i want to give a little bit of background before we dive too deeply into this topic uh a history lesson if you will we're going to focus on sort of necessary information to treat stroke and tia and we're talking about some stroke syndromes we're talking about aca distribution mca distribution pca distribution that kind of stuff but if we really want to dive into what is a profoundly dynamic area of medicine this is a really great place for the advanced bootcamp course and to give a little bit of overview and where this is coming from in 1995 or so there was the publication of the nin's one and two trials and these trials were published in the new england journal of medicine and this was the first time we ever saw a really large randomized control clinical trial looking at the use of thrombolytics for the treatment of patients presenting with stroke within a three-hour window and that was a trial that had a lot of problems with it there were problems with how patients were allocated their baseline morbidity at enrollment there was a lot of debate as to what the best primary outcome was what is a good outcome in a patient with stroke who's receiving thrombolytics is it that they are perfect and have no residual neurologic deficits is it that they score a certain number on a modified rank in scale and neurologic grading criteria is it that they move from really bad to a little bit better is it that they exist in one dichotomous category or another so you can see right off the bat that when we begin to talk about what's a good and successful outcome in stroke following thrombolytics right away we don't even know what the end zone is right because you're uh you may disagree with me as to what's a good outcome for a stroke um you may set a different bar for um deeming somebody a successful treatment with tpa so in 1995 these trials came out and there's been a number of trials since then 13 in fact most of which have been generally sort of neutral trials and that haven't driven the literature base in one way or the other but overwhelmingly this is a very difficult literature base nonetheless since 1995 we sort of developed this massive world of stroke intervention right we all are familiar with the window of tpa intervention we're all familiar with comprehensive or basic stroke centers all across the country this is a multi-billion dollar industry that was born from really one small trial fast forward then about 20 years 2015 or so we saw the publication of three trials mr clean extend ia and escape these were the first three trials that really began to look at neuro intervention sort of fishing up there with a wire grabbing that clot and either spraying it directly with tpa or grabbing it and pulling it out and these trials really began to reformat the conversation and address a lot of the consternation that had gone on in the 20 years precluding you know so much of the conversation in emergency medicine is uh angst with these trials that have suggested that tpa may be beneficial for patients who present within a certain time window but what these last three trials what these three trials in 2015 began to show us is that the long held time is brain mantra may be an incomplete approach to how we see patients presenting in the emergency department with stroke and specifically what we began to learn with the publication of mr clean extend ia and escape was that perhaps the approach to patients with stroke leverages our new and evolving technologies and changes from a time is brain mantra that every second that goes by you'll lose another additional 9 million neurons to a risk benefit analysis based off a neurogeographic model of ischemia and infarction it's a lot of big words but really what what did it land us on well when a patient presents to your emergency department 20 years ago with concern for stroke generally speaking they got their two and a half slice ct and a decision for tpa administration was based off of a time-based formula well with the publication of extend ia escape and mr clean what they began to use was new and evolving ct and mr technology sort of ct perfusion or mr diffusion-weighted imaging the type of imaging that is able to show us an infarcted core but is also able to show us an ischemic penumbra surrounding that core so instead of simply saying listen it's been three hours and one minute since your stroke so you're out of luck now we're able to look at this imaging and say okay look i can see a clear mismatch between a dead infarcted core and an ischemic and endangered penumbra and therefore i can say oh listen if your ischemic core is really small and your penumbra is right up against it and you have no salvageable tissue well the risk-benefit analysis of tpa or intra-arterial intervention or really any other intervention whatsoever clearly isn't there right there's clearly no benefit to be had you've infarcted your brain you don't have much time left that sort of your brain is dead and we're going to talk about the other things that can be approached for stroke rehabilitation and success but then also what if you come in and you have your infarcted core but then you have this profound and large ischemic penumbra and over here is you know how to walk and over here is how to sing and over here is love i don't know how the brain works but what you can clearly see is that there's a risk neurogeographic risk benefit analysis to be made and this has driven a whole new world and a whole new precipice in how we approach stroke in emergency medicine so there are two types generally of strokes there's ischemic and hemorrhagic strokes when we talk about ischemic stroke which make up about 80 to 90 percent of strokes that we encounter these can be thrombotic or embolic they can come up from the heart the heart throws off a clot they can start from atherogenic plaques in the brain but ischemic events usually prevent with a constellation of symptoms that point you toward a neurogeographic distribution of ischemia and that helps us make the diagnosis of stroke when a patient presents with complaints that are not in any neurogeographically similar or consistent pattern then we begin to think of other causes for their change in neurologic presentation the brain vascular anatomy helps us understand where the clot could have gone or where the clot could have been born and it helps us make these diagnoses within the vascular distribution of wherever a patient is presenting with neurologic compromise typically we begin to think of the most common areas where strokes can occur within the middle cerebral artery distribution but the anterior and posterior cerebral artery distributions in their clinical syndromes are important as well we'll talk of course about vertebra basilar syndromes and the vertebral basal artery as well as the lenticular striate arteries as well the middle cerebral artery and presentation of the middle cerebral artery is really the most common presentation of patients presenting with ischemic stroke this will be a contralateral presentation where the arms and the face are more affected than the legs the facial droop is a common and sort of classic presentation of patients presenting with middle cerebral artery stroke and the big key that we like to highlight here is that the facial droop typically and most often spares the forehead and the reason for this is because of dual innervation of the muscles of the forehead coming from dual innervation this obviously contrasts of patients who are presenting with facial droop secondary to bell's palsy which does not spare the forehead because the facial nerve itself becomes paralyzed ipsilaterally contralateral hemianopsia is commonly found in patients who are presenting with severe mca strokes remember eyes will point toward the side of the lesion middle cerebral strokes have contralateral findings and what you can see here is a picture of what you may have remember from way back in school a picture of the cerebral homunculus the homunculus which helps us understand where a patient is going to be most significantly affected from their stroke syndrome so a middle cerebral stroke most commonly affects patients with upper extremity weakness greater than lower extremity weakness and when we look at ct we can begin to see some of those changes on neuroimaging where here we see a ct of a large area of infarction almost certainly began with a clot in the middle cerebral artery leading to profound neurologic change the anterior cerebral artery makes up a minority of patients who are presenting with ischemic stroke and presents with contralateral weakness of the legs more so than the arms in the face and they have a sensory deficit in the same distribution this is in contrast to patients with pure thalamic strokes which we'll talk about in just a minute posterior cerebral artery tias and strokes are much less common and more often will have contralateral homonymous hema homonymous hemianopsia they'll have visual agnosia but they'll generally have minimal motor involvement vertebral basal arteries are often involved in patients who are presenting the with complaints that may be suggestive for central causes of vertigo when patient and we had a fantastic vertigo lecture earlier yesterday but an important reminder that when patients present with vertigo or virtiginous symptoms parsing out the central etiology or the possibility of a central etiology for their complaints is important and then finally there are the lacunar tias and strokes which often can be a bit more difficult to diagnosis patients will present with a pure motor syndrome if it's a large ischemic insult they'll have a pure motor hemiparesis with no sensory involvement whatsoever but pure infarcts in the lacunar area of the brain more often result with pure motor symptoms in patients presenting with stroke so these are our stroke syndromes but what about our tias most often can be much more difficult to make a diagnosis of tiaa because of symptoms that a patient present with that are often gone the patient's symptoms are gone and we're forced to make a diagnosis off of a base off of a patient's descript description of an episode the tia is described as described and defined as a transient episode of neurologic dysfunction caused by focal brain spinal cord or retinal schema without acute infarction and therefore we begin to recognize then that a tia's diagnosis has always and consistently had this neurogeographic and tissue based diagnosis component to it as opposed to stroke which has always had a time-based component to its intervention and diagnostic milieu but what we see here is that to make the diagnosis of tiaa you have to have imaging because you have to have neuroimaging which demonstrates no evidence of infarcted brain tissue this is often symptoms of a ti will last less than 24 hours but can last much shorter than that but symptoms typically last less than 30 minutes and often less than 10 minutes a consideration of a tia can be extremely difficult once a diagnosis that is often made on history alone and often an oscillating or different history an exam is typically normal or markedly approved from what a patient had initially described there are many symptoms which are not suggestive of tia and one of the pet peeves of mine is when i often hear a presentation of a patient who had a sinkable episode or loss of consciousness and on that differential from a resident or another practitioner is often stroke loss of consciousness stroke or tia which makes very little sense when we think about the neurogeographic distribution of what is going on with a patient remember that consciousness is supplied in the brain stem the reticular activating system and interruption of the reticular activating system or ischemia to the reticular activating system would be a stroke of the brain stem resulting in profound neurologic deficit often locked in syndrome alternatively the other way that you could suffer syncope and loss of consciousness from a stroke would be bilateral simultaneous mca cerebral infarctions extremely unlikely loss of consciousness is extremely unlikely to be suggestive of a tia or a stroke there are other things which are not suggestive of a tiaa in isolation alone very commonly we think of tiaa as more commonly subtracting from a patient than adding to a patient a patient will lose their ability to feel to move to see but very infrequently we'll have something added on to them for example paresthesia alone is a very uncommon presentation of tiaa and is more likely indicative of something other than central cerebral ischemia loss of balance tinnitus as we talked about previously amnesia syncope none of these things bring to mind tiaa or stroke at the top of the differential diagnosis but of course in our current climate we must always be considering the broad differential diagnosis that comes with stroke and tia hypoglycemia will always lead the top of this list and there's not an emergency clinician anywhere i think who hasn't been prepared or already called a stroke alert on a patient who comes back with a blood sugar of 16 a few minutes later the key is to hopefully get that blood sugar of 16 before you get the ct on a patient but an important reminder that a patient who presents with consigns and symptoms concerning for stroke we always return to our abc and d's airway breathing circulation and then dextrose for patients who are presenting with stroke-like symptoms and then the other big sort of mocker here the the one that we want to keep on our list is patients presenting with todd's paralysis or a post-seizure transient localized paralysis more common in the pediatric population but a todd's or post-seizure transient localized paralysis is quite common and really needs a detailed history to understand if the patient had signs of symptoms which would be consistent with a seizure episode prior to their paralysis which would more appropriately suggest todd's paralysis than tia or stroke when a patient presents to our emergency department with tia or stroke we are it is incumbent upon us to document a full and detailed neurologic exam including the presence or absence of carotid breweries including the presence or absence of a regular heart rate of course we know that all of these things if diagnosed or elucidated from physical exam can help identify the underlying etiology of a patient's stroke and get them definitive treatment a little more quickly and that drives the ed evaluation but also the subsequent inpatient evaluation an ed evaluation of a patient presenting with a ti or stroke as we discussed should really always begin with that rapid glucose that airway breathing circulation and then dextrose to ensure that hypoglycemia is not the uh the arbiter here the mass cause of the patient's neurologic symptoms and ecg is important to obtain for a number of reasons and when you dive down into the literature as to why an ecg is obtained in patients against presenting with ti or stroke you actually get different answers the common sort of snap back answer that i hear so often is what you want to get an ecg to see if they have atrial fibrillation because an irregular heart rate could lead to embolic stroke and that's absolutely correct but i don't need an ecg to make a diagnosis of atrial fibrillation i need fingers on a wrist or a monitor an ecg should also be obtained because there is a concomitant incidence of acute coronary syndrome in the setting of patients presenting with neurologic syndrome in fact in some cohorts up to five percent of patients presenting with acute stroke had simultaneous acute coronary ischemia and it drives the importance of a comprehensive workup of patients presenting with stroke symptoms and then finally a head ct without contrast no patient should be administered tissue plasminogen activator or any thrombolytics prior to a head ct without contrast and as we enter a new world of neural intervention you're going to want to have a detailed conversation with you in your own hospital system about other advanced neurodiagnostics which may be warranted at the time of presentation there are many hospital systems throughout the country that when a patient presents with signs and symptoms concerning for stroke or tia the patient immediately obtains either a cta or a cta as well as advanced ct imaging ct perfusion imaging to get a better idea again of that neurogeographic risk benefit analysis and then i want to talk a little bit about moving this neurogeo this neurologic imaging into the field a little bit more and many of you may have seen over the past five to six to seven years an explosion across the country of what's called mobile ct or ct-based pre-hospital ambulances these are ambulances that are equipped with a ct scanner and often a radiologic technician as well as a neuroradiologist on call to rapidly evaluate the head cts of patients in the field who are presenting with signs and symptoms which may be presenting with stroke this was born out of berlin in germany where the stemo program drove a giant ct scanner around berlin for a year and did everything they can to get the patients more quickly so that they could image them more quickly and then ostensibly administer tpa more quickly this has been extrapolated across the united states texas new jersey michigan colorado california many of these places have ct ambulances in effect now unfortunately never has a ct ambulance or a ct ambulance program ever been shown to have any benefit to a patient whatsoever they do cost on average about two million dollars and yet we have proven really time and again now that the the time savings they bring to any patient leads to no clinical improvement whatsoever and they are unfortunate a lot a very costly intervention that perhaps that money could be diverted elsewhere to more relevant and impactful programs but you do have a rolling dirty bomb rolling around your city so there's that tias the management of blood pressure in the emergency department is a tough one we have been assaulted in this newfound nihilism of asymptomatic hypertension and emergency medicine and everybody here has heard or should have heard by now that a patient presenting to the emergency department with asymptomatic hypertension there's a very outstanding and excellent asep clinical policy that guides our decision making in these patients you know long story short says you don't have to do much in a patient presenting with asymptomatic hypertension really regardless of what their blood pressure was and that nihilism sort of extends into tia and stroke and we know that lowering blood pressure acutely in tiaa and stroke may come with it some adverse events certainly anti-platelet therapy is warranted in tia and stroke once the ct demonstrates no bleed and if a cardiogenic source atrial fibrillation and clots from the heart are indicated anti-coagulation is likely to be brought on board early but not in the emergency department why do we care about tias we obviously care about tias because they're a harbinger of stroke right they could be a warning that stroke is just a few days weeks or months away and for so long we have thought about the abcd2 score risk scoring algorithm to determine what the risk of a patient converting to stroke in the next 30 days is throw it out get rid of it don't use it forget that it ever existed abcd2 is not reliable it's not has not been externally validated and it's not a good indicator of what a patient's risk factor is going to be in the coming days and the risk factor for stroke what do they do in the hospital once this patient comes in we call them tia we admit them to the hospital most of these patients get an echo most of them get carotid ultrasounds despite again the literature demonstrating that at a population level intervention most of these interventions do not change outcomes for patients or change the trajectory of outcome for them in any way shape or form the stroke belt this is a fascinating evaluation of epidemiology and stroke and since i've moved into the world of public health i've become more interested in understanding the underlying factors which drive morbidity and mortality in different disease states and this is the stroke bout which ever since really the 1960s has been designated and recognized as an area of the southeastern united states where mortality with stroke is significantly higher than the rest of the united states and there's many people in this room right now where you're looking at this map and say i live right in the maroon and if that's the case you got to be a stroke expert this is where people are dying from stroke at rates much higher than other parts of the united states you have to ask yourself why is it because of the geography is it because of the food is it because of the politics is it because of accessibility to the hospitals and this has been looked at time and time again and it's truly fascinating that within the stroke belt we see consistent signs of decreased access to comprehensive stroke care we also see higher rates of poverty higher rates of patients with poor access to primary care and this area of the united states has continually been identified as an area where stroke survivors have i'm sorry stroke sufferers have poor mortality what does a patient look like when they present with a stroke they have neurologic deficits and for the longest time we've really discussed the time is brain mantra and we're going to talk about that because it's still kind of the general approach to things in emergency medicine but you need to begin to understand that our understanding and our comprehension of stroke syndromes has really evolved from the simple time is brain mantra right it's probably not completely accurate it probably is a much more complex and interesting interplay between time as a contributor of course but a neurogeographic risk benefit analysis using our newest technologies to get a better insight as to what we can do should we intervene in any way shape or form these patients if they are altered and can't maintain their airway should be intubated if possible itominate is a reasonable drug to use we do try to limit ketamine utilization in patients who are being intubated in the setting of neurologic compromise because ketamine is thought to potentially increase intracranial pressure now how that parlays down the road to clinically apparent and clinically important outcomes for the patient is kind of yet to be seen but automate is generally thought of as the preferred induction agent in patients with stroke and then succinylcholine or rock uranium as appropriate for paralysis and then there's the monitoring of the blood pressure and we'll talk a little bit more about blood pressure management and stroke it's extremely controversial and generally speaking we don't treat blood pressure and stroke and when we ask ourselves why should we but why are these patients hypertensive to begin with we begin to pull out a bunch of different theories patients who present with stroke often are found to be hypertensive and there's three leading theories as to why that is the first is that the body is increasing the blood pressure to better perfuse a hypoperfused area and that makes a lot of sense the second is that the stroke could have injured the body's own ability to auto regulate and cerebrally auto regulate and that's a possibility and speaks toward the possibility of us intervening and we'll talk about how you intervene if you're going to intervene and then the third possibility and it's probably a little bit of all three let's be honest is that the anxiety and excitement surrounding their presentation to the emergency department their diagnosis of stroke is almost certainly to raise their blood pressure a few degrees as it is and so for the most part we don't treat blood pressure in ischemic stroke certainly if it's under 220 over 120 there is an exception here and that's the administration of thrombolytics the administration of thrombolytics does call for the patient's blood pressure to be less than 185 over 110 and says you have to get there without aggressive blood pressure management now i don't know what aggressive blood pressure management is i don't know if it's a single agent two agents three agents or more i don't know if it's me getting creative with the blood pressure cuff or quite what exactly it means this is an area where there's a little bit of clinician judgment to be had but generally speaking what we've learned is that if patients require blood pressure lowering in the acute stages of stroke to bring their blood pressure below 220 over 120 or below 185 over 110 for administration of thrombolytics the preferred agent is a calcium channel blocker most commonly nicardipine nycardipine has been shown in a number of trials particularly the clue trial as well as some other trials to be the preferred agent for blood pressure management in patients presenting with neurologic hypertensive emergencies and the alternative agent is clavitipine which is a newer dihydropyridine calcium channel blocker which is a bit more titratable but also a lot more expensive and can be used at the bedside to dial in blood pressure quite easily other patients who are not receiving parenteral antihypertensive agents are generally treated with oral ace inhibitors ace inhibitors have been shown to be particularly beneficial in this patient population and often these patients will simply be started on lysinopril and sent on their way in a few days hemorrhagic strokes are a bit different and another area of controversy in emergency medicine there are a number of trials which have looked at the management of blood pressure in patients presenting with hemorrhagic stroke we think of the atach2 trial which looks at should i aggressively manage this blood pressure and drive it below 180 or should i drive it even more aggressively and get it below 160 and the data has been a little bit back and forth but generally speaking what we've landed on is that in patients who are presenting with hemorrhagic stroke lowering the blood pressure below 160 to 180 is safe and effective for decreasing hematoma size in the brain moderate modest lowering of the blood pressure targeting of systolic blood pressure about 160 has been shown to be safe and again the preferred agent is nicardipine or clevelandopine we talked about stroke imaging and i want to review it really briefly as we begin to enter our grab bag of neuroscience and psychiatry at the end of the course here always look at your own cts and your own mris of course look for evidence of hemorrhage of course when we look on a ct evidence of hemorrhage shows up at that white stuff in the top of the brain and of course it looks terrible if the patient is not a excuse me if there's no hemorrhage identified on ct that patient would then become a candidate for fibrolynic fibrolytic therapy and then of course when we're administering fiber analytic therapy we can go through the exclusion criteria i would urge you never to memorize these and every single time look up the exclusion criteria for thrombolytics thrombolytic treatment of stroke requires an informed conversation with our patient and this is extremely difficult and requires that we be informed if we're going to have this conversation with the patient it requires us to understand the evolving literature basis since 1995 which has discussed the use of tpa for the intervention in patients presenting with stroke we know that some patients are likely to get better with tpa administration these are likely patients when you do neuroimaging who have profound mismatch between their ischemic core and their i'm sorry their infarcted core and their ischemic penumbra we also know that there are patients who are going to get worse after thrombolytic therapy here we say it's about six percent and that's about right patients who will suffer intracranial bleeding following administration of tpa or profound large volume gi bleeding and have poor outcomes from same and so administration of tpa really begins with this informed consent with the patient this is one script that we've provided with you which you're more than welcome to discuss and it it sort of bridges the divide between the difficulty and scientific language that we're confronted with from the medical literature and the language that we're required to have at the bedside to discuss this with a patient and have an informed discussion the dosing of tpa and stroke run by the nurses of course out to place is the go-to but recent literature has really begun to suggest that nectar plagues may outperform outer place as the preferred thrombolytic agent in the first three hours for stroke but then finally we moved to endovascular therapy the whole new frontier and whole new world in patients presenting with large vessel occlusion to our emergency departments extend ia escape and mr clean taught us so much about the future of stroke and what it's taught us is that brain perfusion studies and intra-arterial intervention in patients with stroke is really teed up to have profound improvement in outcomes over the next five to ten years where we're seeing this evolution of the treatment of stroke begin to resemble the treatment of myocardial infarction much more closely where we began with the treatment of myocardial infarction in the world of fiber analytics and have moved to percutaneous intervention much is becoming the same for stroke and while extend ia escape and mr clean all included tpa prior to intra-arterial intervention in these patients who has been a number of trials since which have excluded the initial intervention of tpa and are consistently demonstrating that patients do extremely well with intra-arterial intervention without thrombolytics beforehand and these patients can have really great outcomes a note there has been a lot of oscillation in society-level guidelines surrounding stroke over the past several years and in the past few years there was a large redaction of a lot of information in the aha guidelines surrounding strokes things talking about blood pressure management and time management and what all of that is begin we say all of that to begin to inform you that we are poised at the precipice of a new world of stroke care in the united states we are looking at an evolution from 20 25 years of a time-based approach to stroke that exclusively used fiber analytics for all comers to a new world that is a neurogeographic risk benefit analysis that harnesses new technologies to lead to better outcomes for patients it's exciting it shows the value of literature and the value to sticking by our evidence-based guns in the conversation and it shows that patients with stroke have an optimistic future ahead of them that's all i have thanks guys