All right everyone able to hear me. OK. So thank you for having me. My name is Lorna Collins. I am a PGY 3 rehab resident at New York Presbyterian Columbia and Cornell in New York. And today I'm going to be presenting one of our research projects which is the Mississippi aphasia screening test or the mast and evaluating its validity on admission to inpatient stroke rehab. Just a little background on the mast itself. It was really designed to be a brief repeatable language basically screening test to help detect a wide variety of language impairments in people with different brain injuries. So whether it be stroke trauma mass lesions there's a lot of different conditions that it can be applied for. But it was really developed because a lot of the pre existing aphasia screening tests that were out there can be very burdensome for a lot of these patients particularly in this acute post you know injury period. They can be very lengthy they can be very taxing kind of mentally and if these patients have impaired attention impaired you know behavioral or cognitive issues it can be really difficult for them to tolerate some of the longer screens. So that's kind of why this one was developed and it's it's widely used I think for that reason but it's not really been formally well validated in literature in the US on specifically acute inpatient stroke rehab admission. So that's what we wanted to help to provide some evidence for. So our hypothesis was really looking within the while Cornell Medical Center is acute inpatient stroke rehab database looking at the mast and we hypothesize that the mast will more strongly correlate with language tests than with non language tests. So for methods we used our prospective database ultimately two hundred and eighty three subjects were included and these were people who were admitted to the unit and administered the mast on basically admission evaluation by either speech language pathologists or occupational therapists and how to diagnosis of a stroke. Some of the demographics so it was fairly evenly split forty five point nine percent of our subjects were female forty six point three of them forty six point three percent of them were diagnosed with a left hemispheric stroke. Average age was sixty nine point eight years the test batteries that we chose to compare basically the mast against for a certain language and non language tests was the Boston naming test which is a well validated language study the FIM score the functional independence measure and kind of breaking those down into the expression comprehension and motor sub scores and then the Berg balance scale which is essentially testing functional balance and mobility as a non language test. And we wanted to use the correlation matrix with the Spearman's row on all of those assessments as well as a man Whitney you analysis which we kind of looked at stratifying the participants based on their total mass scores so looking at those who scored high on the mast versus low. Do they have any difference in how they did on these other assessments. Moving over to the results on the top right overall kind of scoring 34 percent of our subjects did score essentially a perfect score a max score of 100. So that was our ceiling effect. Our median score was a score of 96 so 52 percent of our participants scored above that 96 level and about 48 percent below and there was no floor effect noted so no one scored a bottom score of 0 to 5. Highlighting most of our results are going to be the tables in the middle. So the table on the left table one this really shows our primary correlation matrix that's kind of the bulk I think of our results and kind of generally you can see that the shading is what's indicating different statistical significance levels. So blue shading squares are going to be P values less than point 0 0 1 green shading is going to be P values less than point 0 1 and then if there's no shading there's no statistical significance. And I think it's interesting in this table there is a level of statistical significance for all of the scores comparing the masked total and the expressive and receptive sub scores when comparing them to the three language tests in the first three in the first three rows the FIM comprehension FIM expression and Boston naming test as well as the bottom two rows which are non language scales that's the Berg balance scale and the FIM motor scores. But there is a stronger level of significance with the language tests in general evidenced by the blue shading. And then I think you know one of the reasons that we wanted to use a correlation matrix is to really show the strength of the relationship. I think that's more clinically relevant for us so you can see by the blue shading that it's a stronger correlation and stronger relationship with the language tests than the non language tests. And one kind of last final point with that table is I think it's interesting that even the types of language did correlate with each other so the masked expressive core scores had a stronger correlation with the FIM expressive scores than the comprehension and kind of vice versa. And then table two on the right that is our man Whitney you analysis so that's looking for differences in scores on these assessments when you're stratifying those who scored really high on the mast and you know may not have language impairments versus those who scored low and kind of as expected you can see that there's a statistical significant difference with the language tests but there's no real difference at all noted with any of the motor scores which provides evidence for us. So kind of in conclusion consistent with our hypothesis it seems like the mast is definitely more strongly correlated with those language tests than the non language tests. So there's concurrent and convergent validity between the mast and the Boston naming test the FIM expressive and comprehensive sub scores. There's divergent validity between the mast and the Berg bound scale and the motor and then there is moderate effect sizes and moderate correlations with all of those language tests. We did kind of discuss as we looked through all of the data and the results that we got looking at the ceiling effect and you know how how maybe effective is the mast at teasing out some of those more subtle language deficits because I think initially it was developed as you know a broad comprehensive screen to look at receptive and expressive language it looks at repetition naming fluency kind of all of that but maybe it's better used for more moderate and severe language impairments. So I think further research there would be needed to really determine the impact of that ceiling effect and whether it can be useful to tease out more of those subtle effects. But overall I think our study definitely provides evidence that the mast is a valid screen of aphasia on admission. Yeah. Your study was retrospective, I'm going to assume. Yes. And you use FIM instead of GG. Is there a correlation between FIM and GG? That, I don't know. A quick question for you, how did you measure the inter-ratel reliability between the occupations? Yeah, I mean, the MAST itself, if anyone wants to look at it, it's really a fairly straightforward test. It's really developed for, I think it was a fifth grade literacy level and education level. So it's supposed to be and kind of meant to be able to be administered by a wide variety of different healthcare providers. It's not necessary that you need specific training on how to administer it. So as far as my knowledge, there really wasn't that much room for any kind of bias or difference in administration. Beautiful. Awesome. Great job. Thank you. Yeah. Three. Three. So now you have a project for PGY from now till next year before we meet in San Diego that we can think about getting you approved. Maybe it's a good idea to do a study of the inter-rater reliability either amongst or between the different therapists who do it. Yeah. That actually would be interesting. Yeah. They can study and they don't have to even know their subjects. You already have it. I already have it. And you can even add to it and just increase your end and, you know, we're going to start asking for submissions in a few months. So it gets you another thing and a free trip. Thank you so much. I'm going to switch gears to the next presenter. So we're going to talk about the effect of a powered bilateral hip exoskeleton on walking speed in chronic post-stroke individuals. Dr. Alberto Eskenazi is going to take the lead. Thank you very much. It's a great pleasure to be here with you, with few of you, I guess. Let's see if we can get out of this and open the next presentation. Here you go. So I had actually sent three slides, which are not here, because I had broken the data so that you could see it in a better way. I'm going to see if I can do a little trick here, maybe. Yes. So I'm going to. Good. So this study is an in-progress study. We're looking at this powered bilateral hip exoskeleton as a way to address walking velocity in patients with chronic stroke. And what we know for a fact is that patients who have had a stroke tend to have decreased power generation at the ankle and hip as the major sources for the reduced walking velocity. And reduced walking velocity has a few other implications, including the fact that it reduces. When you have a lower walking velocity, you tend to have less capacity to be independent. There is also an issue with satisfaction, life satisfaction. And so there has been approaches to try to address this from the point of view of the ankle. And the intent of that was to create power generation. And so there are a number of those devices. I'll mention one in which we were involved directly, the Restore. And the device does produce increased ankle power generation, and patients can walk faster. We know that from the data that we collected. But it's a device that requires that you set it up, you measure, you adjust, and it takes time to do that. It also adds a mass around the pelvis. And sometimes patients get a little bit off bounds when the device is running the system. So we decided to look at a different approach. And that was, could we instrument the hip, which then it puts the device closer to the center of mass. It allows us to control the hip by essentially injecting power, both during swing and stance. So that was the intent of this study. Of course, when you are trying new devices, one of the things you want to be sure is that the device is effective and that the device is safe to use. And so we selected a bunch of patients. Our intent is to collect data in 20 patients. We've collected data in five subjects. And that's what I'm sharing with you today. So again, this is a preliminary study. What you see here is the device. And what the device does is essentially has two motors independently controlled. And the motors can generate force into flexion or extension. And the innovative piece about this is that you can walk with this gadget. The gadget collects information as you're walking. And then it looks at an algorithm that will tell you what's the right dose and direction. When do you inject the power in flexion or extension? And then you can modify the ramping, meaning you could make it faster or slower. And so that's the intent of this. There is a paper, the reference number six. I encourage you, if you're interested in understanding how that algorithm works, look at it. You'll find that to be an interesting paper. So what we did is we essentially walked this patient's, oops, sorry. I didn't do this. I don't know what happened here, but there you go. What we did is we walked this patient's without the device, collected temporospatial data. And we collected also kinetics and kinematic data. And then we applied the device. We let the device run in what's called transparent mode. Essentially, the device judges what's the effort of the patient and reduces the effort to zero so that the load of the device does not create any differential or any change in the walking pattern. That's the intent. And then we use the algorithm inside the system to generate the curves for power application. And so we have a mode that it's called transparent, and then we have a mode that is called active. And we collect the data in both of those modes. And so when we looked at the data across, and we know these are few patients, but we have additional data from the original studies that were done, we clearly can see that patients increase their walking velocity. There was no real adverse effects with this. The patients increase their walking velocity when they are wearing the device in active mode. And they increase their velocity after training with it with the device in transparent mode. We did not see a difference yet in the number of sessions that we provided in using the walking without the device. And so that's the area that I'm most interested in from the therapeutic perspective. The only other important factor here is that patients who walk with a stiff knee gait, spastic patients who walk with a stiff knee gait, and those that walk with not a stiff knee gait need different patterns of acceleration for the power generation. And it's very interesting. We don't quite understand yet why, but you're able to alter that pattern. So we can alter the pattern of stiff knee. So thank you to my collaborators, which are really an international collection of individuals, and to the sponsor of this project. So thank you very much. If there are any questions, I'm happy to answer. Yes. So the subjects screened for sedation at the sterile hand or relative control of trunk? Relative? Were they screened for abilities to control their trunk and or sensation? So these are not acute patients. They were all six months out. And they were already ambulating. So they were ambulatory. They just did they walk very slow. And we were able to modify their walking velocity from average of 0.4 to an average of 0.6 meters per second. The average age for this group is in the 54-year range. Young? Yeah, they're young. Yeah, these are all the patients are from MOS at this point. The device was developed in Italy. The application initially, they're going to be opening a trial with the exact same protocol in Italy, but they're running behind schedule. That'd be great, wouldn't it? And eat some of their great food. Not yet, but I'm looking forward to that. I think that if I get to 10, then I get to go. Future travel plans. Yep. Just made it up. I have a question. Go ahead. Has there been any evaluation of fall risk assessment before and after? Yeah. So we do a false assessment for these patients, and we have not found any difference and change in that. These are patients who are ambulatory, so they were walking. The risk of falls increases for every patient who has had a stroke, but we have not seen a difference. The objective was not to improve balance, really, was to increase walking velocity. That was the objective. Gotcha. Awesome. No, that's phenomenal. Thank you so much. Thank you. All righty. So coming to our final talk, it's going to be around Blast from the Past, Auditory Conditioning as Traumatic Brain Injury Prophylaxis by Aria Kishore. The floor is yours. Good afternoon. My name is Aria Kishore. I'm a fourth-year medical student at Philadelphia College of Osteopathic Medicine in Georgia, and my research was Blast from the Past, Auditory Conditioning as Traumatic Brain Injury Prophylaxis. So traumatic brain injury—let me make this bigger so you can see all of it—so traumatic brain injury is a common diagnosis following bomb exposure among military personnel, and many of these personnel go on to develop secondary complications such as tinnitus and depression. So tinnitus development is multifactorial, but one of the known etiologies is physical damage to the hair cells, which in turn causes hyperexcitation in the auditory circuitry, and this is what is perceived as phantom sounds or tinnitus. So currently, the treatment for tinnitus is tinnitus retraining therapy, and this is when patients are exposed to a 90-decibel broadband noise for 20 milliseconds with 50-millisecond intervals for one hour, five days a week, for 10 weeks. So we asked if this treatment could be done prior to blast exposure in order to decrease the incidence of tinnitus and depression. So in order to do this, we used a mouse model, and we divided the mice into three categories. We had a treatment group and two control groups, one control group having no blast exposure and no auditory conditioning, the other control group having blast exposure and no conditioning, and the treatment group with both. So in order to kind of mimic the bomb exposure and pressure wave setting, we placed mice in this induction chamber, and they were exposed to a 20-psi pressure wave. So following this pressure wave exposure, we screened for tinnitus and depression. We had the baseline results prior to the blast exposure, and then we measured again afterwards, and tinnitus was measured using an acoustic startle chamber. So in this chamber, the mice are placed inside, and a white noise is played, and there's a brief pause in the white noise prior to a startle stimulus. So this pause acts as a kind of warning sign for the mouse and kind of alerts them that something's coming, and then when the startle stimulus is played, they don't jump because they were already more alert. In mice with tinnitus, this gap in the white noise is filled in with their own phantom sounds that they're hearing with their tinnitus, so they don't get this warning, and they do jump when the startle stimulus is played. So that's how we looked for tinnitus, and we measured depression in the mice with a forced swim test. So the metrics that we used for that is the time that they're mobile as well as the distance traveled. So using these metrics, we analyzed all the mice, and what did the results show? So the results showed that there was no significant difference between the treatment group and the control group when it came to tinnitus. There was actually a slight increase in tinnitus among the mice in the treatment group. When it came to depression, however, there was a significant decrease in depression with a 0% incidence among the treatment group. So based on this, we came to the idea that although you can't use auditory conditioning as prophylaxis for tinnitus, it can be used to decrease the severity for depression and other secondary complications of traumatic brain injury secondary to pressure waves. Thank you. All righty, that's interesting. Any questions? Hi. Hi. So it's great that it's done on a mouse. It's great to understand what's the translation between a mouse and a human ear, and how similar are they, dissimilar? And what's the expectation that with this, we're going to progress this to humans? Yeah, so that's a great question. So again, one of the reasons that we didn't really try this on a human model was the implications of causing further damage, especially with personnel who don't already have tinnitus and possibly developing tinnitus if they do get this auditory conditioning for five days a week, 10 times a week. So I'm not... The mouse ear is similar to the human ear? Yeah, the circuitry is similar in terms of the auditory circuitry, but I'm not sure how directly this would apply to a human model. I'm not worried about a mouse getting traumatic brain injury so much. I'm worried about our soldiers. Yes. So this is something that, of course, would need to be looked into more in the human model. And one thing that when we were discussing of how this could be... I concur, to be honest, because when you were presenting, I was like, okay, treating brain injury with auditory tinnitus issues is like, you're thinking from central and peripheral, are we missing any pathology? You're involving other healthcare providers like ENT, and figuring the source kind of guides you to the treatment. So doing this prophylaxis beforehand, is that something, it didn't, again, as you said, it just helped their depression symptoms. What sort of depression sub-symptom has helped, did they, did it, what particular symptom did it kind of got improved with this therapy? So for, in the mouse model, the way that they look at depression is just with how much they're moving, so the time that they're mobile, and the distance that they're traveled. So in the human, of course, that's different, and with us, it's measured using different screening. So it's not a specific symptom of depression that we knew that it fixed, it's just that the, with the mice, where there was a decreased incidence of depression, they had a increased, a decreased distance traveled in the control group, and increased time mobile in the control group, whereas they didn't in the treatment group. Okay, but that couldn't be, I mean, again, me kind of thinking out loud, that could be, not be related to depression per se, that could be related to any other physical damages that happened from the blast. Yeah, so the blast, the mouse, so in the chamber that we built, they were strapped to what was essentially a mini skateboard, so that they're not feeling physical implications of that blast, just the auditory, so they would kind of move with the pressure waves. So they didn't have any physical, like, damage, no movement problems when we were doing the swim test, so it was assumed that the reason that they're not moving isn't due to a physical damage. Okay, okay, again, any other, yeah? You know, your study is actually quite important, and we have a clinic for veterans and first responders, and one of their major complaints is the sense that they can't keep track of what's going around them when they get in a busy environment, and that may be in part auditory, and part may be related to their vestibular system. So this is an interesting study, but I think the questions that are being asked are very appropriate, which is, how do we translate this from an animal model to a human model? And it's not an easy request, but it's certainly something that I think may be of great value to the military population that we serve. Yeah, absolutely, and definitely worth looking into more and more research in the area. Yeah, no, it's very interesting. Thank you so much. Any other last-minute questions? Yeah, so the main campus is in Philadelphia. I'm at the satellite campus down in Atlanta, but yeah, I get that question a lot. Thank you. Thank you, everybody, for joining us in our Best of the Best NeuroRehab Research Projects, and any last-minute questions, any concerns? So if none, you folks are free birds. Thank you so much.

neurorehabilitation

Mississippi Aphasia Screening Test

bilateral hip exoskeleton

walking speed improvement

auditory conditioning

traumatic brain injury