 Hello friends, I must thank Indan Miller for giving this opportunity to talk on stroke, what I'm going to do, which we talk about basics of stroke imaging and part two will have majority of recent advances and future of stroke imaging. So let's start with part one. What is the definition of stroke? Stroke means patient coming with focal neurological deficit in hyperacute, acute or subacute stage or even chronic stage. When we see 100 patients with stroke, 80 of them would be of ischemic ethylurgy, then we have parankamal hemorrhages, six will have subarachnol hemorrhage and four would be stroke mimics. So this could be anything like subbillum, atoma, hyponatomia or even estrogen present in life stroke. What we are going to cover today is ischemic stroke, which forms about 80% of all the patients coming with focal neurological deficit. What is the definition of stroke? It indicates reduced blood flow and perfusion, which is caused by either thrombosis or hemorrhage in artery or hemorrhage. There are three zones of stroke in the brain. The ischemic core where flow of blood flowing through that particular portion of brain is less than 12 ml of blood flowing through 100 grams of brain per minute. Ischemic penumbra is where the flow is between 12 to 20 ml of blood and oligemic tissue is in the area where blood flow is more than 20. The normal flow of blood in the normal brain parankamal in normal human being is between 40 and 50 ml. There is saying in English literature, which says that what you want is what you get and evolution of stroke imaging is really reflective of this same. What begins together from the time city came up in the 70s, role of neuroimaging in stroke was limited to extruding hemorrhage and stroke mimics. There was wide window of when you could image these patients because the findings did not really alter the treatment much in ischemic stroke. With efficacy of thermolytics proven beyond doubt in the first weekend after 2000, it really did redefined neuroimaging and now for us whose practice stroke very, very prominently in hospitals, it is race against time. So, when there are no thermolysis available, imaging you should take 40-45 minutes and we did it, did not really matter. And now we have stroke protocol in Germany where a spoken city goes to patients home where it is not possible for patient to come to hospital. Also, debate of what is better and quicker between city and MR is waging for almost 10 years now and we will try and answer what is better in later slides. So, role of neuroimaging which was purely to depict, and evidently the impact had changed from simple endemic depiction of the impact to identification of region at risk of infarction. Detection of cause of stroke in the same go and try and predict the outcome if you thrombolyze this patient in the same go. Something more that we as radiologists need to know is what are the pre-hospital stroke management. There have to be typical implementations of strategies for emergency medical services within stroke systems of care. That talks about time between the receipt of call and dispatch of response team which has to happen in less than 90 seconds. EMSS response time should be less than 8 minutes in a stroke ready hospital. Radio diagnostic management is where we should focus on and we should be completely aware of. First we must know what is the goal of imaging. The first goal of imaging is exclude primary intracranial hemorrhage. Assess the alternative technologies of symptoms and treatment contraindications or thrombolyzes. Once you do that you move on to goal 2 which is infarct care transition. Identification of core, quantification of core volume, imaging of enombra, imaging of pile polarity vessels is what is important today. So when we image patient with hyperactive stroke there are a lot of questions that we need to answer and that is what we will do in two parts. First and foremost is when patient has spoken knowledge with deficit. Is there an infarct? If there is an infarct what is the cause of infarct? Is it reversible or not? What kind of intervention would be useful in the given patient? When can be done? What is the outcome of the thrombolytic therapy? Can we predict post thrombolysis hemorrhage? Can we detect outcome of stroke before it happens in high risk patients? These are the questions that are going to pose to you and we need to answer them smartly. So we will start off with answering the first question. When the patient comes to you with open neurological deficit does he really have an infarct or something else? Currently to answer this question across the world clean CT scan is the most commonly performed study because it has 100% sensitivity to detect pancam language. It is widely available. It is quick. It is relatively inexpensive. Problem with CT scan today is when you are performing anti thrombolysis treatment you have to be sure that you document the size of stroke, core, penumbra, etc. In that situation finding in plain CT will be showing that finding will be a significant challenge because almost in 60% cases CT would be normal in first few hours. In 40% cases where you are going to see findings these are going to be very very subtle. Previously normal CT scan was good enough to document and exclude hemorrhage. Today in the era of thrombolysis this is not what the neurologist treating stroke would be interested in. Let's look at the findings that we should be looking for in less than 6 hours when the patient comes to you. You should be looking for dense artery sign, obstetrician or maybe for nucleus and insured liver sign and these findings are going to be very very subtle and if you don't know the history and if you don't sit on the console and try and change window width and centre for the subtle findings you are more likely to miss them than pick them up. And these are three technical signs that we should be looking for. Hyperdense artery sign, whether it is thrombocyl MCA, Hyperdense basal ganglia sign when the basal ganglia hyperdense compared to the counterative side and insured liver sign where we are looking for dark insular. These are three technical signs of hyperdense fog on plain CT scan. When infarct moves from hyperdense to active stage this hyperdensity that we saw in the previous slide gets more prominent, easy to see, mass effect on the adjoining subsurface of ventricles become apparent. In the subacute stage that is wave 127, this wave shaped hyperdensity becomes more and more dark. Mass effect initially increases then subsides. Even if the transformation whether these patients are treated or not will be seen in 25% cases and if you contrast these patients you will see guided form enhancement because of luxury perfusion and break in bloodstream barrier. Compared to CT scan a plain MRI even without diffusion will be positive in about 80% cases in the hyperactive stage. It also has potential to provide evasion of tissue activity by doing perfusion imaging and basal pregnancy by doing MRNGO and hence today it is called as one stop shop for hyperactive stroke imaging. MR is also good for small occult cortical and lack of infarcts which will be difficult to see on CT scan in a patient who has murky infarct status. Also it can rule out hemorrhages and micro hemorrhages quite accurately and at times better than CT scan. What are the basic MR sequences when you are imaging hyperactive stroke? Diffusion is by and large the most important syphilis infarct very accurately so it is called as the stroke sequence. Flare is important especially in wake up stroke because you try to look for flare diffusion match and mismatch. I will explain this to you later. SWI or susceptibility related sequence is important to look for micro hemorrhages and hemorrhages. For fusion with or without occult cramps it will be important to differentiate ischemic core from penumbra and ginger is required to look for thrombus in the major artery. So these are five important sequences and these have to get over in a reasonable time of 10 to 15 minutes if you are about to do this as a primary imaging in hyperactive stroke. And here is a real time example of a patient who was admitted in our hospital for acute myocardial ischemia. He also developed focal neurological deficit and we scanned him within about 35 minutes of getting it. And what you can see here is the small which appear of the diffusion in the right way of the area which is not seen on T2 or flare. So almost 97% of infarcts would be detected in hyperactive stage on diffuser weighted images compared to 58% on plain MRI. Diffusion is also important and very well sensitive in the posterior posterior infarcts also. And this is an actual example of lateral medullary hyperactive stroke in all the right half of medulla flare negative. As infarct moves from hyperactive to acute stage diffusion abnormally gets more intense and brighter. On flare and T2 it will be seen as a wretched hyperintensity. There will be circular festment, gyroedema and loss of gray white matter. The measurement remains simple. You have to multiply the anterior posterior, lateral medial and superior inferior dimension divided by 2 for quick calculation. When you have a small infarct that is less than 10 midway meters in volume, it has very very good outcome. When it is moderate sized, it has lesser outcome than the small one. But if it is a large volume infarct measuring more than 100mm, it has worse outcome and chances of hemorrhage. So the cutoff to differentiate malignant mc infarct from benign mc infarct is a threshold core volume of 82mm. So anything less than 92mm can be treated aggressively more than that has poorer outcome. On the concept of flare match and mismatch that I talked about, when a patient has wake up stroke flare is the saviour for us. If it is a flare negative diffusion positive infarct that means you are dealing with an infarct of less than 4.5 hours duration which can be treated aggressively. If it is flare and diffusion positive that means you are dealing with an infarct of duration of more than 4.5 hours. So you have to go less aggressively treating them. Little bit about hemorrhagic infarct and hemorrhagic transformation of an infarct. There is lot of controversy on that. But what is malignant mc infarct if the hemorrhage transformation is less than 1cm in one area anti-platelet therapy can be continued rather than that anti-platelet therapy has to be stopped for time being. As it goes from acute stage to early subacute stage on MRI that is between day 1 and 3 you will get intra-ascular gel enhancement. It initially increases and then begins to decrease. You will get early parancameral enhancement without mass effect and signal abnormality and this is how it looks. It is because of break in blood blood barrier and lingerie perfusion. As infarct moves to late subacute stage that is between day 4 and 7. This which is high for intensity on flare and tattoo becomes hypo on P1. And you get intense heterogeneous enhancement if you contrast which can at times simulate tumors or infections. So you should be careful about the history. In the chronic stage that is between few months to 2 years you start getting encephalomerase changes, volume loss, aceratolamidation of adjoining ventricles and so on. And what are the inhibitions of the laminate tract? So this is first question answer. Is there an infarct? The second question that you need to answer simultaneously is what is the cause of the infarct? And for that you have option of CT-NGO and MR-NGO both. CT-NGO is absolutely quick. It has much higher resolution compared to MR-NGO. It differentiates calcific class from soft class quite accurately. And it is as I said quite quick and gives you information that you need. But if you are going to MR-NGO, it also gives reasonably equal information as CT-NGO. The advantage of CT-NGO is in addition to showing the major issue of occlusion, it also has what is called as collateral scoring system. And that allows us to understand the outcome of thrombosis. So if collateral scoring system is closer to three and four, that means there are good collateral. It will have better outcome compared to absent four collateral. So score zero is myelin profile, arrest is benign profile. With multifaceted CT-NGO now available, so if you have phase one, two, three to look at on CT-NGO, you can differentiate the outcomes into patients having good collateral, having the best outcomes, four collateral, seven worst outcomes and intermediate outcome with intermediate collateral. MR-NGO as I said on a good machine can happen in two or three minutes along with diffusion and major issue of occlusion and AC perfusion. It gives you a fairly good idea as to how you are going to treat these patients. A lot of people used to do contrasting on MR-NGO in stroke, but that is now given up. It gives you tandem regions better, it gives you more accuracy of severity of narrowing, but that is no more considered important in two ways. The third question that we need to answer when we are looking at hyperactive stroke is how much of it is reversible. For this, you must understand the concept of perfusion imaging. Perfusion imaging defines ischemia better. So ischemia as I said in the beginning is defined as ischemia when serving blood flow falls below the threshold of blood flowing through 100 grams of brain per minute and that is 18 to 20 ml to call it ischemia. Because that is the minimum blood that is required to maintain basic cellular activity. Now when ischemia remains for more than 4 to 8 minutes in one row, the ischemic area turns into infarct because that causes irreversible cell damage. Idea of doing perfusion imaging is differentiating ischemic core from ischemic penumbra. Ischemic core is defined as ischemic core where cell death has happened and membrane failure has already ensured. Penumbra is defined as penumbra where the brain can be marginally perfused, metabolic way unstable, but no cell death has happened. So it is a potentially salvageable brain if you re-perfuse it. Perfusion imaging acts as a complement to diffusion. It will show decreased CBV, increased empty and diffusion-perfusion mismatch is an area which has salvageable penumbra. And I'll show you a few real examples. We buy and large do ASL imaging for compassionate perfusion investment. Here the patient having multiple hyperactive lacrimine fox in left MCF territory and left posterior watershed zone. On ASL perfusion imaging there is large area mismatch. Compare this patient with the next patient where diffusion abnormality is almost 110 cc, perfusion abnormality is 130 cc. So if you symbolize this patient, his outcome is going to be worse compared to this patient where diffusion-perfusion mismatch is large. This patient's outcome is going to be very, very good. ASL is also useful in post treatment situation. So this is a patient who has such premismatch, thrombolyzed and MRI and diffusion was repeated after six months. And this particular patient where the area of perfusion abnormality is large, most of it has reverted back normal. In fact, in places there is re-perfusion or luxury perfusion. Today we have moved much beyond just mismatch. We tried to divide the extreme brain talentament four zones. Core, diffusion abnormality, perfusion abnormality and began oligemia. I am going to explain this in details in stroke imaging part two. There are several perfusion parameters that we need to understand when we are doing contrast enhanced perfusion. So that divides the perfusion abnormalities into CBV abnormalities, CBF abnormalities and transistor abnormalities, TTP abnormalities. And based on that, you can differentiate brain talentament to normal, benign hyperlemia, at-risk ischemia and infarction. So to conclude this particular part of stroke imaging, imaging plays a very critical role in stroke management. Diffusion is the stroke sequence with ongoing advances in imaging protocols dissipating more robust and rapid. Penumbra mapping should ideally be a part of all imaging protocols in stroke and what we must not forget is by this brain. So don't waste a second also. Thank you for your attention. We'll cover the rest in part two of stroke imaging. Thank you again.