Good morning, everybody. Welcome to the American Academy of Physical Medicine Rehabilitation CNS Member Community Day. I'm very excited about this meeting today. First time ever for a virtual platform. Please forgive us if we have any technical glitches as we go along. Hopefully, this will go very smoothly. But if not, just please have patience. I'm going to take about 10 minutes and discuss some CNS member community business. And then I'll turn it over to our speakers for our educational session. Just real quickly, the business that we're going to discuss today, primarily discussing elections for some open positions. This is more of just an FYI. We've spent some time in the last year developing some bylaws for the CNS member community. Those can be available for anybody who wants to review those. And then, of course, the primary goal of this meeting is the educational session. I'd like to give a plug for my co-executive committee members, Kristen Caldera, who's the Vice Chair of Education, and Sherry Jun, who's the Vice Chair of Communication. Really have had a great time working with this panel over the last year. We've accomplished a number of things, including the presentation that you're going to see today for the member community meeting, which is our educational session for the membership. I mentioned that we've also developed some bylaws. We've been publishing some things on FIZ Forum. I hope everybody's been able to see those, including some reviews of some articles and so forth. So really proud of the things, the objectives we've achieved over the year, and looking forward to the next year for continuing the growth of the CNS member community. Without further ado, I'm going to get on to the elections. The positions that are open right now are Chair-Elect, Vice Chair of Education, and Vice Chair of Membership. You can see the candidates below. Kristen Caldera, who's currently our Vice Chair of Education, will be moving to the Vice Chair-Elect if everyone selects her. And then we have three candidates for Vice Chair of Education. Marilyn Pacheco, who's at the Heinz VA here in Illinois. Subhadra Nori, who's at Queens and Elmhurst Hospital and at Kahn School of Medicine at Mount Sinai in New York. And then Diane Mortimer, who's at the Minneapolis VA University of Minnesota. And then we have a candidate for Vice Chair of Membership, who is Heidi Fusco at Rusk in New York. The election, I don't know why I keep saying education. The election is on SurveyMonkey. If you have a QRC reader on your cell phone, this is kind of cool. You can just point it at that QRC code, and the survey opens right up to vote. There is a link here. I'm going to publish all of this on FYS forum after the meeting. And the elections, you don't have to do this right now, but the elections will be open through Saturday at 7 p.m. Central time. So you don't have to make your decision right now. There is a little blurb from some of the candidates about their interest in the position there. And so this will be open and published several times throughout the week as the meeting goes on, so you can have an opportunity to vote later. Without further ado, I'm going to move straight to the educational session and introduce my colleague, Dr. Richard Harvey, who's going to start the session and introduce the rest of the speakers. Dr. Harvey is a professor of physical medicine and rehabilitation at the Feinberg School of Medicine at Northwestern University, and he's chair of the Brain Injury Center of Innovation at the Shirley Ryan Ability Center in Chicago. So I'm going to end my slide and turn it over to Dr. Harvey if he's ready. Richard? Yes, I am. Hello, everybody. Thank you for joining our session today. We had been very interested in trying to put together a community session that would bring more CNS people together, and what we've done is we've combined stroke and spinal cord injury, because last year we had more of a focus on traumatic brain injury. So we decided to focus on the brain stem and high cervical cord and how that impacts the lives of people with stroke and spinal cord injury, focusing specifically on locked-in syndrome caused by stroke or TBI and high cervical injury. And we're going to talk a lot about brain-machine interface in the context of that and how that might be utilized for research and also for technology management. So we're going to... We had originally planned on a bit of a longer session, but now we're at 90 minutes, so we're going to get started right away. Our first speaker is Dr. Alan Anschel, and, Alan, if you want to share your slides at this point. He is an assistant professor and a colleague of mine at the Shirley Reinability Lab in Chicago and Northwestern University Feinberg School of Medicine. His clinical specialty is spinal cord injury, so he's going to talk about cervical spinal cord injury and the issues that surround that diagnosis. Great. Thank you, Dr. Harvey. Good morning, and thank you for joining our session. Dr. Harvey, can you see the slides okay? No, not yet. Not yet. Okay. Let me see what I need to do. You hit share screen. Yeah, there we go. Okay. There we go. That's it. Okay. Great. Okay. You can hear and see them okay? Yes. Great. Okay. Thank you. Good morning. Thank you for the introduction. Thank you for joining our session. I have no financial disclosures. So the rehabilitation of high cervical spinal cord injury is obviously a very large topic, but for the next 15 minutes or so, I would like to talk about some broad themes, challenges that we often see in this patient population. We'll start off by looking at the epidemiology of traumatic cervical spinal cord injuries and then talk a little bit about how the respiratory system is impacted after these kind of injuries and then look at briefly the rehabilitation approaches for communication and mobility. So when looking at the etiologies of acute traumatic spinal cord injuries over the last five decades, we see that the number one cause is motor vehicle accidents followed by falls and then violence. And when we look across neurological category, we see about 35% of the patients are tetraplegic, with just about 4% of them requiring mechanical ventilation. And when we look across etiologies, traumatic cord injuries are a disease predominantly of males and motor vehicle accidents, sports and falls are more likely to cause traumatic neck injuries as opposed to violence, which is going to cause more paraplegia due to gunshot wounds to the thoracic and lumbar spine. Tables 85 and 86 kind of just remind us that those patients who do come in on mechanical ventilation to an acute inpatient rehab hospital have a really good shot of being liberated from the vent or at least weaned towards positive airway pressure by the time of discharge or at least one year post-injury. And when we look at the SMR, the standard mortality ratio, the actual death is over expected deaths, we see that those who are less than 31 years of age on mechanical ventilation have about a 51 times higher mortality than those who don't have a spinal cord injury when you control for race, gender, and age. And diseases of the respiratory system remain the number one cause of death in this patient population. And when we look at median days hospitalized in the acute care hospital, for complete touches is around 21 days and for incomplete touches around nine days. And then median days hospitalized in the rehab setting is about two months or 61 days for complete tetras and about six weeks or 44 days for incomplete tetras. So this slide's here just to remind us that after a high-level cord injury, the autonomic nervous system is obviously greatly affected with resulting in unopposed parasympathetic tone. And as mentioned, we're going to focus mostly on the respiratory system. So there are significant changes to our pulmonary physiology after spinal cord injuries, neck injuries. There's impairment of ventilatory muscle performance. The higher the level of injury, the more complete the level of the injury, the more the respiratory muscle dysfunction is going to occur. And because or due to the inability to inspire to total lung capacity, the rib articulation sites become stiff and in some case ankylose causing a decrease in lung and chest wall compliance. And for reasons not entirely understood, our ability to respond to hypercapnia is reduced. And as mentioned, due to the unopposed parasympathetic tone, there is airway, bronchohyperresponsiveness or bronchoconstriction. It's also useful to think about the pulmonary physiology on time from injury. So immediately following the spinal cord injury, there's period spinal shock where you have flaccid paralysis affecting muscles caudal to the level of injury. And then by six months, one year, we know that the pulmonary function increases. There's increase in vital capacity. And partly we feel like this is due to retraining of deconditioned muscles, the evolution of flaccid dyspastic paralysis and descent of the neurologic level. Now, cervical spinal cord injuries have an increased risk for sleep disorder breathing. Certainly chronically, it seems to be the obstructive form is most predominant. And Berlowitz looked at a couple of studies or published a couple of papers about the prevalence of OSA and the cervical spinal cord injury population. And he observed that at least chronically that 90% of patients with neurologic complete cervical spinal cord injury had OSA. And then another cohort he looked at and then in a different study, he showed that around 62%, about half of patients at four weeks post injury had some form of sleep disorder breathing. And by one year, they also had about 60% had sleep disorder breathing. And certainly cervical compared to thoracic cord injuries had a higher prevalence of sleep disorder breathing. So why does sleep disorder breathing occur? Well, they don't entirely know, but the thought is that perhaps time in supine sleep position is increased, causing an increase in upper airway collapsible forces. There's the unimposed parasympathetic tone that promotes bronchoconstriction. It's partly due to the medications we use, such as opioids, baclofins, benzodiazepines. And in some cases, there's some preexisting traumatic brain injury that can also contribute. So the mechanism for the increased prevalence of sleep disorder breathing after a spinal cord injury is not entirely clear, but evidence seems to point towards this combination of hypoventilation, neuromuscular weakness, and upper airway collapsibility. So how do we manage this on the acute inpatient rehab floor? Well, polysomnography is the gold standard for studying sleep quality and diagnosing sleep disorder breathing, but we know it's expensive, time-consuming, labor-intensive, less readily available, requires regular monitoring, and certain expertise. Pulse oximetry is cheap, reliable, simple, quick, and a valuable screening tool for us to get at the ODI, the oxygen desaturation index, and the AHI, the apnea hypopnea index, and help to screen for mild, moderate, and severe OSA. And then with consultation with pulmonary, we're able to prescribe non-invasive ventilators to help manage and treat it on the floor. So airway clearance is obviously so important and critical to this patient population to prevent mucus plugging, atelectasis, and pneumonia, and there are various devices that we can use, such as the Medineb, the mechanical cough assist, and the EMST. The Medineb is a lung suspension therapy that provides high-frequency oscillations along with nebulized medication to promote airway clearance. And the EMST is a low-cost device-driven therapy where patients can expire against a one-way spring valve to strengthen the expiratory muscles, improving both cough and swallowing function. And you can see that these devices can be accessed through the trach, through face masks, or through mouthpieces. So communication is obviously very important in this population who are in mechanical ventilation, and certainly things like lip reading, facial expressions, gestures, communication boards can all be helpful, but one of the most helpful techniques is leak speech. But the problem is that during mechanical ventilation, the trach cuff is inflated and there's inadequate subglottal pressure to cause vocal cord vibration. And so the solution revolves largely around reestablishing air flow through the larynx and by lowering the trach cuff, increasing the tidal volume. But the kind of trach that's in place really does matter. And so in this picture, you can see that the Shiley cuff is in place, the Shiley trach is in place, but when the cuff is deflated, there's still a large amount of plastic residual in place, obstructing airflow. So changing them to a TTS system, a tight to shaft system that's shown here on the right in the lower corner where the balloon incorporates into the trach is very helpful to facilitate airflow within the larynx and allow for vocal cord vibration and vocalization. Now, for those who can be weaned off the vent and can progress with their trach, then you can see with the inverted one and three, there's the one-way speaking valves, the Passamere valves, and then progressing towards trach capping, in which we monitor for ventilation, oxygenation, airway protection, and secretion management. So the diaphragmatic fracture can be used, got a couple of videos here, let me just mute them. So the diaphragmatic pacer can be used for those patients who can't be weaned off the vent, but are able to, but there are means to reduce the need for ventilatory support. And so here you see in this video, the surgeon cutting down the fasciform ligament, exposing the diaphragm. And in this video, we can see the surgeon is looking for areas of maximum contracture of the diaphragm and greatest change in intradominal pressure. There we go, sorry, the video froze for a minute. So here you can see the surgeon mapping out the diaphragm, looking for those areas of maximal contracture. And in this next video, you can see the surgeon is attempting to pass the device through the diaphragm. As he mentioned in the video, there's often a lot of atrophy that works against us when placing the devices. And in this video you can see that the wires are pulled through and then placed externally where they can be connected to an external device. So the power wheelchair obviously is the mobility device of choice for this population to navigate the environment. There are various configurations with mid-wheel drive, front-wheel drive, wheel-wheel drive, and they all have their advantages and disadvantages towards indoor and outdoor navigation as well as turning radius, driving stability. But one of the most important features is the tilt and space feature that is shown here on the left that allows patients to perform adequate pressure breaks. And then here is a video demonstrating the sip-and-puff control system where the user provides positive negative pressure through a straw that allows the driver to drive forward, backwards, turn, and initiate tilts. And then here in this video we can see the head array system where the user can facilitate controlling the chair through a series of toggles that are right next to their heads that allows them to drive forward, backwards, turning, tilting. And then here is an example of the goalpost joystick where someone who's at maybe at the C6 level, this provides a large surface area for them to rest their hands in a neutral position and then they use shoulder protraction and retraction in order to drive the wheelchair and it doesn't provide a pincer grasp. Okay, thank you. Those were my slides. We have a few minutes for questions. If you have a question, you can put it into the chat and I will read it out. And if there are no questions, we will just move on to the next talk. And if you do have a question, I'm going to go ahead and move on, but if you do have a question, but if you do have a question, go ahead and put it in the chat. We'll catch up with it a little later. Okay. I almost left the meeting just now. Instead of sharing. Okay. Get to the right place of my slides. Okay. All right. Can I assume everybody can see this? My fellow speakers just tell me that they see. All good. All right. Thank you. All right. So I'm going to move on and talk about locked-in syndrome and I'm going to talk about it in the context primarily of stroke, but locked-in syndrome can occur from traumatic brain injury, from ALS. I'm also going to contrast locked-in syndrome a bit with what you just heard from Dr. Antrill in terms of management of high cervical spinal cord injury. Locked-in syndrome is a bit different in quite interesting ways that impact medical management. Locked-in syndrome became somewhat popular or entered the popular world when Jean-Domique Bobet wrote a book back in the late 1980s, I believe, called A Diving Bell and a Butterfly, where he wrote his own autobiography of his experience with living with locked-in syndrome. He spelt out the book letter by letter to an assistant. It's a short book, probably because of his limitations with writing, but it's a very interesting book. Later it was made into a movie, which was nominated for Academy Awards. And I have to admit, I do locked-in syndrome care pretty routinely. So I actually have never sat down and watched this movie, mostly because it's sort of like going back to work again. But someday I'll actually see this movie. So what is locked-in syndrome? It's a medical condition usually resulting from a stroke that damages part of the brainstem, in which the body and most of the facial muscles are paralyzed, but consciousness remains and the ability to perform certain eye movements is preserved. There are three ways to classify locked-in syndrome, and I think it's really important to do this when discussing this diagnosis with clinicians, especially when we talk about rehabilitation. The first is the classical locked-in syndrome, which was actually described by Plum and Posner in 1966, which is quadriplegia, that was their term, mutism, cranial neuroparalysis, with preservation of upper eyelid function and up gaze. Most patients actually are incomplete locked-in syndrome, which resembles a classical locked-in, but with some additional remnant preserved movements. And in caring for these patients, any preserved movement is of value. And then the last one is total locked-in syndrome, which is really uncommon in stroke, but can be seen in ALS, where you have complete paralysis with no means to communicate. These patients are often confused with being in a coma. Fortunately, that's the most rare. The cause, as I implied, is primarily stroke and followed by traumatic brain injury, which constitutes a third of these. In fact, I currently have a patient in-house who has a locked-in syndrome from traumatic brain injury, but interestingly, the trauma led to trauma of the vascular system, which resulted in a dissection and a stroke. So it's kind of a mixture of both. In data that actually came out of, back then, the Rehabilitation Institute of Chicago, they did a long-term follow-up and showed that the five-year survival for locked-in syndrome is 83%, with the 10-year survival about the same, and then 20-year survival is 40%. Their risk of death is usually due to things like pneumonia. And in terms of outcome, looking at motor recovery, the majority have minimum recovery of motor function, but a good percentage will have moderate recovery. No recovery is seen in about 20%. In terms of quality of life, there was a French study that just looked at 17 patients, but this is the only one I am aware of, that interestingly showed the locked-in syndrome being in the white bars, showed that mental health versus controls is about the same as anyone else. Where you see that a decline is, or a lower rate, is in once-perceived physical functioning, where locked-in syndrome patients pretty much feel they have no physical functioning worthy of quality. In terms of life satisfaction, just over half find that their life is satisfying. And most, more than half, never have a depressed mood, and only half have ever even considered euthanasia or decided they wanted to do euthanasia. Now, I have to qualify this, is that these were likely people who were at home, living with family, as opposed to those who ended up in institutional care. So, the anatomy is, really focuses on the pons. You can also have incomplete locked-in syndrome from the medulla injury, the bilateral medulla injury, but more commonly you're going to see bilateral pons. This is a patient of mine who had pretty much wiped out her pons and part of her cerebellum due to a basilar artery thrombus. And what this does is it knocks out both corticospinal tracts, as well as the abducin nerve in blue and the facial nerve in green. You also lose a part of the paramedian pontine reticular formation, and this is why you have only preserved third cranial nerve function in classical locked-in syndrome, where you can raise your eyelids and look up. Since this is more often incomplete, you will often have patients who have diplopia because they have some ability to do some horizontal gaze or down gaze that is not conjugate, and they may end up with some diplopia. You can also get some nausea and vertigo because of some of the injury around the pontine region. So, I'll move on to medical issues. One thing just coming, when patients come into acute rehabilitation, you have to consider some of their cardiac issues. Orthostatic hypotension is common, as it is in high cervical cord injuries. And, you know, but the difference is that in patients with stroke, most of the time they're on a ton of antihypertensive medications because they were very hypertensive in acute care, and the first thing you can do, rather than put abdominal binders on and compression hose, is to reduce their antihypertensive medications, trying to normalize their blood pressure when they're more in the upright position. And this often is sufficient, but at times you may have to use some compression stockings and abdominal binder, usually only temporarily. Tachycardia is common due to loss of vagal tone because the vagus nerve is in the region, so you'll end up being tachycardic for usually some time. It's usually addressed best with beta blockers, and ultimately, the heart rate will come down and weaning out the beta blockers is possible. On very, very rare occasions, you can get paroxysmal autonomic instability with dystonia. It is rare. The one case that I had of it was severe enough that ultimately we had to put a bath up and pump in, which did resolve the problem. The other thing is, you know, acutely the patients are intubated primarily to control the airway, because these patients generally will aspirate at the time of their stroke. In rehabilitation, of course, you want to keep patients in an upright position, suction orally because they usually cannot handle their oral secretions due to oral motor paralysis and tongue paralysis. And because the patients cannot communicate well, many times they can't even use a call light because of lack of mobility. Frequent nursing checks are necessary. I usually have my nurses check on these patients every 30 minutes if they cannot adequately use a call light. Now, what makes locked-in syndrome different than spinal cord injury is that they ventilate. They always ventilate, and they ventilate with fairly good diaphragmatic movement, but they do it automatically. They're in automatic tidal breathing. If you ask a patient to take a deep breath who has complete locked-in syndrome, they will not be able to. They will just continue breathing at that normal, tidal breathing pattern. What that does is it puts patients at a risk of lower lobe atelectasis. Now, they will think Now, they will spontaneously cough at times, and that may be a very weak cough. It may be a very strong cough. They may yawn sometimes, but for the most part, they're in tidal breathing. And because of the atelectasis, I almost always will use a cough assist until the patient's x-rays show absolutely no atelectasis in the bases. A lot of people will use drying agents because these patients will aspirate their own secretions and therefore produce a lot of secretions, but I would be very careful doing that because if you dry them out too much, they can get a mucus plug, and these patients cannot manage a mucus plug very well, especially if they have atelectasis in their bases. So in a sense, you kind of want to have nice loose secretions and use drying agents only if it becomes to the point where it's just way too wet to be able to manage them. So in terms of tracheostomy management, very similar to cervical cord injury, that we like to use the TITUS shaft tracheostomy tube pictured above rather than the kind with the more plastic cuff. This allows you to work on airway management just like Dr. Anshul described earlier. You can use one-way valves or you can cap them off. This is more to get them to practice with breathing through their normal airway. They may not be able to vocalize because of their stroke, but in some cases patients may recover sufficiently enough to vocalize, but I think for the most part vocalization is still not possible, and their oral motor function may not allow them to talk. But it is part of the process of weaning the trach, and you can in many cases wean the tracheostomy tube on these patients if they're not aspirating liquids anymore. So this usually requires that they initiate swallowing again. Another key area is eye care, and because they have bilateral facial palsies or at least or they may have unilateral facial palsy or they may not have facial palsy at all, they often will not be able to close their eye all the way. And I've had patients come to rehabilitation whose eyes look like the one on the left there, which is unfortunate. It just means somebody did not pay attention to eye care. So what you need to do if they cannot completely close their eye, you do need to use regular eye drops and you need to use ophthalmic gel and patch at night using a nice secure system of patching as shown. In severe cases if the eye is not doing well they may need a tarsoraphy. Another option is to use airtight protective goggles which are easy to apply and do protect the eye. Patients may not necessarily like these, but if it does help their eyes feel better then they generally do appreciate them. As I mentioned earlier, patients can have diplopia and so we frequently will use Fresnel lenses, which are shown on the right there, which add prisms to one of the eyes. These are easily applied. They can be removed and changed as the patient's eye movements improve. And they don't work perfectly well as somebody who's had a cranial nerve palsy before that affected eye movements. They help a little bit, but they, you know, eye movements are very dynamic and these prisms don't perfectly correct. They just help a little bit. You can have definitive corrective surgery after about 6 to 12 months when the patient is at their maximum recovery. So let's talk about some of the rehabilitation. There are several ways to communicate. I'm sure most of you are familiar with the one in the middle which is the AEIOU board. We often use quick and easy picture boards that help with stuff you might experience in a hospital like need to reposition or, you know, having some pain. And the ways that these are done, of course, is the patient will move their eyes as you go sequentially through each of the letters or the pictures. The one on the left there is called the ETRANS. And this one's an interesting one. It's a lot quicker to spell out because what you do is you look to the color, you know, the color that you want, say red, and then you look to the color that indicates the letter in that red block. So if I wanted the letter E, I would look to the red, which takes me up to the left upper corner, and then I would look to the purple which tells that it's the letter E. Now what you need to be able to use this is good head stability and ability to look horizontally somewhat with your eyes. Lacking horizontal eye movements, you really cannot use this very well. And then the one on the right, of course, is a computer interface that can be used with eye tracking, head tracking, and switch and switching as well if you have a, let's say, finger movement or something like that. And speaking of finger movement, of note is that bilateral pontine strokes will generally recover distal to proximal and may not ever get a lot of spasticity. So really what you're looking for motor wise is can they, you know, twitch a finger or move the thumb. And you'll probably see this before you see shoulder movement, which is the opposite of what you typically expect with stroke patients. Not to say they won't get spasticity, many of them will show synergy movements and hypertonia, but that's not the general rule. So we progress upright position over time, dealing with the orthostatic hypotension. Once we can get them upright completely, we'll use a stander. And we've been using some functional electrical stimulation on a tilt table with pedaling as well as a sort of pre-gait sort of training approach. Dr. Antle mentioned the wheelchairs. I don't want to reiterate what he said already, but I will say that many patients will not be able to use a power chair because they lack the head control and they lack the ability to gaze in directions for directional driving. So a tilt in space manual chair is appropriate. If they do get enough head control back or the ability to move a finger and the ability to gaze in enough directions to avoid objects during driving, then they may be able to use a wheelchair, usually with a head array, but possibly with a joystick. Swallowing, of course, is an issue. Swallowing is what keeps these patients from weaning their trachs early on. They have poor oral motor control, poor tongue control, facial weakness leading to poor control of secretions. However, patients can get their swallowing back, and I've seen it many a time. It may be spontaneous swallowing at first and then voluntary swallowing. So we use the usual approaches. We may use functional electrical stimulation. We also work on tongue pressure because their tongues are weak using this device here where they press pressure down with their tongue onto this bulb and we can progressively measure their pressure, give them targets to work towards, and approach therapy that way. So this can both help with swallowing and also control of secretions. Finally, the key thing with patients who are locked in ultimately is their ability to maintain connection with the world, and we're so fortunate now to have the World Wide Web and easy connectivity through computers. This allows communication, it allows emails. My patients do email me at times, writing, some express themselves in writing because they can't express themselves in other ways, reading, videos and movies, television, online courses, and even just messing around with the internet. So this is a very important piece to their home life and their ultimate quality of life. I showed this MRI earlier with this diffusion scan showing a complete wipe out of the pons. This is a patient of mine who's on the right here who is in her 30s and she had locked in syndrome, recovered adequately to get the tracheas removed, the feeding tube is removed. She can eat, she can communicate with an electronic communication device, and a friend of hers modified a bicycle to create this tricycle that she can use, and she actually can tricycle down the street with the minimal but sufficient leg movement that she has. She loves her life, she loves everything that everyone has done for her, and she's just a wonderful person, and she sort of motivates me to keep working in this area. This is two other patients of mine I just want to show you. The one on the left is a patient who was locked in, but now he has sort of a spastic tetraplegia with ataxic components, but he was able to walk with a walker. He once got in his truck and drove it down the street, much to the frustration of his wife. He was a welder, he was able to weld things together, made some toys for his grandchild, so he's staying very active. The one on the right is a classic locked-in case, and I'm just going to point out one thing that I didn't mention earlier. He doesn't move anything. He can move his head, he has better vertical eye movements than other eye movements, but he smiles. If you ask him to smile, he cannot smile, but if you tell him a bad joke, his whole face lights up. Patients can often have inappropriate laughing, inappropriate crying, so they can have what I call, as opposed to pseudobulbar affect disorder, I don't call it that because A, this is real bulbar affect disorder, the bulbar nerves are involved, and secondly, it's more in the area of pathological laughing and crying. It can be treated with SSRIs. In some cases, you can use quinine with dextromethorphan combination as well, but I tend to go with the SSRIs more often, especially since dextromethorphan is an NMDA blocker that can affect motor recovery, so I don't use that early on. So that's my talk. I have been focusing on that and not on questions, so let me get back into my Zoom and stop sharing. Let's see, there's some questions here. Is there a respiratory benefit or other benefit to power recline on a power wheelchair in addition to a power tilt for high quads? Alan? Certainly for the high quad, high tetraplegic, you really would want that tilt in space mostly for skin protection and being able to adequate pressure breaks since pressure ulcers are such an issue. I can't think of an immediate benefit to just having that power recline. I feel like I've seen that used more in maybe someone who has kyphosis where positioning and posture in the chair is important, where they're kind of bent so far forward that the tilt is there to kind of get their eyes back up to horizontal positioning. Another question is, I love the elevating seat for patients with lower level quadriplegia to help not only with socialization, face level, but for function, reaching cabinets above counter height, reaching counters, how do you get it covered? Most insurance companies say it's only socialization, not functional, but I disagree. Any pearls on getting elevating seats covered? This is a very challenging area. I did have some luck this year having one patient get it covered, but it did require a series of letters from me, so from the doctor, and the patient did hire a lawyer to kind of help collect all the paperwork together and advocate for the patient and the need. One of the underlying unique features was that the patient had chronic pain while sitting in the chair, and it was only with elevation and standing did they get good pain relief, and after a series of medication changes, pain programs without any relief, we were able to then kind of justify it from a chronic pain perspective. Okay, thanks. That's all the questions right now, so we'll move on to our next talk, and our next speaker is Dr. Kristen Caldera. She's an assistant professor of physical medicine and rehabilitation at University of Wisconsin-Madison, and she's also, as you heard earlier, the vice chair of education for the CNS community and soon-to-be chair because she's the only candidate, so I assume she's going to be voted in, and so she's going to talk about brain-machine interface and its use in research. All right, can everyone hear me? Yes. Yes. Excellent. So thank you for that introduction. Again, I am Kristen Caldera, and I need to get my, there we go. Okay, and yes, I work at the University of Wisconsin-Madison. I want to take just a moment to say if you're enjoying the presentation, we still have two more parts to go, and please start thinking of what you might be interested in hearing about next year. I practice a little bit of everything in neural rehab, spinal cord stroke. I have a large group of adults with developmental disabilities, and I've also become more involved with a research project looking at brain-computer interface, which I would like to speak about today. I have nothing to disclose. The group I work with does have some NIH funding. The objectives for today are to talk about the ABCs of BCI, brain-computer interface. It's a bit of an alphabet soup, and I'll try to put all the parts and pieces together as we go. I'd like to really give a bird's eye view of what brain-computer interface is. I'd like to give some examples of the end goals of BCI, one being to drive neuroplasticity, which I'll speak more about, as well as to control an external device, which my next co-speaker will speak about. I'll give some examples of using BCI to promote neuroplasticity in stroke, as well as some of the results that we've had and some of the limitations in the research we've been doing, and discuss some of the future directions. I'd like to go back and talk a little bit about where this definition of BCI started. There was a conference in 1999, and it was the first international brain-computer interface technology conference. They decided that they wanted to further define what brain-computer interface was to differentiate from some of the other technology that was out there. They defined it as a communication system that does not depend on the brain's normal output pathways of peripheral nerves and muscles. This is a technology that uses brain signals themselves to measure an intention or even a thought. This differentiates it from the technology that we were talking about earlier with the eye-gaze system. There's no muscle input needed here. Brain-computer interface uses the brain itself as the signal. So back to 1988, it was Farrell and Donchin who conceived this P300 Speller system. This system reads intention without action. You can imagine how this could be helpful in the patients that have Lockton syndrome that don't have motor capability. In this system, the subject or the patient identifies a letter. So in this instance, they're looking at the letter P. That letter creates an evoked response, which is read by EEG. That evoked response is then fed into a computer, which prints out the letter P. This goes on for different letters with the letters making words, the words making sentences, and the sentences purveying thoughts. So in this simple algorithm, you can see there's three main parts to brain-computer interface. There is the recording of brain signals, and these can be done in a number of different ways. I'm going to talk about electric signals, but also magnetic or metabolic. These signals are processed through a computer algorithm, and they are translated to an output device, which could produce an action. This slide here, I took from Dr. Marcia Bachbreder, who will be speaking next. And this is from our journal, the PM&R Journal in 2018, written by a number of our colleagues. And I thought it was a really nice way to put together a bird's eye view of what brain-computer interface is. So in the red box, you can see the different inputs. And as I said, I'll speak about EEG, but there's also a lot of other things that you can do And as I said, I'll speak about EEG, but there's also fMRI. There's both non-invasive and invasive ways of measuring brain activity. So these signals are recorded. And then in the blue boxes, this is where the magic of the computer happens. The signals are processed, they're computed, they're decoded. After the computer does that, the code is given to an end-effector device, which is in the green box in the middle. You could see that this could control a computer screen, it could activate an FES, it could activate an exoskeleton. Interestingly, in addition to having an end-effector device, it can then feed back to the system, such as direct current stimulation, and close this loop. So two of the applications for BCI, neural prosthesis to replace locked function, or in what I'm going to follow, to promote neuroplasticity and recovery for motor difficulty. I work with a large group at the University of Wisconsin on this research team. Yes, there's physiatry involved, but there's also neuroradiology and our biomechanical engineers, therapists, kinesiologists. It really takes a team to run this lab. So our goal at the University of Wisconsin is to restore upper extremity motor function after stroke. This is the group that we're working with. The intervention is a closed loop, non-invasive, EEG, BCI, FES intervention. As I said, it was a little bit of alphabet soup, and I'll get to all of the different parts and pieces. So first, let's start with the two paths of motor recovery that we are looking to bring about. The first being the restoration of function of the surviving neural architecture following a stroke. The second, promoting neural reorganization of the proximal architecture. We're doing this through the process of two ways, one being heavy and learning, the second being deep learning. The process of two ways, one being heavy and learning, the second being classical conditioning. And they do feed upon one another. Heavy and learning essentially rewards cortical activity. So our cortical activity is measured by EEG. If the person can produce the rhythm that we want for EEG, then an effect will happen. And that effect, for instance, could be stimulating an electric stimulator device. So we're pairing what we want from somebody with an end effect. So we ask them to do this over and over. We like to say practice makes permanent. Where classical conditioning comes in is we want that practice to be goal related. We want them to practice to make something they want to do permanent. We don't want to promote maladaptive activities. So this is a picture of our setup. And here you can see the EEG cap. We have superficial EEG, and there's 16 electrodes. In the middle of the screen, the signals from the EEG are fed into a computer. The computer decodes the signals, and there's two output devices which we have. We have a computer monitor, and we set this up as a game to maintain the person's interest. The game will ask the person to move, for instance, their right hand. If they make the EEG signal to move the right hand, the ball will move to the right of the computer screen. In addition, they will receive a stimulus from the FES. So these are the two parts that they need, which ends up closing the loop. So to start, they're asked to do an activity. They do the activity, and that closes the loop. The outcome measures that we're looking at are many. In the area of behavioral motor outcomes, we are looking at the ARAT, or the Action Research Arm Test. There are 57 points. And just to remind people, 57 is the highest score that someone can achieve. And you can see the box here with the wood blocks and the cylinders. It's measuring grasp, grip, pinch, gross motor movement. So the subject is asked to do a number of tasks with these different objects. And if they score high, they are less impaired. In addition to looking at this test, we also wanted to look at the person's experience. So the stroke impact scale really measures someone's personal experience. Questions on the survey are things like, how difficult is it to move your hand? How difficult is it to eat? How impaired is your hand? And again, the higher they rate this, the less impaired they are. We also looked at nine-hole PEG test as well as grip strength. In addition to these behavioral motor outcomes, we looked at outcomes of brain activity as measured on brain imaging. We looked at MRI, functional MRI, and structural as well as EEG. So briefly recall that functional MRI measures brain activity associated with blood flow. So we couple blood flow with brain activity. EEG also measures brain activity, electrical brain activity. Our study design is a randomized controlled crossover study with recruitment ongoing. There's two phases, a control and a therapy phase. During the control phase, we are obtaining the behavioral outcomes as well as the imaging at various times where you can see on the screen T1, T2, T3. Before they enter into the therapy phase, they again receive the, they are tested for their motor outcomes and undergo the imaging. They then will have two to three weeks of this intervention, which I talked about, and in those two to three weeks, two to three times a week, they're receiving an intervention session. So about halfway through, they repeat their motor outcomes and they also repeat the imaging, go through another two to three weeks, repeat the imaging, and then there's no therapy for four weeks. And again, we repeat the outcomes in the imaging. So there's three topics that we looked at that I want to briefly talk about today. And one of that, one of them being with our intervention, I'm going to call it our BCI therapy, so I don't have to continue to say EEG, BCI, FES. So with this intervention, are there changes in the motor behavioral outcomes? Number two, is the brain wiring changed as measured on functional MRI? And number three, are there changes in EEG over the affected area after intervention with brain computer interface? So our first question regarding motor behavioral outcomes. So does this intervention change motor behavior? We had 21 participants who initially had some upper extremity paresis secondary to stroke. We employed the brain computer interface intervention. 14 of these patients at the very beginning, before they had the intervention, had already, or I'm sorry, 14 patients at the time did have room for improvement on their ARAT. And of those 14 participants, six of them did show an improvement in their ARAT as a primary outcome. The second question we called has to do with the wiring of the brain. And we wanted to look at, does a change in wiring correlate with behavioral change, if in fact there is a change in the wiring? So we had nine participants, and the intervention was the same, brain computer interface. Functional MRI was done before, during, and after the intervention. The behavioral measures, as I talked about, were the ARATs. And in particular, with the stroke impact scale, we looked at the domains of hand function and ADL. Again, we measured functional MRI. These functional MRIs were then put into a whole brain functional connectivity analysis in the motor network. So remember, functional MRI measures blood flow when an area of the brain is in use. So increased flow, increased brain use. Functional connectivity, which we're looking at, is when two areas of the brain are active simultaneously. So when we took these fMRIs and looked at functional connectivity, we looked at specific areas of the brain targeting motor recovery or motor performance. So those areas are the bilateral thalamus, motor cortex, and the cerebellum, and the right supplemental motor area. The programming was looked at, and what they found is that there was increased functional connectivity, in particular, in the thalamus. So where the thalamus is reaching out to these different area connections, and that was found a change from mid-therapy to post-therapy. Interestingly, it was found in both sides. It was found in the affected side, the ipsilateral thalamus, as well as the contralesional thalamus. So we said there seems to be increased functional connectivity. We see this in both ipsilateral and contralesional sides. So was there a correlation with behavior? And yes, there was an improvement in the subject's performance of the nine-hole PEG test, as well as in the domains of activities of daily living and hand domains on the stroke impact scale. Interestingly, there was also a negative correlation. So with increased functional connectivity, or two parts of the brain activated at once, they did worse on their ARAT, as well as on their subjective view of their strength. So it's possible that there could be both adaptive and maladaptive sources going on, and how can we try to change those forces? The third part that I wanted to look at is EEG. So we've looked at behavioral outcomes, we've looked at functional MRI, and functional connectivity, and now we're going to look at EEG. So the question is, does the EEG change over the motor areas when we employ brain-computer interface? And here, I'm going to talk a little bit about desynchronization. So back to our EEG 101. So this is an EEG. Desynchronization, think about synchronized swimmers. When swimmers are all synchronized, you don't really notice one particular swimmer. When they desynchronize, you can pick out that specific swimmer. We're doing the same with EEG. So we wanted to look over the motor and sensory areas. You can see in the head with the colored area, those are the sensory motor cortex. We then asked the patient to perform activity. And in this instance, it was to move the right hand, or to move the left hand. And when they do that, they create a specific rhythm, which is called a mu rhythm. And that's what you see marked in the yellow box. It's called mu because it looks like a Greek letter, mu. So we had 21 stroke survivors. They had 18 to 30 hours of intervention with the BCI device. We looked at their function baseline, mid-therapy, and end-of-therapy. And during the therapy, their EEG was recorded. The outcomes that we looked at was, was there a change in desynchronization of the mu rhythm following therapy? Another colorful picture. So on this picture, what I want you to look at is that dark blue is more desynchronization. And I told you that desynchronization occurs during attempted movement or movement, which they're doing during this therapy. Please appreciate that in the pre versus post, whether they're trying to move their left hand or their right hand, there is more blue. And this change in desynchronization after using brain-computer interface was significant. This did also correlate with a change in their ARAT. The more desynchronization, which you can see on the bottom, correlated with an improvement on their ARAT. So it seems that increased desynchronization over the motor sensory cortex following brain-computer interface does correlate with an improvement in the ARAT. There is a lot of work to be done for our group and all the groups out there working in this area. If the brain-computer interface does indeed form new brain connections, can this really carry over to functional activities? And if it does, can this response change, response remain over time? Which lesions are most responsive to BCI? We have a variety of lesions and impairments in our group. Is there a dose-response relationship? Technology continues to improve. As I said, we're using superficial EEG. If we used invasive, would it be different? Could we still do this work? And could this therapy be paired with other rehab therapies? Some final points to remember. Brain-computer interface is a computer system that permits brain activity alone to control the external device. There's no motor with this. It can be used with a normal motor cortex to drive an external device. But as I've shown you today, there's growing evidence that brain-computer interface could improve neuroplasticity after stroke. That we've looked today at functional motor activity, changes in functional connectivity on fMRI, and changes in EEG patterns. There's still much to be done. A brief thank you to the team that I'm working with. They let me go through their work quite a bit and all the different parts and pieces. Thank you to my CNS community members and to my co-presenters. Thanks a lot, Kristen. I actually have a question, which is, when you're looking at the patients who did the ARAT and the other measures, the nine-hole PEG test, what was their baseline coming in? Are we talking about fairly low-level patients? Are we talking about higher-level patients in these studies? All of the above. You had a pretty wide spectrum across. The early work was really done under a pilot grant as well. We took really all comers, anyone that had a stroke and had some degree of their strength affected or their use of their hand affected. In that slide I showed you with the motor outcomes, there were a number of people that had a maximum ARAT. They weren't included. We had a large ceiling, but also a large floor. I guess small numbers, so you can't really answer this definitively. I would think that the higher-level patients probably wouldn't get that much out of using brain-machine interface because they could just practice conventional hand training. I'm thinking lower-level patients might be more appropriate. I don't know if you saw any trend in that direction. We would love to see actually mid-level patients. Those are the patients that seem to have the most improvement. It might be that they just have the most room to improve as well. I do think that it's really interesting if you recall the stroke impact scale that some patients actually felt like they did worse. I wonder that a little bit about brain-computer interface too because we're asking someone to do something. I've tried this machine. I think you saw the picture where I had it on. There's definitely a learning curve to a normal brain as well. I wonder if some of it is someone seeing, I'm supposed to be moving this ball to the right, and my hand is not moving, and just that frustration of, yes, now I'm really appreciating how weak it is. We do have small numbers. As you saw, it's a really long intervention phase with multiple functional MRIs and multiple times with the computer. We're still collecting people and data and looking at them in all different ways. We look forward to seeing more results of this. Great. Thank you very much, Kristen. That was a great talk, a great introduction. We're going to continue on this topic of brain-machine interface. Our next speaker is Dr. Marcia Bachreiter from Ohio State University, where she is an assistant professor in the Department of Physical Medicine Rehabilitation. I'll let you take it from there, Marcia. Thanks. All right. Give me just a second. I want to change my pointer to the laser because I'll be pointing at things here. Everyone, can you hear me all right? Yes? Yes, we can. We see your slides. All right. I am going to give a brief history of some of the proof-of-concept cases where people with either ALS or locked-in syndrome or cervical spinal cord injury are using the different versions of brain-computer interfaces to do functional things. Then talk a little bit about what is the future of people with these injuries using this in their daily life. In my clinical work, I am board certified in brain injury medicine. I sometimes also cover the spinal cord injury medicine service. However, I actually am lucky enough to be 100% funded for research at the moment. I have several of my funding sources up here. I also want to point out that I will be talking about products that are investigational and that no product endorsements are implied. Briefly, my objectives. Thank you, Kristen, for going over the background of BCI. I'm going to assume that we've talked about the concept of BCI and the magic of the translation process that the computer does when a user is thinking about whatever they're thinking about that gets translated into the output. I'm going to talk a little bit about technological tradeoffs of wearables versus implantables. Again, give you some examples of how BCIs are used for things like controlling a cursor or a robotic limb or a person's own paralyzed limb, a vehicle, and then into what is cutting edge, restoring sensation, and also this idea of the closed loop feedback with sensory information. And then we'll talk about the future. First of all, as we discussed earlier, there are a number of different ways to actually record the neural signal from the EEG setup to something that's actually implanted in a person's cortex. All the people that I will show you here have given permission for you to see their faces, and they're all people who were involved in proof of concept studies. This person is a person who participated in my lab for five years in an intracortical brain-computer interface study. This is the implant that he has, it's called a Utah array, and it's implanted in his left motor cortex in his hand area. This is the piece that sticks out of his skull that connects up to the computer system. And like the previous study, we're giving him FES, and the goal here is he thinks about a movement, it gets translated through the computer, and then that movement is produced through neuromuscular stimulation of his forearm. So on the level of the neural recording, you can do this either very invasively with a cortical implant like we have here, or something that is less invasive like the EEG system, and there are pros and cons to this. So what's practical depends on what setting you're thinking about using this. If you're thinking about using such a system in daily life, and you have a spinal cord injury, it may not be possible to set something like this up on. And that is one of the reasons why people would consider something like surgery to do a permanent implant, to increase their independence and be able to use a system like this for more independent living as opposed to short-term in therapy. Obviously, there are drawbacks to having something implanted. If there's a component failure, you need surgery again. If there's an upgrade, you would need surgery again. And our participant has also found that some people refer to him unkindly as a cyborg, which is a little odd, but he also has told us that really using the system over the course of five to six years, he's really integrated it with his sense of self. So there may be some truth to that. The opposite end of the spectrum is something that's wearable, more like clothing. And then practical constraints, like how do you protect against the shock hazard for something that's implanted versus wearable? And where do you put the power supply? And how big is the power supply? Similar concepts also hold true for the output options. So using the case just of neuromuscular stimulation, there is a version called the nutwork neuroprosthesis that is fully implanted, meaning that someone would actually, who has, for example, cervical spinal cord injury, have the nerve cuff electrodes or electrodes that stimulate muscles implanted directly into their body at different regions that they were hoping to control through the BCI. This system also allows control of diaphragm muscles and potentially also bowel and bladder. So this is really the hope for the future, really, in terms of a system that gets around a broken spinal cord or potentially a pontine stroke. Intermediate is this sort of thing, which is a system that requires an engineer to set up. And each of those circles is an electrode that can activate the muscles under the surface of the skin. And the other extreme is something like this, which is really more like clothing and a wearable device that maybe you wouldn't need an engineer there along with you to use it. So examples of BCI goals, definitely controlling a cursor, a vehicle or the arm. And there have been some groups, these groups are in Brazil and Peru, respectively, who've shown that you can use the EEG type system to do the equivalent of pointing and clicking, which as you've seen, can be used to spell words for communication. It can also be used to replace some of the switches that are on wheelchairs so that a power wheelchair can be translated into something that is a brain controlled device. But with the EEG system, there are some limitations. And so typically, the response time is a little bit slow. So you wouldn't want to be going very fast as an example. And some of these groups have also integrated things like robotic arms. So this arm is programmed so that it has some semi-autonomous features. The person basically actuates it with their EEG cap, and then the arm does its thing to reach out and grab, let's say, a glass of water to bring it back to the person who might be thirsty for a drink. The other way that this type of system could be used is to interface with environmental controls, or more colloquially, a smart home. So turn on or off lights or furnace or things like this. Another thing that's been done with the, and this is out of Europe, so Germany and Austria, there is a group there that got funding from the EU to make something that they call the Think2Grasp, EEG BCI orthosis with FES. And that morphed into this system, which is called the MoreGrasp. And the idea here with this system is they designed it so that the EEG system acts as a switch. They're looking at basically the idea that with the EEG, you can distinguish between moving your right arm, your left arm, or your feet, and that allows you to choose between a few different options. That allows you to say, I want to control my elbow joint versus my grasp. And in this case, they also used a shoulder sensor as an analog control to say how much they wanted to stimulate the FES. So this was the early version. And now they have done some work with the EEG to be able to distinguish specifically forearm rotation, pronation, supination, two different types of grasp versus a hand open versus no activity at all. And you can see this is the sleeve that has some large pad electrodes over the larger muscle groups to get some of the arm movements for pronation and supination. And then some smaller electrodes up here that allow things like finger movements. So this has been tested with a handful of patients with spinal cord injury. Some of the things that are important to note is that with people with spinal cord injury, it turns out not every healthy person can use an EEG system in order to actuate anything. And the accuracy with people with spinal cord injury is even lower. So if you were thinking, for example, of someone with FES, what are your other options if you, let's say, didn't want to put an EEG cap on every day? Well, one option is something that's called an ECOG array that sits on top of the cortex. And this woman has her ECOG array sitting over her sensory motor area, and it picks up her thought of moving her right arm. And when she moves her right arm, she's done some training with some of these games so that moving the right arm generates a response that is similar to a click with a mouse. And doing that sort of training allowed her to use a spelling system similar to what's used with the EEG. And as a result, using the system, she was able to actuate the sequence of letters that communicated to her research group, we'll get there. That's the first thing that she said. So this is available in the Netherlands, it's not available in the US. The cool thing about the system is it's wireless, it's fully implanted, it works 24-7. The tablet itself scrolls through the selections, and the user just basically clicks on what they want. So what else is out there? There are some intracortical implants that are in the motor cortex. And this is again, the Utah array that I showed you a picture of earlier. And this person has two or had two implants in her motor cortex hooked up to a computer system that interpreted her brain activity when she was thinking about moving her hands. And that was translated into actual movements of this robotic arm. And over time, she initially used a virtual reality setup to learn to move this robotic arm. But then over time, she was able to actually move the real life robotic arm. So pretty cool. And again, this is a person with tetraparesis. And she's just thinking about doing the movement she actually wants to make. And that's effective. So this is a person in my research lab, he has one array and his motor cortex on the left side. And using this array, he was able to think about making different hand grips. And after practicing for about a year, was able to use these hand grips, switch between them, and then on cue, choose the grip that was appropriate to whatever he was trying to do in that particular situation. So there is a test called the grasp and release test. It's got six objects. And what you're seeing here is the training for the cam object. So he sees on the left hand side there, a hand do an action that he has to repeat. Once he's done that training, he actually can use that programming of the computer to replace the trained object with another object. So this is an example of him using a peg training profile to manipulate a toothbrush. This is the so called fork object in this task. And what he's learning to do is basically squeeze with his hand and then press down with his shoulder and he has active shoulder and elbow flexion. But using this you can see he can he can grip a fork and actually bring food to his mouth. Now on the left side, he can't grip without using the FES system. And you can see the ease with which he can grasp and release this fork with the FES system. So the next thing that we asked was, all right, if we can train movements like opening the hand and closing the hand and pronating and supinating, can we use those movements to control other things? And it turns out that we were able to get our participants to successfully navigate a it's a driving simulator system, it's called Carla. And also you'll see at the bottom right of the screen use those same signals to control a vehicle, a remote control vehicle in real time. So this is ongoing research that's happening now in my lab. And I'm going to move on to tell you about some other labs that are doing work. So this is out of case Western, this is BrainGate2. This is a gentleman who has had two motor cortex implants. And here you can see him training to move his arm so that his elbow is in the position that that he wants it in and to open and close his hand. The top line is real time of the brain activity and then the lines below it were activations of the FES stimulation. So he had surgery to implant all of those FES electrodes in his arm, as well as surgery to implant the recording electrodes in his brain. In addition, he's got a mobile arm support that's powered, because he is not able to lift his shoulder. And what you'll see for many of these patients when asked what they'd like to be able to do with their arms, a lot of times it's ADLs, like feeding themselves, eating, drinking, grooming. So this is a wired fully implantable system. And this is the system upon which the the network neuroprosthesis is based basically, it's part of the network neuroprosthesis. So moving on to another lab, this is Pitt UPMC. And the innovation that this lab did was actually not just to implant and motor cortex, but also to have some electrodes over the metasensory area that stimulates the brain. And what you're seeing is their participant is getting brain stimulation that corresponds to the area on the robotic limb that is actuated. And that's mapped to the corresponding fields in the brain that evokes a percept in that person's hands. And so he is able to report what movement is happening in the in the robotic limb, because the feedback is going through the computer to some electrodes that are stimulating over a sensory cortex. We have about a minute left. Okay, thanks. When you close the loop in this fashion, what you find is that people are much more skilled at grabbing and transferring objects. And then I'll stop here. The other thing that we found in our lab was that if you pull the signals off of motor cortex, what you can do is actually separate some of the sensory signals that our participant couldn't consciously feel from the motor signals that are happening there and provide feedback to him. So this is subconscious level perceptions that are that are showing up in motor cortex that we're able then to use to give him feedback with stimulation in his arm that he can sense. And that gave him an increased sense of being in control of grasping. And it also gave us a way to automatically modulate the grip strength, which made him faster at transferring objects. So I'll stop there. Great. Thanks, Marcia. Unfortunately, I don't think we have any time for questions. I don't see any in the chat. I will I'm going to share this this slide that Dr. Ripley had up earlier for voting, just so if you didn't catch the If you didn't catch it, you can you can use the scanner there to get the survey. And Richard, the link has also been published on FizzForum. So it's available outside the meeting and will be published several times this week as the meeting progresses. So This is my only time to vote. Thanks. And I want to thank all the presenters today. This is a really interesting and educational session. I'm going to put a plug in to the members. If you have any other ideas for our talk next year, please get back to us. We probably will publish another survey later asking soliciting ideas for next year's educational session. And again, thanks to all of the presenters. Great job. And I hope you guys enjoy the rest of the Academy meeting. Thank you. Thank you. Bye, everybody. Bye.

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