do the, why is the flexors typically the spastic muscle?
Samuel Milton (05:12.07):
Right, generally those are the anti-gravity muscles. So those muscles that fight gravity are the ones that tend to be spastic. For example, even if you look into the upper extremity, you’re going to see, stroke patients, we’re going to have a classic, what we call a flexor synergy, flex at the elbow, flex at the wrist, hand in a fisted posture. The lower extremity is the opposite, where the leg goes into extension and the gastrocs is, so in other words, pointing downward. So I look at it as the muscles that typically fight gravity every day…
Our muscles aren’t equal in strength, so those muscles that fight gravity every day are much stronger than the muscles that don’t. So if you look at your arm, for example, the muscles that actually grip something like if you’re going to hammer something or play tennis, well naturally you want those muscles stronger than those muscles that want to release. So those muscles that tend to fight gravity or be those strong flexors will be stronger than those extensors. But we don’t know that on a day-in and day-out basis because our brain controls how we move and they control the fine coordination of these muscles and how they interact.
Henry Hoffman (06:13.646):
Yeah, it’s like you’re…
Henry Hoffman (06:26.406):
Right, and it’s almost like you’re already fighting a losing battle just because the flexors are stronger than the extensors. When we, if you ever lived in a third-story walk-up and you have groceries, you’re going to hook them with all your fingers into a flexed grip and start, you’re not going to carry them with your extensors. So we’re already fighting a losing battle because the flexors are so stronger than the extensors. And then of course, you have a stroke and you go from the stages of flaccid to emerging spasticity.
Samuel Milton (06:40.812):
Henry Hoffman (06:57.246):
And then the hope is over time, which we’ll get into through some treatment interventions, we can kind of break out of that spastic pattern and get some more recovery there. So moving on to common treatments. Now if we can just think about it from a medical perspective, the different buckets of treatment. So I don’t want to say too much because you’re the guest and you’re the one who’s the expert in spasticity.
Samuel Milton (07:11.95):
Thank you, that’s it.
Samuel Milton (07:20.712):
Henry Hoffman (07:26.746):
Chemotherapy, or any other, you know, just oral, pharmacological. What are the major buckets? So a patient comes to you and they have spasticity. You know, what are the solutions and options for them?
Samuel Milton (07:39.871):
Well, the first bucket I always think of is therapy. So that’s the very first bucket. And then depending on the patterns of spasticity, you move into oral medications as one method of treatment depending on the type of spasticity. And then more recently, which became FDA approved, you look at chemo denervation where this is more designed to treat focal spasticity of one or two muscle groups. Then the last option, well, I don’t wanna say last option, but another option would be surgical intervention where you’re releasing tendons. Sometimes, depending on the expertise of the surgeon, they’ll do transfer of tendons or to take advantage of some of the overactive muscles or a combination of all these above, all of the above.
At it mostly now is a combination of all the above.
Henry Hoffman (08:41.546):
Okay, and so we’ve all had patients, whether they come in with baclofen, it’s more systemic, or you’re using medication versus a focal. How do you determine if you’re gonna give a patient a medication versus going with a focal chemo? One of the examples is Botox, it’s not the only one, but that’s the one that all the patients commonly know and have heard. How would you determine who’s gonna get medication versus getting Botox? For example.
Samuel Milton (09:01.95):
Samuel Milton (09:09.87): Well, first of all, you have to appreciate whether or not the patient has more generalized spasticity. So in other words, if they are fighting with spasticity in their leg as well as their arm, this can be very difficult to try to address with Botox every spastic muscle many times. So you may want to attack it using a systemic agent to try to then isolate or make more prevalent those muscles that you can now address with Botox.
Limitation of how much Botox you can give safely. So if a patient has diffuse spasticity, I’m going to offer an oral agent first and then use the vocal treatments with chemo denervation or Botox.
Henry Hoffman (09:53.506):
With the medication route, what are like one or two of the common side effects if a patient wants to get medication for systemic, you know, upper and lower extremity spasticity?
Samuel Milton (10:03.39):
Right. Well, the most common medications that we use, Baclofen or Tizanidine, we also use some anti-convulsants that can help, but they all act centrally. What that implies is that many times these central acting agents can cause drowsiness and make people actually feel weaker. Sometimes they don’t tolerate these side effects whatsoever, especially when you’re looking
Henry Hoffman (11:32.986):
It’s the date of side effects. So at that time, we’re left at trying to use other modalities, which primarily would be chemo denervation. I even have had patients who’ve had strokes have an intrathecal baclofen pump because their spasticity is so severe in their lower extremities. Many times if you can take care of the bigger problem, then you can focus the neurolytics on the focal problems.
Henry Hoffman (11:32.986):
So before we jump into the neurolytics, can you briefly explain what intral fecal baclofen pumps are and how do they actually implement that?
Samuel Milton (11:43.83):
Yes, so intrathecal baclofen pumps, we usually reserve that for patients who have severe spasticity. So how that medication, how that type of treatment works is that there’s a catheter that goes into the space of the spinal cord, the intrathecal space where the fluid is, and we actually administer baclofen. Now the good thing is that the baclofen there is going to be 100% bioavailable, meaning
Samuel Milton (12:13.81):
Exactly where it needs to go. When you take an oral baclofen, only about 30% of that actually goes to where it needs to go. So therefore, you’re left dealing with the sedation and the fogginess, the brain fog that’s associated with the oral medication where we’re using a hundredth of a dose. So we don’t have to typically worry about the sedative side effects and it’s very
in reducing spasticity, especially in the lower limb. And it does require a surgical procedure, and usually, we do a trial first to assess whether or not this would be appropriate for the patient.
Henry Hoffman (12:58.126):
Okay, interesting. Well, let’s switch gears then and talk about chemo denervation techniques. Basically, those are local injections, like you said. You know, it kind of gets a bad rep. Some patients think that they’re putting poison in their body, you know, for the audience Botox as an example. It’s not the only one, but it’s a drug made from a toxin produced by a bacterium, clostridium, right, botulin, foodborne intoxication.
Samuel Milton (13:24.515):
Henry Hoffman (13:28.686):
Called botulism. So can you discuss exactly what neurolytics are? And obviously, I brought up Botox as an example and maybe curb the fear that some of these patients may have regarding, hey, you’re injecting poison into your body.
Samuel Milton (13:34.714):
Thanks for watching!
Samuel Milton (13:45.37):
Sure, sure. So first of all, you’re right. Botulam is derived from a Clostridium botulinum, which is a bacteria. It’s in soil. It’s actually ubiquitous in the soil so that anytime we eat fresh vegetables, we actually consume a little bit of this all the time. Botulism becomes a problem or poisonous when someone does not can a say peaches or can
Samuel Milton (14:15.49):
Or toxins just multiply and multiply. So you really have to consume a lot really to get sick. But it is a toxin. But in how we use it in injectable form, it’s a very weak toxin. But it has a very strong effect on the membrane of the muscle. It blocks the receptor from releasing acetylcholine so that the muscle can no longer produce a response.
Binds to that irreversibly, but over time, our nerves grow around that blockade and re-innervate that muscle. But the dosing we use is very safe. We just inject into the muscle. We do not inject into the blood vessels or anything of that matter. But usually, I explain that botulism or the clostridium botulinum is actually ubiquitous in our soil and we actually are exposed to it
Henry Hoffman (15:15.886):
Okay, that’s helpful to have that explanation. Now what other forms are out there, neurolytics and community, you know, local injections should one consider besides that one.
Samuel Milton (15:27.17):
Right. If for some reason a patient’s allergic or they’ve had or cannot have Botox or a botulinum toxin, then alcohol injections can be used. The downside of using an alcohol injection is that it is a permanent blockade. So you have to; it takes a long time for the nerve usually an irreversible pathway because it actually destroys the nerve.
Henry Hoffman (16:04.386):
Wow, interesting, I didn’t know that. So with alcohol, the potential risk is, and for some this might be not a reward, but a potential risk is it’s not gonna be just three months like Botox and it wears off, where it’s a temporary paralytic, this is almost a permanent paralytic, if you will.
Samuel Milton (16:25.85):
Correct, correct. The benefit when I explain about doing it using a botulinum toxin is that if we don’t like the result, it will wear off. And therefore, but using alcohol, then it does not wear off and you have to live with that result. So sometimes that is a tough sell sometimes.
Henry Hoffman (16:50.086):
So is there any other ones? I mean, I’ve read stuff on phenol. I mean, is it just pretty much botox? Oh, so it would fall under the.
Samuel Milton (16:55.55):
Well, phenol isn’t alcohol. Yeah, phenol, so that’s the brand, right. So those are the two major ones. There are two or three brands of botulinum toxin on the market, and phenol is the alcohol that we use for those types of injections. Now, many times I’ll use, sometimes use a, sometimes you can use a combination of both.
Henry Hoffman (17:02.593):
Henry Hoffman (17:13.626):
Got it and what percentage of…
Samuel Milton (17:23.05):
Yes. So in my practice many times if the patient has a really tight peck and I’ll use phenol there so that I can reserve the botox in the lower arm where I may need it. So I have used both in combination in the past.
Henry Hoffman (17:43.906):
Okay, and what percentage of your patients get phenol versus Botox? You know, if you’re looking at your…
Samuel Milton (17:55.052):
A very small percentage, phenol, you have to have the capacity to store it, it has a very short half-life. So I would say that’s a very small percentage, like less than 5%. So most of my patients I’ll use a brand of botulinum toxin primarily.
Henry Hoffman (18:14.966):
Okay, and as far as their number one complaint, are they coming because, what percentage are coming because it’s a painful problem versus it’s a tight problem?
Samuel Milton (18:27.67):
Excellent question and it can be a combination of both things. However, since you mentioned that, really what’s really important when you’re looking at a treatment plan using either medications or injectables or anything like that is that you want to have a goal in mind. What are you, the therapist, the patient, and caregiver, what are you trying to accomplish? But getting a patient fitted for an orthosis. It can be from a family member because they are having difficulty with getting a patient dressed in the morning because they can’t get their arm in position or pain. They can’t get deodorant under their arm. Or it can be from significant stiffness and tightness that leads to discomfort. But you like to have that conversation
Henry Hoffman (19:38.726):
Yeah, I know you’re bringing up a good point. From the therapist side, you know, this is not a fixed cure, a panacea. The research is very clear on what these types of techniques can do and cannot do. Just like the research is very clear is from a therapist perspective, you know, sadly there’s not a lot of good options for reducing spasticity. And we’ll talk about that in a second. But as far as, you know, positive, I guess a positive case study example for you would be
Samuel Milton (19:57.932):
Thanks for watching!
Henry Hoffman (20:08.686):
Hey doc, great, I can now open up my hand to do hygiene, or hey, this is wonderful, I can now sleep at night without pain in my shoulder, or guess what, because of this Botox, I can get my orthotic on much easier. You’re probably looking at those goals as the classic success story versus, hey, I got my hand back. You probably don’t hear a lot of, because of this Botox, I can now open my fingers and button my shirt. You’re not getting a lot of those testimonials, right, because I’m not getting those either.
Samuel Milton (20:41.73):
Right, no, you’re correct, you’re correct. I would say that the testimonies, as you mentioned, I can get my brace on; it’s not as uncomfortable, but I also get them from the caregivers who are helping them get dressed. Now I can get his shirt on without causing a lot of discomfort and pain. I can get, you know, the hygiene is much better in the hand and underarms and things like that. So I also get it from the caregivers as well.
Henry Hoffman (21:07.506):
Yep, yep. Now there is one, I don’t know if it’s a myth or if it’s a fact, maybe you can address it. Electrical stimulation provided to the site where the botox was injected. Have you heard where, if you do electrical stimulation with a site where the botox were injected, let’s say the finger flexors, long finger flexors, the extrinsics, that could help speed up the reaction. Is there any truth to that?
Samuel Milton (21:30.69):
I have not read anything other than anecdotal, nothing with any double-blind studies. So I haven’t really, now my injection technique, again, without any evidence is that usually after I inject, I will pretty aggressively stretch the muscle because Botox diffuses pretty readily in the muscle. And I do that to help with the spread of the muscle, really stretch the muscle out as much as I can, after I do an injection. But I have never set up a patient for immediate eSTIM after injection.
Henry Hoffman (22:01.311):
Henry Hoffman (22:06.306):
Okay, well, one a follow up since you brought up your technique, you know, I’ve seen and we’ll explain this to the audience. And you can dive deep. There’s the biofeedback guided injection where you’re looking, you’re waiting, you’re listening, or watching the signals of the muscle activity where it’s hyperactive and to help guide where you need to go. There’s ultrasound guided. What is your technique? Can you share just briefly, if a patient’s going to get Botox, what would they expect if they were coming to see you?
Samuel Milton (22:37.55):
Yes, so depending on the problem, so if I have a patient who has more spasticity or synergistic pattern of movement that’s creating problems, I will use an electrical stimulation technique where I’m stimulating the muscles that I want to inject. Now I’ve also had patients who’ve been very fortunate to gain that weaker side of recovery. In other words, they’re gaining some finger opening but they can’t realize that because the flexors are just so strong. Well, in those cases I’ll use more of a feedback technique like an EMG where I’ll ask the patient to open your hand, bring your wrist up, but I’m located in the flexors to see what muscles are fighting against me. And so in those cases I want a finer control because I don’t want to take away all that good flexion that they’ve gained but I’m trying to sort out what
Samuel Milton (23:37.49):
An extension or opening of the hand. So in those cases I tend to want to be very very local and or focal with my injection to those muscles that are particularly causing a problem.
Henry Hoffman (23:50.126):
Is EMG still considered the best way to get as exact as you can before injecting? Okay, so what about the ultrasound guided? Is that?
Samuel Milton (23:57.13):
Yes, yes. But either way, I, well, I mean, I don’t use ultrasound guided. I use EMG in STEM depending on, as I described, it’s exactly depending on what I need to do. Remember, using the STEM method, because the Botox spreads very readily in that muscle, that means I’m not really concerned about getting too much in that flexor they’re so tight. However, if I do have someone who’s experiencing some movement, they’re using the hand, I’ll tell you a funny story in a moment, then that’s when I’ll use eSTEM. I had a very pleasant lady who had a stroke and she had her typical elbow flex posture. She comes into the office and wants Botox and of course I go ahead and tack those elbow flexors and she comes in very upset with me.
Henry Hoffman (24:56.106):
Samuel Milton (24:57.19):
Upset that I went after her her arm that holds her purse so you know you want to make sure you get your patients into it yes
Henry Hoffman (25:02.417):
Sure. Well, remember.
Exactly, and there’s benefits of having spasticity, right? It’s not just always a negative where you don’t want to be 100% flaccid. That’s not where you want to be in your life. I’d rather be spastic than flaccid, right?
Samuel Milton (25:10.091):
Samuel Milton (25:17.33):
In this business, many times you find that when patients or loved ones go through a scenario like this, they want the opposite. So if their hand is now starting to close and all of a sudden they say, well, I need Botox, but at the same time, their hand is just starting to close. So I may not want to jump in there and necessarily do Botox, especially if the range of motion is full. You know, now they’re starting to get some return. Let’s see where this return takes us. And if it’s a problem, then we’ll address it. That right away if they’ve been slow to have a, like I said earlier, I’ve been doing this for 30 years, every stroke victim recovers differently. I’m sure the therapist in your audience will agree, every patient is different. But you sort of want to be cautious, like you said, you don’t want to take away the good tone. There are some benefits to tone and spasticity.
Henry Hoffman (26:07.806):
Yeah, so that brings me to the next point. You know, I don’t know if you have therapists ever in your clinic when working with one of their patients to be part of the team. I know when I was treating patients back in the day, and I did this with a lot of the SIBO therapists that were in different parts of the country, some of them had fantastic relationships with the physiatrist, and they’re working with these patients almost on a daily basis. So they know, for instance, when they were using a device called the SIBOFLEX, that is a spring-loaded wrist, hand, finger,
Samuel Milton (26:35.281):
Henry Hoffman (26:37.886):
Because a lot of people with spasticity, they can’t, and for the camera, they can, you can see they can squeeze, they just can’t open. But when you go to the, let’s say go to get your injection, if you take away their PIP flexion, they’re no longer going to be able to use their hand for three months. And we don’t want that either. So the therapist would go in with the patient, they would show the product, this is a functional orthosis, they want to be able to grasp. So please, doc, you know, titrate, don’t do as much.
Samuel Milton (26:39.634):
Samuel Milton (26:46.736):
Samuel Milton (26:55.87):
Henry Hoffman (27:08.066):
That’s the middle joint that bends. Try not to do too much because if you take that away then you’re going to be firing other muscle groups and for the therapist they would be doing more of an intrinsic plus where they would no longer have PIP flexion so they would represent if you’re watching the video you’re representing this type of positioning which is that limber called intrinsic plus position and if you’re in that position you’re definitely not going to be using disabled flex for those three months it becomes a paperweight. So my point is I don’t know if it’s advocated
Samuel Milton (27:35.57):
Henry Hoffman (27:37.806):
Much but it should be if it’s not having that neuro therapist available with the patient to go see the doctor because remember you’re only seeing this patient every three or four months for 20 minutes where the therapist is seeing this patient for hours per week so they know what’s going on do do you guys have those conversations with the therapist and I know you know where to inject but usually there’s more to the story sometimes
Samuel Milton (27:49.39):
Samuel Milton (28:02.41):
Yes, well, luckily for me, in my situation, my clinic and their clinic are right next to each other. So we have those conversations very frequently. Now that we have electronic medical records, they’ll just tell me what they want. The therapists will say, I need this, this is the problem, or please look at this. Sometimes they’re nice about it, but they’ll let me think I have a decision here. No, but yes, it’s very important that, especially if they’re using this device, because I find
Henry Hoffman (28:15.286):
Henry Hoffman (28:21.789):
Yeah, yeah, yeah.
Samuel Milton (28:32.47):
Phenomenal. It gives the patient world of confidence and self-being and so you do not want to take you know go backward. I should say in those patients I definitely use bio EMG feedback to make sure that I’m not overdoing it with the flexors and the flexor compartment.
Henry Hoffman (28:48.906):
Yeah, no, I agree. Okay. Funding. Sometimes I’ll talk to patients and they’re saying it’s not covered. Is it a problem getting Botox covered for stroke survivors? I don’t even know if it’s, maybe Medicare covers it, but private insurance doesn’t. What is the reimbursement situation?
Samuel Milton (29:08.57):
Well, Medicare does fund it. Medicaid, state Medicaid also funds it. The private insurance companies, now that it is FDA approved with appropriate documentation, also fund it. The Allegan, the company that produces Botox or manufactures Botox, they also, because many times there’s high co-pays. We didn’t talk about the co-pays that sometimes go with the treatment programs to offer financial assistance for the copays. And if you do have a doctor who’s doing it you can ask them about that resources for that or how to apply for those funds.
Henry Hoffman (29:51.786):
Okay. From a research standpoint, when you think about OT-PT, you’ve been around the therapist for a long time, how do you think, you know, the OTs and the PTs can best treat these patients suffering from spasticity with a combination of a neurolytic? We talked briefly about the goals. The major goals are not a lot of the goals at the end of the day that are home run. You know, we talked about pain management, which is a big one, no doubt about it.
Henry Hoffman (30:21.906):
An AFO or a hand splint or keeping the foot loose as well. We talked about just trying to have more flexibility in the limb. You know, the home run is getting the hand back. And you know, if you comb the research, and this is more also for the patients here, if you comb the research, you know, people confuse spasticity with stretching, thinking stretching will help reduce spasticity.
Samuel Milton (30:35.966):
Henry Hoffman (30:51.966):
A contracture is not a spasticity problem. Those are two different things. So when they think, you know, the only way to, if they, you know, if you think about it from the patient’s perspective, if you suffer a stroke and you’re weak and you can’t move your limb and you start to become spastic over time, you’re gonna create soft tissue shortening which will lead to contractures. So then you’re gonna try to address the contractures. And this is where it gets a little confusing for patients and therapists in your role.
So, can we stretch muscle and tendons? Yes, we know that you can do serial casting. We know that you can, you know, there was a study done, you know, I think it was in Brashear’s book talking about more than 48 hours of constant stress to the muscle-muscular tendons junction will lead to increased sarcomeres in series. Conversely, if you’re shortened for more than 48 hours, it can lead to reduction in sarcomeres.
Samuel Milton (31:22.85):
Henry Hoffman (31:52.566):
In range of motion. But that has nothing to do with spasticity. Once you stretch and reverse a contracture, you’re still spastic. Because that’s a brain problem, not a peripheral joint problem. So when I think about research, I think about OTs and PTs, you know, obviously stretching comes to mind. People want to splint thinking splinting is going to reduce spasticity. Again, we’re still, are we going to affect sarcomeres? Are we going to affect the ability to improve range of motion? Yeah. But what do you think is going to happen?
Samuel Milton (31:56.35):
Thanks for watching!
Samuel Milton (32:00.955):
Henry Hoffman (32:22.506):
E-STIM, same thing. I do E-STIM a lot. I’ll E-STIM, for instance, if they have a hard time opening their hand and they have spastic flexors, I’ll put E-STIM on the extensors because every time they fire their extensors, they’re relaxing the antagonists in that position. I like to stretch and do E-STIM at the same time. But a lot of these things, they’re inconclusive when it comes to did we have long-term benefit when it comes to reduction in spasticity. So, yes, stretching can reduce reflex hyper-excitability, but temporarily.
Samuel Milton (32:24.033):
Henry Hoffman (32:51.786):
I can weight-bear for 30 minutes and I’ll get some, you know, by the time I’m done weight-bearing, the patient’s nice and loose, but by the time they get to their car in lot C, 30 minutes later, they’re tight as a drum again. So from my perspective, the only true way, and this is a long-winded way of asking you, to reduce plasticity is if you can manipulate and affect neuroplasticity, right? So in order to, because if you…
Samuel Milton (32:53.95):
Thanks for watching!
Henry Hoffman (33:21.826):
Potentially doing ESIM, any way to reduce the tone, it sets the patient up for task practice or functional training, which the brain wants. The brain wants to have a meaningful functional task that’s purposeful, and if I can stretch that handout for 30 minutes and get it loose for 30 minutes, couple of Botox, or I can put them in a SableFlex that allows them to grasp release, the hope is through what the research says, by you doing meaningful purposeful tasks repeatedly, that we can rewire the brain, and if we go through those brunstrom
of recovery, we’re going from flaccid to spastic, well the next stage is you start to reduce spasticity. And that’s what we’re hoping on that level that Brunstrom stage, you know, going from four to five and then finally to six. So I guess my point from your perspective, since you’re knee deep in this and you work with therapists, you know, how do we get that breakthrough to no spasticity long term? That’s just not temporary. Is it through the rewiring process that I explained or is there some other magic bullet that we haven’t touched on?
Samuel Milton (33:58.75):
Samuel Milton (34:19.05):
Thanks for watching!
Samuel Milton (34:22.27):
No, no, I mean, you explained it very well because as I teach my residents that a spastic muscle is a weak muscle and really the more spastic a muscle is, the weaker it is. And as we go through neuroplasticity and motor recovery, well then that spasticity starts to abate. The problem is that, as I said, alluded to earlier, every patient is different and they develop different types of problems due to spasticity.
Samuel Milton (34:52.189):
Your case is that I’m letting the patients know that I’m reducing the muscle tone temporarily but we have to really get this tendon moving. Reducing the pull of the muscle now will allow the therapist hopefully to get this tendon stretched, reset a little bit longer because the shorter the tendon is the more likely you’re able to activate that velocity stretch reflex. You’ve got to try to restore that muscle tendon.
A lot of the research indicates that prior when I started doing Botox back in the 90s, I was finding that doing Botox earlier can be really much more helpful than waiting longer to do it during the recovery, you know, during the rehab process. And I totally agree with that because once you get behind, it’s really hard to catch back up.
Samuel Milton (35:52.329):
Had this, somehow got this recovery late in their process, yet their tendon is so contracted. And look, Doc, I can use my fingers now, but their tendon has become so contracted that we can’t use it until we have to use a more aggressive surgical method. But those break my heart when, you know, the only thing you have to do is try to get them on a good program, and then they had this unrealized recovery. So I do believe that, yeah, I do believe the research
Henry Hoffman (36:16.886):
You bring up a good point.
Oh, sorry for interrupting. Go ahead.
Samuel Milton (36:22.793):
Earlier is better as far as intervention.
Henry Hoffman (36:25.566):
Yeah, sorry about that. So spontaneous recovery may be for the first three months, let’s say. When would, how soon can you actually administer Botox? Is there any guidelines behind that?
Samuel Milton (36:39.23):
I usually will wait until one or two months after. Usually by that time, I mean, like I said, it depends on where the stroke is. Usually these strokes in the basal ganglia tend to develop tone really fast versus some of the cortical strokes where they’ll be really flaccid for a long period of time. And you’re just hoping for some tone to come to some tone to kick in. But usually these strokes that are current in the basal ganglia usually develop tone really right away.
I’m looking forward to, okay, I’m gonna need to do both types. Luckily, because I see them on the inpatient side, I have a good flow or continuum of how they are and how their tone is emerging. As the patients who’ve been out for a couple of years, that I really struggle with their treatment plan and really need a bimodal approach or a multimodal approach. But luckily, seeing them from day one, I can get a good feel within the first couple of weeks what their tonal pattern is going to look like over the next few months.
Henry Hoffman (37:40.406):
Yeah, that’s great. Well, you know, I think this podcast was really helpful from many points of view. It hopefully opened the eyes for patients to consider Botox and other techniques that they haven’t potentially tried before. I think for therapists, they have to realize it’s not going to, stretching is not the magic bullet, so don’t spend 45 minutes doing a stretching strategy that’s, in calling it a skilled service, because it’s definitely not a skilled service. We have to come to the conclusion that,
If you give your patient the best chance to reduce spasticity, we have to rewire the brain. So we have to do neuroplastic strategies. And the strongest evidence to date are things like constraint-induced movement therapy and task training. And if you don’t qualify for constraint-induced movement therapy and you don’t have the wrist or finger extension, then you’re going to have to consider, you know, eSTIM and functional bracing and other ways to get the hand involved so you can actually grasp and release or fire muscles. You need that contract and relax. You’ve got to get that limb involved somehow and stretching is not going to do anything other than temporary relief. So I think this has been fantastic, especially going over the contraindications, indications, the surgical options, as well as the different type of systemic medications. Dr. Milton, this was just, I could do this for three hours. I know you’re a busy guy as well, but I really appreciate your time today. I know the audience has. We’ll definitely put your contact details in the show notes and we’ll also put in some research articles and links for the audience.
Samuel Milton (38:40.65):
Henry Hoffman (39:10.466):
A word as far as hope for patients who are battling spasticity that might be helpful for them to hear today.
Samuel Milton (39:17.31):
Well, I think that having access to an academic center like Emory or academic center in your area is very helpful. These are people who see stroke victims every day, all day. There are some new techniques, vagal nerve stimulation, things like that we didn’t even touch upon that are helpful for recovery. That’s a whole different topic for another day. But that’s where you’re going to find that probably the most skilled providers is in academic setting like this.
Henry Hoffman (39:49.126):
Wonderful. Yeah, thanks for talking about vagal nerve stim. We’ll definitely have to have that as a future topic as well. Well, Dr. Milton, thank you so much for joining us on the Notepad Plateau podcast. I really appreciate it. I know the audience appreciates it too. And I hope you have a wonderful week doing the great things you do.
Samuel Milton (40:08.27):
Well, thank you, Henry. It was my pleasure, definitely.
Henry Hoffman (40:11.206):
All right, take care.