Thank you all for joining. This is Maximizing Stroke Recovery, Debating the Controversies, and I am Joel Stein, the course director. I'm going to turn over the podium, however, to Dr. Michael O'Dell, who is moderating this session, and I will serve as one of the panelists. The basic format here, just very briefly, is that we have a number of case vignettes that are constructed to stimulate discussion about these controversies. Each of the vignettes will be discussed by the panelists, and we would welcome questions, I guess, after each vignette would be good. Maybe when we've had an initial conversation, we can pause for questions. And then at the end, if we finish the vignettes, we'll have time for other questions on any topic related to stroke rehabilitation that folks may want to raise. So with that, I will turn it over to Dr. Michael O'Dell. Dr. O'Dell is Professor Emeritus at Weill Cornell Medicine from the Department of Rehabilitation Medicine, and he'll be introducing the other speakers. Thank you, Dr. Stein. So I want to introduce our... Good afternoon, first of all. I want to introduce our panelists for this afternoon. You just heard from, and to my immediate right, is Dr. Joel Stein. He is Professor and Chair of Rehabilitation and Regenerative Medicine at the Vagelis Columbia College of Physicians and Surgeons in New York City, as well as the Chair and Professor of Weill Cornell Department of Rehabilitation Medicine. He's also the editor of the primary textbook in stroke rehabilitation in the field. Preeti Raghavan is the Sheikh Khalifa Stroke Institute Professor of Stroke Treatment, Recovery, and Rehabilitation, and Associate Professor of Physical Medicine and Rehabilitation at Johns Hopkins University in Baltimore. And to the end is Joan Stilling, Assistant Professor of Rehabilitation Medicine at Weill Cornell School of Medicine. Dr. Stilling is particularly important because she came to Cornell and allowed me to retire, so she's my favorite person in the world. So our format this afternoon is we have a series of cases. We may get through them all. We may not get through them all. I will read the case. The case will be also on the screen for your consideration. And then we'll start out with one of the panel members. The case will then be discussed among the panel members. As moderator, I retain the right to jump in and stir the pot if need be and ask a question to either challenge or change the scenario a little bit as need be. And I will also try to keep time so we move from case to case. So case number one, upper limb splinting. A 69-year-old woman with right internal capsular stroke six months ago has residual left hemiparesis with minimal motor control of the hand and some increase in tone, modified Ashworth of 2 over 4 in the finger flexors. She performs self range of motion reliably and has well-preserved range of motion. She's been using a resting hand splint at night since her stroke. Does she still need it? And how do you decide who needs a splint and when to discontinue it? Dr. Agravan. Thank you, Dr. O'Dell. So here the question is about somebody who's had a stroke six months ago and she has minimal motor control. So what we do know from the literature is that the greater the degree of motor impairment, the more likely they are to develop spasticity and muscle stiffness over time. So she was prescribed a night splint. She's using it. Her modified Ashworth score is 2 out of 4. So she's beginning to develop that stiffness. What's the best thing to do? Well, I think the most important thing... So this is controversial only because the literature is all over the place. There was a systematic review in the American Journal of Occupational Therapy in 2020 where it's a bit difficult to interpret the findings of the review because they talk about stretching and static splinting and dynamic splinting. And they talk about it in the context of spasticity, hand function, and motor recovery. And it seems like different things are important for different aspects of what we need for the patient. So my overall take on it is to the greatest degree possible, we should preserve muscle length and flexibility. And so if the patient can do self-range of motion during the day, that's great. We need to teach her to preserve... The flexors are particularly prone to shortening, but the extensors can get stiff as well. So moving the joint in all directions possible is important. And so I would say continue to use the night splint, especially if she tends to flex her wrists at night or sleep in an extremely flexed position, but during the day to continue a range of motion. And if during the day she tends to get into a flexed position, then maybe a dynamic splint is a good thing to bring back muscle length to resting length. So that's my take on it. Dr. Stilling, would your approach be the same, or would you tweak that a little bit? Yeah, I think it would be similar. I think that in this patient, I'd really try and figure out whether or not she was tolerating wearing the splint at night. I think there was an RCT at one point that showed that there was no significant difference between groups of people who stretched and used the splint at night versus just stretched during the day. So that was just one RCT. I don't know if that could be extended to all scenarios. But I think trying to figure out from the patient's perspective if it's burdensome for her at night to be wearing it. If she's developing any pressure injuries, for example, she's in pain wearing the splint, and then kind of go from there. If she's able to tolerate it, there's obviously no harm in continuing on with it, and it's going to preserve her muscle length, which is great. But if she is finding it painful and she isn't getting well-rested, then I think it's reasonable to stop. Dr. Stein, would that be your approach as well? Yeah, I'd go just a little. The longer I do this, maybe the more conservative I get. But I tend to favor getting rid of devices if they're not really doing anything useful. I would be inclined if the patient expresses any desire to get rid of this at night to see how she does without it, but to monitor her range and see if she's getting tighter. Certainly if she has any pain or issues that are resulting from discontinuing it, I would certainly resume it. But many patients can maintain their range of motion perfectly well passively. Her tone is increased but not exceptionally high. So I would be inclined to give her a shot without it to see if she can manage. I have a lot of patients that self-discontinue splints and do just fine. No one ever gave them permission to get rid of it. They just decided themselves they didn't need it. I think we should be trying to work with patients that way to reduce equipment when it's not clearly needed. Preeti, wind the clock back a couple months. Let's say she's just starting to develop tone, but let's add a fairly substantial sensory loss on that same hand. Are you going to be reluctant to prescribe that splint in the first place, or are there circumstances under which you would feel comfortable doing that? That's a really good point. If she has sensory loss, I might be a little bit more reluctant to prescribe a splint only because she may, especially at night because she may hurt herself. She may not feel the discomfort or the pain, so maybe I'd think twice. The flip side is sometimes when patients have neglect early on, sometimes it sort of protects the hand. I've seen patients who sort of end up with their hand in very strange positions, their wrist hyperflexed or whatever. That's not a sensory loss, but it's more of an attention deficit. But I think that there are some patients where it may be protective, early on especially while they're in inpatient rehab. Good. Shall we go to a case that I'm sure anybody who's involved in an inpatient rehab hospital or unit faces about three times a month? A 72-year-old man sustains a left MCA stroke due to a newly diagnosed AFib. He remains in the acute care stroke service on day number five post-stroke and has been receiving NG tube feeds due to dysphagia. A modified barium studies shows aspiration with thin liquids and penetration with thick liquids and a strong spontaneous cough that allows him to clear the aspirated materials. He is otherwise ready to go to a rehab hospital, but they have requested placement of a G-tube prior to admission. Is G-tube placement appropriate in these circumstances? How do we decide who and when to place a G-tube in patients with a reasonable prognosis for ultimately returning to oral feedings? Dr. Stein. Yeah, I can't believe I wrote this because now I don't know how to answer it. But this is a really thorny question. I think that we really struggle with this for many reasons. The first is that malnutrition is a real issue in these patients. There's a lot of patients who are unable to take oral feedings adequately early on who simply become malnourished because they're not getting enough food by mouth if they can't take some or their NG tube is always out or always clogged. And so I think we need to keep our eye on the ball and not allow patients to become malnourished. On the other hand, there is some significant morbidity associated with G-tube placement, and I think we tend to sort of understate that a little bit. I looked it up and I found a reference that found a mortality rate at 30 days of between 1.5% and 2%, which is not nothing. That's a significant risk you're exposing a patient to to put in a G-tube. Of course, there's morbidity and potentially mortality associated with NG tubes as well. I didn't look that up, but that's certainly an issue. The Heart Association guidelines, stroke rehab guidelines, are clear that some sort of enteral feeding should be initiated within seven days post-stroke for patients who can't swallow. That's pretty obvious. I think that, frankly, if you wait seven days, that's an awful long time. So I think that some sort of enteral feeding is needed in this kind of patient. Those same guidelines suggest that a NG tube be used for short-term, two to three weeks nutritional support for patients. And I think this patient may fall in that category, and I think we should be careful about not jumping to a G-tube. Most patients with MCA strokes do have a favorable prognosis for recovering swallowing function, so I wouldn't be in a rush. On the other hand, a lot of rehab facilities don't want these patients who have NG tubes because they worry they're going to come dislodged, they have to send them for an X-ray to reconfirm placement, they'll get clogged, all those issues. So it's a challenge. I think that my bias would be to try and temporize here to avoid putting in a G-tube. I'm not sure that's always been my practice over the years, though. I bet I've put a lot of G-tubes in patients like this. Joel, do you think the threshold should be different if somebody's going to a rehab unit within a hospital versus a freestanding rehab hospital? That's a great question. I think that the question is maybe restated as, does the resources available at the facility matter? And I think it does. I mean, I think, first of all, if you decide you need to switch gears and someone's in a hospital-based rehab hospital, rehab unit, it's very easy to go get the G-tube. It's harder if they're in another facility. X-rays, on the other hand, may or may not be available in a freestanding facility depending on what they have to, say, reconfirm a replacement of an NG tube. So I think it probably does have some impact, and I think in a hospital-based rehab unit you can probably put this off a little longer more easily. Preeti, how would you handle this at Hopkins? Yeah, so luckily I don't see inpatients. You know, there was a study published in 2020 where they developed a prognostic risk score exactly for this purpose to see who might be at higher risk of the morbidity and mortality, particularly the 30-day mortality. And it seemed that, like, older age, this gentleman is 72 years old, and atrial fibrillation, so this gentleman has atrial fibrillation, and short time between the stroke and G-tube placement were prognostic of a higher 30-day mortality. So, you know, I might sort of lean a little bit towards what Dr. Stein was saying, and see if we could delay the G-tube placement potentially since he has a strong cough and is otherwise doing, you know, seems like he's doing pretty well. I would maybe plug in the scores in the prognostic risk indicator and see what it suggests to. Joan, you trained in Canada, and now you've been in the United States for a few years. I mean, to put you on the spot, do you think this would be handled differently in Canada than it would be in the United States? I don't think so. Well, I can talk from my experience in residency training in Canada, but as well as doing inpatient in a different state in Maryland, at Johns Hopkins. I feel like in Canada most patients would come with an NG-tube, but it wouldn't be as much an issue. In the states at Hopkins, I was there when the thinking was shifting. So almost every single patient coming over to the inpatient rehab unit within the hospital had to have a G-tube, and then during the course of my time there, it transitioned to where we started taking patients who had NG-tubes because of the risk associated with it. So we would really have to fight with the neurology team to try and prevent the G-tube from being placed before because it was a discharge barrier. So we'd have to intervene quite early to try and advocate for those patients who, for example, in this case, the patient does have a good prognostic indicator of he has a strong cough. If you could get the speech therapist on the acute unit to help talk to the team, you could maybe avert getting the G-tube, but it's something that I think has to be considered strongly because on the inpatient rehab unit side, if you don't have therapists who are able to do a modified barium or a freeze or something on the other side, then you're kind of left with that same decision on the acute rehab unit of how to send the patient home. I'd love to ask a speech language pathologist how much the NG-tube interferes with their exercises for dysphagia as well. I don't know the answer to that question. All right. Any other comments? That's a tough one. That's a real tough one. And a very practical case that we deal with all the time. Next case, medications for recovery. A 59-year-old woman sustains a large left basal ganglia hemorrhage and requires a hemicraniactomy for decompression. She's now day number 10 post-stroke and remains hospitalized in a step-down unit with reduced level of alertness and severe mixed aphasia as well as right hemiplegia. Her daughter has been exploring options on the Internet and inquires about using medications to enhance recovery. In particular, she is asking about imantadine, modafinil, methylphenidate, or fluoxetine. How do you respond? Would any of these be appropriate to facilitate her recovery, help her participate better in rehab, or might they be harmful? Dr. Stilling. Sure. So starting with the first drug that's listed here, I think it's important to take into consideration the clinical context. So this is someone who has a hemorrhagic stroke, who's had a hemicraniectomy, and she's fairly early in the acute phase. She's 10 days post-stroke. It's difficult to say from this exam that's given whether or not she's— it sounds like she's not minimally conscious or in a vegetative state, so that may influence some of the medication choices. But in any case, thinking first about imantadine, there's the first trial that came out showing efficacy of imantadine in the TBI literature, prescribing 100 milligrams twice a day in people who had disorders of consciousness, and it helped to expedite their emergence from either a vegetative or minimally conscious state. So translating that over to the stroke population, from what I could find, there was only one retrospective review that was looking at imantadine in the stroke population, and they did have a 50% response rate for improved wakefulness using imantadine. They also compared it to monotherapy with modafinil as well as a joint imantadine and modafinil, and they didn't find any benefit with modafinil alone. That's in contrast to another study that was done, the MIRA study, another retrospective review that did find improvements with modafinil for improving discharge outcome. So I think the evidence is a little bit mixed for both of these. I think it is important to consider the side effects from the medications. The biggest with imantadine are causing rebound spasticity, agitation, and change in sleep behavior. So it's always important, if you are to consider this, to prescribe it in the morning at 8 a.m. and 10 a.m. or 8 a.m. and 12 p.m. and to not have nighttime doses. And to be aware of some of these side effects. The last thing with Mantadine, it can prolong your QTC interval, so making sure that their QTC is within the right range. So that's a Mantadine and a Modafinil. Going on to Methylphenidate. I think there's only been one study that I could find at least that showed benefit of Methylphenidate for stroke patients. It's an older study, but it did find improvement for patients who had fatigue by prescribing five milligrams up to 30 milligrams per day. And that's something that I know I have clinically used before for patients who kind of are stalling in their rehab or they're not quite showing enough energy or motivation to participate in rehab. It's fairly well tolerated. One thing with Methylphenidate that you do have to be aware of is it can increase your heart rate and your blood pressure, so making sure that's within the appropriate range. And then finally, moving on to Fluoxetine. I'm sure many people are aware of all the different trials associated with Fluoxetine, the initial FLAIN study that was positive and then subsequent negative focus, affinity, and effects trials. And so it really has fallen out of favor for promoting motor recovery. That's not to say it can't be used for post-stroke depression. And then there's other medications not listed here that could be considered. I know that Lexapro has shown dual benefit for post-stroke depression as well as post-stroke aphasia recovery, so that could be something that the family considers in this patient who had mixed aphasia. Yeah, that's my take. So would you agree with my assessment from an evidence standpoint, you are really on thin ice? Absolutely, yeah. So from that standpoint, what level of unalertness do you think it would warrant a medication trial? How bad does this patient need to be before you think the potential benefit, whatever that is undefined, would be worth whatever side effects you might see? I think it really would involve talking to the therapist to see how well the patients are participating in rehab, if at all, and if they're sitting on a step-down unit at day 10, not getting any rehab, then I think it's something to consider to try and wake them up enough to at least get a bit of therapy in that acute phase. And then weighing the side effects, watching them closely if you are to start a medication, and just monitoring to see if there's any adverse effects. Dr. Stein, what would your approach to this patient be? Well, I think we're, aside from the fluoxetine, we're largely in an evidence-free zone here. Fluoxetine, I think, is one of these interventions that's at least, or SSRIs in general, that have at least been reasonably studied. I think, clinically, if somebody is able to stay awake, participate in therapy, seems to be engaged, even if they fall asleep in between and are sort of napping throughout the day, I could tolerate that without treatment, but I think if they can't make it through a therapy session, they keep falling asleep, or can't attend, then I would be inclined to try something. I'm a little bit partial to methylphenidate by prior experience and sort of habit, but I think imantadine would be a close competitor there. I don't have a strong feeling. I've always been a little bit less inclined towards modafinil and related medications, just because they, in some ways, have a rather more restricted effect. They affect wakefulness, but not really attention in the same way, and I think here, we probably want the broader effects of something like methylphenidate that both tends to make people more alert, but also helps them focus their attention more, so that's why I would favor one of those, and it would be for a patient that really is struggling to get through a therapy session. Preeti? Yeah, so I guess my take on it is that if the person does respond to a stimulant, then the literature shows the retrospective study you cited that came out in Neurocritical Care in 2021 shows that they might be able to be discharged home or to acute rehab, so it's rather than go to a subacute or stay or not do well at all, so I think it's worth taking the risk to try one of the neurostimulants. I think as Dr. Stilling and Dr. Stein mentioned, maybe I would go with amantadine because the literature favors it so much, and if they didn't respond, maybe admodafinil, and if neither of them worked, maybe go with methylphenidate because she did have a hemorrhagic stroke and I would be a little bit more concerned about the hypertension, so that would sort of be how I weigh the evidence. So Preeti, the daughter is engaged but she's not dumb, and so she brings her lawyer to have this conversation along with her. So what's your CYA discussion with the daughter in terms of kind of venturing into this very little literature to support using these medications? What's that conversation with the daughter sound like from your standpoint? Well, that's a good one. I think it's important to lay out everything and allow them to make the decisions, but yeah, we'd have to tell them what the evidence suggests and what the benefits and risks of using the medication versus not using the medication are and let them make a decision. Really tough. Sometimes the internet cannot be our friend. Let's move on to case number four. Vagus nerve stimulation versus direct cranial, transcranial direct current stimulation. A 57-year-old man has persistent hemiparesis 18 months after an incomplete left MCA stroke with some mild word-finding difficulties and disfluency, but able to communicate effectively. He is able to grasp and release objects with his right hand but lacks finger individuation and only uses the right upper extremity as an assist for a few two-handed tasks. He appears eligible for vagus nerve stimulation and is considering pursuing this therapy, but also expresses interest in transcranial direct stimulation. One of the academic medical centers in the metropolitan area is now offering T, that's so hard to say, TDCS under medical supervision combined with OT as a self-pay program. He indicates he can afford the program, but these costs are meaningful for him and he is reluctant to pursue without a clear understanding of the likely benefit. What would you advise him regarding selecting between these two treatment options and how much benefit could he reasonably expect from each? I believe this is Dr. Stilling. Thanks. I feel like this is more of a controversial case, but so unpacking the scenario here, we have an individual who's in the chronic phase of stroke at 18 months. They're having, they have word-finding difficulties and disfluency, so speech-related changes, and it seems that they have some motor function in their distal extremity, which suggests a little bit more mild of a stroke in that he has distal motor control. This suggests that possibly his corticospinal tract is intact, which I think makes a difference for when you're considering some of these therapies like TDCS or vagal nerve stimulation. So starting with TDCS, so I think what I'd really try to do is present the literature to this individual and try and help him decide which may be most useful to him from a number of different aspects. So thinking about TDCS, this is not FDA-approved, which is in contrast to vagal nerve stimulation. TDCS devices are considered non-significant risk, and so they're not currently being closely monitored by the FDA, and so I think this is why you see some of these programs popping up that can provide the TDCS off-label to patients. Looking at the evidence for the two treatments, there have been a number of systematic reviews looking at TDCS for the treatment of upper extremity rehabilitation, upper extremity motor function following stroke. There are mixed results, so two to three of the systematic reviews show no significant benefit from TDCS, while the other two do demonstrate that TDCS is effective. In particular, there was a recent network systematic review that showed that nodal TDCS was superior to vagal nerve stimulation, with both improving Fugl-Meier score by about five and a half points. With that network systematic review, I think it was really the only one that did show that drastic change when you're looking at pure systematic reviews investigating TDCS, the improvement in Fugl-Meier score is a lot lower, with mean changes of about one point on the Fugl-Meier score. The benefits of TDCS are that it's non-invasive, and that's a distinctive factor from vagal nerve stimulation. You can undergo one session with TDCS, see if you like it with the occupational therapist, and consider whether or not to continue on with the treatment or not. So I think that for this individual who's trying to figure out whether or not it would be beneficial for him, it is non-invasive, and you're not committing yourself to a surgery and a whole treatment paradigm afterwards. So that would be one of the benefits. On the flip side, it's not covered by insurance, and so I think that that's something significant, and if this patient would have, would qualify for the vagal nerve stimulator through the insurance, it's a really good program. The recent Lancet trial shows significant effect from the vagus nerve stimulator. And then there's been a number of recent follow-up studies published up even to this year with two and three-year outcomes showing ongoing benefit just past that initial phase. I think the other benefit of the vagal nerve stimulator study is it can be used by the individual in their own home, and they can swipe past their device whenever they're doing therapy independently. It could be covered by insurance, which would be great, which would also sign them up for a whole treatment with occupational therapy that may be covered. And so if he qualifies, I think it would be a really good option for this individual, but once again, the downside is it is an invasive option that requires a surgery, and anytime he's going through an airport detector, for example, he'd have to declare it. So it's not a simple non-invasive solution for him. I'm really considering both options, Dr. Stilling. Tell me, how does my arm look different after five Fugl-Meyer points? Yeah, so I think that's a great distinguishing factor. So I think it's still debated within the literature with actual clinically meaningful important differences on the Fugl-Meyer. It ranges anywhere from six to 10 points. So both the vagus stimulator and the TDCS are right at the lower end of the Fugl-Meyer change. I think in some of these recent studies that have just come out for vagus nerve stimulation, it shows that the Fugl-Meyer score is actually additive. So although in the first year it may be only five points, it continues to go up to nine and up to 12 points, I think is the most recent finding at that three-year mark. So I think that would be meaningful for the patient. Yeah, I don't. How would you answer that, though? How does my arm, because this guy's gonna go under the knife. If he chooses vagus nerve stimulation, he's gonna go under the knife and he wants to know how does my arm look different if I do this? Right, so I think thinking about the upper extremity Fugl-Meyer score, you get scored zero, one, or two based on no function, partial function, or full function for a number of different arm movements, elbow, wrist, and hand movements. And so I think what I tried to describe to him is although maybe he's not able to fully hold onto a cup while I'm pulling it, at one point, if he were to improve by a few Fugl-Meyer points, maybe he would get stronger grip strength, possibly a stronger pinch score where he can now hold a pen if he wasn't able to before. You can't really predict what will improve in terms of the Fugl-Meyer when you're doing these treatments, but I think that's what I tried to describe to him is maybe he would now have more arm range of motion and that he's able to move it through the full range as opposed to just partial range. That's pretty good. Yeah, I typically, in these situations, tell the patient when I'm expecting gains in that range that it'll be noticeable, but won't be normal, and I sort of probably don't go beyond that. But you'll notice it, it'll be a little better, but it's not gonna be fine. It's not gonna be back to the way it was. Preeti, you have a huge body of experience in this area. What do you think about this? So both vagal nerve stimulation and TDCS, they only work, they are paired treatments, so they have to be paired with pretty intense occupational therapy or pretty intense task-specific therapy. So I think it's extremely important to explain to the patient that what they do during the stimulation really matters because the stimulation only sort of increases the gain on the plasticity that is occurring as a result of the actual use of the limb. So with that, I would say that given that he has grasp and release, it seems we don't know what his Fugl-Meyers, but I'm guessing it must be at least in the 40s or so. I would say let's do really intense OT, occupational therapy first, and give him a very strong home program that he can commit to and follow and then see how much he changes in terms of his Fugl-Meyer or any other functional battery or is he able to do more in his daily life? I think ultimately that's the most important thing. And if he is still not happy, then I think adding the stimulation to that intensive therapy would be something that could be more meaningful, could get him to where he wants to be perhaps sooner. But I think just making sure he understands that it's definitely, it's a paired treatment would be really important. Any other comments? Just, you know, I agree with everything that's been said. I think that my biases, I guess, match Jones to some degree in terms of maybe favoring starting with TDCS just because it's non-invasive. And the other thing that I would be honest with the patient about is that while the studies for vagal nerve stimulation are well done and certainly show benefit, I don't have a lot of personal experience with it. And we haven't yet had a lot of patients that have gone through this. And so I just want them to understand that it's early in the game and we're working off published literature, but we don't have a lot of personal experience. The surgeons have lots of experience putting them in and I reassure the patient that that's not the issue. But just in terms of who's going to benefit, how much they benefit, we're still getting a feel for that. And so I think it's a little, unless the patient's highly motivated to go through that and committed to the exercise, I would probably encourage first trying the less invasive therapy. And just one last thing. The patient also has word finding difficulties and disfluency and there is evidence in the literature through systematic reviews that TDCS can be paired with not only OT, but speech therapy and PT. So it could be more of a multimodal technology to use. I think vagal nerve stimulation may also improve those areas, but it just hasn't been studied yet. Okay, very good. Next case, what I think is one of the toughest problems to deal with in stroke. 63 year old woman sustains a right MCA stroke and undergoes thrombectomy with good results. She is left with a relatively mild hemiparesis and good cognitive function and returns to her job as a banking executive. She is troubled by persistent fatigue that makes it hard for her to get through the day and sometimes takes naps during the work day on a couch in her office. She does note some modest benefit from caffeine when she drinks her morning coffee, but that does not last very long. What treatment or treatments or other advice would you give her regarding her fatigue? Dr. Raghavan. So cognitive fatigue is pretty common after stroke, but sometimes it's not, patients are not aware of it and some providers may not necessarily ask about it. Recently, actually in 2023, there were a couple of studies that came out really talking about understanding the patient's experience of fatigue. And it seems like, because it's obvious so late in their rehab, it's only when they go home and go back to work and this lady seems to have had a relatively good outcome in that she's returned to her job as a high-level banking executive. The causes of the cognitive fatigue could be, I think the first thing I would ask is, is she sleeping well? So poor sleep is an important cause of fatigue. You know, are there some reasons why she may not be sleeping well, like sleep apnea that may require treatment? The other is, you know, what type of environment is she returning to? She's a banking executive, does she have an office, or is she, you know, on a floor? Is it very noisy? Sensory overloaded environments tend to cause more cognitive fatigue. If they are in emotional distress, you know, she doesn't feel quite ready to get back, but she has to get back, you know, that could be a reason. And if the cognitive task is complex, you know, she's had a bit of a hiatus and she may not quite be ready for it. So the treatment that I suggested are, you know, find the cause and then teach the person to pace themselves. You know, don't take on everything all at once. So maybe one advice would be to start part-time before going back to full-time so that the person can sort of gradually phase into their previous role. And then to also increase both physical and mental endurance, right? So are they able to exercise? That may help them sleep better, have more energy. So those kinds of interventions could be really important. I'm sorry if I missed this, but is there any role for the input of a neuropsychologist in this case? That's a good point. You know, there may be. It seems like she has good cognitive function, at least that's what it seems to say here. So if it's just, if some of these interventions don't work and we need to delve a little deeper, then yes, then at that time I would refer her. And a related question, sounds funny. Do you always believe the patient when they tell you they're not depressed? I think it's very important for us to screen for depression and to ask them, do I always believe the patient? Well, I think it's a valid question. We probably need to probe a little bit to truly understand if they are depressed or not. Depression could be underreported, right? It's remarkable to me how many times I ask a patient whether they're depressed and they're shaking their head no and their spouse is sitting right behind them shaking their head yes, absolutely. So you get that disagreement. Yeah, I definitely think asking a family or friend informant can be very illuminating when you're not sure. Joel, how do you approach fatigue? So I guess at what point, first of all, I agree with what Preeti has said. And I think though there is a little bit of a cultural issue in America around napping, which is considered a moral failure. But really, it's okay. Maybe she should schedule a midday nap, not have any meetings, tell her assistant, don't let anybody come in, close the door, pull the shades and take a midday nap. And I think that there's sort of a, she's entitled to a lunch break, why can't that be a nap? So I just wanna sort of point out that part of this is cultural in terms of our unwillingness to give someone a chance. Napping is often very restorative in these situations. I do think also pharmacologically, caffeine is not a solution, it's not a treatment for the underlying problem, but it may help her manage it. Maybe she should have her caffeine later in the day, a cup of coffee after lunch or something to help her get going. I would be hesitant to use other pharmacotherapy, but certainly people have done that in cases. I do think Preeti's points about making sure she's sleeping well at night are really important. And that she's got good sleep hygiene, that she doesn't watch TV or do other stimulating things right before she goes to bed and that sort of thing to improve the quality of her sleep. But I do think that frankly, I often advise patients like this to build a nap into their day, I think it may help. I just got back from Italy, don't try to get anything done between two and five in the afternoon. Joan, anything you would add on top of this? Just to add in that I think I would also screen for depression, anxiety. Also do basic lab work to make sure they don't have anemia or thyroid dysfunction as other causes of fatigue. And I think there is some evidence for cognitive behavioral therapy for post-stroke fatigue. And so maybe seeing a neuropsychologist could be helpful with regards to giving an appropriate program for that. I have found that the neuropsychologist can be very helpful on mood issues in addition to cognitive issues. And in that case particularly, if I can't figure out what's going on, their input, at least in ruling out certain things can be very, very helpful. Any other fatigue comments? Are we fatigued of that? I wanna point out, it's already late in the day here, so be careful about fatigue questions. All right, let's move to more of a medical issue. DVT prophylaxis. 79-year-old man sustains a right basal ganglia hypertensive hemorrhage with resulting severe left side weakness. His hemorrhage is managed conservatively and he's admitted to the rehabilitation unit on day eight post-ICH. He is transferred with pneumatic compression boots for DVT prophylaxis. Is this an appropriate therapy for DVT prevention in this circumstance? For patients who receive sub-q heparin or other medications for DVT prevention after a stroke, how long should this treatment be continued? Is it based on mobility level? And does the discharge destination, home versus skilled nursing facility, impact the duration of prophylaxis? I believe this is Dr. Steins to start out with. Thanks, Mike. So this is a very common scenario and I'll think I'll touch on both ischemic and hemorrhagic stroke because we struggle with both in terms of prophylaxis. So first I'm gonna ask the audience a question. We don't have an audience response thing here but a show of hands. How many in the audience have patients on their rehab units that are receiving pneumatic compression devices on a regular basis? Okay. How many see those devices used properly? Yeah, okay. Well, whoever raised their hand there, amazing. I gotta go to your hospital. But I have to say I have never seen them used properly. So I'll get back to that in a second. But the risk of DVT after acute stroke is estimated, I should say clinically evident DVT, is estimated between one and 10%. But there's a lot of clinically non-evident ones. So this is a very common problem and sometimes the first indication is somebody has a pulmonary embolism and sometimes a massive pulmonary embolism. So it's a really serious issue that we need to address and get ahead of. And it is clear that hemiparesis increases the risk. That's not surprising. And interestingly, the risk is associated with the severity of the weakness. Again, not surprising. But the more densely plegic you are, the greater your risk of DVT. And as you might expect, the risk in the paretic or plegic side is greater than the other side. Again, not surprising. It's estimated that between 13 and 25% of the early deaths that occur after stroke are due to pulmonary embolism. So this is a cause of death. Despite everybody knowing about this, it's in all the guidelines, it still represents a significant percentage of the patients who die after stroke. And the reality is that this should be preventable in the vast majority of cases. It is worth mentioning, I think, that elastic compression stockings don't work. Don't use them. I tell people that they use them because they're cosmetically attractive. Some people like white stockings, but TED stockings are otherwise useless. And I think the real issue is the intermittent pneumatic compression devices, which have been shown to be effective in clinical trials, but mostly those are in the ICU settings where they're worn 24 hours a day. The patient's not getting out of bed, they're not moving around, and they're not getting therapy. And so they work when they're used in that way. But the patients in the rehab setting, we hope they're getting out of bed, we hope they're going to the bathroom with help, we hope they're getting therapy, and they're always getting disconnected and they're never getting reconnected. And these things also move all around their legs, they're around their ankles, they're around their knee, they're in bad places. So I think the issue around pneumatic compression is not whether or not it works, but whether or not it works as actually implemented. And my impression is the answer to that in a rehab setting is typically no. For patients who are, the guidelines, as best I could determine, there's multiple guidelines for intracranial hemorrhage, generally do recommend initial use of intermittent pneumatic compression, which makes sense in the ICU. But then to switch probably to a low molecular weight heparin or to sub-q heparin somewhere between one and four days post-onset. Obviously there's some clinical judgment there, the neurosurgeons have their say in this, some patients of course will have a neurosurgical procedure. So I would, in this particular patient, probably favor switching them to either a lower dose of a low molecular weight heparin, like Lovenox, 40 milligrams, or sub-q heparin, either 5,000 twice or three times daily. In terms of patients with ischemic stroke, there is some thought that with patients on dual anti-platelet therapy, which is quite common these days in the early phase, that maybe adding these heparins to that could be risky. So some people favor intermittent compression in that setting. I don't know the answer to that. I think probably I'd still favor sub-q heparin in that setting, but maybe 5,000 BID for somebody who's on a dual anti-platelet therapy regimen. And then I guess the last comment I'll make is we have no idea how long to continue this. It's really a hash. I think what most of us do clinically, again we're in evidence-free zone here, is that we do this until a patient walks out of the hospital or is rolled out of the hospital. So essentially while they're under our care we continue it. When they go home we generally stop it. And for patients that are there for whatever reason, for an extended period, maybe they have a social issue and they're regaining ambulation, let's say independent ambulation, then stopping it then. But I've been unable to find any real evidence to support those practices. It's just common practice. So 150 feet is poppycock. I haven't seen the evidence for it. Maybe it's there, but if you find it let me know. And second issue, particularly for patients coming from the neurosurgery service, would you touch base with the neurosurgeon before you change prophylaxis? Yeah, if you want to keep your job. I think it's polite. I think that probably the way I'd frame it is I'm planning on putting this patient on sub-q HEPRIN. Any concerns? That's just me. Joan, any comments above and beyond? I have nothing to add. Anything? Yeah, me neither. But I would say that he's 79 years old. Hopefully, now that he's in the rehab unit, he is moving a little bit. I would just, regardless of the DVT prophylaxis, encourage him to move his ankles, even when he's seated, even when he's in bed. And you know, there's a device that I recommend quite frequently. It's basically a plantar, it's a bilateral foot rocker that, it basically allows you to keep your ankles mobile, even if you're plegic on one side. So things like that, anything to keep them mobile, I think is extremely important, especially when he goes home. You know, you don't know what he's going to be doing. It's really quite remarkable when we know so little about something that's really so important and potentially so impactful. All right. Case seven, complementary and alternative medicine. 34-year-old woman sustains a peripartum stroke with resulting left hemispatial neglect and cognitive impairments. Her mother has quit her job to live with the patient and the patient's newborn child. She has severe upper limb spasticity and has been receiving botulinum toxin injections, which alleviate her tone to some degree, but she remains without functional use of the limb. Both the patient and her mother are frustrated by her persistent limitations more than one year post-stroke and are seeking alternative therapies. They've heard from a friend about hyperbaric oxygen and from another friend about neuroephra. They're inquiring about intravenous stem-to-cell therapy and found a clinic in the Caribbean that reports great success from this technique. What would you advise this patient and her family? Dr. Stilling. All right, so this is a little bit different since it's a young patient who, it sounds like, has severe spasticity and limited use of her upper limb. So some of these other treatments that we've been talking about, I don't know what her Fugl-Meyer score is, once again, so it's a little bit difficult to determine whether or not, for example, she'd benefit from the brain stimulation treatments like Vagus Nerve or TDCS. But they're seeking these alternative therapies that, at least on my literature search, don't have a lot of clinical evidence to date, or at least not randomized controlled trials that prove any benefit or harm. Hyperbaric oxygen therapy has a lot of data that is being used in the acute phase. I couldn't find as much use in the chronic phase, and it has been shown to be not effective in the acute phase of treatment. Neuroephra, I wasn't familiar with this therapy, so I had to look it up myself. And it seems to be more of a integrative approach to treating the patient, so I think that it's more of an intensive rehabilitation program where the patients would go and be seen by a number of different therapists in one stay. And when you look on their website, at least, it seems to be quite personalized in how they approach their treatment, but it's all video-based, and I didn't see any trials related to it, so I can't comment too much on that. And for stem cell therapy, I think that there is promise, especially in some of the animal models, as well as early kind of pilot studies for stem cell therapy. More so are what are called muse sales. I think there's a clinical trial underway for this one. There haven't been any benefits using neural stem cells in terms of functional recovery, and I think I'd reiterate that to the patient, but I think it's just too early for a more aggressive therapy like stem cells for me personally to be recommending any of these things, and so I think I'd try to indicate that to the patient. I'd suggest she try to engage in some of the other options that may be available that aren't covered by insurance first, prior to going down this route of therapies that don't have the clinical evidence. I think for this patient, trying to really try and aggressively address her spasticity would be important. I know she is receiving Botox injections, but seeing if there's anything else we could do to augment her spasticity management would be helpful. Do you have experience with acupuncture with spasticity management? I do not. Someone else may. So the question was acupuncture. Well, some people report that acupuncture is, there is literature suggesting that acupuncture may be effective. Again, I think the situation here is that she's really young. She's already one year post-stroke, and she has severe spasticity. As Dr. Stilling mentioned, there's a risk. Patients want to try anything and everything, and you feel their pain, but you have to also advise them that some of these treatments may not have the evidence that they need. Neuro-IFRA is actually interesting. I've come across a number of practitioners in New York. It's kind of a specialized OT training, so these are occupational therapists that are specifically trained. They report that they have wonderful outcomes, that they can actually promote functional recovery over time, but they're extremely expensive, and they actually provide very intensive therapy. It seems that the way the occupational therapy focuses a lot on scapular stabilization, and there's a lot of manual work that goes into it. I've seen some patients who swear by it, and others who weren't particularly impressed. It's that way with a lot of emerging treatments where there aren't trials, unfortunately, and so I think I would err on the side of saying, what can we do for you that would help with the spasticity? What's your approach to CAM, Joel? So I think that my big concern with these things is often maintaining patient safety. I recognize that we in standard medicine don't have what this patient needs. I don't have a cure for this patient, and so I appreciate their desire to try other things. What I don't want them to do is get hurt in the process, and so I think that's my first perspective is to try and steer them away from things that I think are particularly hazardous, and then acknowledge the other things that may be without evidence, but at least are not likely to hurt them. You asked about acupuncture, and I think acupuncture is generally acknowledged. If appropriately done, it's safe. And there's some evidence that it may provide some short-term relief of spasticity. I've seen that in my patients a lot. I have to say that I haven't seen anyone that's kept up with it for very long. They tend to get frustrated because it comes back the next day. The neuroifra, as Dr. Raghavan was saying, is a sort of intensive therapy. It's certainly not hazardous, and I've seen some patients that feel like they benefit. So I wouldn't sort of steer away from it that strongly. There's no published literature on it. And some of the practitioners are very dogmatic in some aspects. And so we'll say, for example, no oral anti-spasticity medications. I've seen that. No Botox. You have to use their kind of bracing. So it's a little bit of a cult or a religion in some ways. But that said, for some patients, it works OK. And I certainly wouldn't be worried about it. I just would advise them to take it with a little bit of a grain of salt. The intravenous stem cell thing really just gets my blood pressure up. I don't want to end up as a patient here. But this is a presumably unlicensed Caribbean clinic. And I would tell them, under no circumstances should they go there. I think it's quite likely that it's ineffective and potentially hazardous, not to mention probably horrendously expensive and poorly regulated. There are legitimate stem cell clinical trials in the US. And so if they really want to pursue this, I would advise them to try and find one of those. But they're mostly in very early phases and really have not yet been kind of reaching prime time. They're certainly not available clinically yet. So I would only advise stem cell therapy in the context of a clinical trial at a reputable center. And then the hyperbaric oxygen, there is this one paper that was in PLOS One that claimed these sort of very impressive and, I think, not terribly credible results. So I tend to discourage it. I do remind people that there are some associated hazards, including barotrauma. And of course, it's expensive. There's been reports of seizures. But it's probably not as dangerous as, say, the intravenous stem cell therapy. So I put that in sort of the intermediate realm. One last point about this is that I really try and maintain a therapeutic alliance with these patients, no matter what therapy they go for. And I think that oftentimes, you have patients that will feel like they're going against your advice. And therefore, they can't come back to see you. They've kind of, you know, I didn't listen to my doctor. And therefore, you no longer can be my doctor. And so I will tell patients in advance, you know, if you choose to do this, please let me know how it goes. I want to hear about it. I want to learn new things. And even though I might be advising against it, it's no reason. I'm still happy to care for you, even if you decide to pursue something I've advised against. I think that's important. I think we sometimes forget that step. And patients automatically assume, you said no. I'm saying yes. And therefore, I have to sever the relationship, which is unfortunate. Very good. Last case. We did make it through. Spasticity management. 72-year-old right-handed man had a subcortical stroke several years ago with a residual left hemiparesis. He has some ability to close his hand, but cannot open it without assistance from his other hand. He has had botulinum toxin injections performed every three months for the last two years and finds that these relax his hand, but do not improve his ability to use it. He is wondering if there are better treatments and mentions an OT suggested he try a Sableflex device or possibly therapeutic electrical stimulation device, such as the Bionass. He also searched online and found references to hyaluronidase, cryoneurolysis, and shockwave therapies. How would you advise this patient? Dr. Raghavan. Okay, so this gentleman is 72 years old. He can close his hand, but he cannot open it, and he's in the chronic stage. It seems like it's been several years. So he's had the standard of care, which is botulinum toxin, and it seems like it helps with his, it just doesn't, it hasn't been very effective. It hasn't restored his function. So I would say that if he wants to improve, so the reason that botulinum toxin may not have improved his function was maybe because it's inducing some weakness. So the question is, is it, what is it that is limiting his function? Is it weakness? Is it the spasticity? Is it muscle overactivity? Is it that the muscles are shortened? Or it's just, is it limited motor recovery overall? I think it's important to parse this out so that we can suggest sort of the right next step. You know, we had a session yesterday about sort of doing assessments when you're doing any kind of treatment for spasticity. So I think this is a case in point where if you don't assess, then you don't really know why the patient is not getting the response that they need to get. So I would say that if he's stiff in his flexors and he needs to be able to open his hand, the SableFlex actually uses the tightness in the flexors to help with release so that, you know, it's basically like an elastic band. So your extensors are stretched when you flex, and then through the device, it sort of helps you release the ball or whatever you're working with. Is it really going to restore his function? Well, it might if he practices with it. It's relatively, it's an intervention that he could certainly try. Bioness, electrical stimulation, you know, I see Dr. Shea sitting here. You know, there have been devices with electrical stimulation, especially to help with hand opening. You know, so you could try electrical stimulation to help with hand opening, and that is definitely something that has support in the literature. If muscle stiffness is an issue, if that is the reason he can't open it, then, you know, SableFlex is noninvasive, not SableFlex, shockwave therapies, they can basically help reduce some of the muscle stiffness, but it may not last very long, right? Hyaluronidase, well, thank you for that trick question. It's still in the experimental stage, so I'm happy to see somebody for a clinical trial at Johns Hopkins, but it's not yet something that has all of the evidence through a randomized control trial. It's ongoing, but it's something that, if it can address stiffness, if that is potentially an issue. Cryoneurolysis, again, it's new. It's approved, FDA approved for pain, but not yet for spasticity, and it can, you know, it does, it works with, it's a neurolytic agent, so one has to sort of ask, is there weakness? What is the real problem here before one decides on the treatment? So that would be my take on it, to really try to hone in on what the real problem is, and then take it from there. Joan, would there be any other direction you might suggest for this patient, if they came to you? Another direction, in terms of treatment options? Yeah, other than what was kind of mentioned here, are there other things, after these two years of injections without much improvement, what are the other things that might be on your radar screen? I think just in terms of the botulinum toxins, maybe cycling through one or two or three different types of toxins to see if they respond to one over the other would be something to initially try, possibly, but I think all of these other options that are non-invasive, like the Sableflex or the Bioness, could be done in conjunction with that. With regards to some of these other therapies, I think they are new, but if you've gone through all of the different types of toxin, and they're still not showing much improvement, then there are these clinical trials that the patient could be a part of to see if it would help for them. Joel, how would you? I don't have much to add. I think we probably were getting close to the end of the session. Maybe we'll open up for questions at this point, just people from the audience. Right in the middle of the room is a microphone. Anybody have any questions? It doesn't necessarily be about the cases that we covered. Stroke, rehabilitation, recovery in general. I think anything is fair game. We have three incredibly smart people up here. You can ask questions on any topic. Thank you. For someone who has, they've tried the botulinum toxin in the past. It looks more, the spasticity has nothing to do with stroke. It's an MS patient. But anyway, it didn't help. And it looks more like it's permanent contractures. Is there anything that could be done to help with that? So if I understand the question is, some patients have contractures as a result of spasticity and what do we have to offer there? Is that right? So I think that that's actually a tough situation. If it's not too severe and not too longstanding, then stretching may be helpful occasionally. Dynamic splinting has a role, or rarely serial casting. Surgery has a, it's an option, but I think you'd have to really have a clear functional goal. I mean, if somebody's skin breaking down or really having problems, you wouldn't want to subject somebody to that just to make their hand look pretty. But yeah, I don't know. Other thoughts? Yeah, I just want to say that sometimes when somebody's extremely stiff, we might think they are contracted, but contracture is a diagnosis you couldn't make by physical exam alone. So you might want to do an ultrasound to see the echo intensity, the echogenicity of the muscle. So if the muscle is truly, really very white with ultrasound, then you might, you know, you may lean more towards contracture. But very often, these individuals are just stiff. You know, they may not be contracted and, you know, aggressive treatment could help. Just one other comment on that, which is if you're not certain if it's severe spasticity or actual contracture, a local anesthetic, you know, proximal nerve block can be helpful to sort those out. Yes. Hi, to revisit the question of patients who have decreased wakefulness or arousal during their period of inpatient rehabilitation. As we mentioned, or as you all mentioned, we don't have great, you know, evidence-based treatments from a pharmacologic standpoint to turn to. I think a lot of us probably do use methylphenidate. And I'm wondering how the three of you approach how to start with dosing. So, you know, I tell my residents we could start with, say, five milligrams twice a day and, you know, see how they tolerate it and then uptitrate. But, you know, with limited time in inpatient rehab, sometimes you risk having an ineffective dose and then having to increase. You could start with a standard adult starting dose of 10 milligrams twice a day and see how they do with that. Or we can extrapolate from the brain injury population with some evidence for weight-based dosing. So I'm curious of how you all might approach that. Thank you. Yeah, I typically would start with five milligrams, you know, as you indicated, either once a day just to kind of test it or, you know, twice at 8 a.m., let's say, and 12 noon, and then titrate up. I realize we don't have a lot of time with these patients, but at the risk of going in with a high dose and having, you know, cardiovascular side effects, you know, you got to be careful. Yeah, if they respond, they respond fairly quickly. So that's the good thing. Yeah, it doesn't take that long to see if it's working. And if they're inpatient rehab, they're going to get their vital signs taken 500 times a day anyway, so it's going to be very closely monitored. Thank you for the presentation. Just have a question about a patient with kind of decreasing response to botulinum toxin. So kind of in thinking about making a switch to a different toxin, do you ever consider testing for kind of the presence of neutralizing antibodies, and when does that kind of come up for you in practice, if at all? So just one small point, which I don't think that that assay is available anymore. I think it had been commercially available from one of the labs, and unless someone else has reinstituted it, but you can't actually test for those anymore. They stopped doing that. So I think people just tend to empirically change from one toxin to another. Maybe from botulinum toxin type B. I don't know, Myoblock, other thoughts? Mike, you have anything? Yeah, I would just switch from one to the other. And there's still a role, of course, for ethanol or phenol in some patients, depending where their spasticity is and which muscles are involved. But I think we tend to sometimes forget that, and not as many people in this room probably are familiar with how to do that and are comfortable with it, so it can be an issue of access as well. Thank you. In the second or third case, when you were talking about patients with aphasia, one of the nerve stimulants not mentioned, like, is there any indication for denepazil? And then I even think I saw some European studies where they were looking at the drug class, like with Keppra. Any indication for both denepazil or that drug class? For what indication? For, like, aphasia, post-stroke aphasia. Aphasia and denepazil, not that I'm familiar with, but I don't know the literature that extensively. I think that there is some for denepazil and cognitive impairment post-stroke. Right, that I've seen. And also for dopamine agonist, I think that there's a literature there. It's sort of, it's just not a very robust literature, so I think some people will try it, but it doesn't feel very evidence-based. Thank you. Dr. Smith? Hi. How long do you wait after starting imantadine before you switch to another agent if it's not doing the trick? I've switched to which? Sorry, so for neurostimulation, how long would you keep a patient on imantadine before you would consider, you know, oh, this maybe didn't work, let's switch them to Ritalin? I feel like this is something I encounter a lot in disorders of consciousness, especially. It's a tough question. The question is how long would you wait before you added something else? I typically wait three days or so, three to four days, but that's just how restrained. I don't know if it's evidence-based. Yeah, the literature that we were citing suggests that you could start a stimulant on, you know, between days three and five, and then, you know, if there's no response at all, then every three or four days, you can titrate. And sir, you get the distinction of being our last question. Thank you for a great presentation and panel discussion. In the setting of stroke recovery, especially with spasticity involvement of the lower limb, has there been any role in CPG, specifically exobionic, early onset in the inpatient setting showing an impact on, you know, reduction of spasticity and also involvement of better gait patterns? I'm not sure I heard the question. Sorry, there's an echo. We're just having a little trouble hearing the question. We apologize. Maybe slowly and louder. Sure. Any role for use of, like, exobionic or other CPG type of intervention from therapy to reduce the incidence or prevalence of progression of lower limb spasticity post-stroke? Got it. Okay, so you're asking about lower limb exoskeletons? Is that the question? Yeah, more about the spasticity involvement of the lower limb and use of CPG, like exo, I don't know if the mic's working right, exobionics. Yep. So I think that, I'll comment briefly and then maybe others have thoughts. We don't know. I mean, I don't think there's a lot of evidence there. You know, in general, any motion, any passive motion or active motion, for that matter, is good for spasticity. So in principle, it seems reasonable. I think, you know, the problem with these exoskeletal suits for patients with stroke is that there's a lot of time and effort involved in getting someone into it, using it, and to some degree, it takes the place of more active movements. So I would be a little worried that you're maybe taking away time from real walking. You know, for a non-ambulatory patient, maybe it's a different story. If somebody can walk with assistance, I would probably favor that over trying to introduce an exoskeletal system. Yeah, so I think the key point is that motor recovery and spasticity are, you know, inversely related. So the greater the recovery you can promote, the less likely they are to be stiff and spastic. So, you know, for chronic stroke, a recent FDA-approved device, you know, is using rhythmic auditory stimulation, right? So basically, anything that will get them to move more is positive. Again, I don't know. I would, in spinal cord injury where you have paraparesis, you know, using these exoskeletons is much more, it seems to be something to try. In stroke, I know there've been some studies, but I think one would have to look at the studies or see who's doing the study to use the devices. Thank you very much for joining us this afternoon. Make sure you go online and claim your CME and have a great rest of the day.

stroke recovery

panel discussion

splints

G-tube

medications

vagus nerve stimulation

post-stroke fatigue

spasticity management

stem cell therapy

aphasia management

individualized treatment