hello newbies welcome to the exciting field of stroke my name is Igor ribbon ik and I am a vascular neurologist at Rutgers Robert Wood Johnson medical school and the neurology clerkship director over the next 90 minutes you'll become a stroke neurologist for managing patients with various server vascular emergencies so keep you hands and feet inside the vehicle at all times and have fun I have no irrelevant conflicts to disclose so the objectives of this talk are to review the vascular Anatomy and vascular syndromes to discuss the diagnosis and management of acute ischemic stroke to review the five mechanisms of ischemic stroke with a specific focus on diagnosis and stroke prevention to discuss the diagnosis and management of acute hemorrhagic stroke and to review the three mechanisms of hemorrhagic stroke with a focus on diagnosis and prevention so before we get to the fun stuff we do have to review server vascular Anatomy yeah I know what you're thinking that is so last year second year of med school called and once it's pile of information back unfortunately anatomy is still important for every day stroke care and we have to crawl before we learn to walk pretend this patient is looking directly at you I haven't chosen this view by chance you'll see this view in various vascular studies you can see the arch of the aorta on the bottom of the screen a giving rise to anterior and posterior circulation vessels common carotid arteries typically arise from the brachiocephalic trunk on the right and I or t'k arch itself on the left they bifurcated into external carotid with Rogers in the neck that's how you know they're external and internal carotid that ascent all the way to the brain in the back of the neck vertebral arteries arise from subclavian branches of the aorta and supplied the posterior circulation so far so good great now let's take a look at the intracranial vasculature and the Circle of Willis the two vertebral arteries we spoke about are visible here and with an important perforator called posterior inferior cerebellar artery or pike up which you guessed it mostly supplies the posterior inferior cerebellum and lateral medulla retrievals then joined together to form a basilar artery with major branches including the eicha or anterior inferior cerebellar artery the SCA or superior cerebellar artery and at its tip the basilar bifurcates into posterior cerebral arteries it sort of looks like a palm tree from the posterior circulation posterior communicating artery connect PCAs to internal carotid arteries and the anterior circulation is basically comprised of icas which bifurcate into middle cerebral and anterior cerebral arteries and anterior cerebral czar in turn connected by anterior communicating artery there's quite a bit of variability in the vasculature and only 1/3 have a complete circle of willis who you're still with me and now for the PSA as he stones vascular territories you can see them coming into view as I scroll you can actually refer to the legend on the right side of the slide to see which vessel corresponds to which colour so the medial frontal lobes are supplied by the a CAS medial frontal lobes are important for contralateral led control motivation and the memory circuit so as you can imagine a CA infarcts cause abulia an unmotivated state contralateral leg weakness and amnesia mca supply the vast majority of the hemispheres an occlusion of these vessels causes quite a bit of symptoms including contralateral hemiparesis face Paris's gaze Paris's sensory deficits field cut and in non-dominant lesions and neglect and in dominant hemispheric lesions aphasia with those symptoms you can throw in dysarthria which is non localizable and can occur with any damage to the motor tracts and difficulties with skilled movement called apraxia now PCA supply the thalam I so called the switchboard of the brain as well as occipital lobes and large parts of the midbrain so it's not surprising that PCA territory infarctions can be very diverse they can cause sensory loss on the contralateral side but also field cut amino PIA occasionally neglect if you damage the non-dominant thalamus and transcortical aphasia if you damaged the dominant thalamus and behavioral abnormalities the patient can look frankly psychotic with thalamic damage now as we go lower if the midbrain is involved in midbrain here is pictured in blue it looks like a head of a Mickey Mouse you can get contralateral hemiparesis from crus cerebri involvement apes a lateral third nerve palsy and contralateral ataxia from red nucleus damage the basilar artery supplies wait for it the base of the brain well mostly the pons in some anterior medulla to be precise so unsurprisingly it can actually cause contralateral hemiparesis with or without facial weakness any sensory loss intranuclear ophthalmoplegia that's when both eyes are not moving in synchrony and that's from a medial longitudinal fasciculus damage it can also cause if so lateral symptoms including horizontal gaze Parris's from pontine para media and reticular formation damage they taxi for damage or fibers that are going to the cerebellum lower motor neuron facial weakness from cranial nerve nucleus of seven damaged facial sensory loss with cranial nerve nucleus of five damaged as well as nystagmus next SCA it supplies the anterior superior cerebellum it's all in the name and infarcts occlusions of that vessel can cause a taxi ax lower down you see anterior inferior cerebellar artery Eike pictured here in light blue now it mostly supplies the cerebellar peduncles so i co territory infarcts are very similar to SCA in farts causing epsilon ataxia however eicha actually gives rise to labyrinthian artery which supplies the inner ear and occlusion of eicha can cause epsilon all hearing loss and finally Baike pictured here in purple PICUs applies the lateral medulla and the posterior inferior cerebellum so occlusions of pica can actually cause cross signs so you get contralateral hemifield lamech track damage but you can also get epsilon oral facial sensory loss from cranial nerve nucleus of v damage you can also get tongue deviation a Horner's syndrome from sympathetic damage and a taxi a' from cerebellar damage you also get bull bar signs the so called for the bulb and bulb is the medulla so you can get dysarthria dysphagia hoarseness lower down perforating branches of the vertebral artery supply the medial medulla and stroke in that region can actually cause Hemi Parris's due to pyramidal damage I hope this was a review and now you're still confused but as Enrico Fermi puts it hopefully confused but on a higher level otherwise you may need to rewatch the segment in slow motion also consider pausing that Netflix show that I know you're simultaneously watching while watching my podcast okay so now that we understand the vessels involved and the symptoms their blockage may cause let's jump right into a case so we have a case of a confused man he's a 74 year old man with hypertension dyslipidemia coronary artery disease who develops acute confusion left facial droop left-sided weakness while driving his car he's able to pull over to the side of the road and bystanders who witnessed this event actually called the ambulance he arrives to the emergency room one hour after symptom onset he has no headache and he's able to protect his airway you're examining him in the emergency room and you notice that he's alert awake he's oriented to place person and time he has no aphasia but his speech is slurred he has dysarthria and profound neglect he doesn't even recognize that he has left-sided weakness he also has right gaze deviation and no matter how hard you try you can't get him to cross midline with his eyes he also has a left field cut left facial droop and flaccid left hemiparesis so what is the differential diagnosis of acute focal neurologic deficit well that is actually a relatively short list with of course cerebrovascular disorder right there at the top ischemia or hemorrhage but the differential actually includes also seizures with postictal paralysis hypoglycemia brain and neoplasms demyelinating disorders such as multiple sclerosis infections such as brain abscess encephalitis meningitis and complicated migraine just to prove my point on the right is the MRI of a patient who presented very similar to our patient but was actually diagnosed with a tumor in the parietal occipital region with quite a bit of subcortical white matter edema now was seen here in bright white edema creates a hyper intense signal and you can probably make out the eye so intense around mass in the middle so what's the next best step in the management imagine the right MCA gets blocked as pictured in this illustration so almost immediately some part of the brain usually the deep structures which rely on that blood flow die pretty quickly and that's called the ischemic core it is an area of the brain that suffered irreversible ischemic damage however there is a large part of the hemisphere that is surviving on blood flow from collaterals and that is called ischemic penumbra collateral flow is not as robust as direct blood supply via the MCA think of it this way if a main highway gets blocked by an accident you can still get to your destination by side streets but with much more difficulty penumbra can become viable tissue or permanent infarction so the primary principle of acute stroke therapy is to re-establish blood flow before the brain and fart and the clock starts now so our patient arrives at the hospital and to facilitate stroke care a stroke code is called by the way is scrub still a thing well a stroke code brings the entire team together to the bedside we usually want to know a brief history what was the last time known normal and contraindications to TPA we need to get a quick neurological examination sort of to get the lay of the land and obtain imaging to rule out hemorrhage and there is usually one person who is lost during the code like dr. Kelso here who is asking for free muffins National Institutes of Health stroke scale is a standardized focused neurological exam that was developed to be able to rapidly assess and follow a stroke patient it consists of 11 domains level of consciousness orientation command following gaze visual fields facial palsy motor strength of the extremities limb ataxia sensory loss language this is expressive language dis are three articulation extinction and intention which is essentially neglect now the actual scoring is not as important as describing the deficits just note that the higher the score the bigger the stroke so NIH Stroke Scale of zero maybe normal or near-normal patient in a stroke scale of 42 is a very severe stroke please note that gait and reflexes are missing from this list NIH Stroke Scale does not replace a full neurological exam but it allows you to examine and treat a patient faster so let's get back to our case remember our patient had dysarthria profound neglect and no signature right gaze deviation left homonymous hemianopia left facial droop and flaccid left hemiparesis so that's out of the score for the level of consciousness the person was normal orientation was normal as well and so was his command following but on the gaze he could not cross midline forced gaze deviation so he earned two points their visual fields he had a partial field cut one point he had a partial or lower face facial palsy one point on motor strength of the arms and legs essentially the right side was normal so he receives zero points there but the left arm and leg had no effort against gravity it did have a twitch of movement so he got a three on for both out of a possible for limb ataxia there was no ataxia out of proportion to weakness sensory loss it was pretty dense so he earned two points there his articulation was impaired so he at one point but he had no aphasia he was able to express himself zero points there and he had of course profound neglect two points so when you add up the entire score it's about 15 points which correlates with a large infarction so far so good by the way you're still on the clock so don't think about pausing this presentation to go get some coffee it's about to get more fun to proceed to treatment we first need to exclude intracerebral hemorrhage in a non-contrast head CT is excellent for that purpose with over 95 percent sensitivity let's take a moment to learn how to read CTS so let's focus on the image on the left pretend the patient is lying in front of you on the table with feet closer to your face and head further away from your face the patient is lying face-up so you're looking at the patient's brain through the bottom of their jaw so the eyes should be facing towards the top of the slide and the patient's right side is on your left the bright outer rim is the dense skull now look at this axial slice through the basal ganglia do you see anything abnormal is there a problem on the patient's right side is there a problem on the left side is there no problem well if you said that this is a completely normal study you are correct but you say to yourself self how can the CT be normal isn't the patient having a stroke in an acute ischemic stroke patient early head CT is normal pause on that for a second ischemic neurons cannot maintain sodium potassium gradients and as a result take on water becoming a demitasse over a course of hours today's hit demise fluid fluid looks dark or less dense on CT so it typically takes about six hours for a cat scan to develop a hypo density corresponding to the ischemic tissue our patient presented within an hour after symptom onset so his stroke has not yet set in so a normal head CT does not mean no stroke but instead it's actually reassuring and it's telling us there's brain left to save if we were to proceed to treatment Oh head CT you sly devil you you won't trick us by the way take a look at the image on the right there is a hyper dense region in the Sylvian fissure do you know what that is you're right of course it's blood or clot to be more precise that's contained within the middle cerebral artery this is called a dense vessel sign it's quite specific and very helpful when you see it but it's not very sensitive you can see these dense vessel signs and other vessels not just the middle cerebral artery so the head CT is the best initial test because it's very good at excluding hemorrhage but should be completely normal in early ischemic stroke with a head CT we also typically get a CT angiogram it's a pretty rapid study that follows a bowls of contrast to trace the lumen of head and neck cerebral vessels leading the brain it's an excellent study to document large vessel occlusion on the left you once again see the axial cut the patient is looking towards the ceiling you can actually see the eyeballs facing the ceiling and on the right is the coronal cut where the patient is actually facing you so take a look at the image on the left do you see the robust flow in the left middle cerebral artery now compare that to the right something's missing isn't it there's a thrombus occluding flow through the right MCA and the same can be visualized on the coronal cut now back to the case do you remember the primary goal of acute ischemic stroke treatment that's right remove the obstruction and restore blood flow to save the ischemic penumbra so to recap our patient was delivered by an ambulance to the hospital his symptoms were recognized as a right MCA syndrome and a stroke code was called a rapid neuro exam the NIH Stroke Scale defined his deficits and Ct confirmed absence of hemorrhage and CTA confirmed right MCA occlusion so the next step is treatment administering IV TPA in order to give TPA the patient has to be within a four and a half hour window so establishing the time last known normal or last known at baseline is crucial here we typically check a finger stick because hypoglycemia is a great mimic or stroke elevated blood pressure is very common in stroke patients and is the single most significant risk factor for bleeding after TPA so we have to lower the blood pressure to less than 185 over 105 the contraindications to TPA by the way can actually be summarized as two statements are you currently bleeding or are you likely to bleed so the head CT can exclude intracranial hemorrhage but if there's acute internal bleeding giving a thrombolytic that activates plasminogen and lysis clots is not a good idea if a patient has a condition that predisposes them to bleeding for example full dose anticoagulation IV TPA is contraindicated as well please note that although labs are typically sent during the stroke code we don't have to wait for results to treat the patient unless there's a history or suspicion of quiet allopathy so let's get back to our case TPA was started and neurological examination remains unchanged so have we accomplished our primary goal well obviously not CTA told us there's an occlusion in the right MCA and unfortunately TPA works about 1/3 of the time on the lesion like this it's time to get a lot more aggressive we review illegible 'ti for endovascular which in a nutshell means a previously functioning patient now with disabling deficits whose penumbra or area at risk and also the area that we can save is nearly twice as large as the ischemic core or area of irreversible damage our patients fit the criteria and we prepare him for intervention by 60 minutes from arrival to the emergency department the patient's groin is punctured a catheter is ascended through the femoral artery up the aorta brachiocephalic trunk right CCA right ICA and eventually reaching the right MCA clot and thrombectomy is performed and clot is removed using suction or one of these modern stand retrieval devices that's pictured on this slide these therapies actually pretty effective over 80% of the time in fact these are probably the most effective treatments in all of medicine with a number needed to treat of two to three to help one patient a chief functional independence that's pretty remarkable now you've been paying attention and I know what you're thinking if therm ectomy is so wonderful and IV TPA doesn't always work why not just skip IV TPA and go directly to thrombectomy valid question my young padawan the problem is that even when the stars align it takes 30 to 60 minutes to assemble the end avascular team and puncture the groin look at this time circle here also about one-fifth of the patients may have difficult Anatomy making tharam ectomy a nightmare so IV TPA is always much faster and can continue to work while arrangements are being made for into vascular intervention remember the ultimate goal is opening the blood vessel so we don't wait at all after IV TPA before proceeding to therm ectomy but say you're still not convinced what difference does a 60 Minutes make imagine you see our patient arriving at the ambulance Bay in the emergency department well in that second of right MC occlusion the patient has lost 32,000 nons you decide to introduce herself hello mr. Smith I'm doctor ribbiting that little delay cost the patient two million neurons so we really no longer introduce ourselves to the patient until the treatments been started if you wait an hour before beginning treatment that patient will have lost 120 million neurons which is equivalent to the same number of neurons a patient would lose with nearly four years of aging and in an average stroke a patient may lose over a billion neurons so pretty much every second counts while if graphs get you excited this one illustrates the same point this is data from Hermes collaboration including modern endovascular thrombectomy trials on the y-axis are the odds of patient improving and on the x-axis is time from symptom onset to the start of intervention the longer we wait the less chance for improvement and at around 7 hours from symptom onset the risk of Thurm back to me begin to outweigh benefits remember the stroke neurologist mantra time is brain say it with me time is brain now I did promise something cool these are the images of a cerebral angiogram just to orient you the patient's looking directly at you the x-ray shadow in the middle of the screen is an endotracheal tube the endovascular catheter is resting in the in carotid artery and the dye is injected and x-ray images are obtained in rapid succession to track the flow of dye and consequently the flow of blood in real-time so take a look do you see a problem just as we suspected the right MCA still occluded now take a look at what happens after the clots been removed we have restoration of robust MCA flow and if we keep scanning we can even see the blood travel from the arteriole face across a capillary network into the venous sinuses and out of the cranium through jugular veins now is this not the coolest thing you've ever seen take a look at the clot that's been removed so let's get back to our case and the vascular therapy was successful and neurological improvement was noted after the procedure and patient was admitted to the ICU now that the flow has been restored what are the new goals of treatment once where perfusion has occurred we are now focused on prevention of secondary injury remember that blood pressure is an important permanent of bleeding risk while we generally want permissive hypertension in acute ischemic stroke we must no lower the blood pressure to avoid post refusin hemorrhage blood pressure targets post intervention are a bit of an educated guess surrounded out with some wild speculation supposed to TPA the blood pressure goal is typically set at less than 180 over 105 if we managed to open a blood vessel and restore perfusion the blood pressure goal becomes 140 to 160 systolic now this patients of course must be closely observed in an ICU setting with frequent neuro checks we typically use NIH Stroke Scale to reassess stroke patients and get worried if the score increases by four or more points multiple neuro protectant trials failed in the early 2000s and it was generally a disappointing decade in stroke research so the best neuroprotection we have so far is homeostasis making sure hyperglycemia is corrected fevers are addressed and targeting normal cap Nia and normal NAT remya on top of that cerebral edema usually rears its ugly head and Peaks over the course of three to five days and at times it becomes so severe that it needs to be addressed but once we get the patient over the secutiry 'add the goal now becomes to prevent recurrence and the gooey chocolate center of that goal is of course stroke workup now that brings us to a discussion of stroke workup mechanisms and prevention strategies and to keep going with my chocolate metaphor I'm gonna borrow a phrase from Forrest Gump my mama always said stroke was like a box of chocolates you have to do an MRI transesophageal echo and mobile cardiac telemetry to know what you go and get so let me ask you a question why do we need to do a stroke workup a study was never done to prove that doing all those tests improves outcomes and stroke patients well to that I say there's no study on the effect of parachutes on mortality in patients skydiving at 13,000 feet are you gonna stop using parachutes until such a studies done as stroke neurologists would sort of intuitively understand that stroke workup changes management so the idea is that three-quarters of patients may be at low risk for and stroke but one quarter may Harbor a dangerous source of clots which needs to be addressed more aggressively so we absolutely must find the wolf among the Sheep so who remembers the ver cows try it rudolf ludwig car lover cow was a 19th century german physician among other things who proposed a simple idea that in order to form a thrombus the body needs three conditions abnormal stasis of blood in the heart for example increased clotting potential and endothelial injury of vessel wall injury so in a nutshell stroke risk comes from disorders of the heart blood vessels and blood itself it's not rocket science so to expand on virchow's theory ischemic stroke the most common kind of stroke may be caused by vessel disease cardio embolism rare causes such as hypercoagulability and genetic derangements and in one third of the patients even after extensive stroke workup we never prove a cause and those are known as cryptogenic strokes although recently they've been reclassified as embolic strokes of undetermined source because they look embolic so let's tackle the thrombotic mechanisms first which patients get thrombotic strokes well there's a common risk factor profile for both large vessel and small vessel strokes a typical patient is older has multiple vascular risk factors such as hypertension diabetes dyslipidemia smoking so a hypertension patient for example is at risk for both small vessel and large vessel strokes the key clinical differentiator between these subtypes requires an understanding of what's meant by large vessel and small vessel any ideas well I'll give you a hint large vessels are the ones that have proper names carotid artery vertebral artery proximal middle cerebral artery etc small vessels are unnamed perforators coming off of those named large vessels these small vessels supplies subcortical structures like the basal ganglia thalamus pons deep cerebellum take a look at this example of perforators off the MCA so small vessel strokes tend to be radiographically smaller and subcortical and clinically milder by the way what symptoms will you never see in a patient with a small vessel subcortical stroke it starts with a C and ends with a article that's right small vessel lacunar strokes generally do not cause aphasia neglect field cut which are symptoms traditionally attributed to the cortex in order to call a stroke large vessel we need to have radiographic confirmation of large vessel disease on vascular imaging take a look at this example carotid artery stenosis is the poster child for large vessel stroke one more important point about large vessel strokes of all ischemic stroke mechanisms this one is practically the exclusive cause of transient ischemic attacks if you're interested in the mechanisms large vessel strokes are typically caused by atherosclerosis and lacunar strokes have multiple proposed mechanisms including lipo halitosis tiny atherosclerosis and Mike ramble I can you guess what the CT is showing do you see the subcortical black holes corresponding to chronically damaged brain what type of strokes are these if you set small vessel you are correct these are small and subcortical and therefore by definition small vessel or lacunar infarcts now this stroke is more extensive and take a look at this mr angiogram image of the common carotid artery bifurcating into internal and external carotid at the arrow you can see the internal carotid artery and it almost looks like as if someone took a bite out of the ica doesn't it this is the classic appearance of a large vessel atherosclerosis causing stenosis stenosis can result in poor cerebral blood flow causing watershed strokes like the ones pictured here or pieces of the unstable plaque can embolize to the brain now let's switch gears to discuss Cardian bollix stroke clinically speaking there is generally a striking difference between how cardio bollock and large vessel stroke presents think of it this way how long does it take to form a carotid or MCA plaque significant enough to affect the blood flow years it's a slow process in that timeframe the brain slowly adjusts by increasingly relying on collateral flow if that stenosis progresses to the point of occlusion the stroke will likely be relatively small since the brain has had a chance to adapt now imagine that our previously normal MCA suddenly gets occluded by an embolus the entire MCA territory starves and the patient will have maximal severe deficits also radiographically Karndean bollocks strokes tend to be larger and may affect multiple vascular territories think shower of emboli and high-risk embolic sources include atrial fibrillation left atrial appendage or left ventricular thrombus valvular disease such as endocarditis structural heart disease paradoxical embolism from the venous system which typically goes to the right side of the heart across a patent foramen ovale which is a communication between two atria to the systemic circulation the left side of the heart a Artic arch plaque and cardiac tumors can also embolize although that's more rare so all of these can cause Q cheesy animation and bollocks strokes so here's the imaging example of cardio bollocks strokes multiple hyper intensities in both hemispheres correspond to acute stroke in various vascular distributions so in this patient transthoracic echocardiogram shown here is the classical four chamber view of the heart shows a large left ventricular thrombus here are some of the more rare mechanisms of ischemic stroke arterial dissection is basically a tear of the intima and the media resulting in hematoma forming to heal the tear but occasionally pieces of that hematoma can embolize to the brain in the process dissections usually happen in younger patients with predisposition I think connective tissue disorder and weakened vessel walls and superimposed trauma by the way trauma doesn't necessarily mean a car accident where a person is thrown through the windshield trauma can be as mild as a violent sneeze or retching and vomiting think of the vessel wall as being Superman weakened by kryptonite and Batman is mild trauma so normally Batman has nothing on Superman but in this situation Batman's punches can surely do some damage other causes include sickle cell disease hypercoagulable states vasculitis vasospasm possibly drug-induced venous sinus thrombosis this is a venous infarction genetics such as mutations and proteins that ensure vessel integrity and complicated migraine which actually causes a leggy Meah or decrease blood flow and sometimes can progress to an actual stroke well that was a lot of information but I know what you're thinking which stroke mechanisms are the most dangerous which ones do I really need to worry about well that's a great question and I'd like to illustrate that concept of ischemic stroke risk with dogs small vessel disease is like a small French Bulldog conferring a stroke risk of several percent per year large vessel disease while here we're looking at a medium-sized border collie three to six percent risk per year cardio embolic stroke is like a large German Shepherd stroke risk of up to 15% per year and rare causes are kind of unpredictable just like this kitten sometimes they have a low risk of stroke of less than 1% and sometimes they can increase the risk of stroke tenfold depends on the cause now that we understand the possible causes of stroke remember why we embarked on this discussion in the first place to find the wolf among the Sheep a patient who is at high risk so a typical stroke workup consists of a brain MRI without contrast which is the gold standard depending on the clinical history in MRI you can suspect a certain mechanism or mechanisms typically you would also need to do vessel imaging for Cardian Baalak workup every stroke patient gets a transthoracic echo and an EKG and some in hospital telemetry cardiac monitoring but if you truly suspect a Cardian bollix source you would need to go further to transesophageal echocardiogram and extended outpatient cardiac monitoring modifiable risk factors such as dyslipidemia diabetes and smoking be assessed and addressed in certain patients where rare stroke mechanism is suspected we may have to check for hypercoagulable state or genetic vascular posses and occasionally invasive procedures like a cerebral angiogram which is really the gold standard of vascular imaging and a brain biopsy which is the gold standard of gold standards may be necessary for diagnosis for example if you have a case of CNS vasculitis so the gold standard of acute ischemic stroke diagnosis is specifically diffusion-weighted imaging sequence on the MRI now I'm not a radiologist I just play one for the purpose of this podcast DWI essentially shows area of energy failure when neurons can no longer maintain sodium potassium gradient and water does not diffuse along that gradient and creates a bright signal or an area of restricted diffusion DWI becomes positive within the first 30 minutes and stays positive for approximately a month after the stroke onset and in order to confirm true restriction of diffusion DWI is checked against its evil twin apparent diffusion coefficient or ADC pictured here on the right true stroke is bright on Twi and dark on ADC by the way since MRI is quite a bit slower to acquire than CT it's typically done after acute treatment to avoid delays our options for non-invasive vascular imaging are essentially CT angiogram and mr angiogram you saw that our patient got a CT a during the stroke code and here's another example CTA is very quick it has slightly better resolution than MRA especially for distal small branches of cerebral blood vessels but CTA is susceptible to bony artifacts it requires radiation and it carries a risk of contrast nephropathy so CTA is perfect in a neurological emergency where you quickly need to know the vessel status MRA on the other hand pictured on the left side of the slide is slower but safer it gives you a beautiful picture of proximal intracranial vessels without any contrast so MRA is preferred in non-emergent situations and in patients who should not be repeatedly radiated think of kids cancer patients and pregnant women they probably would rather avoid a CTA Oh an MRI doesn't image bone so no bony artifacts the third option for vascular imaging is ultrasound specifically transcranial Doppler and carotid ultrasound combination but that modality is best used for confirmation or follow-up of known lesions because it's operator dependent and can only visualize certain portions of the vessels and not the whole vascular tree this is Emery of the neck the images take longer to acquire and we have to use gadolinium contrast to avoid artifact but in return we get a beautiful picture of the vascular tree all the way from the aortic arch to the brain do you remember us going over a cerebral vascular tread the beginning of this talk while this is that same view the patient is still looking at you with the aortic arch all the way on the bottom carotid and vertebral x' in the middle and Circle of Willis towards the top so compare that with a CTA on the right which is a little more detailed but it's definitely contaminated with bony artifacts and veins bottom line there's no clearly better study and each study has strengths suitable to certain use cases like each member of the Avengers superhero team except Hawkeye no one really knows how he's lasted this long battling gods and otherworldly beings with a bow and arrow is anybody else confused okay that was a very long detour but remember we still have a patient to treat so back to our case CTA was done an admission and there was no carotid stenosis echo showed normal ejection fraction and mildly dilated left atrium and telemetry monitoring showed paroxysmal atrial fibrillation so what's the appropriate stroke prevention regiment Before we jump into the prevention regimen let me ask you a question what do you think is the number one risk factor for stroke in general did you say hypertension what about number two risk factor nope still hypertension what about number three still hypertension hypertension increases the schemings stroke risk fourfold and hemorrhagic stroke risk nine fold then there are the other well-known vascular risk factors so the four major pillars of stroke prevention include blood pressure control statin therapy not so much for the cholesterol but it confers anti-inflammatory plaque stabilizing effects antithrombotic therapy which in our case is actually going to be an anticoagulant for atrial fibrillation smoking sensation and glycemic control in diabetics now let's say we flip the script while we are running around getting those CTS CTAs TPA all the deficits in our patients miraculously resolved within 30 minutes how does our management well first we don't give TPA it's hard to make somebody more normal than normal the clock is reset and this becomes the last known well time so if the symptoms return within four and a half hours the patient can still be treated with TPA and finally the workup is the same as if the patient suffered a stroke so let's talk about transient ischemic attack for a second TI a has become sort of the wastebasket of medicine disorientation after opioids dia episode of slurred speech during dialysis dia transients sleepiness Ti a transient tingling TI a 60 seconds a word finding difficulty TI a transient facial droop well it's very easy to turn off our brains and call everything at TI a but the vast majority of those events are not server vascular in nature a true transient ischemic attack is a very worrisome it's basically brain pain it signals that a stroke is coming remember that earlier in this talk we spoke about large vessel disease while cia's occur almost exclusively in patients with symptomatic large vessel disease like carotid stenosis if you don't identify the stenosis and address it you may be dealing with a full blown stroke pretty shortly so in the modern era a good definition of TI a can be found in something called the ABC d squared score so a transient event is more likely to have been served or vascular if the patient is older has risk factors such as hypertension and diabetes you have the symptom lasted 10 to 60 minutes and preferably included unilateral weakness or speech disturbance well that was a lot of information I realized that let's arrest your brain with this fun clip from the movie Dracula dead and loving it [Music] gentlemen you are about to observe your first autopsy it is not unusual for some members of the freshman class to feel a bit faked during this procedure so this is where we begin to separate our future physicians from those who just wanna play doctor no one seems to be standing hello I am still standing professor van Helsing why don't we have a look at the naked human so good morning whoo well that concludes the first six months of a vascular neurology fellowship hopefully you still feel confused but like I said before on the higher level about more important things now let's switch gears and discuss hemorrhages 59 year old man with uncontrolled hypertension and frequent binge drinking was found by his wife on kitchen floor with left-sided weakness headache and lethargy after she heard him fall there were no previous such episodes family history is unremarkable and just as before our patient arrived to the hospital within one hour after last seen at baseline in the emergency department he vomited twice on the neurological exam the blood pressure is elevated but our patient is still protecting his airway his lethargic response to voice but disoriented when he's awake there is no aphasia or neglect but he does have moderate dysarthria left facial droop and flaccid left-sided weakness and numbness so what's the next best step in the management well stroke code of course we can't be confident whether this is a scheme ER hemorrhage just on the basis of symptoms alone stroke code head CT was done can you see the abnormality I bet you can see it halfway across the room there's an acute left Allah make hemorrhage and some Mass Effect on the right lateral ventricle so we talked about the primary goals in the management of ischemic stroke but what about the primary goals in the management of hemorrhage of the early goal in the treatment of acute hemorrhage is preventing expansion and secondary injury because that's most likely to kill our patient aggressive blood pressure control and reversal of coagulopathy our like Iron Man and Wonder Woman very indispensable unlike ischemic stroke where cerebral edema peaks at three to five days hemorrhages create mass effect much faster sometimes even within minutes which we often need to address thankfully this is not an issue in this case so that's a nice cop out for me to leave the management of cerebral edema and intracranial pressure to a whole different talk except to say that the misty procedure is the most promising intervention which we're going to talk about in the next slide homies thesis is just as important as the management of ischemic stroke and finally the goal now becomes diagnosis and prevention of recurrence so say you have controlled the hypertension perverse the coagulopathy and verified stability with the repeat head CT that blood continues to sit in the brain for weeks and ayran within it is actually toxic to neurons and glia so we intuitively believe that removing the blood should be beneficial but invasive surgical procedures such as open craniotomy and evacuation of clot has not really improved outcomes probably because of surgical trauma that's inflicted on the brain just trying to get to that hematoma the most promising surgical procedure in recent years is the minimally invasive surgery with TPA for intracerebral hemorrhage otherwise known as misty a catheter is placed through a borehole directly inside the hematoma and low doses of TPA we're talking about one milligram or so are used to dissolve and passively drain the hemorrhage out of the brain over a course of a couple of days now I know what you're thinking am I crazy didn't I just say not to give TPA two hemorrhages it used to be that a student would fail or rotation immediately for suggesting such an action but it's a brave new world now so as you can see over the course of several days the hemorrhage is drained out as a result of this procedure there's a dramatic reduction in the hematoma size and mass effect so that brings us to a discussion of stroke workup mechanisms and prevention strategies charts and pictures comin right up so hemorrhagic stroke is less common than ischemic stroke and includes bleeding in the brain parenchyma itself or interest cerebral hemorrhage and bleeding just outside the brain in the subarachnoid space or subarachnoid hemorrhage subarachnoid hemorrhage deserves a couple of its own slides so we'll tackle that in a moment inter cerebral hemorrhages are essentially classified by their location deep versus low bar now hemorrhagic transformation of ischemic stroke while it's certainly considered under the umbrella of intracerebral hemorrhages is basically a bleeding in the necrotic tissue it's quite common and it doesn't really behave like spontaneous industrial hem it's not likely to kill you so we'll leave that out for now deep bleeds are the most common and they're sort of analogous to the small vessel type of ischemic stroke only in this case these fragile perforators rupture instead of occluding so the most common location for these hemorrhages are basal ganglia internal capsule thalamus this type of hemorrhage is actually often nicknamed hypertensive remember because hypertension is the strongest risk factor for small vessel disease and actually increases the risk of such a hemorrhage nine-fold lobar hemorrhages on the other hand unfortunately have a variety of causes ranging from vascular malformations tumors cerebral amyloid angiopathy does this look familiar looks quite a bit like ischemic stroke workup doesn't it we start with the MRI of the brain but this time we use gadolinium gadolinium typically sits inside blood vessels but does not enter the brain unless the blood-brain barrier is broken so it's excellent for enhancing tumors but MRI also includes a gradient echo or susceptibility weighted sequence to assess for other microhemorrhages microhemorrhages basically mean that the vessels are weak and a prone to rupture a vascular path of sorts so we also need to exclude vascular malformations and for that we can use MRI or CT a of the head in the cases where endocarditis is suspected a thorough workup with a transesophageal echo and blood cultures is in order now a modifiable risk factors should be addressed and in certain patients we may even need to go further performing genetic testing angiograms and even a brain biopsy i gave you an example before of CNS vasculitis which can cause hemorrhagic and ischemic strokes here's one example of a lobar hemorrhage AVM so typically arteries communicate with veins via capillary network which slows down the blood and decreases the pressure in an AVM arterial pressure is directly transmitted to a vein which is really not equipped to withstand it and AVMs are prone to rupture and bleeding look at the slide here you can see arteries and veins right next to one another that should never have but there should be a capillary network between them so ATMs essentially appear like a tangle of vessels on a CTA this particular AVM is probably fed by the MCA branches and drains into superior sagittal sinus here's yet another example of a cause of lobar hemorrhages this is the gradient echo or GRE sequence of the MRI and you're looking at different axial cuts on the same brain it's especially good at detecting hemosiderin which is a byproduct of blood as you know so here you can see a plethora Nahum multitude in a cornucopia of tiny subcortical and cortical microhemorrhages these look like hypo intense spots but because we're in med school and need a ten-dollar phrase that describes them we call them areas of susceptibility so this is the hallmark of cerebral amyloid angiopathy when it's seen an elderly person who's also demented remember amyloid the same protein that can cause Alzheimer's disease by damaging neurons can also damage the small blood vessels causing them to be brittle and bleed so now that you understand the differential diagnosis what is the mechanism of our patients hemorrhage think about it you're absolutely right his hemorrhage is due to small vessel disease or hypertensive so back to our case MRI of the brain with gadolinium showed no evidence of neoplasm the GRE sequence of the MRI showed no other microhemorrhages so we're not thinking CIA CTA of the head was negative for vascular malformation the final diagnosis in this case is hypertensive right basal ganglia bleed also known as small vessel disease and patient was discharged to rehab with a blood pressure of 125 over 70 so just like with ischemic stroke you're probably thinking which of the hemorrhage mechanisms are more dangerous so I'd like to illustrate the concept of hemorrhagic stroke risk with cats small vessel disease is like a Lynx dangerous but relatively small risk of recurrence now low BER hemorrhage is on the other hand carry a much higher recurrence risk now that lion is pretty hard to miss so we can probably run away in time but he can still bite us if we don't treat him appropriately we are coming to the end of our journey together in the next few slides let's talk about subarachnoid hemorrhage quick refresher by the way subarachnoid space is located between the pia and the arachnoid the important point is that blood vessels and cranial nerves run through the space bathe by CSF all caught up great now when a vessel ruptures in the subarachnoid space the blood mixes with CSF and causes chemical meningitis which in turn causes the typical symptoms worse headache of life neck stiffness lethargy nausea vomiting by the way Sbrocco and hemorrhage does not have the market cornered on the worst headache of life can you think of any other disease processes that can cause a thunderclap headache that's going to be your homework for today let's get on to the causes trauma is actually the most common cause of subarachnoid hemorrhage but ruptured saccular aneurysms are the most common cause of non-traumatic sah now these occur at the branch points in the Circle of Willis where the hemodynamic stresses of turbulent blood flow are the greatest makes perfect sense vascular malformations such as the AVM as we discussed can also rupture into the subarachnoid space so the three feared complications of aneurysmal subarachnoid hemorrhage are rebleeding especially in the first 24 to 48 hours obstructive hydrocephalus caused by clotting blood and vasospasm caused by chemical meningitis by the way vasospasm risk tends to peak around the first week but can last for as long as 20 days so subarachnoid patients may be in the hospital for a long time after their aneurysm has been fixed here is an example of subarachnoid hemorrhage on a non-contrast head CT you should be a professional by now you know that you're looking up through the jaw of the patient the eyeballs are pointing up to the ceiling and the patient's right is on your left these are two different axial slices from the same patient on the left is a slice through the basal ganglia and on the right it's through the midbrain how should this all say look if you direct your attention to the ventricles you can see that CSF is very hypo dense or dark so the salsa which are bathed by CSF should also be hypo dense can you see the abnormalities now all of the salsa are actually hyper dense because they're filled with blood it's as if every crevice of the brain has been outlined by chalk hopefully the treatment approach should be familiar at this point the early goal in the treatment of acute aneurysmal SAH is basically preventing rebleeding and secondary injury presumably a non-invasive vascular imaging study like CTA will already have been done to diagnose the aneurysm early aggressive blood pressure control and reverser of coagulopathy is still the key just like in any hemorrhage and then you need to direct your energy to securing that aneurysm early once the aneurysm is secured the patient should be on hydrocephalus and vasospasm watch occasionally subarachnoid hemorrhage is so severe that the obstructive hydrocephalus may need to be addressed early for that we have to make a burr hole in the skull and place an external ventricular drain that does exactly what the name suggests diverts CSF flow from the ventricle outside to kind of circumvent the obstruction for the Prevention of vasospasm the patient is treated with calcium channel blocker and emotive beam but if that fails patient may need to be treated with intra-arterial that is through the angiogram or intrathecal inside the ventricle infusion of calcium channel blocker finally prevention is extremely important even in our day and age 1/4 of the patients died enroute to the hospital so once you've treated a patient with subarachnoid hemorrhage you definitely don't want to see that patient go through this again smoking must absolutely be stopped there's actually increasing data that aneurysms are not just the product of hemodynamic stress but actually have inflammation in their domes inflammation that aspirin may be able to mitigate so it might be a good idea to treat these people with aspirin as well also don't forget the surveillance and repair of other unruptured aneurysm z' whenever appropriate so congratulations you made it to the end of the talk I realize that you're probably feeling information overload at this point here's some takeaway points of how to become a stroke neurologist so remember your anterior versus posterior acylation and remember the deficits that correspond to different vascular territories remember that acute ischemic stroke is a neurological emergency we have to call a stroke code time is brain so we are focused on rapid diagnosis and treatment with intravenous TPA and and the vascular Tim Beck t'me ischemic stroke workup is really necessary to find the wolf among the Sheep and to decide how to properly prevent stroke in patients Cardian Baalak stroke has the highest risk of stroke recurrence it's the large German Shepherd of strokes and also don't forget that Mel Brooks is an awesome writer and you should definitely see all of his movies now on the hemorrhagic front acute hemorrhagic stroke is also neurologic emergency obviously you have to treat aggressively but in this case we're trying to prevent rebleeding or expansion so we need to reduce the blood pressure and reverse coagulopathy misty is shaping up to be a promising surgical procedure for evacuating intraparenchymal hematomas to prevent secondary injury aneurysms need to be secured early and patients should be monitored for vasospasm and obstructive hydrocephalus and hemorrhagic stroke workup is necessary for effective secondary prevention of bleeds lobar hemorrhages typically have the highest risk of bleed it's the lion in the room thank you for your kind attention and as always please let me know how I can make this talk better you