You as a doctor give hope and health to many each day, there are many more to give hope and health to and with Fujifilm we are doing that together. So let's go ahead with this topic, the topic is stroke protocol and update. So there is nothing new to it as such in the way that it's not a rare case or something which we don't know how to diagnose but it is something which is evolving the concepts are evolving. Before we start I would acknowledge all my learning to my mentor Dr. Deepak Patkarsar and contributions to this particular talk to Dr. Sushin Kumar and again Dr. Pradyumna Oak our neurologist who is also teaching me a lot of new things in stroke with his all clinical experiences. So how do we define stroke? It is reduced blood flow and perfusion which is caused by a thrombus or embolus or can be because of hemorrhage. Whenever a particular brain parent timer undergoes stroke there are basically three zones which are created. One is the ischemic zone that is the zone which receives blood supply less than 12 mL per hundred gram per minute of perfusion, second is a penumbra and third is oligemic tissue. So we are going to see these in details. What you want is what you get. So evolution of stroke imaging has been really marrable in the past few years. Earlier it was just CT scans and that too very low quality CT scanners which we used to have and what CT used to do was just it was ruling out hemorrhage but now we are shifting to an era of multitude and multi parametric MRI in stroke imaging. So we have something like mobile stroke units which carry CT scanners with them to save time. So from time is brain to physiology is brain. So lot of papers coming up and even the window period which we used to talk about that was earlier like 3 hours then 4.5 hours even that is expanding to up to 6 hours. So what is role of a neuro imaging guy in cases of stroke? First is first of all you have to identify that yes there is an infarct you have to locate an infarct then you have to identify the area at risk that is whether there is a salvageable penumbra or not. Then you detect the cause of the stroke and then you predict the outcome of this particular stroke. Let's see how we can do it. So these are the various questions which we can answer through our reports whenever we are reporting stroke. The question is is there an infarct? So CT if we start with yes because of its availability definitely many protocols in stroke are based upon CT even if you see the guidelines and recommendation by national and international communities they also recommend CT. But the reason might be very simple that MRI is not available MRI may be time taking. The disadvantages with CT is we can easily miss hyper acute infarct and in that ways we can easily miss a lot of neurons and because time is great as we know. Therefore CT is just helping us to rule out that there is no hemorrhage but it does not pick up infarcts. There are typical CT findings in a case of acute infarct like dense MCA sign, obscuration of lentiform nucleus insular ribbon sign but I must acknowledge these signs are basically for maybe for exam purposes because with a higher slice machine with particular hemodynamic changes in a person this hyper dense MCA is many times seen in various normal CT scans also. So now let us come to what we do and we practice at our hospital which is MRI based protocol for stroke imaging. So MRI as we can call is a one stop shop for imaging a patient in suspected stroke. This is how we carry out our stroke protocol sequence. We call it as code white. We have created a code white particulars alarming system whenever a patient with stroke reaches the hospital accident and emergency or even information wise code white is activated and all the radiologist consultant as well as neurologist ICU team gets a call out of it. This is our sequence which we follow. This is a tailor made protocol which ends in about 12 minutes. The satswit diffusion goes to an angio sequence then sworn then flare the neck angio and ASL. So we just see why do we do all these sequences one by one. So diffusion weighted imaging as we all know is the stroke sequence. So it is based upon the microscopic motions of water molecules as we have already seen what Amit told us in the first talk in the beginning. This is a very fast rapid quick sequence. All of us know it gets over within a minute's time. So we take almost 40 seconds to complete diffusion on our 3 Tesla scanner. We always do a B value of 2000. So it's like how we have tailor made our protocols. We try not to waste time with a B value of 1000 directly go for a B value of 2000. Diffusion is very sensitive and can pick up hyper acute infarcts. Infarcts which are seen only as a restricted diffusion area and not seen on T2 or flare images. It's very good even in posterior fossa infarcts. Like these are two patients, two different patients. You can see small area of infarct or restricted diffusion in the medulla. This is an obvious large area of infarct in the MCA territory. But it is hyper intense on T2 as well. So how sensitive is diffusion? Sometimes we might think that will diffusion pick up everything or is it that it can miss few infarcts? So various studies, it's a thing which is already reliable and established. But still let us see that sensitivity wise diffusion for identified ischemic stroke is 92% sensitive and 75% specific. So specificity might be low, but sensitivity is quite high. So therefore see this example. This is again a very recent example which we did yesterday I think. And so we did this diffusion weighted stroke protocol and we said that nothing normal. But the neurologist felt that no there has to be something and in such situations we usually say that fine we will repeat diffusion after few hours. Then this was repeated and we could actually see this small area of infarct in the medulla. So when to expect negative diffusion weighted images in stroke and TIAS. So yes there might be some infarcts which diffusion misses, but maybe because of the time period. One second maybe because of the location. So if we see these kinds of study they talk about a diffusion missing these infarcts. Maybe one because the B value was lower. Second the infarcts are in the posterior force or posterior circulation. Third they are small infarcts like lacuna infarct. So like in this case. So if you see retrospectively you can still say that yes there was something there in the right half of the medulla earlier as well. So yes diffusion is reliable and has to be the first sequence in any MRI protocol. Actually there are many centers who have combined CT with diffusion. So they call it CT and diffusion screening MRI for stroke. So now coming to the next sequence very important one is flare. We do flare one to pick up weather. We can see what we are seeing on diffusion on flare images or not. This is very important in cases of wake up stroke because that time the time interval cannot be just based upon the clinical findings. Because the patient was sleeping and when he got up there are features of stroke. So that time the neurologist definitely relies on what we say. If we are saying that it infarct is flare negative they confidently go ahead with an active intervention. If we say that no it is flare positive then they expect that there might be hemorrhages post thrombolosis and they don't go for any active intervention. Next component of the stroke protocol is SWI or sometimes we can also use GRE sequence. So here with our 3 Tesla scanners we use so on images. SWI has several advantages over routine GRE which was used as the basic thing. Yes SWI helps us to find hemorrhage within an area of infarct. But secondly it also can detect very accurately a thrombus and intra arterial thrombus can be picked up very nicely with SWI. So this is an example here we can see the arrows pointing out a small band like area of blooming along the course of right MCA. And beyond that particular segment there is no flow on the corresponding 3D tof angio images. So this is because this was a intra arterial thrombus which was seen very well on SWI. So we start with diffusion the second sequence which we run is SWI. Because if the patient suppose starts moving or cannot continue with the scan these two sequences give a lot of information. Next is prominent vessels sign. So there is something called as diffusion swan mismatch. So some centers and studies have established the role of swan in establishing penumbra. Because there is congestion and a lot of prominent vessels can be seen in cases of hyperacute stroke. And therefore swan can also be a secondary marker to delineate the penumbra. It was about our sequences. Now coming to the next sequence which was a part of our stroke protocol which was MR angio. So why do we do angio? Because we need to say what is the cause of the infarct coming next to MR angio. MR angio what we do is definitely non contrast of sequences. We have changed the parameters a little bit because here we are not concerned about getting very beautiful images. What we are concerned about that we should be sensitive enough to show the vessels and at the same time not waste time. So here our angio sequences both together are finished in five minutes. We start with brain angio neck angio is the last sequence of the protocol. Because even if we don't do it that may be fine. So brain angio is done and we can actually see that where the arteries blocked or whether the collaterals have formed whether the supply is good or not. Contrast enhanced MR angio is not a part of the routine stroke protocol because sometimes giving contrast might be an issue. But yes we did a study for almost about 20-25 patients where we used time result imaging of contrast kinetics which was definitely more sensitive to pick up smaller areas of narrowing for these particular cases. Next way of how to determine the cause of stroke. Sometimes it's not only vessel occlusion or embolic stroke. Sometimes you see the distribution of the infarcts in different vascular territories and that time you can say that it is an embolic phenomena. If it is bilateral various territories far apart then you know that it is something cardiovascular. So most of the time they can correlate with 2D echo and find some or the other cause in the cardiac system. They can be vasculated infarcts, they can be infective infarcts or they can be just restricted diffusion because of N-capillitis. Next question which we can answer is reversibility. So will your intervention help or shall we go ahead with any active intervention or shall the patient be just kept for just simple medical management and follow up. So that is based upon the phenomena of salvageable penumbra. So as we all know whenever there is vascular occlusion a particular part of the brain is almost dead what we call as the ischemic core that we see as restricted diffusion.  But definitely there is an area beyond that area of restricted diffusion which we call as penumbra which is the area at risk. Timely interventions can definitely save this large area of salvageable brain-parent kinam. So that is based upon the concept of perfusion and perfusion-diffusion mismatch. So what we use is something called as arterial spin labeling. I'll just take through a few slides and explain what it is. So we actually presented this paper as well at RSNM. So arterial spin labeling is a non-contrast MRI perfusion sequences and it has a lot of application particularly in patients with stroke. So here is an example patient A, small area of restricted diffusion. On ASI image which is a rainbow-based color spectrum what we are seeing the area which is blueish in color or towards the violet spectrum is hypoperfused. And here we can see the sizes are usually almost the same. But in the second example which is patient B, restricted diffusion almost same as the first patient. But a fairly large area on ASL is hypoperfused. That means there is significant perfusion-diffusion mismatch and definite salvageable penumbra. So this gives us a lot of advantage. It's just a four minutes of an extra MRI sequence and no contrast is required. So many a times now our neurologists they know the importance of ASL and they ask for it and their basis on the ASL they take decisions whether to go for an active intervention or not. This is how we quantify though it's not very sensitive or a good method of quantification we will discuss why. But yes you can roughly quantify the mismatch as well. Second application of ASL is that ASL can also show you whether there is a thrombus within the vessel or not and that is called as the bright vessel sign. So here you can see so on images lower bottom right side which is showing that intra-aterial thrombus and same patient ASL showing a bright dot. So that bright dot is actually the site of thrombus. And another application is once the treatment has been done or whenever you are following up the patient you can actually see the perfusion coming back. So sometime it is auto perfusion or what we call as luxury perfusion. Sometime it is after treatment when we call it as reperfusion. So it's really rewarding to show the patient as well their relative. Let's see first of all you had an infarct there was something which was at risk and we did something actively and your brain has been saved. A lot of damage has been saved. So various examples now we have over 200 cases of similar results. So you hear also pre thrombol is pre thrombectomy and post thrombectomy. First side we can see there is hypo perfusion and a mismatch and after the procedure the vessel has opened up and also the perfusion is back. So this is the comprehensive answers to why did we do all these sequences for our stroke protocol. Now can we tell them what kind of intervention should they go about. So definitely you can help them take decisions but this is what neurologist and the neuro intervention guy decides. So there are a lot of options available like IV thrombolysis, intra arterial thrombolysis, bridging thrombolysis, thrombectomy, mechanical thrombectomies etc. So when you give them exact information when you grade whether there will be hemorrhage or not they can confidently decide for the patient. And the question of the golden window period. So yes window period is widening so you should not deny at least a scan or bringing a patient to the hospital just because 3 hours have passed.  But do image these patients because for mechanical thrombectomy there are studies coming up that beyond 6 hours also they have been successful results. Especially in posterior 4 hour stroke there is a longer window period which is taken. Can we predict of thrombolysis or can we tell them the risk of hemorrhage post thrombolysis. Yes we can that is based upon where exactly the thrombosis is. So whenever there is occlusion of a larger vessel when there is a larger infarct there is larger chance of post thrombolysis hemorrhage. Whenever there is no occlusion of the large vessels or a smaller infarct the prognosis is better. There is something called as aspect score which you all must be knowing and that is used for CT scans. But actually can be extrapolated to diffusion as well which is called as DWI aspect score. So again by giving this score you are making your reports more comprehensive and robust so that your clinician can decide confidently on the management options. Other things they have to consider before going for an active management and that depends on age and various other comorbidities. Let us now see how can we predict and how can we grade post thrombolysis hemorrhage. Because your work does not tend just by diagnosing you have to follow up. So when you are at particularly you are working for institute or at a hospital centre the patient is admitted. After thrombolysis post 6 hours thrombolysis they will follow up with a CT scan what we do and then after 24 hours we do an MRI. So some kind of imaging follow up is always there. So these are four types of four classification of post thrombolysis hemorrhage the terms which we can use. One is HI1, HI2 which is HI1 is a particular hemorrhage infarct. HI2 is a particular hemorrhage throughout the infarct but no mass effect. What is pH1, pH2? pH1 is parenchymal hematoma with minor mass effect. So it's like a hematoma but minor mass effect less than 30% of impacted area. And pH2 is parenchymal hematoma more than 30% impacted area involved and major mass effect. So I would request all of you especially the residents to give on-call reports to use this term. Because if you just say that there is hemorrhage in infarct post thrombolysis the clinician might think that some large area of hemorrhage has developed and they might stop the active medications. So if you use these classifications they are at a better place to understand your reports. There are various other predictors as well so size yes. So if the area involved is more than one-third area of the territory they say that more chances of post thrombolysis hemorrhage. Aspect score less than 7 is a bad score. So more than 7 is good less than 7 is a bad or poor prognosticator score. So we see we saw the answers to so many questions. Now let us go ahead and see can we predict that this person will have stroke. So not directly but yes some risk factors we can definitely see. So somebody who has developed a lacuna infarct or small infarct always do an MR NGO. See for any obvious vessel wall narrowing see for any obvious sorry vessel wall thickening or luminal narrowing. And thereby you can predict that this person is at risk of future embolite upstream. And they can actually do a stenting for these patients and can prevent such events. So this already Sikander sir has taken in details so I am not going into the depth of this. There are few new advanced sequences not yet in practice but for those who are exam going these are questions for your exam. And definitely you will be working with these sequences maybe five years down the line. So something called as diffusion kurtosis imaging and something called as pH imaging. So kurtosis imaging is based upon the Brownian movement of water molecule. So that was when it was in a Gaussian distribution that was DWI when it is based on non Gaussian distribution which is more close to reality then that is called as diffusion kurtosis imaging. So various models rat models various studies are coming up. But I will just tell you in brief what actually you can just remember out of this kurtosis and pH imaging. So one is pH imaging as well and pH drop precedes the drop in cerebral blood. So I think the next speaker has put on his microphone. So what you can just remember is here till now what we are determining is restricted diffusion one we call it dead brain or we call it the core and second we call it is a penumbra which can be saved on perfusion. But actually these are not two things these are four things just remember this. So actual diffusion beyond that a smaller area is of kurtosis diffusion. Actual penumbra inside that there is a small area with pH mismatch and just two sentences if you want to write your answers at least. So diffusion kurtosis is equal to true in fact core what you see there and that is smaller than actual diffusion. So this is the basis of diffusion reversal phenomena. And second pH is equal to true penumbra and that is smaller than the what perfusion you are see now coming to something very recent very ongoing which is impact of COVID-19 and increasing incidences of stroke. So yes I think all of you must have experienced this also in your practice that lot of different kinds of strokes are coming up in that flash three question which we had the quiz question that had that was very odd. So a lot of you had written venous hemorrhagic in fact we also thought venous hemorrhagic in fact the patient was COVID positive and maybe because of that or some reason there was a lot of hemorrhage in that acute phase also. So to conclude time is brain yes physiology is brain so you have to be very skeptical very sensitive about your stroke protocols I must acknowledge that he takes all the efforts in our department that all of us are sensitized for stroke patients. MRI based protocols are better than CT based protocols if you can tailor made them and you can actually be dynamically guiding your technicians and residents and fellows to take care of this particular protocol. Every case gives you a learning point try to answer why this patient had a stroke that will help you learn a new point and try to learn to treat stroke so this is something I would like to add because I feel that its neuro intervention is something what radiologist can do and should do if we can diagnose stroke we can treat them as well.


Up next is Dr. Doug Wieb, who's a professor of epidemiology, it's like having to do that to church service where you have to read from the book of Ecclesiastes. But a professor of epidemiology in the School of Medicine at the University of Pennsylvania, also the director of the Penn Injury Science Center, one of nine injury research centers funded by the CDC. And growing up in Canada, his primary sport was volleyball. He was a member. I think he's proud about this. He was as he should be. He was a member of the University of Calgary Dinosaurs team, Go Dinos, that won the national championship in 1989. So Dr. Wieb, please bring some dino magic to your presentation. Thanks to Lauren Peerpoint and to the organizers for the chance to be here. I'm here representing the Ivy League Big Ten Epidemiology of Concussion Study, and that study is operated by the TBI Collaboration. The TBI Collaboration is hosted by the Big Ten Academic Alliance, and that was created in 2012, and participating institutions are all of those in the two conferences, Ivy League and Big Ten. And the goal is to increase collaborative research on sport-related concussion and to collect data that can inform practice. The epidemiology study was initiated in 2011. Data collection began in 2013. Schools in the Big Ten started to join in 2014, and in 2017 the Data Coordinating Center was moved from the Ivy League office to our offices at the University of Pennsylvania and the Pen Injury Science Center. Participating sites in this study at present are the eight schools in the Ivy League and 12 of the campuses in the Big Ten. And high-level overview of this study. It's a prospective, obviously multi-site observational study. It's a surveillance system and a prospective cohort study. It was started using informed consent of student athletes across all participating sites, and participation is estimated at over 90% of athletes who sustain a sport-related concussion. The data that are collected include demographics, circumstances of the injury and mechanism of injury, and information on the impact of the concussion, and return to academics and to athletics. Also, athletic exposure information is collected to enable calculation of rates. The study is in its eighth year of operation. We have an asterisk on the current year for ending early, and at present, total number of cases in the database is 3,006. You can see the, of course, the majority are sport-related concussions, but the database also includes non-sport-related concussions that are captured across all sites. And 27 sports are represented in this study. It was just last year that we published the first report, high-level overview of findings from the study, and detailed information on the history of the study, and on the methods that are used. That study reported on concussion rates by competition and practice and overall for sports. It reported high-level information on the symptom, the prevalence of symptoms. Symptoms are collected using the SCAT, and we reported on time to a number of outcomes. Here is time to symptom resolution for four different sports, time to return to academics and to exertion and to competition by sex. These are crude Kaplan-Meier curves, and there is much more to be studied with these data. From an epidemiologic standpoint, and also from a policy standpoint, another report that we put out in the last two years was conducting an evaluation of the experimental kickoff rule that was introduced in the Ivy League in 2016. We did that rule using a difference in differences analysis, comparing changes in rates of concussion during kickoff returns in competition to changes in rates in sport-related concussion during all other types of plays. We found that there was a large excess reduction in sport-related concussion rates during kickoffs over this time period that we attributed to that experimental kickoff rule. That was a nice start and a very good example of how this study, because data are being collected across conferences and over a considerable period of time, are in a position to really inform policy decisions and practice decisions, and try to find ways to make participation in varsity athletics. Now there are many opportunities for learning about risks for concussion and risks for prolonged recovery following concussion, and also for the prevention of concussion. And analyses are planned for a number of these items, and in the long run much more can be explored and data collection is continuing. Sex differences is something that will be exploring important issue of club sports compared to varsity sports, and perhaps different risks of concussion or different types of management for sport-related concussion, because typically the lack of athletic trainers assigned to sports, club sports across campuses, exploring different helmet types and risk of concussion, exploring the tackling robot, for example, that was introduced at Dartmouth, and more. Zooming in on a couple of them, one example of work that can be done next is looking at mechanism of concussion, and here we've taken a first pass at looking at that in four different sports. Basketball, lacrosse, soccer, and water polo, where we have both women's and men's teams. And quick snapshot of findings here from a descriptive perspective are that in basketball there were differences in mechanism of injury by gender. We also saw that in the cross, for example, where the most common mechanism was contact from a ball or from a person, but more men sustained sport-related concussion from a person or person during a ground ball compared to women, and more women had contact with a sticker ball compared to men. For soccer there were also sex differences in the mechanism of injury, but we didn't see sex differences in water polo, perhaps because being immersed in the water largely leveled the playing field. So opportunities to look even closer to think about how the games are played and whether there are opportunities to make these sports safer and identify what is it specifically, what's happening on the field when concussions are sustained in these sports in women and men. Abby Bretzen is a postdoctoral fellow with us and a certified athletic trainer who completed her PhD at Michigan State. And this is a poster that she presented in February this year at Big Sky. And she was exploring the non-sport-related concussion data. In the top right you can see that there were 415 non-sport-related concussion cases captured in the database so far. Mechanisms of injury included moped and scooter from a fight, some were alcohol involved, some were car crashes, some were falls, and in considerable time out of sport resulted due to these non-sport-related concussions. So more to be explored and for example we can look across campuses and see if any of these mechanisms are disproportionately happening on different campuses maybe due to different ways campuses or laws are enacted there and chances or opportunities for prevention. At Rutgers they have introduced use of the guardian cap in practices in football and what catches our eye is that a handful of scarlet knights have been assigned the guardian caps to see if those might reduce the risk of concussion in practice. This is such a tightly knit group of campuses that are participating. I think that we're actually in a position to do even more and rather than look retrospectively and treat some of some changes in practice like this as a natural experiment. We could even consider introducing countermeasures like this with randomized designs and if there is an interest in having all athletes receive an intervention and not have it held back from any of them even using for example a step wedge design over time to introduce a countermeasure in a systematic way and have a really robust test of whether that might reduce the risk of concussion. So there's potential for this kind of countermeasure to be evaluated with rigorous methods beyond observational studies. So many people to thank for the collection of data and the creativity that goes into ways to to make that happen and have the data be valid. In particular I want to thank Bernadette DeLonzo who is the lead research coordinator on this study sitting there in the front row on my left. She will be starting the PhD program in epidemiology at Penn this fall and also thank you to Abby Bretzen back row on the left who's with us and who's been working very very closely with me and Bernadette for the past eight months. And thank you to the athletic trainers and team physicians and researchers across the collaboration who continue to collect these data and put so much hard work and creativity into it and we look forward to further participation and research collectively as a group to keep on trying to find ways to make participation and athletics safer. Thanks again for the chance to be here.


Going on everybody got Sean and Kyle here relating sports cards are from one box for Taiyuan seat. It's gonna be a top scone black Good luck. Good luck. Let's see what we got Got a Garrett Cole One's gonna be Adley rushman a nice one there on the rookie silver Be refractor Adley and so 199 is Miguel Cabrera Miguel Cabrera to 199 and some 99 the green is gonna be a Prince fielder auto for the Brewers I have not seen a Prince fielder auto in quite a while Go to 99 The one is 21 of 99 for the brew crew and get that right out to you All righty, Taiyuan appreciate you on the tops chrome black get it right out


Hi everyone, Joe for jaspyscasebreaks.com with a quick number block randomizer for these following teams right here. You guys know how this works. There it is. There's the directions, instructions, and there's all the names. Thanks to these folks for getting into this one. There are the numbers right there. Let's roll it. Let's randomize it. Four and a three. Seven times for each list. Two, three, four, five, seventh and final time. I think this is the first time we've had two different Rolando's in the break. We've got Garcia and Lewis. Welcome. Four and three, seven times. All Rolando's welcome. One, two, three, four, five, six, and seven. After seven times, we've got nine down to three. For zero gets all redemption, so that would be those blockchain cards. So zero will drew. You'll get any and all redemptions for those teams down there, including one of one redemptions. Ray, you'll get all the other live one of ones. Aaron with nine. Josh with eight. James with two. Renee with four. Ray with one. Rolando with seven. I had a friend named Rolando, by the way. Rolando Garcia with seven. Josh with six. Drew with zero. Rolando Lewis with five. Aaron Pettit with three. So let's sort these by number. And in a separate video, if you're watching the replay of this in a separate video, will be the break itself. So check that out. Jaspy's casebricks.com.