Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

Anatomy, the radiological anatomy, when it comes on, the imaging is a little bit tricky and overwhelming to some point in the initial stages of the medical school and then in the radiology or your subspeciality. So I'll try to start it from there first. So can you see my screen moving actually? Yeah. So cool. So uh starting with the basic soft cerebral hemisphere. So how it works. So, cerebral hemisphere, as we all know, basically, there are two brain is divided into two lobes which we call hemispheres the right and the left and both of these are connected, they are divided in the mid sagittal plane by what we call a hemispheric fissure. Like there is a fissure between the two lobes and they are interconnected by corpus callosum. So internally those both hemispheres are connected. What is corpus callosum? It is a structure which are just the uh commissural fibers. So these are the commissural fibers, which is the largest white meter tract of the brain which actually connects the two cerebral hemispheres. So they are interconnected. And I think we all know the commissural fibers. I'm not going to detail of that. So what we need to remember in from the aspect of the um the clinical side is they are connected by the corpus callosum. And this is the largest white matter tract which keeps uh and that is the track, which is then further the basics of the responsibility of when we say that the patient is having something in the like uh parses or hemiparesis or quadriparesis on the left side. And there are uh issues or the injury is in the right hemisphere of the brain. So these are interconnected by the various, there are various white matter tracts and one of them and the most important one is the corpus callosum. Now, after that, there are two divided into two lobes. The whole brain surface is covered by the meninges, which is basically just membranes, meninges itself is further made of three layers, which is not the scope of our today's discussion. But yes, it is covered by the meninges, which actually works as a cushion to protect the brain cortex from several injuries and from drugs and infections with T virus is entering into the like making the blood brain barrier and letting it not enter into the brain cortex. Then the surface of the cerebral hemisphere is itself, it's not a smooth surface, it's made of sulci and gyri. What Sulci in gi is basically, it's sulci are the grooves like at the at the outer surface. If you consider it uh imaginatively on the outer surface of the brain, the outer cortex indents into the inner core of the brain. And the indentation itself is called the sci. And when it indents and the area of the brain cortex between the two, these two indentations, the the bridge of the brain cortex is called guide. I, I'll show the picture and it would be easy to understand. Then now each cerebral hemisphere itself right and left, both are divided into four lobes which are of unequal sizes. We all have heard of these names. The frontal lobe, which is the largest comprising 41% of the cerebral hemisphere. Then comes the temporal lobes, 22% parietal lobes, 19% and occipital lobe which is 18%. Now first, I will try to show you the little bit of sulci and guide. So if you see this white thing is the bone, it's the CT image. So it would be like that. So this is the bone, just ignore it. This whole thing is the brain. OK. So from this outer surface of the brain, you can see this dark gray area and this light whiter portion. So this dark portion is the outer surface of the brain you can see here it is indenting into the white surface. Yeah. So this one is the CCI if you can see my arrow, this is the cell side which is dividing the brain cortex, the surface of the brain into this ridge till we see the next sulci. So this, these are the Sulci, these darker portions and this is the gyrus. So this is a very um commonly used term by radiologist in their reports, Sulcal gal effacement or describe any uh pathology with sulcus and the gyrus. So this is the basic concept that this is a sulcus. This area of the brain is the gyrus that rich. And again, this indentation is the sulcus. Now I'm giving um starting with uh I will show a few static images and then I'll show you uh scroll down images how we actually see the CT scan just for the purpose of showing you the cerebral hemispheres anatomy. So starting this is just consider that you are going from cranial to caudal, which means it's from head to toe. And I'm starting to show you from the very top part of the head, which is the vertex when we cut the slice as an axial CT scan. So on the surface this bone and this is the brain. So in the start, what this is is the frontal lobe and this is the parietal lobe. Now how we can differentiate what is the frontal lobe and when it ends and when the parietal lobe starts. So these are divided by a central sulcus. Just ignore all these precentral and postcentral details. Just focus what I'm telling for now. So there are multiple CCI all of this going into the brain. The first foremost major important thing to understand the anatomy of the brain is to know what and identify where is the central circus. Because it is the biggest landmark in the brain anatomy. When you look at all the cells which are starting from this lacri going into the brain surface like this medially, the largest one here in the right and then this largest one seem just parallel and opposite to the in front of the other in the left side is the central circus. How you can identify the central circus? Number one, this is the largest circus you can see largest circus in which thumbs don't consider this one because it's going from an interior towards posterior, consider the ones which are coming from lateral towards the midline. So this is small. Then here comes the central circus. This one is small. This is also small. This one is small. So main central circus is the largest one coming from lateral towards the midline. It is not combining each other. They are not meeting each other in the midline, of course, because this one is dividing the right cerebral hemisphere into the right frontal lobe in front of it and parietal lobe behind it, same is on the left side, frontal in front of it, interior to it and posterior to it is the parietal lobe. So this is the main basic landmark. Now, if we remember from the basic like first two years of the medical school, we used to think about the gross anatomy of the brain. And we got to know that there is motor area, the area of the brain which actually controls the motor movement of the body and then sensations of the body. So that also can be identified with the help of the central sulcus in interior to the central circus. This gyrus which is called pre means interior to the central circus, precentral gyrus is a motor strep area and posterior to this, this post central virus is the sensory cortex. So whenever patient presents with a history of problems in the sensations, like um pain or sensational issues, tingling, sensations, loss of sensations. By the first thing by the help of the history, what we think of is that there is something going on in the sensory cortex, which is the post central guidance. And when it comes with hemiparesis quadriparesis, we think of the motor strip area of the brain. Now it's not that just this part is motor strip and this is the center strip, the sensory strip, we all know that there is it's very complex division which we used to um know with the help of Homan by which they divide the area which controls the um the speech, the visual, the sensations, uh auditory cortex and all of that, that is the part of gross anatomy. Ok. So that is the basic when we are looking at the patient presenting with complaints in a and that is an emergency and trauma and we are looking at the ct brain, OK. Now again, it's just to simplify it a bit more. This is the sulcus, this red is the precentral postcentral. Now, I would just try to just this midline is basically just considered it as a midline separating part, separating the right and the left. And as this is the area where there is separation between the two hemispheres. So this the meninges which covers the brain, it also indents into this area like meninges go in, there is a layer which goes in indents in and then it indents out. And the space between this mening is basically when because the venous sinus spaces of the brain which makes facial sinus that is a bit more complex. So just focus on the basic anatomy of the cortices, same frontal parietal. And this is the central circus here and this is the central circus here. OK. Now I am moving my, this whole images are actually starting to move from the headed first sequence from the headed. Then I moved a little bit down on CT scan. And here comes this level, moving a little bit down, same level. And then when we move down, if you all must have seen the CT scan images at any part in your clinical practice, here comes when there are these dark areas and then there is differentiation in the various shades of gray between the CT scans. So these ones, these darker ones are the ventricles. Like there is a ventricular system of the brain in which the CSF flows. And this CSF flow ventricular system, it comes starting with the lateral ventricles. One later ventricle, which is called right lateral ventricle. This black portion and then left later ventricle at the level of the ventricles. When we start to see the ventricles comes the gray matter nuclei. What are the gray melear? These are basically now, this part is when we have moved down more into the deeper surface and deeper part of the brain. So these are the deep uh located gray mei which are called basal ganglia, basal ganglia comprising of the cordate nuclei and the lentiform nuclei, lentiform further is divided into two which we will discuss in detail further. So at the level of the ventricles, we divide the deep nuclei. This would remain like gray and white matter and the cortic is like frontal lobe and the parietal lobe same as we discussed. Ok. And then in the deeper area of the brain, that was the superficial one in the deeper area comes we divide it as these blue ones which are the cord nuclei more interiorly along the frontal horns of the lateral ventricles are these cod nuclei. And then this whole part is with the lentiform nucleus and more meal part just along the midline are the two. The further going down, just ignore this herniation. This thing where we know we all are aware of the skull bones. So where it comes the squamous part of the temporal bones. Here it comes with the temporal lobe of the brain. And when we identify the temporal bone, it has the temporal lobe, then the occipital bone has the occipital lobe. It's the easy way to actually build the knowledge uh bear the information further on your previously existing knowledge that the temporal lobe uh bones and occipital bones of the temporal lobes corresponding in the occipital lobes. And when you start to see the temporal lobe and the occipital lobes, this chemo appearance is of pons. Here we start to see the pons which is the hindbrain part and um sorry midbrain part. And this one as the cerebellum go a little bit further down and you can appreciate this one's more prominent here. This is the temporal lobe. Now, this thing was the part of the frontal bone. This is the temporal bones. So temporal lobe pons and the cerebellum and as your brain is divided into two, this is the midline structure. But these two again comes down as right cerebral hemisphere and left cerebral hemisphere. Now, I would like to share a video from one of the sources where we can actually scroll the images. And first let's check if it's if you can see. Yes, so you can see the video moving. Yeah, we can. OK. Yeah. Yes. So this is basically from uh site radio pia. You can all see that. And this is a very good site. If you want to have the like they have articles which are divided into the basic um knowledge for nonradiologic, the basic uh imaging knowledge. And for the few of the major pathologies of the brain and then for the more complex one, this for the anatomy purposes, this is good. If you can always go and search for the annotated images, I'm unsure if you can see the annotated images. If you are not the, you don't have a membership. But otherwise all of us can see without annotation. So now I'm starting with brain surface from the top part bone moving down here, start to cover the brain surface. OK. So will have a frontal lobe, parietal lobe. And where is the central circus this bit? It's starting we start to see the central circus right now going down see this is the central circus parietal lobe, frontal lobe fox, which is also called interhemispheric fissure with the meninges. OK? I am moving from head to toe cranial to caudal central circus, getting more prominent frontal lobe, right lobe moving further down. Same I just showed the same image I took it from here. The static one because I was unsure if we can scroll the images. Frontal parietal central circus, keep going, keep going again. This is the same thing. This was the central circus here. So we are moving frontal parietal, frontal parietal. Now parietal has taken more portion. This ho is parietal frontal, parietal, going down frontal right now, here, can you see this thing a little bit of change in the gray color is when we start to see the ventricles go a little bit down ventricles and this is a midline and then we reach the inner cortex or deep part surface of the brain within the core of the brain. Here comes the corpus callosum, what I mentioned in the start, corpus callosum. What was the function that it was basically interconnecting the right and left cerebral hemispheres. And these are just the commissural fibers which are made of white metal tract. So here they cross like that in that part is the corpus callosum and these are the ventricles. The blue ones keep going down, your ventricles, going down a bit more prominent and we start to see the corded nucleus. And when they reach this level, see this is the ventricle corded nucleus as I showed you in the previous images, corded nucleus. And here comes lentiform nucleus, corded nucleus. This blue one is lentiform. Now, if you, I'm unsure if you can appreciate a little bit of change in the shade of the grape. This light part is the corded nucleus. This whole bit is the lentiform nucleus. If you can follow my arrow, the inner darker portion of is called the globus pallidus of the lentiform nucleus. And the outer more later and lighter portion is the. So this is the corpus callosum coded nucleus. Here you can see lentiform nucleus, globus Validus, put him c corded nucleus, globus pallidus, putamen and the thalamus as we already have seen in the previous image, keep going again. I'm not going into the details of the inter limb internal capsule and the external capsules because that would be a too bit, too much temus, a little bit with the ventricles. I would like to share these were the later ventricles in the midline. When we start to see over here, we can slightly this streak of a bit darker gray color. This was the appearance of the y then third ventricle going down, third ventricle. This is again the lateral ventricle horns just ignore the arteries and stuff. It's more complex. Left third ventricle, later ventricle. OK. We are still going down this bit. I would like you if you can just appreciate. This is the wind fissure and the insula or the insular cortex because it would be helpful further when we go into the vascular ries of the brain. So yes, this is the area that I mentioned as we are going to start to have pons. And these horizontal lines when we start to have cerebellum occipital lobe, this was the temporal bone. So this is the temporal lobe, sea pons, occipital lobe. And these horizontal lines start to see as the cerebellum pons until here responses. And if you go down midbrain occipital lobe, cerebellum, keep going temporal lobe, occipital lobe, midbrain and cerebellum further go down, keep going down. Temporal lobe, think I'm going up. Yeah. Fourth ventricle, midbrain and cerebellum and then it comes down cerebellar uncles fourth ventricle once Sveum pons, cerebellum, right and left, right, left cerebellum and pons medulla when the cerebellum til the level of the cerebellum anterior to the cerebellum would be the pons and midbrain. And then at the end comes the midbrain pons and then the med oblongata ending of the cerebellum going more quad is the metal block and then the brain, this is the level of where our neck going to start and head is and like the base of the skull from where we can then appreciate as an extension of the me oblongata starts as the spinal cord. So same would be the cerebral hemispheres. Anatomy is more appreciable, like more distinctive in MRI as compared to the CT brain. But we are discussing CT. So I would not be interested to show it more complexly in the MRI. But I can show you that if again, you can look at the radio pia annotated images. So they have the annotated anatomy of the brain in a bit more detail because it's on MRI images. And if just have to have an overview of the lobes, so that by the end of the session, you can please remember the lobes frontal, it's color-coded. So you can read it from here, frontal parietal and then when you have been scrolling a lot of images and a lot of imaging you are seeing in your daily routine, you don't always have to look for the central circus. It would be a second habit to identify where is the frontal and where is the parietal lobe. So this one just has uh indications of the lobes. So just focus in that frontal and parietal. There comes the lateral ventricles, corded nuclei, this one the corded n and then the lentiform nucleus thalamus see as we are moving down bones are changing. So frontal and parietal and now we start to have the temporal. Here comes the temporal lobe at the level of the lateral ventricles and as we go down, but after the lateral ventricles, we keep starting have the temporal lobe. Ok. So temporal lobe, frontal parietal temporal and also starting the occipital lobe in front of the within the occipital bone, keep going again. Cord it basal ganglia thalamus. I am focusing on those parts in which we tend to see the emergency injuries or emergency pathologies in the en which is important for that aspect. Going down frontal, temporal occipital midbrain that start with the midbrain as you know, midbrain. This is a part of the cerebellum, occipital, temporal, frontal, little bit of frontal, temporal occipital and here comes the it was the midbrain to this level as we start to see the cerebellum and we are moving a little bit two or three slices more down. It starts with the pons continue as the pons Savella, cerebellum becomes more prominent. Is the pons, temporal occipital moving down in the cerebellum. Still the pons, occipital lobe is almost gone. You can see the difference in the in the anatomy. See the cerebral hemispheres, I mean these just identify them as horizontal lines. Ok. The fibers of the cerebellum and then these of the lobes, occipital lobe keep going down, occipital is gone. Temporal is like bit a little bit. This hole is the bony part. This is basically the and squamous part of the temporal bone cerebellum pons. Now, we can't see anything more other than the posterior fossa. We are sitting in the posterior fossa with the pons and the cerebellum going down more cerebellum, posterior lobe. And here it starts to have the mental oblong down, keep going down and there the base of the skull. And further after that, we will start having it, we will continue as a spinal cord in there. OK. So going back to the presentation, OK, with the arterial territories, I don't intend to discuss them in detail. But regarding that, I would like to mention the main thing that we need to know for the very basic CD interpretation of the head is the basic arterial dries. As we all know, interior carotid, middle carotid and posterior carotid. That is for the purpose of basically to look for the MC when we encounter patient with in the en with the history of uh hemiparesis or cores. And we are suspecting an infarct or a stroke. And we want to know how much of the brain has gone or how much of the brain um area has been injured in that it's been affected by the ischemia. Then we used to write it down in the report as MC or AC or PC. In fact, it helps the stroke team and the clinicians basically to know which part of the brain is involved. So here I'm not going into the whole teeny tiny small arterial vascular territories, just the bigger ones. ACMC PC. OK. And then we can always if we want to go in detail, starting from the circle of Phyllis and track from the circle of hyllus towards more peripheral and more um smaller branches. So it is the brain surface. So you need to think of this image first. This is the main brain surface where you can see it's just um where not even ventricles is there, it's just the start. So the m this is the interhemispheric fissure, the midline fox. So in the mid sagittal area, more towards the midline, which we call the medial is the area of which is supplied by the AC, which is interior carotid artery on lateral sides of the both cerebral hemispheres. The lateral surface of the brain is supplied by the branches of MCA. They are further divided into like MC with further six MC segments, AC A with 3 to 4 AC A segments and same with the P AC. We are not going into the, just remember the midline medial portion. If you see something in here, the stroke going on in here, more mid sagittal, we think of the ac, more lateral think of the MC and more posterior and midline think of the PC, posterior cerebral artery. These are the vascular tree. And if this is on the, you know, on the level of the vortex at the level of symptoms, and you will, when we have not down into the deepest structure of the brain, this you will keep these are the basics and their branches. And these segments are supplying the main inner and deeper cortices and surfaces of the brain. So this one at the level of the ventricles. If you see again, these are the branches of PC and this is the branch of the AC and some part insula is supplied by the branches of the M CM that would remain the same. But see mid sagittal part is with the AC, a lateral, with the MC and the posterior mid sagittal part with the PC. And that remains almost the same. If you even move at the level of the ventricles, the later part MC, the interior part ac, the P part by the PC and with the corded nuclei, all of the corded nuclei like oh sorry, basal corded and the lentiform nucleus, putamen and globus pallidus with the various small branches from the AC A and MCA both. Now, this was the basic anatomy. Now we will go down and um emergency CT heads. So when a patient presents in a, like an er or A N, what we do, what we tend to do if patient presents with any possible thing like um mentioning hemiparesis, quadriparesis, confusion, headache, ses anything related to neurosensory system, Anything related to CNS? The first instance in the A&E is after doing that, ABCD, checklist of stabilizing the patient and ensuring all the ABC signs, airway breathing circulation. What is the second instance in the case of anything presenting with the CNS symptoms is go for an imaging to see if there is any injury, if there is any acute event happening in the brain. What acute events can happen in the brain? The most acute, uh the acute ones which we most encountered is a stroke or a bleed. These are the two things we think of first and these are the things which are emergency to be treated in a patient requiring a CT head imaging. All right. So that comes with um and in the emergency situations. The first imaging, uh the first line of imaging is noncontrast CT head. Now that is a separate discussion when we need a contrast enhanced scan and when we need a con noncontrast enhanced. But in the emergency, if you want to rule out if there is stroke or a bleed, these are the emergencies, right? Uh Looking for a tumor or looking for a cancer, looking for a malignancy, any space occupying lesion, this is not an emergency, we are not going to treat it overnight. So this is not an emergency. The emergency is basically should be defined as well. I would say with all our clinicians and medical and surgical colleagues, the emergency is def defined as something in which the immediate intervention is going to cause a major life change in the management of the patient. Right, a major thing that can cause the change in the management of the patient. A major diagnosis that can change the whole of the course of the management of the patient and that results into the complete change in the course of life, considering comorbidities or mortalities or life saving things. So first thing is the noncontrast CT head and a and should be it is to rule out acute intracranial events which would, as I discussed, ischemia, bleed, bone fracture, sinus thrombosis. And when we can request an emergency ct head, we all know the indications in UK are like nice guidelines. I'm not going into details in the nice guidelines, but they are very like very comprehensive and very thoughtful guidelines that are made according to all the possibilities that can happen with the patient coming with anything, any symptom like co headache or anything that can be related to the brain and when we can have them um when we need the imaging to rule out that acute intracranial events. So I would be uh mentioning the ischemia, stroke hemorrhage. There are things for which we do the CT heads overnight and out of hours in the hospitals starting with the ischemia. Now we have stroke, that is a layman term, that patient had stroke, stroke can be further divided into ischemic and hemorrhagic. But normally in, in the medical term, when the patient has ischemia, we call it a stroke. And when he has bleed, we just call it as a intracranial bleed or intracranial hemorrhage. But the both of them are actually causing stroke in the patient, like actually causing the injury of the brain parenchyma, either by blocking the vessels and causing ischemia or by tearing of the vessels and causing bleeding in the brain. But both results in basically stroke. So start the ischemic stroke and I would appreciate if any of you have any question or want to go back to the slide, maybe just put it in the chart box or you can unmute and ask me to in the middle of it. Ok. So starting with the ischemic stroke, I'll just read out the sudden focal neurologic deficit where the exact clinical features depends on the specific vascular territory involved. What does that mean? That means whenever patient presents with a sudden focal neurologic deficit, like patient presents with sudden paralysis or a sudden loss of motor function in the left side of his body or in the right side of his body or one side of the face or patient presents with facial drooping or inability to speak or slurred speech. All of these things comes into when we defined it as a sudden focal neurologic deficit. And here what important is if a patient presents with or loss of like motor power is three by five or two by five or zero by five. In the left arm or left leg or whole left side of the body, you need to identify in which vascular territory there is an injury or an acute event happened which is leading to the injury within the brain. Now, first thing is that the time of onset is important when considering the treatment. All of my colleagues, all of our colleagues, which are part of the stroke team always know that the first thing they ask the patient or they ask the A&E doctor is for how long the patient is having system uh symptoms because it changes the management altogether. It's divided. It's like mostly like first one hour, first three, couple of hours, then for six hours. And after that. So why it is important time of onset is important because then they know how much uh brain damage has occurred in that time lapse. And according to that, they give thrombolysis or thrombectomy or anticoagulation, how it's treated as altogether a different thing. So how ischemic stroke happens? What is the pathophysiology? First thing is that obviously, it is ischemia. So what happens is loss of blood flow and loss of oxygen to the brain parenchyma to a certain part of brain parenchyma. How it happens? Obviously, usually due to an artery being cued either by a thrombus or uh embolus. Like patients with afib history of heart diseases might are more prone to have strokes because they are more prone to have thrombosis and embolism, which can cause the brain parenchyma to be dead or at least partially dead because of the occlusion or because of the deprivation of the blood flow and the oxygen which causes the cell death in any part of the brain uh in any part of the body. It can cause cell death in the brain cells as well. So that cell death results in edema and swelling. Now, on the pathophysiology, we know that ok, brain paran comma is going to be dead. How we are going to see that this brain paran comma is dead or it has um um happened to have the ischemia is we can see the cell death in any part of the body by edema and swelling specifically in the brain. We interpret there is edema change, there is swelling of the brain parenchyma. So it could be stroke. What are the common causes of the stroke? Like I mentioned atrial fibrillation, patients with heart diseases, carotid artery stenosis why? Because carotid arteries is the main artery dividing into IC and EC. And that IC is going into the brain and major blood blood supplies by AC A and MC. As we have discussed in the territories, they are the branches of the carotid arteries. The internal carotid arteries or Cervi artery dis dissections because the cervical artis further go make up like vertebral arteries, vertebral arteries make the basilar arteries which further contributes in the posterior circulation of the brain. If you remember the circle of vous posterior circulation of the brain was like vertebral arteries, both going in meeting to form basilar artery, basilar artery going in dividing into two posterior cerebral arteries. And these were the posterior circulation of the brain. So everything that can affect the circulation of the brain just start to just think about the root cause where it is coming from. And you can identify the cause of the um cause of the injury or cause of the thrombus. Now stroke, the first thing, stroke is a clinical diagnosis. That is very important thing. It is not always the imaging diagnosis. Imaging has you to understand how much and has already occurred, how much time has lapsed, which part or which artery can be um can be involved to cause the ischemia and stroke. But the first thing is because many of the times if you remember there was a term transient ischemic attack in that kind of TI S, we don't see anything on the imaging because it's transient, it's a transient ischemic for a few seconds or minutes of the brain parenchyma causing clinical symptoms and then going away. Ok. So first thing is stroke is a clinical diagnosis. If you suspect clinically by the patient's history, which can be focal neurologic deficits, uh et cetera, then we suspect or if it's involving the frontal lobe, then it can come with seizures. Then we think of the clinically, if we think that it can be a stroke underlying stroke, then we can go to look further in detail on the imaging two broad categories. II said ischemic stroke and hemorrhagic stroke, it should be over here. Actually, I guess now CD has the advantage to look for the stroke. CD has the advantage of being available 24 hours a day and it is the gold standard for stroke, hemorrhage and everything. Ok. Hemorrhage on the MR images can be confusing, I think, yeah, we can just skip this one and continue with ischemic stroke first. So yes, ischemic stroke. So ischemic stroke, as I have already mentioned, it is episode of the neurological dysfunction. What happens as we can see the ischemia, the word in the ischemia is due to focal infarction in the CNS which is attributed to arterial thrombus embolization or hypoperfusion, noncontrast CT scan. As we discussed initially in the stroke, it is a mainstay of imaging in the setting of an acute stroke. OK. What are we looking at on the CTS in acute setting? First thing is we exclude if there is any hemorrhage because if there is any hemorrhage that would preclude the thrombolysis, we are not going to do a thrombolysis in a patient who has a hemorrhage. And then we look for early features of ischemia. Now, what are the early signs of ischemia on C scan? This is more important because the main uh thing, What? So the main thing, what stroke team is um interested into when we they request a CT scan from A&E is the early sky signs because then the changes in the brain parenchyma can be reversible to some extent, thrombolysis, thrombectomy would be helpful to change the patient's management drastically. So the main thing is when it's already an established stroke or a chronic stroke or a late stroke, then the damage has already been done. You cannot, you can put the patient on supportive treatment to avoid further uh future strokes and stuff. But it does not mean that there is something going to happen with the present clinical condition of the patient. Early signs is important because when the brain damage is reversible. So what are the only signs? Number one Hypoattenuating brain tissue, what happens is Hypoattenuating means hypodense, the brain parenchyma becomes of lower shade of gray, a little lighter color, lighter, not in the sense of lighter like hypodense. So a bit darker as compared to the rest of the brain branchy, which is also called loss of gay white matter differentiation. Like you, there is a blurring between the brain and KMA between the the various shades of the brain brain and KMA. OK. Then comes the obscuration of the lentiform nucleus. That's why I was mentioning the uh of the lentiform nucleus all and um uh poin that that is an early sign of the ischemia and CT scan dense MC sign, dense MC sign means middle cerebral artery signs, then comes with the insulin sign insula was the insular cortex which we saw near the sylvian fissure and then comes the sulcular ment sulcus. We have already known and discussed what the sulcus is and how it looks like on the brain parenchyma and CT scan. Now, I would divide one by one of these Hypoattenuating brain tissue. When we can see the hypertense brain tissue. It means that the brain damage has already been done and it is irreversible. So the area of the brain which has been damaged by the ischemic stroke is dead now. And what further is to just avoid the complications caused by that stroke and to avoid any further stroke in the future. That's the mainstream of the stroke team treatment. This is highly specific fit for irreversible ischemic brain damage. If it is detected within the first six hours, then we can consider thrombosis and thrombectomy. So if we look at these images from the CT scan, just because on this left, in this left, you can see differentiation between the shades of gray, this gray metal. On this white metal, there is there is some heterogeneity within the shades of gray in the left side. And if you compare it with the right one, this whole area, it is, it looks different, it catches your eye, it looks different as compared to the left one. What happens is here, you can see the sulcus and the gyrus differentiation. This is the gray matter. This is the white matter over here. Can you see the circle gyro differentiation? There is blurring of that. Can we differentiate the gray and white matter differentiation? No, we cannot see that. And this is Hypoattenuating hypo means hypodense. So it is a bit darker as compared to this, it is a bit lighter. This is a bit darker, this part, even on the right side is lighter, darker, lighter, darker, this is a bit lighter. So this is an area of hypoattenuation which appeared within first six hours and it is highly specific for brain damage. This is the area where the radiologist would mention it in the report. OK. There is an area of hypertensity with loss of gray white matter differentiation in the frontal in the brighter lobe or front to brighter lobe in the territory of MC. Suggestive of MCA infarction because we discussed midline parasal area. This part ac, a lateral part MC and this part PC. So what it comes MC in OK. And here is why territorial vascular is important. All right. Now, moving on to the next one, see loss of gray white matter differentiation in the left insular cortex. Now, look at this image, look in the right side first, this is the fissure OK. This is the sulcus in the fissure and here this bit follow the arrow. This is a bit whiter and this is a bit more gray dark. And if you look over here, OK. And this cortex, this white part, can you see it in here? It's a bit blurred. You can see this gray over here, but the white part is not visualized here. So there is loss of white gray matter differentiation in the left insular cory which is an early sign of it is very subtle. It it is an early sign of infarction. Now, moving to the second sign, what we discussed was obscuration of lentiform nucleus, lentiform nucleus part of the basal ganglia. This sign is also called blood basal ganglia. Now, when I was telling you in the anatomy of the lentiform nucleus, I said that it would be a bit media darker portion which was globus pallidus and a bit lateral and a bit lighter portion, which was put in that differentiation, which is obviously not too looking at your face, not too much. But if you set your eye to look at it, you will start to see the differentiation that would be lost, which is called blood basal ganglia. This is the mo earliest and the most frequently seen sign and it is almost always involved in MC infarction because this is a part of MC territory. So, can you see this is the ventricle? Ok. This was the lateral ventricle here. It was, it should be, this was a corded nucleus, this whole area where I am drawing a line with my arrow. I'm unsure if I can. Well, this is a P DFI cannot draw a line. So this part should have this part a bit darker Globus pallidus, a bit lighter. But I mean, and there is loss of that. So it looks like blurred basal ganglia or obscuration of lentiform nucleus. Third comes with the insulin sign in the insular cortex. There it is and it can be missed many times, but it would be hypodensity which would be very subtle. But the main thing is to look for any swelling of the insular cortex. And we can always compare it on the right side, on the opposite side, right or left. Whatever it is, you can see this was the s fissure, this is the insular cortex. So if you look closely, this is the more zoomed in image, this is hypodense. Yeah, it's a bit darker than the rest of the surrounding parenchyma and this area looks more swelled. So this is the insular enzyme. This area is also lateral part of this brain surface So MCA infarct, then the next one is dense MCA sign. What was the C and C dense MC means just look at the words MCA, middle cerebral artery would look dense. Now, one thing important dense MC sign would be visualized on noncontrast CT because we know when we don't give contrast vessels does not enhance, they do not look, they do not appear white on the CT scan because there is no contrast. So on a noncontrast CT scan, if you can see a white vessel, it is called dense vessel, which is the dense MC sign. Now, here as the right and the left, you can see the white part within the left MC. And here we cannot appreciate anything white in the MC. We cannot even appreciate the MC. So distinctively, even if, if it is not a den NC sign on a non contrast image so dense means this is a thrombus in the MC. And this is also one of the earliest sign when there is a thrombus in the MC, but it has not caused a visible damage to the brain parenchyma. So it's not established. In fact, it's just a very acute time maybe within an hour or two when we can see this thrombus within the MC. And this is just a grass picture where I just intended to show that if it is the dense one dense and see how it looks like you can see the right MC going all the way nicely here. And in the left T here, we can see the MC and then it's lost. So there is a clot in here, that's the angiographic image. So there is a clot in here, we cannot trace it. And here we can see the clot in here on the non contrast CT scan again, I with in context with this slide, this was the on the non contrast CT scan where you can see the dense and what happens with the contrast enhanced CT scan. Now, in contrast in hand, there would be contrast within the vessel. So normal vessel will be visualized and thrombosed vessel would not be visualized. So you can see the right normal MC and you cannot appreciate the left MC. This is the hypoenhancement of the left M two, this part here. So this is the dense MC sign on non contrast image and on post contrast CT scan, it's not visualized thrombosed MC. No, I would move towards the edges of infarct because in the A ne when patient presents, they want the radiologist to comment if this is an acute, in fact, subacute or chronic because it will affect management for the stroke team. So ages of ischemic infarct first, it when a patient presents within first few hours of the start of the symptoms is the early hyperacute within first few hours. What we will see loss of gray white matter differentiation or we can see the blood lentiform nucleus, which is hypertension of the deep nuclear, they will be hyperdense, lentiform nucleus. That's how we see the hyperacute then comes the acute ones. In the acute, we start to see the swelling and hypodensity within the brain parenchyma. So when the brain parenchyma starts swelled and it appears darker, it means that it is an acute infarct, the acute and fog because it's swelling of the brain at that time. As we say, whenever there is ischemia, we see as edema and inflammation and swelling. So it will cause significant mass effect on the rest of the brain and comma. And basically this mass effect and the acute infarct is the major cause of the secondary damage, which happens to the rest of the brain pa and comma in the large in fox. No subacute sub, it is a bit later than the acute. But before being chronic, subacute is when the swelling of the brain, it starts to subside. It's not complete necrosis, brain parenchyma, which is called glassy, but it starts to subside and the affected cortex in that duration. After the acute stage, it sometimes appear a bit normal as well because now with the hyperdense, the slight hypodensity which was apparent and the acute is starting to subside. So we might not appreciate it in the subacute phase and then comes the chronic one in chronic. And what happens since it's chronic, significant time has lapsed. It's after a few days. So what happens, the swelling, the residual swelling has passed and gliosis sets in that the plan is gliosed now and it appears as a region of low density without a mass effect. So there won't be any mass effect because mass effect is because of the swelling and the swelling has subsided. So Hill is the case where you can see that is the don't read down. So the the two CT scans of an 80 year old male that presented with the left sided. So that was a day one ct scan where you can see the hypertense right C here appears hyperdense and there is a subtle loss of gray white matter in the right basal ganglia. Here, if you see in the left side, white, dark, on the right side, there is no differentiation between dark and lighter. So loss of gray white matter differentiation in the right basal ganglia. And here the insular here, the insular can you appreciate here, the insula as well? Not the same one if you look at here, not. So this is the one when patient presents. And then this was the acute mc right-sided infarct and then the repeat CT scan after three days, the day third here, just ignore the left one. We are discussing the right features. What happens there is extensive ischemic changes in the right ear distribution and you can see there is hypertensity loss of gray white matter differentiation and it's a bit more darker. So it's not acute anymore. There is no mass effect here. We can't see the swelling over here. It looks subtle with dense sign here. It's more darker and it is now going towards the size stages of subacute to chronic. Ok. Not completely chronic because there is no gliosis but not acute. It is in between, that is subacute on day five on day three and in the left one actually over here, it has no signs of ischemia in the left, but later on, it actually starts to have left-sided, in fact as well in the MC, but it can only be apparent on day three. So we can't compare it. The only thing I want to show was in the early stages, it is dense MCA sign and loss of gray white matter in the basal ganglia. And then this is how it looks after three days brain damage. Anybody can see that. Now look at the next case, it's on the left side. There is loss of gray white matter differentiation and why I put it in if you pay a little bit attention, this is all hyperdense loss of gray white matter differentiation with there is swelling of the brain parenchyma because it is in acute stage. So there is swelling when it swells what it causes. When the brain parenchyma swells, it causes compression effect on the surrounding brain structures. So in all of this part, there is compression of the brain parenchyma, not only compression. It is also causing mass effect and it is causing shift. If you draw a line starting from here, a straight line from interior to the posterior on the F I cannot draw it over here. Unfortunately, but if you draw a straight line, you can see that this central part of the ventricle which was normally in the center, it appears to be shifted towards the right side. This is what it is reported as midline shift and it is a part of it is a feature of secondary feature of acute infarct or acute ischemic stroke. When there is hypertense hypoten loss of gray white matter differentiation, swelling causing mass effect and midline shift towards the left side. So it is causing the rest of the brain unaffected brain parenchyma, it's compressing it and causing it to be shifted towards the right side, opposite side. Now, uh one thing which is very important clinically is. So these are basically the ischemic stroke features the and then we discuss the ages of infarct on the CT, acute hyperacute subacute and chronic. And there is a scoring system for basically the MC at tear because we discussed that MC is the largest territory we see on the images. So there is a scoring which is called the aspect scores, Alberta scores, which is uh basically 10 point quantitative topographic on CT scan, we score in which we score and it helps the stroke team and the clinical team. The physician to actually assess how much of the brain area is damaged. They have divided the MCA territory area of the brain into six parts. Every part is given score one and whatever part is involved we will minus cause minus one from total of the 10 and the rest of us is the aspect score out of 10. And as where the aspect score is, it is in contraindicating the thrombolysis or thrombectomy. This aspect score is all adjusted for posterior circulation as well, but it's clinically, it's more common commonly assessed and demanded in the reports for the MC to inform one point is directed from the initial score, as I have mentioned uh where are the territories? So there are two levels divide into M one to M six and how it's divided, you will scroll your CT scan at the level of basal ganglia where we can see the ventricles, the basal ganglia. Now, in the basal ganglia, we know this part was AC AC, this was MC. So divided like that the NT MCA cortex M one here comes the insula insula ribbon or insular cortex lateral to the insular ribbon is the M two. And where it comes, the temporal lobe is M three initially, how you can score it is whenever you have a CT scan, open it on the Google or save this image and you can use this to correlate it with your CT scan to report. What is M one M two M three M one is involved minus one from 10, 2 minus 13 minus one. So it would be all three involved seven aspect score of seven out of 10 minus all of this 14 is basically a bad aspect score. We don't have to go to zero. Aspect score four is even bad. Ok? Now at the basal ganglia move a little bit Ranier at the level of Corona radiata, which means that when we just start to have these lateral ventricles bef superior to the level of basal ganglia. Here here comes M four M five M six. It is at the level of the ventricles immediately above the basal ganglia. So M four, if you compare these two images, M four seems to sit just superior to M one. Similarly, M five lateral MCC to M two M six. Again, post the MC terit super to M three. So go to two levels at the level of basal ganglia divide the MC terit into 123 and minus the score, go to the radiator level, divide the MC Terry into three minus them. So if all of this is involved, a large hole, almost whole MC is involved, it would be a spec four. OK. Right. Means thrombectomy cannot be done. This was with the ischemic stroke. Now I will move to the hemorrhagic stroke. So with the hemorrhagic stroke, as we can see with the name it is hemorrhage, which is bleed. Obviously, it means that there is no thrombosis in the pathophysiology of this because it's causing bleed. So it's either tearing, rupture, aneurysm of any artery which is causing bleed within the brain parenchyma, resulting in damage of that and affecting the surrounding area. So, again, patient presents with sudden neurologic deficit depending on where the hemorrhage is within the brain. Other than that, the patient would have symptoms of obviously reduced conscious state, headache, nausea, vomiting and seizures may also be present. Well, that is one thing, it's not a hard and fast rule. But if the patient, if you are suspecting a hemorrhagic stroke, it would be having a history of more commonly with nausea and vomiting in and headache in the hemorrhagic stroke rather than in the ischemic stroke. Ok. And how it caused it is caused by a spontaneous rupture of a small blood vessel within the brain when it can rupture hypertension. The most common cause hypertension, high BP causing rupture of any small of the blood vessel causing a hemorrhagic stroke. Less common cause includes vascular malformations like avm, cerebral venous thrombosis leading to hemorrhage, that is intracerebral hemorrhage. And now again, as I discussed in the stroke, whether ischemic or hemorrhagic main stay of investigation is unenhanced CT scan. One thing in that is just remember, do not ask for a contrast enhanced scan when you are suspecting bleed. Why? Because blood can be seen on the CT scan as white as hyperdense. So if you have given contrast in the CT scan, you would not appreciate that this hypertensity is of the contrast or it is of the bleed. So whenever we are suspecting blood bleed, go for a non contrast CT scan. So an enhanced CT scan, what would be visualized, visible as hyperdense area that would be bleed. Now around the hemorrhage, there would be surrounding hyperdense edema because there is brain damage. So, brain damage, edema and swelling in both types of stroke. Again, brain damage, swelling causing mass effect like ischemic stroke leading to complications like midline shift. If this blood is going into the ventricles, it will cause dilatation. Obviously, ventricles are supposed, they are built to keep a specific amount of CSF in them. If the blood enters in them, intraventricular extension, hydrocephalus, more volume within the ventricles and herniation. Now, two things hemorrhage can occur with the trauma which makes sense and nontraumatic as well. The nontraumatic intracerebral hemorrhage, it would be classified by location and with the location, it changes varies by the logic association. It can be lobar, it can be nonlobar, lobar, any lobe of hemisphere in the cortico or subcortical location. Nonlobar, what would be nonlobar areas involving the deep nuclei, deep hemispheric fissure like basal ganglia, thalamus or internal capsule or the brain stem involving the pons midbrain medulla or in the posterior fossa involving the ce, they would be non lobar lobar would be frontal lobe, parietal lobe, temporal lobe, occipital lobe, if they go into the deep matters in the deep crema, baso ganglia, thalamus interna. Next thing, hemorrhagic size is important. It is the most reliable, independent predictor of IC expansion like when it starts to bleed. When patient presents, it can be a beat of three millimeter fo sorry three centimeter two centimeter. It depends how much, how large is the hemorrhage is a predictor of how much intracranial hemorrhage expansion is going to be in future. How much we can predict it to expand further cause further mass effect, midline shift and herniation of the brain parenchyma. Ok. Hematoma extension. It is measured how we measured in the hemorrhage most of the time, not most of the time, but usually what we do is we do a CT scan on the day of presentation and then they request that oh patient has intracerebral hemorrhage and we want a CT scan, a follow up CT scan on day three or day four. Why we already know there is hemorrhage in the brain? Why do we need a CT scan? Why to see the hematoma expansion? Has it expanded? If it has expanded? How much is the midline shift? Is it increased or is it decrease? Obviously, if it's expanded, it would have more midline shift, more edema, more swelling and more compression of the surrounding brain parenchyma. How it is measured? Not just one or two millimeter increase in the size of hematoma. We would call it as hematoma expansion. It should be at least 33 centimeters, uh 33% from the initial scan. So in on the initial scan, if we have a three m three centimeter hematoma and after three days, it's 3.5 it's not expanded. If it is five centimeters, it means it's expanded. So then we call that there is expansion of the hemorrhage or there is progression of the intracerebral hemorrhage, hematomas with a volume of more than 30 mL S are more prone to expansion as we have already discussed as much larger as the hematoma, more chance of it getting bigger, causing more problems causing more complications. Hemorrhage shape. If the intracerebral hemorrhage is irregular, irregular means that it is caused by multiple leaking vessels feeding the hematoma. So there is not a one small vessel which is damaged, there are multiple vessels which are leaking blood within the brain parenchyma. So it is irregular, multiple vessel involvement means it's difficult to treat it further. And hemorrhages with irregular shapes obviously are more prone to expansion. Then how much is the hemorrhagic extension? As I discussed if the hemorrhage has intraventricular extension located in the which um hemorrhages would be have intraventricular extension, obviously, which are near the ventricles, which have more access to go into the intraventricular spaces like in the deep nuclei like in the corded nucleus. In lentiform nucleus bleed in the thalamus, they have proximity with the lateral ventricle they can go into the lateral ventricle in the pons. They have proximity with the third ventricle, fourth ventricle. It can go in there causing the intraventricular hemorrhagic extensions. Now, we can see few cases with the hemorrhage, how it looks on CT scan. So there is an elderly patient which was on Warfarin, which is an anticoagulation drug. We all know presented with certain deterioration on the in the GCS. So this is the CT scan. How does it look hyperdense content? This is a non class CT scan. We can see hyperdense content, white content in the right parietal lobe. Yeah, we can appreciate it. This is causing here. This is causing mass effect of the surrounding brain parenchyma causing a little bit of swelling. This is a midline, I just told you draw a midline connecting interior and the posterior bit of the F and you can see that it has shifted towards the right side which is because of the mass effect and it's causing secondary midline shift and all of the ventricle is midline in. Ok. So non CT scan demonstrate large intracerebral hemorrhage involving the posterior aspect of the right cerebral hemisphere. And can you see here is the ventricle right? When we see the ventricle at this level, it should come up like this. There should be parietal horns of the ventricle here. Where are they gone? Where is this blood coming into? This is a part of ventricle. There should be a horn in here as well. If you remember the anatomy, where is it gone? So there is white component in this part over here, we cannot truly appreciate it, but obviously, it's gone. So there is a white component extending in which means extension of blood into the ventricle. It was on the right side, it extended into the ventricle, right, and then going through the communication into the left ventricle. So extension in both of the ventricles and subdural space here with the marked midline shift. One case, this is the next case. This is again an elderly male which presented with acute right-sided hemiparesis. So we can see hyperdense content view on the left side of the brain. This is another important thing why we ask for. We should al always consider the history, history is the most important thing because sometimes patient is presenting with a right sided symptoms to look for injury within the left side of the brain. So patient presented with acute right-sided hemiparesis, there is bleed within the left basal ganglia. This is the ventricle I was mentioning in the former case as well. The black one right horns here again, white. So bleed in the basal ganglia which has extended into the lateral ventricle of the left side, intraventricular extension. So, acute hemorrhage centered in the basal ganglia of left cerebral hemisphere extension in the the lateral ventricle. And for now, lateral ventricle is not dilated, no hydrocephalus. With time, it can develop dilatation of the ventricles causing hydrocephalus because there is extra blood going into it more than the space it has. For CSF another case, this is a 70 year old male which presented with axia and impaired consciousness and patient has a history of uncontrolled hypertension. So, con uncontrolled hypertension when you have a history of hypertension, first thing think of the hemorrhage, what is it postero fossa where it is around hyperdense lesion with surrounding edema in the left cerebral hemisphere. And this is causing mass effect on the brainstem on the midbrain. Moving on to the next case again, a noncontrast CT scan and this patient, an elderly patient presented with alter mental mental status and also known hypertension. So what is the hemorrhage? There is uh left nodular hemorrhagic area within the pons again, pontine hemorrhage or pontine hemorrhagic stroke. So this was when we divide the an en patient presenting with focal neurologic deficits and we are suspecting a stroke and we do a noncontrast ct scan to differentiate number one, if there is a stroke or brain damage has occurred. Number two, if yes, then is it hemorrhagic or is it ischemic because it will change the management of the patient. If the if the stroke is hemorrhagic stroke, you can kill the patient by giving anticoagulation because it's already bleeding. And if it is ischemic stroke, you can save the patient by giving anticoagulation because there is thrombus. So it is very important when clinically, you are suspecting a stroke, you need to know is it hemorrhagic or ischemic? And here where comes the importance of the noncontrast ct scan to tell you if there is no bleed. The first question by the clinician is if there is any intracranial hemorrhage, because if there is no beat, they can just give anticoagulation. Even in the case of tia, they can just give anticoagulation to save it from the future stroke or to save it from the recurrent stroke as well. So the first question is no acute intracranial hemorrhage. Then we start to look for any early signs of ischemic stroke. OK. This is with the stroke and now I would move to the next OK. Um section where we say that there is bleed not within the parenchyma but within the dural spaces of the brain. And before that, um I would like to s check if there is any message or OK. So no further questions. So we can start with the extradural hemorrhage. Yeah. So you must have encountered two words, extradural, hematoma, subdural hematoma. In radiology reports presented with a and how we can differentiate them with hemorrhage. Uh just concentrate on this word extra dura. What is dura? It is a layer of me. Uh It is um the meninges like the layer, meningeal layer of the brain. OK? Which is further divided. The main concern is extradural, which means outside the dura of the brain. OK. And subdural, the other counterpart of it is subdural, which means sub to the dura under the dura. So if you can just think of the worldly meaning of these two words, it would be helpful to differentiate, to learn the differences in the appearances of these two hemorrhages, which is quite tricky and confusing at times. But still we can divide it or think of it like that extradural outside the dura. So just figure, look at this figure, this is the bone, this is the brain. OK? And I mentioned that brain is covered with the meninges. So this is the leo the meninges. If you look in this, you can say just this blue one is the arachnoid matter. But this meningeal lay and this is the periosteal uh the brain periosteum meningeal. This red is the blood extradural outside the dura. What is outside the dura outside the dura is the skull. So between the skull surface and the outer layer of the dura collection of blood is called extradural hemorrhage. OK. Now how the dura works dura itself, the layer is tightly adhere to the intracranial bony bony structures here. So whenever there is bleed in the extradural space, it would be confined within that area where dura is adhered to the bone. So it will produce a shape of biconvex or lentiform shape on the CT. OK. Because it is outside the extradural hemorrhage. Now going on with the physiology, extradural hemorrhage is mostly occurs in the young patient. Why? Because dura itself is tightly adhered by nature. Normally, it is tightly adhered to the skull. So it needs a lot of four and a lot of traumatic injury to cause the dura to be separated from its bony attachment, to whatever extent we have the hematoma. So it happens in young patients with a history of significant head trauma. So, extradural hematomas are mostly associated with skull fractures in 75% of the cases because they are high impact injuries. They are caused by high impact traumas like in road traffic accidents. More prone to young patients. Source of hemorrhage is usually arterial and extradural hemorrhage. Why it's mostly involving the middle meningeal artery which is running into that space, how the patient presents headache. First, you have, you would have um history of trauma after trauma, patient presents. So I had a high impact trauma or I had a road traffic x-ray, I was involved in that. Then patient presents with loss of consciousness, maybe headache and sometimes a lucid interval which is also classical for the extradural hemorrhage. Lucid interval is just after the trauma patient had uh uh time period, time lapse when there is no loss of consciousness time. This is classic for hematomas and then we can localizing signs secondary to the mass effect. But the main thing is history of trauma, headache, loss of consciousness, sometimes with the lucid interval where it is located most of the time, 95% of the cases, extradural hematoma is supratentorial and in 5% cases, it can be infratentorial as well. How it looks like on unenhanced CT scans. We have already discussed in intracerebral hemorrhage. That blood looks white hyperdense on the CT scan. So it is again, blood, it will look hyperdense and if there is an active bleeding going on, if the artery is when the patient presents in the A and and you are scanning it in the scanner. If there is an active arterial bleed going on, you can see central dark areas within that hyperdense hematoma. You can see central do dots which is called swine. It is the bleeding artery which is actively bleeding. It is a sign of active bleeding. So how would it look hyperdense? It would be sharply demarcated lentiform in shape. As we discussed, it is extradural outside the dura dura is attached to the bony skull. So it will be accumulating in a tight space and that tight space causes it to expand in a lentiform shape. It is frequently encountered beneath the squamous part of the temporal bone because it is mostly the temporal bone which is tr uh which is fractured in the head traumas uh more frequently. So you can see it over there, blood tends to uh to collect over there uh outside the dura and then depending on its size, the secondary features again of the mass effect and herniation of the brain, cerebral hemisphere would be further in keeping with all the hemorrhagic strokes as well. Secondary features are the same. Ok. So how uh whenever you see uh extradural hematoma in the report, you have to write down urgent neurosurgical referral because neurosurgery had to intervene urgently. In case you can expect there is basically why the brain is being damaged. Why there are because if you think hemorrhage, the blood is outside the brain, this bra uh this blood which is collecting in the potential space is causing mass effect is is compressing the brain parenchyma which is causing or symptoms. Patient presents with headache and loss of consciousness. The reason of this is that if we can solve this, if we can treat this cause, if we can just evacuate this blood, we can take out this blood. We are helping the brain parenchyma to go into its normal position like on this side, relaxing it from all of this pressure and the mass effect which can lead to swelling and further injury of the brain paran comma. So, neurosurgical referral which we just like to go in and they can cause the way they can do a bur hole craniotomy, just evacuate the extradural hematoma and the brain comma itself would be relieved by the pressure, symptoms of that blood. So in extradural hemorrhage prognosis is generally really good because it's even outside the dura of the brain, it's just causing mass effect. Now showing you a few of the cases with extradural hematomas. So you can see on a noncontrast ct head. Can you appreciate the biconvex shape? It's convex in heel, it's convex in heel, a lentiform shoe. Yeah. So it is a massive biconvex, extradural hematoma. I cannot, we cannot appreciate the skull fracture in this because it is not the uh bony window. But if you can see this is a large extradural hematoma which is resulting in massive mark midline shift and hydrocephalus of the la left lateral ventricle, just look at the midline shift. Can you see it's tented towards the left side and to be more sure if you, you can see this white dot of the fox. If you just join a line over here, you can see the midline shift. But if I just this is the whole midline shift. Ok. So massive, even if you can't see the fracture, you need to understand that this is not inside the brain parenchyma, it is outside, but it is causing so much mass effect that the whole brain parenchyma even is involved to that extent that it is causing herniation towards the left side, midline shift and even causing extension and extension of the left lateral ventricle as well. No, here comes another case with 55 years old male with a history of assault. So I'm just giving time for you. Rather than me speaking, the findings, you can have your time to have a look. How does it look like what can be the findings. There are more than one findings, this extradural hematoma other than that you can see further findings as well, no significant midline shift. So no secondary finding but look for the other things. OK? Whenever there is a pair always compare. Yeah. So this is extradural hematoma and whenever there is a pill always compare as a rule of medic medicine. So you have pill see just see is there anything asymmetrical in these two images in right and left? Yes, there is extradural hematoma which is biconvex in shape or lentiform in shape. It is hyperdense means it is acute. What else can you appreciate this thing? I know it's outside the brain, even it's outside the skull. But here it is which is not visualized in here, right? So this is one thing we need to see what it is and this is the bony window of the same. Can you see anything in here? I'm looking at the chat box as well. Yes, it says extra hematoma, right? Biconvex. Yes. Ex OK. So let's go what it is. So three findings. 12 and one in the brain in the bone window. Yes, there is a fracture. Yes, there is extracranial hematoma and soft tissue in the head. That is what somebody has mentioned in the chat box. This is what I'm actually trying to show. We need to look for these things as well. Not just that when there is extradural hematoma, there is a fracture, look outside the brain as well. Look at everything that you can see on the CT images. You can, we cannot say that OK. In the brain, it is this finding and we are not going to look outside the brain. If there is a finding outside the brain, we need to identify what it is because obviously we are not treating the brain, we are treating the patient. So now I have dotted these lines. This this I would start with the middle one. This is extradural hematoma which everyone can appreciate left lateral, moderate, left lateral extradural hematoma. These yellow lines associated with an undisplaced left parietal bone fracture. Here, this is the fracture, these two arrows. This is a small picture I will show you in here. Can you see this line? This stepping there is no displace this uh displacement, but there is a stepping line in that stepping defect. So this is a fracture, left vital bone fracture. And this is the what is this outside the skull outside the bone is a subcutaneous soft tissue. It is a scalp. This line is a scalp. So there is a scalp hematoma or subgaleal hematoma. Sometimes it's mentioned in the report as a subgaleal hematoma and the clinicians are worrying that there is a hematoma in the brain. Subgaleal means scalp hematoma simply. So there is a scalp hematoma in the subcutaneous soft tissues or the temporal bone fronto temporal to some extent. Then there is it must be, if you it must be visualized, it must be palpated on the patient's head like a swelling in the scalp. This hematoma, then there is extradural hematoma, then there is associated fracture. I'm going on to next case here. So if anyone can tell you what is happening in here in the chat box, if anything you can mention the history is same. So just to mention that if we want to speak, we can just unmute and see the answer. Yeah, I can keeping an eye, keeping an eye on the chat box to see the answers for the questions. Just think what you think in that and then I will let you know the answer. Yes, it is right hematoma. Why it is not hyperdense? Yes, there is right-sided hematoma. Why it is not hyperdense? What is the difference in this hematoma? And in this hematoma? And in this hematoma, you have seen this one completely white, this one completely white. Yeah, it is hyperdense. It has a hyperdense component but just not. Why is it? So, so we discussed ages of the infarct. Yeah. So it is the same applying in that as well. What happens is can you see this white line? This white line means there is a hemorrhage, there is a hematoma looking at the shape, it is a biconvex extradural hematoma overlying the right temporal area predominantly is isodense with internal hyperdense component and it is causing mass effect, the mass, not too much Melania. But if you see this ventricle, it is slit like it does not look like the left-sided lateral ventricle. So it has mass effect in that no fracture was in this case why it is. So it is also with the ages of the blood. This hyperdense component is the acute component. OK. So there was a hematoma evolving hematoma with internal hypertense component. We would discuss, we would do it in report like that that there is an evolving hematoma overlying the right temporoparietal lobe with mass effect having predominantly ISOS with internal hyperdense component which means there is af there is a component of acute in that with some subacute component as well. It is not chronic with some subacute component as well going on. But it has this how we can say there is acute complaint. There is this hyperdense content and then there is this mass effect which is a part of the which is indicative of something acute going on. It is causing acute mass effect on the brain branchy in the sub uh extradural hematoma. Now moving on the subdural hemorrhage. So subdural how much look for the wordings. OK. I will show you this image first subdural hematomas like this sub means under the dura. So subdural hemorrhage is a collection of blood in the subarachnoid space under the dura. So it is between the dura and not the br uh bone bone was outside the dura dura and something which is under the dura, which is the arachnoid layer of the meninges. This interpose between the dura and the arachnoid. So you inhale, typically it is crescent because there it's not compressed by the bone crescent shape, more extensive than the extradural hematoma. And it is not limited by sutures, but by the dural reflections that we would be able to understand more once we are looking for the differences in these two, and I'll go back to the subdural hemorrhage. So subdural hemorrhage is a collection of blood in the subarachnoid space between the dura and arachnoid layers of the meninges. It can occur in any age range, maybe an old because it does not always need the high impact injury. Subdural hemorrhage can be caused, not even with the low force injuries as well. Low force traumas. You don't have to have uh high expansion traumas like road traffic accidents for the extradural ones. Now, if we encounter the subdural hemorrhages in Children, we need to think for a non accidental injuries. Ok. In adult, obviously, in the head trauma, it is mainly due to head trauma, of course, but what it means is it is due to he head trauma, but in the head trauma extra is more common and it means more forceful injuries, more high impact injuries in elderly, it can be due to falls just a fall from 22 steps like two stairs, they can fall from two stairs and develop a subdural hemorrhage. Now, extradural cannot be developed by just two uh falling from two or three stairs and it presents with confusion classically dementia. So if the patients are on anticoagulation, they might not be a clear history of trauma. They just, they were standing and they just fell down from standing with the elderly patients like 8090 years old. You should be thinking of looking for the subdural hemorrhages in the brain. How it happens. It happens because of the bridging veins in the subdural space because it it's under the dura. So between the dura lobe, ura and the arachnoid lay, there are veins which are bridging in between those areas. The tearing of these veins causes bleed in that area and these veins are subjected to sharing forces. So it can occur with the low forces in the elderly as well. Again, neurosurgical referral, small subdural, they can just observe with the repeated ct scans, with the larger ones. They might decide to do surgical evacuation, considering the comorbidities, mortalities and other factors of the patient's age and the health condition. So now going and what are the few important points to be noted in that in adults? It's not that you can apply to the imaging, but it's just something that we should, we need to know while we are doing the reporting of the scans for the satisfaction of the search in adults 85% of dural hematomas are unilaterals. But in infants, it would be bilateral in 75 to 80% of the cases. And if in Children, we see an isolated interhemispheric or a peripheral sign subdural hematomas, we should be thinking of non accidental injuries. Ok? Because it's not caused by the accidents how it looks like on an unenhanced ct scan, it's blood, it would be hyperdense in acute phase hyperacute phase. It can be isol in 40% of the subdural hematomas. They would be mixed hyper and hypo denser which would reflect because why there are different ages of blood in a mixed subdural hematoma. Some blood would be un clotted which is just being it actively bleeding from the vessel. Some would be some serum have some clotted ones. So there would be mixed chronic, one would be hyper to the adjacent cortex too hyperdense, maybe. So hypertense CSF like CSF looks dark. Common sides are frontoparietal convexity and Mediterranean fossils. So look at this case. Now, we can see here and can you see the difference in the shape? The subdural extradural was like this by convex lentiform. This one is like this reship. Can you see the difference in the shape? Not a very good drawing but yeah, this is the cresentic one. This is the extra one again in here. And if you look on the left lobe as well again, it's a mixed one with some hyperdense component, some isodense component, but it's bilateral. So there are bilateral subdural hematomas, hyperdense, completely hyperdense on the right side and mixed density on the left side with bilateral edemas and sulcal assessments. So there is there are bilateral hematomas, bilateral mass effect. So, not specifically any mass effect causing herniation in here. But if you look at the lower level, when we go at the level of the temporal bones, we can see that left lateral ventricle is effaced, right lateral ventricle looks fine and left lateral ventricle is slitlike. Mhm Again, in another case, the patient presents with headache after a fall with head strike while snowboarding, few days back. So head strike while snowboarding and it was few days back. Now presented with headache, not a very sharing force, interhemispheric para sign subdural hematoma. Another case, this patient presented with worsening confusion uh after an unwitnessed fall on the background of recurrent falls. Now, I know you all know this is cresentic in shape. These are bilateral. So these subdural hematomas, but if somebody can mention why they are not completely hyperdense. Again, the same formula with that there is a level fluid fluid level. The dependent portion is hyperdense and the independent not dependent portion is the isodense or maybe a little bit hypodense as compared to the cerebral cortex. So there are large bilateral subdural hematomas of mixed densities extending from interior attachment of the f cerebra. It's just a detail in the anatomy up to the posterior medial aspect of the occipital bone and we can see fluid fluid levels. So different ages, acute component with some subacute component, bilateral hematomas. Now we should go with the. So this was with the subdural and extradural. I'm sure most of you have known the differences between these two just to revise the differences. So extradural is extra outside the dura, outside the dura, there is a space between bone and the dura which is a more tighter space. So it is lentiform or bike and reship. This one is cresentic or banana shaped, extra ua is outside the dura. So dura is attached to the bone with sutures. So it cannot cross the suture, it cannot cross the suture line. This is under the dura. So it can cross the suture line. This is also a basic concept that dura is attached to the bone through the sutures. So it cannot cross the at the point of sutures, basically cannot cross the suture line. This can cross the suture line. So you can see a more extensive uh more extensive uh subur hematoma as compared to the extra, 90% are associated with skull fractures. They are also associated with skull fractures in subdural but not as frequent as in extradural hematomas, extradural. 90% are arterial hemorrhages because of the middle meningeal artery involvement, 80% of the subdural are venous hemorrhages involving the bridging veins. Extra prognosis is better than the subdural hemorrhage. And in because we can do evacuation of the clot. It's easy. We are not going through the dura. It's just, just pass the bone, evacuate the clot, release the pressure and prognosis would be better in Subra, we have to go through the dura. So his prognosis is worse than the DH extradural hemorrhage. Now, after the extradural and the subdural, another type of hemorrhage, which is not within the spaces between the dura bone and arachnoid. It is basically within the brain parenchyma but within the venous sinuses, which is called subarachnoid hemorrhage. What is the subarachnoid? It is bleeding within the subarachnoid space in older middle age, typically less than 60 years. We have cases with the subarachnoid hemorrhage. It accounts for 3% of the stroke. These are all the book things to be honest and 5% of the stroke. That's uh because of the subarachnoid hemorrhages. The risk factors are again, hypertension is the biggest risk factor in any kind of bleed rather than is it is subarachnoid hemorrhage. It's hemorrhagic stroke. It's intra cranial intracerebral perinal hemorrhage, hypertension would be one of the risk factors. Of course, family history, heavy alcohol consumption or abnormal connective tissue disorders. What are the main causes of the subarachnoid hemorrhage? Number one is the trauma, trauma is the main cause of subarachnoid hemorrhage and then in nontraumatic causes the spontaneous subarachnoid hemorrhage. The number one causes ruptured bar aneurysm and then malformations how the patient presents for the subarachnoid hemorrhage there is a line in, I guess every book in every medical field is worst headache of the life patient would present with worst headache of the life, thunderclap headache, a sudden onset headache, which is not bearable. All of a sudden a headache be in a middle aged patient associated with the cause of the headache. It would be associated with photophobia and meningism because it's in the subarachnoid spaces. It might be involving meninges. So it can cause photophobia and signs of meningism. Clinically, almost half of the patients can present with associated collapse that they have a patient present in the in with a history of of patient developed a severe headache and then within few minutes collapsed or had loss of consciousness. It is typical classical for looking for a subarachnoid hemorrhage, how it looks on unenhanced ct scan. Again, the blood would always look hyperdense. It's the matter of the area where it is if the hypertense blood is in the outside the dura extradural inside the dura subdural within the brain, parenchyma, intracerebral hemorrhage. And if it's in the subarachnoid space, it's subarachnoid hemorrhage. Simple, like the words most commonly around the circle of illus. Why? Because the circle of illness is the main arterial supply. It's the center. So the injury of the vessels, the bleeding from there would cause the sub fill the subarachnoid hemorrhage, filling the subarachnoid spaces and the barry aneurysms mostly occur in the region of cleopus or in the silvi fissure. So look there, first, complications are again the same hydrocephalus because of the extension, sometimes even not because of the extension. It's in the subarachnoid space. It can cause hypertension, hydrocephalus, elevated intracranial pressure and the prognosis in the subarachnoid space is very variable. It depends on the cause of the subarachnoid space. Either it's a tiny aneurysm of two millimeter or it's a large venue, aneurysm involving the main MC of three of two centimeters. That is because you need to treat the cause, not the hemorrhage. If the cause, if the aneurysm is treatable, prognosis would be better grade of the subarachnoid hemorrhage and then the other pathologies and comorbidities of the patient's clinical condition. This is how a sub noid hemorrhage would look like. Can you see this white? It's not this hyperdense material. This blood is not uh contained within a specific shape like extradural or subdural or within the cerebral parenchyma. It's somewhat disposed a line here. Three here, some lines you know within the CCI see there, these were the cell side in which we can see the blood. And then these are the cisterns, subarachnoid space around the brain stem and then the cisterns here in the insular area, sylvian fissures. So this is subarachnoid hemorrhage. So, but it is extensive subarachnoid hemorrhage around the circle of vilas. There would be area of the circle of vilas and extending into the both svi and fissure interhemispheric fissure. He he it's not that hyperdense in a non contrast CT scan and over the brain convexity. Hi. And if you see ventricles are not that apparent and the temporal horns of the lateral ventricles appear dilated. So it is hydrocephalus causing hydrocephalus as well. In other case, this one was very beautiful and very clear case of subarachnoid hemorrhage, that's tiny subtle one. But in this, I would like to have a look for some time. It's not one finding. There are more than one finding in this case, if anyone can have a look for like I gave you a few seconds to have a look, take two minutes and see if you can find it. What are the your findings in that case, if anyone can answer in the chat box or can unmute them, I can answer it. The findings are all of which we have already discussed during this session. OK? I have not seen any message in the chat box, any answer in the chat box till now? No worries. So can you see this hemorrhage within the Yeah, mest this bit within the sulcus, they sweat within the circus hyperdense content. This is subarachnoid hemorrhage. But other than that, can we appreciate hyperdense content elsewhere other than the sulci as well? What is this? This is not the sulcus, right? This is not the subarachnoid space. This is not the subarachnoid space. This is something else. This is the subarachnoid hemorrhage, right? Frontal subarachnoid hemorrhage. What it is, isn't it subdural hemorrhage? Let me just remove it. Can you appreciate this cresentic shape of the blood? Can we appreciate this shape of the blood cresentic? Not the So what it is subdural, acute subdural hematomas, acute, right frontal subarachnoid hemorrhage. What it is causing mass effect? Sorry, it's very poor but I'm I'm trying to do and if you appreciate there is some mass effect and midline shift, yeah. Not much. But this maybe two or three millimeter midnight shift. And where is the lateral ventricle? Right? One where is the right lateral ventricle? It should be like this like the left one. Where is the right one? Isn't it thinned out or narrowed? So midline shift and compression of the right lateral ventricle. Another case of subarachnoid hemorrhage, it has more than one findings again. But all we have already discussed. So this have this subgaleal hematoma. We already mentioned we already discussed in one of the cases of extradural hematomas, hypertense content in the scalp, subcutaneous soft tissues, right, frontal subgaleal hematoma. Ok. Subarachnoid hemorrhage. A lot of it. Here here here, all the s are and then a crease in shape of subdural hematoma as well and fracture, right temporal bone fracture. So more than one finding. So you cannot always be looking for on a CT scan, thinking only a sub hemorrhage or hematoma or an extra hematoma. It can be more than one. It can be subarachnoid as well as subdural depending on the type of injury patient is coming with for the subgaleal hematoma with a fracture, more than one fractures, maybe fracture over here causing counter injuries. Look for satisfaction of such. Once you have seen one finding, look for the rest of it as well, look over the other scan as well. Now I have it was the think that the images and stuff and now I would like to ask if we have time to go with few of the day to day practice real life cases for relatively interactive sessions that I can show you a few images and then we can discuss the findings and I can tell the reports to you. Do we have time for that? Um I think we can aim to go to um finish at seven. So it's 650 now. So maybe we can do like one or two, II will share one or two scans and then we can have a look at that. Um Will it might take a time for me to share the screen? OK. Because of the confidentiality, I'm stopping sharing my screen for a moment until I have anonymized images. It will just take a moment um while we're waiting. Um Just to mention that um we'll be sharing feedback forms uh towards the end, I'll just share the link now and it will also come to our emails after the event. So please let's endeavor to feel the feedback. It will help with the organization and our speaker. Thank you. So, um I am so, so there are some questions on the, sorry, sorry to cut you. There are some questions on the chat box. I don't know if you start to want to start with that or maybe after this, uh maybe you can ask the attendees, I have not have the liberty to see the questions now. At least until the right now there are questions. That's fine. I can, I can maybe show one or two cases and then we can go back to the question. That's fine. Yeah, can use my screen now, I guess. So this is the case. A few days back, the patient presented an a and with used conscious level and before that, it was an old elderly female, 82 years old. So there was no history of any witnessed fall or any hidrosis. So I'm just scrolling the images slowly. It uh sometimes may take some time. So I have gone to the stroke window. So it would be a bit more easier to pick up the findings. So I have stopped in here so that this is the point where there is the findings on these images. Anyone would like to tell the on or take on the on rhythm, I can take on the findings or should I just proceed with the findings? I think we have a little bit of shortage of time. So just discuss. So if we scroll through if you pay more attention to the right side. So there is apparent loss of gray white matter differentiation in the right side as compared to the left. Can you see it now, there is some hypertensity. There is difference from in the right, from the left moving, moving, moving, that is the ventricles and this is the point of the basal ganglia. Can you see here there is some loss of gray white matter differentiation in the right basal ganglia. There is no mass effect, there is no mid shift, all looks good. And if I keep scrolling here, can you appreciate? This looks more hyperdense as compared to the left one, keep going. I'm looking for. So this is one of the signs I have picked from early signs of ischemia. Now keep looking for the other. See the whole of the basal ganglia appears different from the left. One, there is loss of gray white matter, there is blurring of gray white matter differentiation. And then there is hypo attenuation within the right basal ganglia. Can you see now what it is? I cannot, this is the vessel CMC left. One looks fine, this is calcified, forget it. This one. Can you see hyperdense component of the right MC rather than the left? And just when we see this hyperdense component, and if we track this is the area from where the changes begin, tho hypoattenuation and blurring of any differentiation. So this was acute right-sided MCA infarct. Yes, there is an answer from doctor S yes, this is acute, right MC Infarct and I will show one more scan only otherwise, it would be. So this patient presented with walking down stairs in the train station and developed sudden onset of thunderclap headache, reduced vision photophobia and multiple episodes with background of hypertension. And the query was rule out any acute intracranial neurological abnormality. This is quite evident the abnormalities, just looking at your faces, high evidence content appreciated within the subarachnoid spaces and the sulci significant subarachnoid hemorrhage. OK. Just two minutes left. So I will stop these images. Unfortunately, I had compiled 10 cases to be discussed so that it makes more sense to understand what I'm going to the questions in the chat box. Well, there is a question, I guess on this that the brain looks edematous too. So if you have a closer look, this was a patient. Um 30 years old, uh sorry, 50 years old, female patient. If you have a closer look, the, you can see the cell side and the gyra more evident on the right, obviously, understandably not on the left, but here we can appreciate right. Keep going. We can still appreciate the sai and the gyra. So apparently there is no brain Hypoattenuating attenuation within the brain parenchyma to discuss it as swelling. But if we go down over here in the left, yes, you are right. Brain looks slightly edematous as well specifically on the left side. Yeah, we can see see the difference in the ventricles in the ventricles. In the left one looks a bit affected lateral ventricle. And the right one is more prominent with more dilatation or extension of the temporal horn of the lateral ventricle, which is understandable complication of the subarachnoid hemorrhage. So that was the one question. Yes, MC was involved in the previous case. You were right. And I think there is just one question I can see thing going it. How about contusions and concussions? How about generalized edema? How to differentiate? Ok. So about the conclusions, contusions and concussions. Yes, this is also one of the findings we are looking for on the en CT scans. But due to the shortage of time, we could not cover all of the emergencies on the CT head. We have covered stroke and the bleed, which were our basic concerns and the basic anatomy of the brain. And then how to differentiate subarachnoid hemorrhage from intra. Well, see subarachnoid hemorrhage and intraparenchymal hemorrhagic stroke would be different subarachnoid hemorrhage. You would be appreciating it on and within the subarachnoid spaces. OK. So if we look over here, we know that according to the anatomy, this is a subarachnoid space, ambient CNS and quadrigeminal cns. See it's not involving the brain parenchyma, let me show you a case of brain parenchyma and then you can maybe better differentiate when it is involving the parenchyma. The cortex and the subcortical area of the brain. It's hemorrhagic stroke. In subarachnoid hemorrhage, you would be looking at the filling it in the brain, uh blood with evidence material filling the sulcal sulci filling the subarachnoid spaces filling the cysts. They are going into the venous spaces. Subarachnoid space is not within the parenchyma. See parenchyma is fine. This is the subarachnoid space in the case we saw in this presentation as well. Let me show you that this is not within the brain parenchyma. It is sulcus. If there was a bleed somewhere involving here, a large bleed that would be within the parenchyma because there is no sulcus here. This is within the sulcus. This is subarachnoid hemorrhage. If this is the subarachnoid space, if in this gray part, there is bleed in this w shaped area, this would be subarachnoid hemorrhage. But if there is bleed where there is no subarachnoid hemorrhage, it would be hemorrhagic stroke. So that would be the differ how we can differentiate the subarachnoid hemorrhage from the intraparenchymal hemorrhagic stroke. If you go back on the hemorrhagic stroke images, I'm just doing it quite quickly now. So see this is the hemorrhagic stroke. Why? Because it is not in the sulcal space. If it was in here, it was the subarachnoid hemorrhage. If it was in here, it would be the subarachnoid hemorrhage, it's within the parenchyma. This is within the parenchyma. If it was in here, it would be subarachnoid if it's in here within the parenchyma, it would be intraparenchymal hemorrhage or hemorrhagic stroke. And I think I have answered the questions any more questions. Um I think that's those are the questions um on the chat box. Thank you so much. Any other question anybody has before we um end the session? OK. So thank you doctor far for the session. It was really, really detailed and useful. Honestly, even for me, II still learned a lot from you to be honest. Um I mean, hopefully we're able to do something else and like to cover the parts that we couldn't cover if, if that's possible. Um But yeah, this is what time will allow us to do today. Thank you. Thank you so much. Yeah, so uh please fill the feedback form. Um I've put it on the chat box and it will also be sent to emails of those that attended and the recorded session will also be available um for those that will want to watch the recording. All right. So I'll be ending this session now. Thank you. Thank you so much. Yeah, cheers.