Good morning everybody, welcome, Sadre, I'm Alexios Karanopoulos, I'm the chair of the Evidence Committee at the Academy, and I just want to thank all of you for coming, and also thank all of you who are contributing scholastically to the Academy. We're very pleased this year to get over 1,100 abstracts, and we're very intentionally trying to grow the scientific component of these abstracts to really elevate the level of scholarly activity research in the Academy. You'll see that there are not a lot of case reports that are being presented, they're being presented in a different venue, and again, that's very intentional, not that we don't respect or welcome case reports, but we really want people to look more into the science to advance what we do collectively. So that being said, we're going to go in the order of the app, there's been some changes with some ongoing flex in the schedule, so if you have the app open, you'll be able to see the order you're in. I know there's already at least one group who doesn't have representation, they had to leave, so we will have approximately five to seven minutes per session or per abstract, including discussion, but if we go over under, there's nobody else in this room after, so if you want to stay and talk, be our guest. Okay, so I'm going to welcome Carmen Sertia, is that how you pronounce it? Dr. Carmen Sertia from the University of Missouri Columbia PM&R Program, welcome. So the clicker is here, and there's a pointer too. Okay, I'm honored to be here, good morning, and thank you for coming at this time. So I will talk today about motor recovery and brain excitation inhibition balance in stroke. So I have to point there, yeah? So as you may, stroke is the leading cause of long term disability in US, but also worldwide, and more than 50 patients, 50% of patients, suffer from some motor impairment leading to disability and long term. So a lot of efforts have been made to maximize motor recovery after stroke, unfortunately there are no effective interventions that could foster recovery and complement current rehabilitation or medical, or any medical therapy for stroke motor recovery. Okay, thank you. So do you know why? One major case of that is possibly that we still have a lack of understanding of neural substrates of motor recovery in humans. In animal models, however, there are robust biological events that strongly support motor recovery. One of that is intra-hemispheric and inter-hemispheric excitation inhibition imbalance. I will start with the, oop, the pointer, oop, how can I do this? Ah, point to you? No, because I want to do the, to use the pointer. It's the top button on the, just maybe go up more towards the screen. This screen? Oh, this screen, not that screen. Okay. So on the right side of this graph, you will see an intra-hemispheric imbalance. What happened? In the injured hemisphere, we have an increase in GABAergic tonic inhibition and we have a decrease in glutamatergic excitation. So it's a hypoexcitation in the injured hemisphere. This hypoexcitation in the injured hemisphere will do, will lead to an increase in excitation in the uninjured hemisphere. The recovery of inter-hemispheric balance and intra-hemispheric balance, it parallels the recovery of motor impairment in animal models. So it's important to, it's important to better understand these, the role of imbalance in stroke recovery in humans because it could be a key to optimize clinical care. So my goal is to investigate the nature, evolution, and functional significance of excitation inhibition imbalance within motor cortices after a subcortical stroke. I'm using magnetic resonance spectroscopy because this method allows analogies between humans and animal models of stroke. So what I'm measuring with this is the GABA, major inhibitor in neurotransmitter GABA, that it's a marker of tonic GABAergic inhibition, and the glutamate, that it's a marker of excitation. I put also, okay, it works. I put also here, okay, so the metabolic process releases on glutamate, glutamate, glutamine, and GABA reuptake in glutamatergic and GABAergic neurons and astrocyte. So as you may see, it's a very complex process. However, we have histological and also electrophysiological support of the GABA measure by MR spectroscopy that it's indeed a marker of tonic GABAergic inhibition. However, glutamate here is presented as GLX, that it's a complex between glutamate and glutamine. And it's still debated if the changes in glutamate is reflecting in the cortical excitability. So we measure these in the two major motor areas, primary motor cortex, M1, and premotor cortex, PM, that there are two major motor areas that control, and they have important role in motor control and also in motor recovery, and also they are very well-designed therapeutic targets for non-invasive brain stimulation. So here, I'm sorry for that. It's a graph that show actually is the spectrum that show the, sorry, show GABA and glutamate, and if you, EGLX actually, and if you want any detail how we measure this neurotransmitter, please ask me after. So, as I said, it's a subcortical stroke. Why? Because I want to measure in the cortical areas where it's normal appearing brain tissue and they are not injured by any type. So we have three groups. Twelve subacute stroke, we have 26 chronic stroke, and we have 25 healthy controls that they are age, sex, and cardiovascular, and even medication, antihypertensive medication match it. The patients, in general, they are moderate impaired patients. So our results are, so I'm presenting these graphs. We have M1, it's green color. PM, it's yellow color. In the top of the, oops, sorry. Okay. In the top of the graph, you have injured hemisphere. In the bottom of each graph, you'll have uninjured hemisphere. We have subacute stroke, and we have GLX. I'll present GLX and GABA changes in this group, and we have chronic stroke. I'll present only GLX because GABA, I just developed the sequences to reliable measure GABA in human brain. So what happened in the injured hemisphere, in both region of interest, we have a significant increase in GLX, a significant increase in GABA. However, in uninjured hemisphere, we have a trend to increase GLX. Actually, it's not a trend because it's not significant, but we have a significant also increase in GABA. What happened in chronic? Some patient from the subacute group, also they were evaluated in chronic later on. So we have a decrease, it's still GLX decrease, but I see compared to the subacute stroke, you will see that it's tend to normalize. And we have in the unaffected, uninjured hemisphere, we have a trend to increase the excitability, the excitation of this hemisphere. So why is this important? So as we come back to my first slide, you can see that in the injured hemisphere, we have this balance that I already presented, the intra-hemispheric imbalance. So we have low excitability and increased inhibition, so hypo-excitation in this area, in this hemisphere. However, we didn't find in the subacute stroke patients, several days after stroke, we didn't find increase in excitability. Actually, we have increase in GABA, that we have increase in tonic-gabaergic inhibition. So both hemispheres, several days after stroke, they seem to be suppressed. Why it's important? Because the therapeutic targets in the subacute phase of stroke could be changed in the chronic phase of stroke. If I'm coming back here, you see that in the chronic phase, you have an increase in excitability in the uninjured hemisphere. So what we found also, and it's important, but again, these are preliminary data only in 12 subacute stroke patients. So we found a sex effect on GABA concentration in the premotor area. In both hemispheres, right and left hemisphere, we have a significant increase in GABA compared in male versus female. Again, please take this with caution, because there are only 12 patients. So this is an ongoing study. What do you want to see? It's all the evaluation in the subacute group. It was done, were done at the admission in the inpatient rehabilitation. So we want actually to, we have a longitudinal study, so we want to decipher the function and implication of these measurements, and to inform about the rehabilitation outcomes and discharge planning. This is based on our studies in chronic stroke that we demonstrated that MR spectroscopy could capture information about individual cortical reserve to project the probability of outcome to a therapy. And such models will enable clinicians to optimize rehabilitation, improve stroke care quality, better allocate the rehabilitation resources, and eventually help patient to manage expectation. I want to acknowledge all my funding, and thank you very much. Sorry, I think I'm late. Okay. We'll take the questions now or at the end? Does anybody have any questions? Okay. Thank you. Okay, thank you. Okay, so we're going to welcome Dr. Preetha Dalal, who is here from UCSD, came long and far. She's going to discuss longitudinal assessment of an interdisciplinary inpatient treatment program for pediatric chronic pain management. Welcome. Thank you. Mine is a lot more rehab-based and a lot less scientific, so. We have a chronic pain program, and we wanted to actually publish our data about our outcomes to kind of make sure that what we're doing was helping patients as well. So, in pediatric patients, about 30% of patients have some type of chronic pain at some point in their lives. We define it as symptoms that last for three months or longer. We do differentiate sometimes those acute CRPS as also chronic pain, so those don't kind of fit the criteria of the three months or longer, but we also recognize that that can lead to pretty significant functional disability. There are multiple different treatment models, many different institutions that do different pain programs, whether they're inpatient or outpatient, and so we wanted to look at the data of our program to see if our interventions were actually helping. So, we collected data from 77 patients, basically all of our patients that have been enrolled in our program. Our program started in 2019. And they were treating in our inpatient interdisciplinary team program. Just to kind of give you some information, so these patients are patients that kind of meet criteria to be inpatient, so in the pediatric world, they're not able to do their regular ADLs or their regular IADLs going to school, doing their ADLs, or needing some type of assistive device for their chronic pain. So, those are kind of our criteria for admission. Typically, our program's about four weeks. Some patients end up staying for five to six weeks, depending on their improvement. And we do physical therapy, occupational therapy. Actually, I'm going to skip to the next slide and come back. So, this is kind of our sample schedule of what the patients go through. They typically have about four to five hours of PT and OT a day. So, this is a little bit more intensive than your regular inpatient rehab model. We basically schedule them from 7 a.m. to about 5 p.m. plus an activity in the afternoon to really replicate what you would be doing if you were going to school. And so, they do have some fun things intermixed, and they also have psychology intermixed. So, they typically get about three sessions of psychology a week. Not on this schedule, because pediatrics, we always have to talk about the parents. There's also a parent group every week on Mondays, and then we also have a family meeting to just update the families, because families are not allowed to be here during the program during the day. I'll go back to kind of our methods. So, our psychologist is really working on going over pain education with the patient, and this is individualized. So, based on the patient's education ability and also their time to process and understand more about chronic pain. And then our outcomes measures, we looked at the pain scale, but we always tell patients that come into our program that we actually focus more on function rather than decreasing your pain numbers, but we know, since it's a pain program, we should at least look at what the pain numbers are. We do not ask about pain scale except for admission and discharge and then follow-up visits. I do not ask every day when I see these patients about their pain levels. We talk about easy, medium, hard instead of their numbers. So, this is very much pediatric focus. So, some of the questions on there is being able to stay at school, being able to get on the bus, being able to do your homework, things like that that are really related to functioning for pediatrics. And we collect this information on admission, discharge, three months, six months, nine months, and 12 months. And then I already went over this. So, then our results. So, our pain scores actually did decrease. And this is kind of typical for our anecdotal information. So, they were lower on discharge. They were even lower on the three months. And then if you look at the six and the nine and the 12 months, sometimes things start creeping up as they've been out of our program. They also go back to their lives and there's oftentimes some dysfunction at home or within their lives that sometimes kind of change things. At 12 months, our P-values started creeping back up. So, we've been kind of intervening with the families and kind of talking about what's going on and having a little bit more not just like getting the data for intervention, having more conversations with the family at the 12-month mark to figure out kind of what the things that need to be done to kind of get back to that lower pain level. This is the Functional Disability Index. And these continued to stay significant even at the 12-month mark. So, even if pain levels did go up a little bit during the 12-month mark, their function was still significantly improved. And that means basically that low that they were going to school, they were functioning and they were kind of doing their normal ADLs. So, conclusion. Our treatment at this program does improve pain scores and function and they do persist for about a year. Any questions? Go there. No worries. Okay, well thank you. Go ahead, please. Hi, thank you Dr. Dalal for that presentation. Any information on pain medication usage from beginning to... Very good question. So, we do not add any pain medications during our program. The data is a little bit I don't have it presented here. So, we basically start with, so whenever a patient is admitted to our program, we actually ask them to wean off any opioids. And it's very rare that pediatric patients are on opioids at this point. But we ask them to wean off opioids and then during our program we discuss with the family and the patient about if there are medications that they want to trial to wean off during our program. So, typically we do not add medications. The only thing that as you guys realize that there's a psychological component so if we start noticing that there's a lot of anxiety that's limiting their function or slowing down their progress we will ask our psychiatry team to come and make recommendations. So, that may be the only additional medication that we add on is possibly a medication for anxiety or depression during our program. I don't have the data of exactly how many patients we've been able to wean off of. Usually our more severe patients we're just trying to get them to function again and then we talk about a plan of weaning off of some of the medications as an outpatient as well. Hi. Thank you, Dr. Dalal, for that great presentation. I have just a couple questions, being interested in lifestyle medicine, Dr. Beth Brady's. Do you work on sleep and sleep hygiene is one, and then the second question is just, I saw yoga up there as a way to help them manage stress, also stretch. Do you work on any deep breathing techniques with these young ones? Yeah. Deep breathing is integrated into every single therapy because I can't tell you how many of our patients come in and say, I thought I was breathing, and the PT will be like, they're holding their breath during the entire time they're doing things. And one of our patients kind of had like a slipping rib syndrome, and after they started breathing normally and the way they're supposed to breathe, they were perfectly fine, like within a week. So yes, we do a lot of deep breathing. I apologize. What was the first? Sleep, yes. So our psychologist does biofeedback and then also talks to the patients about sleep. Typically, most of our patients are on some type of sleep medication. It is a hospital-ish setting, so we're in a subacute or a skilled nursing facility, so sometimes sleep's a little bit off because there's other patients that are a little bit louder. It's a pediatric setting. So we don't always wean sleep medications, but we work a lot on sleep hygiene. We do the pain education first, and then we integrate the sleep hygiene within there. We take away phones at nine o'clock, so they cannot be on a screen at nighttime. So we already start with that, but then we also talk about breathing techniques, relaxation techniques, mindfulness, meditation. If they need to use their app, we try to kind of use a different device to try to use an app to try to help with meditation before they go to bed. I had a couple questions. So this is a very, kudos to you for, it's a difficult population. I'm just wondering, in this four-week intensive program, how do you integrate their schoolwork? Yeah, that's a really good question. So I think, oh, it's gone. We usually have, so in most school systems, home hospital is one hour of school per day, so we already have their school scheduled for one hour a day. We recognize that that's not a full school day, but we also recognize they're not functioning, so we're taking some time away from school to actually get them functioning and hopefully get back to school. It depends on their, what's going on. So some of our patients, because they have such severe back pain or whatever their pain issue is and what they're having, what's limiting them from going to school, we will emulate that. So we'll have them sit at a desk. Especially, we do this usually around week three or week four to kind of practice for integrating back into their lives. So we'll do that. We'll also kind of, sometimes, if they have more cognitive difficulties, like one of our patients had functional neurologic disorder and couldn't read. So we did a lot of reading. During all of our therapies, we would have a game that they had to do more of that active reading during their therapy. So they'd be doing therapies, but then they'd also be doing cognitive work. So we'd be kind of integrating both of them. So it's individualized. Very individualized. Every single patient. We know that they have their therapies, but what we're doing is pretty individualized. They do have these, so this is based on the program through Dr. Sherry at CHOP. And so they do these animal walks as their timed activities and some functional tasks, which is like lifting a laundry basket that has a five pound weight in it. So those are all the generalized activities that we have all the patients do, depending on their functional ability. Excellent. My follow-up question. Given sort of the drop-off that you saw in some of the success at a year, is there any component of family education or integration during the program so they don't? Yeah, so we do have family group. The family has to, one member of the family or one parent has to attend parent group meetings every Monday. And so those are a group meeting so that the families can talk to each other, parents can talk to each other. And that's weekly. We also have a family check-in at the end of the week. And then we also have the family come in and watch therapies during that time. But we also recognize that a lot of the reason why patients have chronic pain is sometimes the family dysfunction. And so in the beginning, everyone's kind of like working on doing the things that everyone learned. And then 12 months out, sometimes some of that education needs to be re-gone over again of like, hey, are we still working on these things? Because then we oftentimes like recommend family therapy, things like that. Those interventions trickle off a year later. Understandably. Any other questions? Well, thank you very much. Thank you. Okay, we're gonna welcome Dr. James Eckner from University of Michigan. He's gonna discuss the influence of concussion and collision sport history of later self-reported cognitive and mood outcomes. Results from the Michigan Alumni Brain Health Study. Thank you. Thank you for the introduction. Sorry, that's kind of a long title. Yeah, J.T. Eckner. I go by J.T., University of Michigan. And I'm gonna present preliminary results from our, what we're calling the U of M Alumni Brain Health Study. Funding is not relevant to this. Those disclosures are not relevant, but I do want to acknowledge my collaborators on this project. No research could be done alone. Also want to acknowledge a couple of our advisory board members at the Concussion Center who helped spread the word about this survey and helped us out a lot with our recruitment. So quick background. I think we're all aware that long-term effects on brain health relating to sport participations, particularly for contact sports, as well as concussions, is a big topic. Important in the world of sports medicine and important in society at large. And I would argue that we can say for sure right now, based on the science, that the risk of long-term adverse effects to brain health is somewhere between zero and 100%. And I say that only partly to be a smartass. If you look at the research like the papers on the right here, that's where I get the 0% from. Those are three examples of studies that were done in older individuals who played contact sports when they were younger. And across a number of neurological outcomes, those who played football had basically no increased risk of any of the neurological outcomes studied compared to controls. The 100 comes from studies like the one on the right, I'm sorry, on the left, which got a lot of press when it came out several years ago. That's a study in ex-NFL players who post-mortem donated brains to science, had neuropathological evaluation, and I believe it was 109 out of the 110 had chronic traumatic encephalopathy. So we still don't know. So that brings us to our study. This is a survey. It was based on Qualtrics platform, 25 minutes to complete. To be eligible for this survey, you had to have attended the U of M at some point before 2012. The main reason for that timing is just to avoid overlap with other studies we're doing. We collect a lot of information, but our primary independent variables were the self-reported number of concussions the individual had sustained, as well as self-reported cumulative seasons of collision support participation. Our main outcomes were, for the purposes of this presentation, were divided into cognitive outcomes and mood outcomes. In both categories, essentially one of the outcomes was just a self-reported history of any diagnosis that falls under the cognitive or mood umbrella. You can see some examples on the list there. We also did a PROMIS cognitive outcome measure, as well as a cognitive change index, which is questioned in terms of compared to how you were doing in the past, how are you doing now, with a bunch of cognitive measures. Mood-wise, we also did another PROMIS measure, and we also did the PHQ-8. There's a typo in my analysis line there. We did logistic regression for our binary outcomes, and linear regression for our continuous outcomes. We got a good response to this. We had almost 1,800 responses. After we weeded out those who managed to finish the 25-minute survey in under two minutes, as well as those who did less than half the survey, we still had over 1,000 respondents. We had a pretty good mix based on age, as well as based on sex. Our population was skewed towards being white. It was also skewed towards having a higher income bracket, which I guess, when thinking about the time frame and attending University of Michigan, that kind of makes sense. In terms of sport participation, we had a pretty good mix. 43% did not participate in a sport in college. 34 participated in sports that were classified as non-collision, and 23% participated in collision sports. The four most common sports that were played in college are listed there, football, basketball, volleyball, and soccer. In terms of the concussion history, about 58% reported no prior concussions, and then those reporting one, two, and three or more, you can see the number is 14, 13, and 15%. One thing I'll note is, more than we expected, there was a relatively strong relationship between the amount of collision sport you had played and the number of concussions reported, which did make it a little bit hard to weed out what effects were associated with concussion versus with exposure to the sport. So here's our primary results table. On the left, we've got our cognitive outcomes. On the right, we've got our mood outcomes. If you look at those cognitive diagnoses, there was no statistically significant relationship with concussion or with collision sport. When you look at the PROMIS cognitive T-score, though, there was a statistically significant but small magnitude effect where more exposure to collision sport was associated with lower scores on the PROMIS cognitive outcome measure. No relationship for the cognitive change index. When you look at the mood measures, whether you're looking at the self-reported history of a diagnosis relating to mood, or the PROMIS, or the PHQ, in all three cases, there was a statistically significant relationship with the number of concussions reported, in which more concussions was worse. So to our knowledge, this is the largest population-based study looking at males and females, people who participated in sports at college. I'm not gonna say this is the be-all, end-all study, but our results suggest that collision sport participation, i.e. non-concussion-causing repetitive head impacts may be more associated with the cognitive outcomes, whereas concussions, i.e. discrete injuries, may be more associated with the mood outcomes. Again, the magnitudes were all very small, not really reaching what we would consider clinically significant thresholds. Small effects, but they're there. As far as limitations, this was a survey, so it's subject to all limitations of any survey. There could be potentially inaccurate self-responses. All the biases that come with surveys. Next steps, we're writing this up. We're looking for collaborators, and we've actually been working with the University of Florida a little bit, trying to engage another site. We are currently recruiting individuals for a second phase of this study, where we're bringing them into campus and doing some actual cognitive testing, as well as some neuroimaging. Our long-term goal is to get some funding and do a more definitive, well-powered population-based study, where we can do objective measurements and hopefully get a better answer to these questions, which we think are important. That's what I got. Thank you. Any questions from the audience? I had a question, and it may be just pertinent to surveys. So you excluded, it was the under 50%, and you completed the test in two minutes. Yeah. Maybe you just kind of flew through it and didn't care? Exactly, just next, next, next, next. What was the 50%, under 50%? If they didn't complete at least 50% of the survey. Oh, I see, okay. Yeah, so at least half of it was empty. Okay. Thank you for the presentation. So I had a quick question, and this is more for clarity. About 50% of your sample said no history of concussion. Correct. So was having a concussion not part of the inclusion criteria? No, the inclusion criteria were just having attended University of Michigan. So we weren't specifically looking for individuals that had a concussion history. We were looking for a broader population. So do you think your results could have been affected by the number of participants reporting a concussion versus those not reporting? Or did you control for that as well? History of concussion? History of concussion was one of the primary independent variables in the study. And all of the analyses accounted for a bunch of other covariates, which I kind of blew past, but they were listed on one of the slides. So exercise, sleep, other comorbidities. Got it. Am I getting your question? Yeah, I was just trying to understand, given that part of the sample had not had a concussion, and you're looking at the association between having a concussion and outcomes of mood and cognition. So I was wondering if that had any impact on the outcomes. Yeah, so the variable is coded as no one, two, or three or more concussions. And that was how we analyzed that variable. Thank you. You're welcome. Thank you for this really important work as a mom of a boy who plays ice hockey in college and has had concussions. It really hits home. So one thing is, knowing these boys, some of them don't admit to it. And I'm wondering if, in the future, we need to look at medical records to see who was treated for a concussion and look at the severity of those concussions based on their treatment. Just a thought. Yeah. So you're hitting on a really excellent point, which I didn't address in the six-minute talk, but concussion history is very difficult to obtain. One, we know that a lot of concussions don't get recognized. So even if you had medical records, you're not going to catch them all. I didn't go into this detail, but the way we asked the question, it's taken from another study. One question, we combined two questions. So one was, have you ever had a concussion diagnosed by a medical professional? And then the other one was, here is a definition of concussion. Have you ever had this, but it was not diagnosed by a medical professional? And then we combined the two. What was the time period? I think I missed this. Or what years were the athletes that you collected this? They were a large age range and they had to have attended U of M no more recently than 2012. Okay. And then did you factor in COVID infections? Because knowing that now even those, even people who have COVID infections can have cognitive effects, even if they don't have long COVID. Yeah. So we did ask about COVID, but, and I forget why, we did not include COVID as one of the covariates in this particular analysis. Something that- There was a reason and I don't recall what it was. Okay. Well, thank you very much. Thank you. Okay. We're gonna welcome Abigail Joy Garcia from University of the Incarnate Word School of Osteopathic Medicine to present on long COVID treatment programs for or at top rehab hospitals of cross-sectional analysis. Thank you. Hi, yes, I'm Abby. Thank you all for coming to my presentation on long COVID treatment programs at the top rehabilitation hospitals. I have no financial disclosures because all of my money is borrowed student loans. So with that, we'll get started. All right. So I know I don't have to describe the impact of COVID-19 as I'm sure we all remember the impact and the devastation around the country that was happening at that time, as well as our own personal experiences. I've included two news clippings from that time. The first one's from Staten Island, as we remember, that was the center of the pandemic, at least in our country. And the bottom one is actually from my local newspaper because during that time, me and my dad actually led a team of people to produce over 2,000 face shields and over 5,000 face masks to help in the PPE shortage. So the COVID-19 pandemic really defined my generation, especially of healthcare providers. So not only in this project that me and my dad did, he's sitting right over there, by the way, I started online. I started medical school online and now we're kind of dealing with the aftermath. We're dealing with long COVID. So long COVID can present in a variety of ways, a variety of severities, and it can present with the symptoms you see here on the screen, dyspnea, fatigue, headache, neurocognitive changes. And it can typically last at least three months after testing positive initially for the virus. So the goal of this project was really seeing what resources are available for patients. Patients are now having new disabilities from this condition. So enter us, enter PM&R. So with the project, we wanted to know, based on the list of the top 25 rehabilitation hospitals per the US News and World Report, what long COVID care is available. So here I've given you the list of the 25 facilities, not necessarily in any order. What we did was we looked on their website to see what's available. And from that, we're kind of seeing what the patients are seeing. And from that, we found that only 12 have a dedicated long COVID rehab program. From that on their website, they have a dedicated page. This is our long COVID clinic. These are the members of our team and the services available. Seven of them did address long COVID, but they integrated into a program that addresses chronic conditions such as COPD, chronic heart failure, and et cetera. There were some others here that had, like this one had a post-COVID inpatient rehab hospital, but it was immediately after hospitalization. It didn't really address the three months out or longer long COVID symptoms. Two of them had this short blurb of, yes, we address long COVID in our primary care clinic, but that was it. It didn't really list too much of a rehab type of program. So I kind of grouped them there. And then four of them didn't mention long COVID on their website. So from this, we wanted to see what goals are being addressed in each of these programs. So we looked at what specialties are leading each program. So here I'm showing you the 12 dedicated programs. Four and a half of them were led by a physiatrist. And I gave it a half because one of them is co-led with pulmonology. Same four of these that are listed as primary care, one of them is co-led with endocrinology. The one that was unclear said that they had a mix of clinical rehabilitation specialists, such as PTOT speech and pain rehab specialists. So a little unclear but still present. These are the integrated programs. So these were the seven. One of them was led by a physiatrist but for the most part it was a combination of PTOT and speech. So big picture out of the top 25 top rehab hospitals only five and a half are actually led by a physiatrist. I know what you're thinking that's that's not great but from this we wanted to know how many of them at least have a physiatrist available even if on the website they're maybe not the lead of the program. So on this graph I'm showing you the different specialties that are available along the bottom. Up on the vertical axis we see the number of programs and then the blue programs are the dedicated ones and the green bars represent the integrated programs. So from this only 11 had a long COVID program with a physiatrist at least available through referral through the same system. You can see kind of going from left to right the most common specialties that were available physiatry, pulmonology, cardiology, etc. And this is through the long COVID program. So from this we're thinking that they're working as a team, they're collaborating in this patient's care, not necessarily just referral away and then not communicating between the physicians. So other than physician specialties we wanted to know what therapies are available since oh excuse me before I go on to that. These specialties that I listed here each of them was available at one dedicated program not necessarily the same program but just to give you a full picture of other specialties that were collaborating in the long COVID care. Okay so now we'll talk about the therapies that were available. This graph is similar to the last one we just changed from physician specialties to therapies. Physical therapy was of course the most common but it still was at 17 out of the 19 programs. So still somewhat a discrepancy there. I did include psychology. That was great actually for me to see that long COVID programs that are there are thinking about psychology of these patients now coming with this new disability and dealing with also the uncertainty of it as not many people know especially patients might not know that long COVID is a possible cause of new disability. And finally we wanted to know how many of these rehab programs are participating in long COVID clinical trials. So we looked on the National Library of Medicine clinical trials gov website to see how many of them are participating and only nine. Most of them are participating in these recover trials that I've listed for you here on the slide. Didn't list all of them but just wanted to give you an idea of the main ones. So in conclusion despite the growing prevalence of long COVID the top rehabilitation hospitals show a real a significant gap in long COVID care. In this the natural idea of using the top 25 hospitals was that if the top 25 hospitals don't have it the hospitals that are lower on the list might not have it either. And this this really limits patients access to long COVID care. Not only this but unfortunately a lot of patients and a lot of health care professionals don't know about long COVID as a thing. Unfortunately it's politicized and there's research out there that has shown that rehab is beneficial for long COVID so that's a gap in knowledge as well. So really hospital systems and policymakers have to invest in these rehabilitation programs and development of these rehabilitation programs. And from that there has to be physiatry led initiatives. We're the experts on rehabilitation so we really need to be part of those discussions, have those seats at the table to develop these programs. And finally because long COVID is still very new further research should be done as far as most efficient and most powerful rehab techniques for these patients to improve their outcomes. Thank you so much. Special thank you to my PI and mentor Dr. Gutierrez and I'll take questions. Thank you very impressive. My first question is you are matching NPMNR. Yes yes that is the goal. Well you know the the Academy is doing a fair amount of work in advocacy in many domains including long COVID. How do you think us as ambassadors of PMNR in the room and yourself going into PMNR how can we advocate for what you've discussed in having research available for COVID patients? Thank you yeah thank you for the great question. I think one thing that would be really powerful for us as an organization to do would be actually to infiltrate more of the medical schools. We don't really get exposure to PMNR as a field until maybe fourth year if you sign up for an elective but then not just for people like me that love PMNR because I I took steps to seek it out but for my classmates that aren't necessarily pursuing PMNR they don't really know the role of a physiatrist and may not know this is something that I can refer a patient to. Rehab is beneficial for long COVID. Rehab is beneficial for a bunch of other things like especially spasticity which I also love but in me going out to rotations and I did I chose to do rotations in a medically underserved area a lot of them didn't know what a physiatrist was so I think that would be important too to just expand education of to other specialties as well and it really starts at the med student level. Other questions, comments, thoughts, wonderings, rude gestures. Well thank you. Thank you. So we're next gonna welcome Dr. David Lee who is from the Fullerton Orthopedic Surgery Medical Center and he's going to be presenting to us on a study that's near and dear to my heart. Restorative neurostimulation providing meaningful and durable outcomes five-year longitudinal data of reactivated clinical B trial. And a full disclosure I was one of the principal investigators of that trial so this is very important. Thanks Dr. Karanopoulos, appreciate that and I actually was gonna do that he beat me to the to the punch but I was gonna first and foremost start off by thanking all the authors. I mean it I would have a slide but it's like a laundry list. This data that we're gonna be presenting today has been published as of this year in Neuromodulation Journal and Dr. Karanopoulos was a big part of that study. Dr. Gilligan was the main PI on the study who has presented this data and I'm just a vessel and certainly humbled to be able to do this. Trying to get this thing to advance here, sorry. Yeah I'm pressing the right arrow. I don't think this thing's working. Oh I am. You want to give it a go? Yeah it's not working. Well while he's well Dr. Karanopoulos is working through IT problems here I just want to quickly ask a question. I asked this yesterday too. Oh awesome. I appreciate that. How many of you are familiar with multifidus dysfunction or multifidus stimulation? Just hands in the crowd. Yeah it's okay. I mean that's why we're presenting it. How many of you guys treat chronic back pain? I mean that's that's an easier low hanging fruit question right? I think that's most of us. So just real quick to kind of get through this slide. I came in to this relatively early on the commercialization of multifidus stimulation and when a personal story is when I came out of training you know I came out of physiatry. This was like over a decade ago now but my biggest thing was like I wanted to bring PM&R and interventional spine or pain closer together you know because traditionally it was all anesthesia you know and that's changed dramatically in fact you know we've we're definitely a larger part of that and even early on my career I was attending a NAS conference. NAS is one of the largest neuromodulation conferences in the world and I asked them you know I was part of one of the committees and I was curious I was like how many physiatrists are here you know and I was it was like 30% physiatry which I was like okay that's great. So when I was approached with this therapy when I found out about this therapy I mean I was super enthusiastic and this was even before I started consulting with them mainly because it was utilizing spinal cord stimulation or neuromodulation I should say to actually rehabilitate the back right do stimulation in a restorative fashion versus traditionally a palliative fashion and you know most majority of the things that we do as pain management specialists beyond physiotherapy it's all palliative right if we're medicating it or for you know injecting it or ablating it this is essentially what we had in our utility belt so it wasn't until recently that the utilized stimulation to then stimulate the multifidus targeting the medial branch nerves and that really quickly we talked about the mechanism of action yesterday but I know that there's unfamiliar faces here so the idea with this is that is bred out of this idea of arthrogenic inhibition. So arthrogenic inhibition has been discussed in the orthopedic world quite commonly so you have an injury you know or you have a surgery to the knee specifically is a lot of the literature and the orthopedic world is is focused on and and then you have guarding right we see this you know in our patients they walk in and this is voluntary guarding they don't want to step on the leg they don't want to flex them the leg and over time what what happens is essentially this you use it or lose it type of scenario so then eventually the body becomes accustomed to not activating those muscles and you lose central nervous system control essentially right there's a signal that the typically is being sent to the spinal cord to the knee to move it right and if you don't use that then eventually you lose that control and that that is what's arthrogenic inhibition so they took this idea early on and they thought well maybe this is what's happening in the back we know that the multifidus muscle is the primary stabilizing muscle we know that it's very difficult to strengthen because it's involuntarily recruited you can send patients for physical therapy for eons and you know unfortunately none of us are batting a thousand right this patients come back and you're like I've done everything that you told me to do but my back still hurts right and then of course we go and we block and ablate and inject cortisone you know and into their backs and even then patients come back and they still have chronic back pain so this is idea what you're going to seeing is an implantation so and it is important that will you understand that because of its restorative nature this isn't something that we just put in and take out so these are for chronic back patient the chronic pain back patients the idea with step putting these leads next to the medial branches which we have historically ablated and then stimulating them with a proprietary waveform it's 20 Hertz 214 microsecond pulse width to essentially mimic natural recruitment of the multifidus and the patient activates this twice a day for 30 minutes at a time it shuts off after it's done and the idea with this is to reinvigorate that central nervous system control right to get that response back to strengthen that muscle see you next like thanks sorry dr. Karen opposite you're more of a part of this presentation than you thought so this is just showing you the actual study trial and this is on five years five years ongoing so in originally 204 participants it was a RCT so they split the group to you know a therapeutic group and a non-therapeutic group and and yes for those asking this question is all there all the patients were implanted right and so the implantable group the therapy group actually got the the treatment that I described earlier and the other one got some sham stimulation which really isn't restorative to be restorative so what they've done is they've extended this data from one year which is what I saw initially when I was introduced to the to the therapy to five years and this is for patient for those of you in the in the crowd who don't are not familiar in the pain world like five-year data in the pain world is almost not non-existent why because if we look far enough and especially in neuromodulation usually that's when people start to fail you get X plants for spinal cord stimulations because they did great the trial was amazing you got implanted and then you probably seen these patients in your own clinics they come back and they're like all right it's not working as well anymore okay let's reprogram it come back you know oh it's still not working okay and then eventually it leads to an X plant right and the patient is back to the their same old regimen of home exercise and opioids or whatever gaba pentanoids medications so they so you looked five years out because I think that that's what the field demands we wanted to ensure that there was a restorative aspect to this and it and you'll see here in momentarily that the accrual of improvements in both ODI vast EQ 5d kind of shows that they did it intention to treat analysis as they should because they're when you have a study five years long you're not going to have you know all these patients who continue to follow up there's you're gonna have loss of people from the study so from the original 204 they had about 126 that followed up at the five-year mark and next slide so kind of using Pico criteria who is the population so for those who don't know when we design a study use Pico P is for population so what they one thing that I stress is that you know you're gonna see the data is pretty provocative right and so somebody who's a little bit more skeptical might say well maybe these people weren't that sick right maybe their back pain wasn't that bad so on average these are younger patients in this particular study overseas they've mimicked this exact same results in and in the older population of greater than 70 years old but in this particular US study that it was average age was 47 these patients had 14 years of back pain on average and they had 97% of their days in the prior year affected by back pain so these were pretty substantial back pain patients 100% failed physical therapy obviously so you're not doing this as a first-line therapy whatsoever pain medications over a third of them were on opioids in terms of patient selection they were smart about it they they wanted to make sure that they that just history wasn't just a simple part of it but they were also wanted to get a little bit more selective so they used provocative tests described in the physical therapy world in this particular study they use the prone instability test and there's two other tests that are available out there now presently to evaluate patients for multifidus dysfunction and then 52% of that have failed previous previous intervention so your traditional epidurals medial branch blocks radio frequency neurotomy the exclusion criteria is simple no prior low back pain surgery this was a explanatory trial so they want it to be very clean with it now practice in the real world right now there are patients who are getting implanted with this who have had some you know maybe microdiscectomy or had a one level you know fusion or one level decompression and no leg pain greater than back pain obviously that's not going to help that we're not talking about ridiculous symptoms this this graph is one of my favorites because this shows you kind of the data plotted in a huge slide but again a reminder like when I initially was presented this as a therapy I mean it was a fifth of this slide you know in terms of the length it was that only out to one year a couple quick things so the green line represents the therapeutic group the red line represents the original control group one of the things that we found which was we had we always kind of understood this but there was a huge placebo effect a huge placebo effect so if you look in the first like 30 to 60 days they were the the placebo group and the treatment group are almost identical in terms of their their vast reduction so what does that tell you so if you if you believe that something's actually happening and you want to treat low back pain and you want to design a good study you have to go further than that and so and so they did in 120 day that you could see that the these they started to separate the lines and so much so that the designers of the study were told that they should probably allow patients to cross over so ideally you want to extend this as far as possible to you know because you want to have a control and a treatment group but you know because of you know you have to be sensitive to these patients and you want to be give them opportunities so that they can have therapeutic benefit as well so they let them cross over and what you saw was those patients essentially acting as their own controls you saw that line then all of a sudden shoot down to where the the treatment group is and and so you see those black lines and green lines plotted all the way out to five years in the those data paint those data points continue to remain consistent next slide this these are bar graphs showing the three main outcome measures that were used and tracked during the study dr. Karanopoulos understands this but in the pain world we are kind of moving away from simply just using VAS because we also understand that functionality is extremely important particularly this therapy which is restorative in nature we're talking about re-establishing motor control in the lumbar spine they looked at things like Oswestry as well as the EQ 5d and and what you can see here is across the board the the green are the non-intention to treat analysis and then the gray is the imputations that they made to account for those patients lost. And even when they did that, it was still wildly statistically significant up to five years. Next slide. We can go to this. So this is kind of showing you, this was on the previous slide here, but this is really showing you where the patient started. So on the x-axis you're seeing the VAS, y-axis the ODI. The fact that it's in the kind of right upper corner it shows you how bad these patients were in terms of the disability, but also what they were reporting as their pain score. And then Dr. Karayanopoulos is gonna show this cool graphic. And then you can see that it's dropped down to the left lower corner, which shows that both VAS and ODI were reduced. The amazing thing to me personally is that this graph hasn't changed, right? So we're using this graph a year ago. I mean, excuse me, a year into the study and then the second and third year, fourth year data we were presenting and this graph hasn't ever changed. So this is just, I know this is kind of a busier slide. I think one of the salient points here is that both VAS and ODI improved. When people ask me like what are the, generally speaking, like what are the success rates here? So they used ODI and or VAS reduction as a cutoff. It was almost near 80% responder rate at five years, 80%. The other thing too, and somebody was asking about medication. So the opioid, you know, which is a huge thing in our pain management field and PM&R as well. Gender physiatry often gets stuck having to deal with this because nobody wants to touch it. But 69% of the patients were able to reduce their opioids from baseline. So only neurostimulation device proven for compelling long-term effectiveness for five years. The reason that I included that bullet point is that there is a lot of new data coming out regarding utilizing dorsal column, you know, traditional spinal cord stimulation for the treatment of low back pain. The past two years, they've been, a lot of different companies have been publishing data from that. I think that that's, it's great. I think we need some of the data. But what we're kind of separating here is that that's again still remains a palliative treatment. Right, we're not, we're essentially covering up the signal using like headphones. We're not eliminating the noise as opposed to this therapy, which is really trying to get to the root of the problem. Next. Yeah, so the one kind of final point here is that there have been removals, right? But instead of being removals because the treatment has failed the patient, these are removals for success. So patients have had explantations because their back pain, they had been essentially complete remitters from their low back pain and they no longer needed any therapy. Yeah, and that's it. So again, I wanna, yeah, thank everybody for their time. Thank Dr. Karianopoulos and the other authors for allowing me to present this data. Thank you. Can you elaborate a little bit more on the mechanism of action? Yeah, so the idea again is, so we actually presented this yesterday. So the idea here is that when you stimulate, the idea of stimulating the nerve, you're trying to essentially reconnect, you know, in colloquial terms, the CNS to the low back and essentially re, well, and that's the idea of this, the whole terminology for the therapy, reactivate that system, you know, that reversing that arthrogenic inhibition. I did not attend yesterday, so I'm sorry. Is it more of a gate control sort of mechanism? Is it more activating certain dorsal columns or sensory columns to reduce central sensitization, or is it direct stimulation of the muscle? I thought I heard you say all three of those in your mechanism, like you mentioned, strengthening of the multifidi. So I'm trying to get a more scientific understanding of the mechanism. Yeah, yeah, I think, so if you look at the, and Dr. Karanapos, you might be able to shed some light as well, but if you look at the data, so personally me kind of digesting how this works is that I think in the beginning stages, you do get a gate control, no susceptive, you know, kind of improvement, because if you look, almost instantaneously, patients do well, right? It's not like they're waiting, they're waiting for the restorative mechanism's action to kick in, and then it finally plays in at the six, 12, whatever mark, you know, they start noticing, you know, improvement in central nervous system control. But the long-term aspect of this is thought to be reestablishing control of this muscle, you know, from the central nervous system. So you stimulate it repetitively to regain that. The study that kind of shows the inherent changes in the muscle, so there is some of that as well ongoing, was done in a sheep study, and that was a double, it was a randomized control trial in sheep. So they took sheep, they implanted sheep, they injured their intervertebral discs to promote degeneration of the multifidi, and then they stimulated one group, I think nine, and then the other nine didn't get any stimulation whatsoever. And then they looked at them at the, I believe it was the 90, 120 day mark, that escapes me at the moment, I'm sorry, and they actually saw that the sheep that had stimulation, when they biopsied their muscles, stained them with picoserious red stain and immunofluorescence, they had less connective tissue. So I think it's a combination of both, but the idea here is, yes, intrinsically changing the way that the muscle is how it looks, but more importantly, really motor control from the central nervous system. And just to clarify, so he may have mentioned dorsal column or gait control, but that's in comparison to the palliative spinal cord treatment. Oh, yes, yes. So this is direct muscle stimulation through a training effect. Hi, I'm Alicia, I'm a medical student. I had a question on future applications of this study. Did you ever consider maybe doing like a CBT with this to control for some nosoplastic elements of pain? Yeah, that's a great one. Dr. Karanopoulos, do you wanna take that? I think there are a lot of different avenues that we've considered now that we have this five year data. I think just to establish in the literature that there is a therapy with a longitudinal rehabilitative treatment effect. The graph that showed the sustained benefits at five years is really anathema in the pain world, nothing shows that. So we're building upon that, but there are those studies. I hadn't heard about, that's a great idea, we should get you in touch with our peeps at the mainstay people. But there are a lot of different ways we can expand on this data. It's really relevant to our field, whether you are MSK or TBI or pain, we all treat back pain at some point. And this is a great opportunity to really use your rehabilitative skills and your rehabilitative mindset to help patients longitudinally. There is a pragmatic study that's been followed up. This is usually the cadence of any type of new therapy. You do an explanatory trial, which is very rigorous, then you give it to the world and you see how it works in the real world setting. And so that study is the RESTORE trial, and that's gonna be published within the next few months. No spoilers, but the data's good. But I don't think they use cognitive behavioral therapy specifically on those patients. Some of them may have gotten it, because now you're doing it in a different setting, you're doing it in a real world setting. But I agree, I mean, with Dr. Karanopoulos, it's a great idea. But not to dwell too much on this study, but by and large, we were very intentional with the patients we selected for this study. These were patients who were motivated to get better. And so the nociplastic changes that you would otherwise see in chronic pain patients, that may be a little different. This is not a, because we needed the patients to activate the device twice a day for 30 minutes, you can't pick a couch potato, this is not gonna work. And we didn't wanna squander the opportunity to really get good data. Yeah, that's a great point. Sorry, I know you're gonna say something, but I was gonna actually say that too. The one thing I think that works towards this therapy is that the patient actually has to activate it. It's not passive like traditional spinal cord stimulation where you just turn it on. And then most patients just, they don't, they're not active in terms of the delivery of the process. The fact that the patient has to do it, and then you track them. Because when they come in for a reprogramming, because you can, sometimes with scar tissue formation and fibrosis, you might need to tinker with how many milliamps is being delivered. It's really, really low energy. But when you do that, the rep can tell you like, oh, this patient's been using it like 80% of the time. And so it's an opportunity. I mean, we go in there, I go in there, hey, you gotta be more compliant with their thing. And the patient's like, oh yeah, yeah, yeah. It keeps them accountable. It's kind of weird. I don't want them to come off like big brother watching you and making sure that you're doing things, but it is nice that you can manage that. And you can ask them like, what's going on? Like, oh, my wife got sick, or my loved one got sick. So then you can kind of work through that, and you can kind of better understand that. But I think the fact that people have to activate it keeps them accountable, keeps them engaged. We have time for one more question. Or do you have a follow-up? I just wanted to say thank you. Oh yeah, no problem, thanks. Okay, our wonderful medical student. Hi, thank you. Yes, I also have a question. I feel like I have multiple questions, but I'll just ask one. In terms of the mechanism, and me thinking back to my anatomy classes, there's multiple levels with the multifidus. How do you decide which level to implant it at? And then does it just stimulate that level, or does it activate the entire kinetic chain? Yeah, she's gonna be a future physiatrist for sure. Amazing question. So it is in the same place all the time. Yeah, so they did preclinical studies of where to stimulate this specific level. So we stimulate the L2 medial branch. And the idea with that is that you can get majority of the recruitment of the lumbar paraspinal muscles. That was the intent. So you're absolutely right. I didn't even talk about that from the procedural standpoint of things. This is as simple as it gets. The leads are on the outside of the epidural space. You're placing them at the same location every single time. And so the procedural part of this is very repeatable. It's the same every single time. And you can, I mean, to be honest, they perioperative test so you can actually feel where it's contracting. And it's pretty profound, the contraction that you can feel. It does involve the entire lower back, yeah. Nice. Yeah. Thank you. We need to move on, but thank you. I apologize, a teensy weensy question? Okay. Dr. Lee, thank you for the presentation. If you could give your quick thoughts on, obviously this is a new therapy, but in terms of how we work this treatment into our treatment paradigms for mechanical low back pain. Yeah. Specifically with regards to how we should be thinking about ablating. Yeah, yeah, yeah. Mine's really, that's a really quick answer. So what I do now is, I don't think, I think we have to be careful, right? We don't wanna turn and start criticizing the therapy that has helped us for so long, right? I think that's one of the things that we do have to be very sensitive about. Radiofrequency ablation still works. Data has shown it. There's been a lot of incredible amount of work that's been done by other organizations, including PMNR, AAPMNR, but Ipsys as well. And a lot of that was physiatry-led. But what I do is I will medial branch block them. I will block their medial branches in anticipation that maybe they might be a radiofrequency candidate. But the conversation now has changed, whereas before it was really just vanilla, one-track radiofrequency ablation. I tell them, whether you get a response or not to the medial branch block, you can be a candidate for either of these things. The proposition is simple. If you get radiofrequency ablation, you need to repeat it in, on average, the mean nine months, right? So some patients don't wanna do that, right? They're like, it's just, I don't wanna come back every single year and have this. And then sometimes, to your point, there are diminishing returns with radiofrequency. After a while, radiofrequency ablate somebody like three, four, five times in their life, which is quite common because patients need it every year. Sometimes they say, well, it didn't help as much, right? Well, why is that? Maybe there's something else going on. Maybe that multifidus is dysfunctional and we're kind of, unfortunately, adding to that. So that is a thought. Thanks. And with ablation, it is a palliative treatment. You're denervating the medial branch. So that's, essentially, you're affecting the muscle stabilizer that we're trying to build up with this other therapy. All right, so enough of that. Sorry, we're a little late. I'm going to welcome Hirotaka Nakagawa from Tufts, Systematic Review of RCTs for Use of PRP for Knee Osteoarthritis. Hi, everyone. My name's Hiro. By the time when I submitted this abstract, I was a resident at Tufts, but now I'm a fellow at UC Davis. Do we have a clicker? Oh, sorry. And thank you for all the co-authors. So the background of this research was that many studies on PRP to date have, unfortunately, failed to provide sufficient details about experimental protocols or the characteristics of the PRP product, affecting our ability to really interpret outcomes, compare results among the studies, and also to reproduce the protocols. So in May 2017, AAOS came up with the MIBO guidelines, which stands for the Minimum Information for Studies Evaluating Biologics and Orthopedics, and this was published to encourage improved reporting standards. The objective of our study was to analyze the adherence of RCTs on the use of PRP for knee OA to the MIBO guidelines, and second was to determine if the publication of MIBO guidelines has actually resulted in improved outcomes. So we performed a systematic review, including RCTs on knee OA treated with intra-articular PRP from 2015 to 2022, and we excluded those that were surgical application of PRP and also excluded the combination of orthobiologic products such as a PRP plus BMAC. So 87 studies met our inclusion and exclusion criteria, and each study was put in one of the buckets. The first one's a pre-MIBO group. If the data collection started prior to May 2017, which was the publication of the MIBO guideline. The peri-MIBO group, if the data collection started between May 2017 to December 2018 to give some leeway in case the data analysis or the data designs started prior to MIBO guideline publication to allow some time for the studies to incorporate the MIBO guidelines to the study design. And the post-MIBO group, if the data collection started after December 2018, at least a year after the publication of MIBO guidelines. Each study, two co-authors, we went through each MIBO guideline and then scored and obtained a MIBO score, which was calculated as percent of the checklist items reported out of the 23 checklist items. So let's say if a study had 16 of the 23 checklist items reported, then that would be 16 out of 23, so that would be about 80%. And for each item, we also calculated the item score, which was calculated as percent of studies reporting that specific checklist item. So let's say for checklist item one, if 20 out of the 87 studies reported checklist item one, then that would be 28 out of 87, so that would be about nine or 10% or so. So overall results, we had 51, 19, and 17 studies in the pre, peri, and post-MIBO groups. And in terms of the MIBO scores, we had 72, 76, and 69%. And we did not see any statistically significant differences in the MIBO scores among each group. And for the item scores, we saw particularly low scores for full blood characteristics, which was only reported in 20% of the studies. Platelet recovery rate, which was only reported in 22% of the studies. PRP analysis, 30%, and PRP activation, 47%. This is pictorial representation of our results. We have 87 studies in the column, and then 23 MIBO checklist items in the row. Green representing checklist items that has been fully reported. Yellow if it was only partially reported, and red if it was not reported at all. And I also wanted to, again, highlight the top four underreported items, which are shown here. So we found that we had a poor reporting of key variables, including whole blood characteristics, platelet recovery rate, PRP analysis, and PRP activation. And our conclusion was that, unfortunately, the publication of MIBO guidelines did not improve the reporting practices in studies investigating intra-articular PRP for the treatment of NeoA. We have found that the recent studies suggest that the characteristics of PRP, especially the platelet dosage, played a significant role in clinical efficacy. And the poor reporting of key characteristics negates our ability to interpret the current literature. Here's our reference. Thank you. Any questions? Well, thank you. All right, thank you. Okay, I apologize for the delays here, but we're gonna finally welcome Serena Shine? Shane? Shane. Shane, from St. Louis University. She's going to give us a discussion on direction-specific cortical control of automatic postural responses in Parkinson's disease. Yes, it's very long. I apologize. Hi, I don't, where's the thing? Hi, I'm Serena Shine. I'm a third-year medical student at St. Louis University, and he's already said my very long title, but I would like to thank my PI and mentor, Dr. Jason Longhurst. I have no disclosures. Oh. St. Louis is great. It's getting cold. The trees are really pretty though. It's orange and yellow everywhere. My street is like six different colors. It's wonderful. I am probably going to PM&R. I'm kind of deciding between that and neurology, as this probably makes a lot of sense. My screen is showing something totally different down here. That's okay. I'll just look over there. That's all right. Okay. So kind of a little bit about background and aims here. So as I'm sure you are all aware, Parkinson's disease is a relentless neurologic disease that results in instability and falls. And Parkinson, we don't know very much about the impact on neural control of reactive balance in Parkinson's disease, even though this is what is resulting in this instability and falls. And so the aim of this study really is to understand neural control of reactive balance in Parkinson's disease with the added factor that we're using a relatively new piece of technology known as the functional near infrared spectroscopy device, or FNIRS. And so the other kind of piece of this is, is it feasible to use this new technology to understand what is going on when you put someone in a reactive balance kind of situation? And so the aims are just that, right? Number one, neural activity and anterior and posterior perturbations. Aim number two is being able to characterize the difference between an anterior perturbation and a posterior perturbation and the neural activity associated with it. And the third one is that feasibility piece. How can we collect data? Can we get people to come in for this protocol and complete it and get data that means something? And I don't know if this video will play for you. It won't. Unfortunately, this is a PDF. I had a video so you could see what this looks like. But so for our methods, we had seven participants thus far. This is a preliminary analysis with a mean age of 65 years. They had mild PD. So six of them had Honin-Yar stage one and one had Honin-Yar stage two Parkinson. And then they had fair to good balance with many best test scores from 18 to 27. So you can kind of see on the other side of the screen what the FNIRS kind of does. And so the FNIRS measures changes in oxygenation and blood flow in different regions of the brain where those optodes are located. And so you can see on the screen kind of the top is the prefrontal cortex, then supplementary motor in yellow, premotor cortex is in green. The primary motor cortex is in purple. And then we actually recharacterized. We had sensory area in red, but we recharacterized it more accurately as the superior parietal cortex. And so how we do this, we put Parkinson patients on a treadmill. It is still at the time that they're on it. And then a randomly, temporally and directionally randomized perturbation is enacted to prompt them to take a step. So they're harnessed in. There were no falls. It's very safe. But the treadmill will randomly move backwards to prompt an anterior perturbation and the belt will translate forwards to prompt a posterior perturbation. And so then they take this step and we're able to measure what's going on at the time that they're taking that step. So in terms of our results, kind of we used Cohen's effect sizes given our small sample size. And you can see that we had statistically significant results in the anterior perturbations for the prefrontal cortex, the supplementary motor area and the primary motor cortex. Whereas posterior perturbations, we really only saw that significant effect size in the motor cortex. And then in terms of characterizing the difference between anterior and posterior perturbations, you're seeing that there's really only this effect size in the motor cortex, which made sense given kind of the results that we saw prior. So we took it a step further and we kind of characterized using Pearson's correlations, things that were happening when you look at two different areas and how they're related. And so this kind of goes with the previous slide in the sense that you can see the anterior perturbations are below that gray line. The posterior perturbations are above that gray line. And so you're seeing that with the anterior perturbations, these brain regions are working together. That positive blue correlation is showing that when one increases or decreases, the other area associated with it is doing the same thing. Whereas above this gray line, you can see there's a trend that there's more red, right? They're not working together. And so you're seeing that when one thing is increasing, it's not necessarily meaning the other things are also increasing with it. And then on the side, you can just see some scatter plots to visualize maybe what that data would look like. So what does this mean? This is preliminary evidence that there is direction specific neural recruitment patterns in people with Parkinson's disorder when you put them on a treadmill and there's a reactive balance protocol. This data did mean something. There's trends towards this increased activation in the prefrontal cortex, the supplementary motor area, and the primary motor cortex. The responses to the posterior perturbations seem to rely really heavily on that primary motor cortex, whereas the anterior perturbations seem to be relying on a more distributed network that involves more attention and motor planning. And then this is an initial study. This is a preliminary analysis, but there's further steps we can take. We have videos of participants on the treadmill. So what does the hemodynamic response look like for a certain reactive stepping response? And can we find other cortical regions that we can measure with this FNIRS device? Our data did seem to mean something, so preliminarily it looks good. A big thank you to a lot of collaborators here. Thank you, and I apologize that we're nearing the next session. So excellent presentation. Does anybody have any questions for our presenter? Okay. Well, thank you for your time and efforts. And thank all of you for, those of you from the last session, for your excellent work, and thank you for your ongoing contributions to the academy. We welcome your scholastic efforts.

medical research

motor recovery

chronic pain management

concussion impacts

long COVID

neurostimulation

knee osteoarthritis

Parkinson's disease

brain excitation

pediatric program

rehabilitation hospitals

functional outcomes