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Hi, good evening and welcome to our second part of our essential radiology for surgeons. And this is the second part of our series, which has been running collaboration with the Society for Radiologists and training. Uh The session tonight will follow a similar format to previous evening's. So we'll have and the first set session hosted by Doctor Cameron Spence and we will be discussing principles of neuro radiology. And then the second part of the evening will be hosted by Doctor Sandra, knew who will be discussing the principles of gastrointestinal imaging. As always, there will be a chat box throughout the evening. So if you have any questions, you can put them in the chat box and we'll answer them at the end of each session. And at the end of today, all participants will be issued a feedback link and once you've completed the feedback link uh certificate will then be issued to you. And so like I said, our first speaker tonight is Doctor Cameron Spence. Uh Doctor Cameron Spence is both an S T four in radiology but has previously trained as a dentist as well. Um Doctor Spence is training focusing on neuro radiology and head and neck and we'll be giving us the first error of his evening. Thank you very much. Thanks for the introduction. Uh Let me just share my slides. So you should be able to see my first slide now. Um It's a, it's a pleasure to be speaking here again. Thank you to the attic committee and the S R T for organizing these talks. Um So, yeah, I spent a few years working in maxillofacial surgery before making the switch to radiology. So hopefully there's, I can, I can relay some important tips here for you from a surgical point of view. And there's plenty of questions throughout this presentation to help you recall the important things. Um You might like to grab something to scribble down your answers on or you can just try and answer them quickly in your head and we'll go through the answers and move on so we can try and fit loads of cases in for you today. So are learning objectives today will include the basics of CT and Emma neuroimaging will skip all the heavy detail about imaging physics and we'll focus on lots more examples of common pathologies. By the end, you should be able to understand them and recognize them both in your exams and in clinical practice. So now hopefully you won't be stuck when the radiologist isn't answering the phone. I understand that for your mrcs mrcs exams, you're expected to be able to identify and describe the imaging appearances of things like intercranial hemorrhage and its complications infarcts, tumor's skull fractures amongst other things. So we'll touch on those. So a CT head is the same effective radiation as one year of background radiation or 100 chest radiographs or eating 20 kg of Brazil nuts and one in 10,000 patient will go on to develop cancer as a result. But despite this risk, we do get a lot of requests for CT heads for bleeds and strokes. And it makes up the bulk of our on call reporting. It's easier to do a CT than an MRI because it's a much faster study to perform. We can scan far more CT heads than M R S each day and, and, and enhanced CT heads re quick. It takes about well less than five seconds to do the scan. Um Although MRI showed the brain in better detail, we can only scan a few m our brains per day. So we usually reserve these limited appointment slots for when we have high suspicion. Based on previous CT findings, we don't have enough capacity to do an MRI head everyone. So most patient's get a CT first, you request CT heads to look for bleeds either traumatic or spontaneous. This is intraparenchymal hemorrhage which is decompressed into the ventricles. There's also some extradural hematoma here and we'll review many examples. And by the end, we should be able to recognize the different types of intracranial bleeds. We'll also request imaging for suspected strokes. We would normally do a CT first and we sometimes follow this up with an M R if there is any doubt. And this is an example of an acute left emcee a territory. In fact, we also get asked to look for tumours, for example, in patient's with worsening headaches or confusion with no cause identified. Usually we perform a CT first. So this one is a brain tumor with some surrounding low density edema. And when there's already a known tumor, MRI provides far better detail than CT infection and inflammation in the brain. The better seen on MRI, we also perform CT scans to investigate red flag headaches for suspected intracranial pressure abnormalities. And prior to number puncture for patient's with meningea is. Um so Hounsfield units are really important concept to understand they measure how dense a Vauxhall is on CT and a Vauxhall is just like a three D pixel. So uh imagine we've got a glass of water and then if we put metal in, it will sink to the bottom because it's much more dense than water. And then the same thing will happen if we drop some cortical bone in and then if we pour some fat, uh it will float on top of the water as it's less dense than water. And air will be right at the top of the glass because it's the least dense. These properties show us different types of pathology in the brain. And then we change the windows to focus on the different types of pathology that we're interested in. So this is a brain window and in the brain parenchyma, most soft tissue densities are within a very small window. So we set a very, very narrow window of center 40 with 80 you don't need to learn the numbers. But it what it means is that this image only shows us densities between zero and 80 Hounsfield units. So using a brain window, anything less than zero will appear completely black and anything more than 80 will appear completely white. And all the things between zero and 80 will appear as are different shades of great. So on these brain windows, we get a nice contrast between fluid like CSF and the dumb A which is zero gray matter, white matter and acute blood and acute blood is about 80 Hounsfield units. So in this example, we can see this extradural hematoma separate to the brain. But if we try and use a massive window and show everything on the image at the same time, it squishes together the tiny space between zero and 80 hands field units giving them all the very similar shade of gray. So the human, I can't tell the difference between brain and fluid and blood. So remember we said that with brain windows, anything more than 80 Hansford units will be completely white. We can see here that all of the bone around the skull is white. We can't see any bony definition. Here is the window with is nowhere near the bones normal 700 to 1000 hands food units. So after looking at the brain, we must change our windows to inspect the bone. So this is more like the bone window for, that's exactly the same CT scan. We want the center to be a lot higher because bone is very dense and we also want the width to be very wide. And this is because what we're really interested in here is the difference between normal bone and air or fat. So with that bone window, we can now see a tiny fracture, a tiny bit of fat or air can go into these fracture clefts. And so by having a very wide window, we can see the air or fat in the fracture cleft making the fracture more obvious. So on the bone windows deep to the fracture, we can barely see that extradural hematoma from the first image. But if we change back to the brain windows, we can see the soft tissue contrast much easier to take home message is that we must use multiple windows to see all of the information the bone windows show the fracture but not the bleed and the brain windows show the bleed but not the fracture. Remember on the CT acute blood is bright be for bright blood radiologist also use blood windows and stroke windows. They both do what they say on the tin, they reveal subtle bleeds and strokes by changing the contrast and exaggerating their features. We don't use windowing really on MRI. Instead we run multiple different sequences. The main ones you have heard of A T one and T two weighted imaging plus some variants of these simple fluid like CSF and edema usually has low T one and high T two signal. I remember water is bright on T too because H 20. Apart from blood, most brain pathology shows some edema as in it's T two bright flair sequences are a bit like T two sequences, but they remove the high signal from free flowing fluid like the ventricles and the CSF spaces. So this makes fluid that shouldn't be there that can't move freely like a Dema stand out more. Remember, blood is bright on the CT but on an MRI, it's more complicated as the signal changes as the clock matures. So we sometimes use IV contrast. Normally when you request a CT, the radiologist will decide when we're vetting the scan, whether we need contrast, whether it be helpful based on what you tell us you're looking for. So we would usually use IV contrast when we're looking for vascular problems like strokes and aneurysms. Here is an example of a giant left internal carotid artery aneurysm. We can see it's much bigger than the normal right side. We can also give IV contrast when we're suspicious of tumor's and use iodine based contrast with CT and gadolinium based contrast for Emma, they're nice head injury guidelines are well established. But beyond the scope of this talk, they essentially advise who needs a CT for head injury assessment. And how soon we've seen a skull fracture already, they aren't any different to looking for fractures in other areas of the body, but they can be confused, suture lines in the skull. So check for asymmetry. This example shows a subtle fracture through the left frontal bed. Yeah, we can also use three D reconstructions to better understand fractures. This is a depressed comminuted fracture through the right frontal bay, depressed scone fractures result from high energy impact by blunt object. 75% of skull fractures are in the front of prior to regions. Like in this example, they will often be associated with intracranial hemorrhage either within the brain parenchyma itself, which is called intra axial or outside of the brain, which is called extra axial extracts. Your hemotomas include extradural, subdural and subarachnoid hemorrhage, which we will cover in more detail. This example shows a right frontal extradural hematoma associated with this depressed skull fracture. Mhm We can also see fractures in the skull base where they'll often display classical patterns like the peri orbital bruising, mastoid process bruising and nose or er CSF leaks skull fractures need neurosurgical intervention if there's more than five millimeters depression, a tear of the juror or large volume intracranial hematoma. Now, we're going to discuss the different types of intracranial hemorrhage. These have different complications and are managed differently starting from the outside and working our way. In words, extradural hematoma czar between the skull and the dura matter subdural hematomas are between the juror and arachnoid martyr and subarachnoid hemorrhages between the Arachnoid and Pia martyr. Intraparenchymal hemotomas are a type of interaction or hemorrhage within the brain tissue itself. This is an important diagram. Remember, acute blood is bright on ct, the appearance of a hematoma will get darker as the clot matures by about 1 to 2 hands, four units per day. So immediately after bleeding, the blood is the same density as the brain tissue. But as it clots, it rapidly becomes very bright and stays like this for a couple of days. Then it starts to get darker and then it blends in with the normal brain tissue before finally becoming darker than normal brain itself after about three weeks. So dark that it looks similar to CSF. So subacute blood is very difficult to see on CT. And if we suspectedly that's around a week old, then sometimes we'll choose to use em are to try and look for that hemorrhage instead. So extradural hemorrhage is are usually from high impact trauma and are associated with adjacent skull fractures. 90% of these are due too arterial bleeds. Classically, the middle meningeal artery is damaged. So these arterial bleeds can expand quite a lot quicker than a subdural hematoma. And they need close monitoring. If they're large and causing mass effect, they are treated surgically. Mass effect means something is compressing other structures nearby. For example, squashing the ventricles or other parts of the brain. If the mass effect gets bad, it can lead to midline shift and trans compartmentalize herniation, which we'll talk about later. If they're small, they're treated conservatively. You will have seen these being described as being biconvex or lens shaped. I tend to find it easier to think acute extradural hemorrhage will look more like a white egg. This large white egg shaped extradural hematoma is cited over the left frontal parietal convexity and there is some mass effect with squishing of the left lateral ventricle and contralateral midline shift. Here is another example of a more subtle egg shaped extradural hematoma at the tip of the left temporal lobe as a general rule because they're right next to the skull. Extradural hematoma is usually don't cross over the suture lines because the juror is tightly bound to the skull. Here. This is a common multiple choice question as the answer distinguishes it from a subdural hematoma. Note that in real life, there are exceptions to this rule. For example, if the fracture disrupts the periosteal layer of the juror then confusing the an extradural hematoma can cross each lines. This is a Corona reformer image. Another common MCQ question is the extradural hemorrhage is are able to cross the midline. If you remember that they're right next to the skull, then you can remember that they can jump right over the top of the Folks Cerebri, which is just a double fold of the dura mater that dives down to separate the left and right hemispheres. Here is an example of an egg shaped extradural hematoma which is jumping right over the top of the fox cerebri and crossing the midline. You can think of an extradural hematoma as being tall as it's at the highest point of the inside of the skull. And an extradural hematoma is so so tall that it can jump right over the folks cerebri and cross the midline, but it's too tall to tie, it's shoelaces, sutures, subdural hematomas are usually traumatic or following trivial trauma and patient's with clotting issues in real life. They usually don't occur in isolations in the vast majority are also associated with traumatic subarachnoid hemorrhage and significant intraparenchymal brain injuries. The mechanism is usually due to tearing of the bridging veins as they travel from the brain cortex across the subdural space to either one of the dural venous sinuses. Treatment is surgical if it if it is large or if there's significant mass effect on this example, there is marked mass effect with displacement of midline structures to the other side. Treatment is conservative. If it is only small, an acute subdural hematoma will look like a hyperdense, crescent, overlying the brain. And I like to think of this as being a bit like a white banana as opposed to the white egg of an extradural hematoma. Subdural hematomas are a layer deeper than extradural hemotomas. So they don't sit right next to the skull. If you can remember that, then you can remember that they aren't immediately next to the sutures. So they can pass right underneath the tight dural attachment, suture lines. Remember extradural hemotomas usually can't cross an intact suture line. However, they cannot cross the midline as they are blocked by the folks cerebri. Earlier, we saw that an extradural hematoma can jump straight over the top of the folks and therefore can cross the midline. Conversely, a subdural hematoma isn't tall enough to jump over the top of the fox. So it would have to go all the way down under the fog cerebri. In order to cross the midline, this corona reformatted image shows an acute left parietal subdural hematoma with a hyper dense, thick fog cerebri. This means that the subdural hematoma is tracking down along the folks that hasn't crossed over to the other side of the brain. More inferior lee. You can see the normal thickness of the folks which then merges with the tentorium cerebelli to understand where we might see subarachnoid hemorrhage. We should recall where the CSF goes. This is a diagram in the sagittal plane. CSF is produced in the COVID plexus in the ventricles and then it goes on a long journey, it travels from the natural ventricles, then through the frame of Monroe into the third ventricle in the midline, slightly inferior, early and then posteriorly and inferior early through the Sylvian aqueduct to the fourth ventricle. In the posterior fossa. From there, it can get out of the ventricles and into the basil systems passing through some tiny holes, holes called the foramen A of Lusaka and Majendie. The basal systems are between the skull base and the base of the brain. Here colored in yellow and from there, the CSF goes up and surrounds the entire brain. The CSF is eventually be absorbed by the Iraq annoyed granulations around the brain which drains CSF away via the venous sinuses, subarachnoid hemorrhage can be seen anywhere along that normal CSF pathway. It can occur as a result of trauma or it can be spontaneous in the absence of trauma. These are usually do two ruptured aneurisms of vascular malformations. Trauma usually results in localized blood and a ruptured aneurysm often results in more widespread blood subarachnoid hemorrhage present with the typical thunderclap headache, sustained during vigorous activity. They can be seen anywhere where we would normally see CSF. So we could see blood in the ventricles, the circle spaces, the deep sylvian fissures and the basal systems. Normally the CSF in the ventricles and salts. I are black like these areas, normal areas anteriorly. However, in this example, we can see hyperdense blood in the complexity, salsify and sylvian fissure. It's bilaterally there should, these should be dark and filled with CSF we shouldn't be seeing any high density blood in here. There is also blood in the ventricles, is bright material laying in the posterior horns of the lateral ventricles is subarachnoid hemorrhage. It lays posteriorly like this because the patient is lying on their back in the CT scan. Er This example shows blood around the base of the brain in the basil systems. This is the starfish sign because it looks like a white starfish. This is a classic pattern for subarachnoid hemorrhage laying in the super seller basil system treatment of of traumatic subarachnoid hemorrhage is is often conservative. However, it's that if there is an underlying lesion such as an aneurysm or an A VM, these often need to be clipped coiled or removed as they're high risk for recurrent bleeding. Be aware the car ride plexus, which is where CSF is produced is a bright calcified structure seen towards the back of both lateral ventricles, this is a normal structure. So don't be fooled into calling this intraventricular hemorrhage. It's densely calcified and it's much brighter than acute blood. There's also usually normal dark CSF seen behind the choroid plexus. Whereas subarachnoid hemorrhage in the ventricles, completely layers along the occipital horns right at the back of the ventricles and no normal dark CSF is seen post area to it. So if we see a big subarachnoid hemorrhage on our ct brain with no history of trauma. What do you think would be the first investigation we would do to look for a cause. Well, if we're suspecting a saccular or a berry aneurysm that has caused the subarachnoid hemorrhage, we give the patient some IV contrast and we do another scan before they go back to the clinicians. This is what a secular aneurysm looks like on a ct intracranial angiogram. You can see that there is a small blob at the termination of the right internal carotid artery here. And this is an example of what these aneurysms look like on a digital subtraction angiogram. You might be slightly surprised to know that we still use these two D images in the air in the era of CT and MRI. But they give much better spatial resolution of the vessels than a CT scan, which is very blurry in comparison. Basically, it's like watching Netflix Inglorious four K compared to your childhood TV. So let's imagine we have a patient and based on the history, we suspect subarachnoid hemorrhage. Imagine we perform a CT head and we don't see any blood this time. What's the next step? Well, a CT won't show subarachnoid hemorrhage if it's only small volume as it mixes with all the CSF around it. So the patient will need a lumber puncture to look for Xanthochromia. This needs to be done more than 12 hours after onset time to allow time for the xanthochromia to develop as it's a breakdown product of blood. In CSF the CT can be used to look for contra indications to lumber puncture such as mass effect and brain herniation due to raised intracranial pressure. I remember that a negative CT head cannot exclude a small subarachnoid average. Mhm. So here is an intraparenchymal bleed in the right frontal parietal region. It's very high density compared to the surrounding white matter edema and cortical gray matter. And it looks like a white blob within the brain. You can see dark edema surrounding the blood and the edema is dark like the CSF spaces surrounding the brain because edema is just water. These can be a result of trauma, they can be spontaneous, do type things like hypertension treatment is often conservative but sometimes surgical evacuation is required if they cause significant mass effect. Here's an example of an intraparenchymal hematoma in the left frontal lobe with some surrounding edema. And here's another example of an inch a prank more hematoma in the left temporal lobe with surrounding edema. Sometimes when you see one of these, the pressure inside them will force the blood to try to escape. You may see some blood that is squeezed out of the brain and into the ventricles. Here is a tiny bit of blood in the posterior left lateral ventricle. So this is an intraparenchymal hematoma with associated subarachnoid hemorrhage. So it's summarize intracranial bleeds, an acute extradural hematoma looks like a white egg over the surface of the brain. An acute subdural hematoma looks like a white banana over the surface of the brain. Subarachnoid hemorrhage looks like bright blood where the dark CSF should be an intraparenchymal hemorrhage looks like a white blob within the brain prank more itself. These will stay bright on CT for the first few days but will then become more difficult to see in the sub acute phase. Eventually, once their chronic, they will be dark like CSF. So to recap, what kind of bleed do we think this one is, is this an egg or a banana? This is a left temporary prior to an egg shaped, extradural hematoma. This example also shows a sneaky small amount of subarachnoid hemorrhage in the pace for assistance around the left side of the brain stem. So what are these dark spots behind the extradural hematoma? They are purples of gas. So what else do we need to look for? We need to use our brain bone windows. So this is a skull fracture and when we use a three D reconstruction, it becomes a lot more conspicuous. So what kind of bleed do we think this one is, is this an egg or a banana? This one I think looks more like a banana. So this is a subdural hematoma and this hematoma looks different to the ones that we've looked at so far. Why are there different densities within it? Well, this is the swell sign and it indicates an actively bleeding subdural hematoma. So the older blood has had time to clot and it becomes more dense and bright. But the fresh blood is so fresh that it hasn't even clotted yet. And so it's still low density. Are there any other worrying findings on this scan? Well, yes, there is a severe mass effect here with midline shift, a basement of both of the ventricles and of the right convexity Celsa. So this patient needs surgery of their fit. Here's another example of the swell sign with mixed densities in a banana shaped subdural hematoma. So do you think this one is a subdural or an extra axial hematoma? So this one is a subdural hematoma because it's banana shaped, there's different densities within this one. So, is this another example of the swell sign? Well, no, this one isn't actually because it's not swelling, it's just layering by the hematocrit effect. So, what's happened is that there is some acute blood posteriorly and darker older blood more anteriorly. This indicates a chronic subdural hematoma that has had a recent acute bleed, but there probably isn't rapid active bleeding. So now we'll move on to stroke imaging. We know that stroke can be due to infarct or hemorrhage, they present in the same way, but they managed very differently when a patient presents with stroke symptoms. We do an early ct brain to see if there's a bleed or a thrombus causing a stroke. If it's a hemorrhagic stroke, we definitely don't want to give them any thrombolytics that will make the bleeding worse. CT is also used to identify patients who would benefit from mechanical, from beck to me by a neuro interventional neuroradiologist. If we haven't seen anything obvious on the CT, we can do an MRI. However, if we've seen a massive stroke on CT, we don't really gain much extra information by doing an MRI hemorrhagic strokes. Basically look the same as the intraparenchymal hemotomas we saw earlier, they also look like a high density bright blob in the brain parenchyma. This is a high density, right frontal parietal hemorrhage with low surrounding a low density surrounding edema. There's mild mass effect with some effacement of the right sided sell side compared with the left side. And the surgical CSF spaces aren't as crisply defined on the side of the lesion infarcts are usually tricky to spot that hemorrhagic strokes. The key thing about arterial, in fact is we normally see them conforming to a vascular territory. Here are the different territories of the anterior middle and posterior cerebral arteries. Mhm There are also some smaller uh central perforator arteries which can commonly lead to tiny and farts around the basal ganglia. So within farts, think of it like a city at nighttime. As long as the power is flowing, the city is lit up with lights and it's the same with the brain as long as blood is flowing, it will be relatively bright on CT. However, when the powers gets cut off to a certain neighborhood, it will go dark. And so it is with the brain, when blood stops flowing to a section of the M C A territory, it will literally go dark as in low density on CT. Although we've said we should get a CT early. We if we scanned a patient really quickly, often the brain hasn't had much time to change and we don't see much. If we're lucky, we might see some dense blood clot within a vessel. Remember, acute blood clot is bright but high density within the left M C A is the dense vessel sign and this is one of the earliest signs of a stroke, but we often don't see it as it's quite a small vessel. So the clock needs to be very big and dense to be seen on CT. Sometimes we see blurring of the gray white matter junction due to the edema. This is a very subtle sign and you wouldn't be expected to recognize this for your exams. And often we don't see any signs at all. This CT shows a patient who was scanned within an hour of the onset of symptoms. We were looking for the dense emcee a sign and we're looking for any subtle lot of definition between the gray and white matter at the motor and sensory cortical strips. And on this CT the findings are very subtle at this early stage. But then when we scanned the same patient, four hours after the symptoms started, the difference is quite stark because it's now been a few hours. We can see a Dema leaking out from the infarcted cells in the left M C K territory. There's a loss of power to the neighborhood and the lights have gone out. Starting to learn uroradiology is nice because you're basically just looking for a symmetry. So here's another example, we can see the right sided uh edema and an unclear boundary between the gray and white matter in the right emcee a territory. This is what normal grey white matter differentiation looks like. And we can see faint bright cortex or grey matter going around the edge of this gyrus. But on the abnormal side, we've completely lost the definition between the gray and the white matter. This one is a chronic mature, in fact. So the brain tissue dies and is resorbed cinespace gets filled with CSF and it turns very dark. This is usually fairly easy to recognize as it conforms to a vascular territory. So here's another example of an old in fact, which vascular territory do you think is involved? Well, on this one, there's bilateral mature anterior cerebral artery territory, in fact, and kudos to the sharp I'd surgeons who also spotted this sneaky acute left posterior cerebral artery territory. In fact, we also see a Dema on M R imaging. So remember adama is fluid. So like CSF it will be low signal on T one and high signal on T two sequences. Remember H 20 on T two sequences, fluid like CSF and edema are bright for strokes. We also use another sequence called D WI or diffusion weighted imaging. This just tells us how freely water molecules can move inside the tissue. And when tissues become super swollen, the water cannot move as easily. So diffusion is restricted, an acute infarct, restricted diffusion and is super bright on D W I. Even tiny infarcts really stand out on this. So D wi is useful for patient's with lots of infarcts such as a patient with a F who's throwing off multiple emboli and acute numbers will be very bright on D wi whereas the older in France will now have turned dark. So we can tell the difference quite easily between acute and chronic infarcts. Yeah, you can also get thrombus in the veins to risk factors include your pro thrombotic state systemically on well, patient's or hormonal factors. This presents very differently too arterial strokes without the classic hemiparalysis, patient's can complain of softer symptoms like headaches, confusion and visual disturbance. They can get imaging signs of in fact, but it often doesn't conform to the arterial vascular territories we're used to looking for. So these cases are often very hard to spot. In this case, we can see a hyperdense blood clot in the internal cerebral veins and the noncontrast ct, we can also commonly see clots in the dural venous sinuses like the superior sagittal sinus at the top of the head or the transfer sinus in the back of the head. Mhm. Often it's hard to tell. So if we're suspicious but not sure we can do a CT or an MRV in the ground to check. So in this example, we gave IV contrast through a cannula and waited until the heart pump, the contrast through the veins in the arm, through the heart and the lungs up into the head and through the intracranial arteries and capillaries and at that point, the radiographers trigger the scan. So most of the contrast we injected is within the venous sinuses. And here we can see a filling defect in the vessel. The contrast can't reach it because there's a big blood clots out there. We can see the bright contrast next to the clot in the vessel. A venous thrombosis can lead to infarcts and hemorrhages blood can't flow freely out of the brain because of the clock. So it backs up like traffic on the off ramp of a motorway. The patient gets increased pressure in the veins and capillaries, edema will form in a few hours but it won't conform to a classic arterial territory. So another question, this patient is in a coma and is intubated. Are there any urgent findings on this enhanced CT head? Mhm. They've got a really worrying sign. This is the dense artery sign we were discussing earlier, but they haven't been given any contrast. So why is the artery dense? Well, this is the basilar artery and it's full of thrombus, which is clotted blood. To remember, clotted blood is bright. If we address this quickly, we might be able to salvage some brain tissue. But the prognosis for this is really poor as a basilar artery thrombus can take out the entire posterior circulation including to the brain stem and cerebellum. So basically everything in the posterior fossa infarct, I always think of basilar artery thrombosis in a patient with a very low GCS requiring intubation with no obvious cause. We've now covered bleeds and strokes. Let's move on to tumor's sometimes referred to a space occupying lesions or focal Prank Malaysians, a space occupying lesion is an umbrella term for masses in your exams. The first differentials to think of our tumour, abscesses, brain metastases are far more common than primary brain tumour. If there's only one tumor, it's hard to say, which is which. But if there are multiple, we're dealing with metastases on the contract on the noncontrast CT, we often don't see the mass because they are the same density as the surrounding brain. The big clue of the noncontrast CT is we will often get lots of surrounding edema which is dark sorry to toxic invasive genic edema or important concepts in neuro radiology. The edema. We see surrounding a tumor is different from the edema. We see in this chemical stroke, we call the edema surrounding a tumour vasogenic edema. We can see that it only involves the white matter. It spares the cortex or grey matter on the outside of the brain. The tumor causes fluid leakage between nearby cells but don't actually cause those cells to die. So, the edematous fluid leaks from the tumour into the surrounding white matter but spares most of the cortex. This is because the cortical cells are more tightly brown together and the fluid can't get in between them. And in the scheme, X stroke, we get side too toxic. Kadima. A thrombus stops blood supply to all of the areas surrounded by that supplied by the heartery. So it all dies great and white matter. And we see a dumb a affecting both just remember that having no blood will be super toxic to the cells and they die. Cytotoxic cells can survive next to a tumor. So it isn't as toxic. The edema here is also affected the cortex and we have lost the great white matter differentiation in the tumor. On the right of the screen, the cortex has been spared. So when we see, you know, natural edema within the brain, we must first determine is the cortex affected or spared if the cortex is affected and it affects the vascular territory, then we should be concerned about an ischemic stroke. In strokes, the patient may need an intracranial angiogram. If there is Faiza genic edema, meaning the cortex is spared, then we're more suspicious for tumour. For us, we give contrast and wait a bit longer to take the scan. Usually a couple of minutes. This gives contrast time to reach the tumor and light it up. So in this pre contrast study, we can see lots of vasogenic edema. But then if we give IV contrast and do a scan two minutes later, the tumor lights up more than the surrounding brain and remains surrounded by dark edema. This is a different type of enhancement in a tumor called ring enhancement. And this one turned out to be a metastasis. This is vasogenic edema in the right sided white matter, sparing the cortical gray matter. It's pretty difficult to see the actual tumor on this noncontrast study. But if we give IV contrast, we can see the lesion more easily. This one turned out to be an aggressive primary brain tumor called glioblastoma multiforme me. And if you go to a neurosurgical MDT, you'll see loads of these tumor's are much easier to see on MRI and CT because we get much better soft tissue detail. Also, we can assess them using lots of different sequences like T one T two flare D W Y and cramp trust enhanced T one sequence is the tumour often looks heterogeneous, which means there'll be a mix of different signal intensities within the tumour and they usually enhance with the IV gadolinium contrast. This is a T one post contrast study. You can tell it's to you one because the CSF in the ventricles is dark and all the bright signal is gadolinium enhancement at that peripherally at the periphery of the tumor. This is a T two sequence of a different patient. You can tell it's T two because the CSF and the venture courses bright, we often see areas of very high T two signal within the tumour, which can represent areas of necrotic fluid. So hopefully you can now recognize vasogenic edema as a clue that there might be a brain tumor with that in mind. Here's a few quick questions to help you to recognize them is this cytotoxic or vasogenic edema? Well, there's right sided white matter edema here that the overlying cortex is spared. So this is vasogenic edema due to a tumor. How about this next example? Well, in this example, there is a Dema affecting the right emcee a territory involving both the cortex and the white matter. This one is cytotoxic edema due to an acute, in fact, remember, cytotoxic edema is so toxic that everything dies great matter included. How about this case? Like with the first case, there is right sided white matter edema but the cortex is spared. This is vasogenic edema due to a tumor. In this case, we've got left sided edema which involves both the cortex and the white matter. So this one is side too toxic edema due to an acute in fact, and this is the last example. This one shows left sided white matter edema with the cortex being spared. So this is visa genic edema due to a tumor. Another type of space occupying lesion you'll come across are abscesses. These can be tricky to see on CT. So we usually use MRI to tell them apart. You can see that they look very similar on the T one and the T two weighted sequences. But the key thing about abscesses is that they're full of pus, which stops the water molecules from freely moving within it. So it really restricts diffusion. So we can use the diffusion weighted images to tell the difference between the abscess and tumor's anything that's inside the skull that shouldn't be, there can lead to mass effect and trans compartments or herniation. So this can happen with pathology like intracranial hemorrhage and edema less effect is extremely important to recognize as it can result in severe morbidity and mortality. If not swiftly managed, think about it like compartment syndrome in the leg. As the pressure builds up inside the skull, the brain is under the most pressure gets compressed and we'll get squashed outside of its usual compartment through a narrow opening. For example, it can go through the frame and magnum into the spinal canal downwards across the tentorium in the posterior fossa or across the midline by diving under the folks cerebri, which can lead to massive problems in blood supply to the affected area. The Monroe Kelly hypothesis basically says that there are three things in the skull. Brain CSF and blood. The inside of the skull is a fixed volume and the body cannot make it bigger. So if there is something else inside the skull, that shouldn't be there, like an extradural hematoma, it will squash the CSF out of the skull. So the CSF space is closed, uh then it squashes the brain's places it shouldn't go and eventually it squashes the vessels closed and threatens brain perfusion with high mortality rates of not rapidly decompressed a relatively easy way for us to quickly recognize. This is by looking for shift of midline structures. Here, we have significant contralateral shift of the septum lucidum, which is the thin membrane between the lateral ventricles. It's being caused by this lesion. What do you think this lesion is? It's, it's bright on CT. So it's acute blood and it's shaped like a banana. So this is an acute right sided subdural hematoma. Other clues to the mass effect here is that there is severe ventricular asymmetry. This is because the subdural hematoma is squashing the brain on the right side and as a result, the brain has squashed CSF out of the right lateral ventricle. If the ventricles have been pushed away from the midline, this implies that the brain on the abnormal side is also herniating across the midline. Another clue that there is a mass effect here is that we can't see the dark CSF spaces in Seoul see around the outside of the brain both on the abnormal side and on the left side. Remember the CSF is the brains shock absorber and brain is normally surrounded by CSF on all sides. Mhm. So this is a drawing in the corona plane to does that demonstrate the main kinds of trans compartmentalize brain herniation. Radiologist look for sub Dalcin means underneath the folks cerebri across the midline between the left and right hemispheres. This is what gives us our midline shift and brain asymmetry on the axial images. Brain can also herniate across tiny spaces next to the tentorium, cerebelli and compresses the mid brain structures or or cerebellum. It can also cause herniation of the cerebella tonsils through the frame and magnum into the cervical spinal canal. Any to brain can compress vessels and needs a massive infarction and death. So this quirinal reform matches a large left sided banana shaped subdural hematoma demonstrating the swell sign which means rapid ongoing bleeding. There is clear midline shift and trans compartments or radiation here. Hmm We should also be able to see dark CSF around the spinal cord at the frame and magnum like um this example, if there is something causing mass effect within the skull, cerebella tonsils may herniate in fear really through the frame and magnum into the cervical spinal canal because the cerebella tonsils are now in the frame and magnum, we don't see the normal dark CSF around the cord. We just see if Raymond magnum full of soft tissue. And this is another bad sign. Hydrocephalus is when there's too much CSF in the ventricles. So they look bigger than what they normally do. This can be quite subtle and I wouldn't expect it to come up in your exams and it's much easier to find when you've got a previously normal CT head to compare to. But having said that it's important, you know about hydrocephalus and why it occurs and what we tend to do about it, you can lead to increased intracranial pressure which can also lead to mass effect herniation and infarction very, very rarely. It can be caused by too much CSF production, for example, by a choroid plexus papilloma. Remember the chorioplexus producers CSF. But this is super, super rare. It's much more common to see hydrocephalus when there's a blockage of CSF flow somewhere in the ventricles. CSF then can't move freely through the ventricles. So it builds up and the ventricles dilate. This is an example of hydro obstructive hydrocephalus. You can see here there's a colloid cyst which is a benign nation and it sat in it's typical location, obstructing the frame and of Monroe. So this lesion blocks the main drainage pathway of CSF out of the natural ventricles and into the third ventricle. These natural ventricles are more dilated than usual. This is more like the normal size of the frontal horns. We also sometimes see communicating hydrocephalus, which means all of the ventricles are still communicating as in there's no focal blockage instead in communicating hydrocephalus. The arachnoid granulations that normally resolved the fluid into the venous system are not working properly. And that can be because the patient's had subarachnoid blood or infection or sometimes tumor in the ventricular systems. And so we get hydrocephalus. So it appears that there's loads of blood in the ventricles and blood in the ventricular system will eventually block the macula granulations and stop normal re absorption of CSF. If it gets really bad, the patient may need a temporary intraventricular catheter or even a ventriculostomy, uh ventriculoperitoneal shunt to remove some of the excess CSF from the ventricular system. So, it's important to make sure you've got a structure to make sure that you don't miss anything. And this is a little structure that's basically just goes through all of the different things that we've been talking through today. So I'll run through some examples at the end just to help us cement, are learning now. So what kind of sequence is this? This is a T two weighted MRE sequence. And we can tell this because the CSF and the venture causes bright. How would you describe this lesion? Well, you should pretend you're describing the lesion to someone over the phone who can't see what you're looking at. You want to describe it so well that they can imagine the picture that you're looking at. And most of us often tend to panic a bit when we're asked to describe a lesion in our exams, whether it be on a plain film CT MRI ultrasound or even a photograph and it doesn't sound very polished. It really helps if you can have some kind of structure, you can fall back on. So I like to think of the three S is site size and shape. And then we can describe the characteristics of the lesion from inside to outside. And you can use this structure for any lesion would ask to describe in radiology. So for this lesion, we can say in the left side of the brain involving the deep white matter in the cortex, there's a large ovoid abnormality. The lesion is high signal or hyperintense compared with the normal brain tissue. And on this T two weighted sequence, that means there's fluid here consistent with the Dema this is cytotoxic adama as it's affecting the cortex as well as the white matter. The outer borders of the lesion are well defined as in, we could draw around it with a pencil and there is a mass effect on nearby structures such as a basement of the Sultan ventricles and mild contralateral shift of the septum lucid. Um So how can we decide on the cause of this edema? Well, we've discussed that when you have a Dema from an infarct, you can have a Dema from a brain tumor and you can have a Dema from hemorrhage infection and trauma. The dead giveaway here is that the edema is well defined and conforms to an arterial territory. So this is an acute left M C A territory, in fact. So what do you think has happened in this case? It's always a good idea to look around the edges of the film first. When we shone a case in this example, before we look at the brain itself, we can see there's some overlying swelling over the left parietal area that isn't seen on the right side suggesting this is where the initial trauma was. Then when we look inside the brain, we can see a nice normal cell side and sylvian fissure on the left side. But on the right side, the sylvian fissure is completely filled in with hyper dense material, which means there's acute blood where the CSF should be. So this is a traumatic subarachnoid hemorrhage. The head is hit so hard in the left parietal area that the opposite side of the brain smashes against the right in the wall of the skull, causing trauma to the opposite side of the brain to the initial injury. There is also very slender subcoracoid hematoma on the right side here too. It's much easier to see the subdural hematoma. If we scroll down more in fairly what do you think of this abnormality? Well, this one is a banana shape. So this is a subject hematoma. And why are there different densities within it? And it's made of different densities because it's actively bleeding and the blood clots, it turns hyper dense and the fresh blood hasn't had time to got yet. So that's the dark areas. Sometimes this looks like swelling blood. So we like to call this the swell time. And why else might we be worried about this case? Well, this lesion is causing severe mass effect. We draw an imaginary line across where the folks should be through the middle of the brain. We can see that there's severe contralateral shift of midline structures. This patient needs surgery to decompress the intracranial contents if they're a surgical candidate. Mm This case also has mixed density but there's no swell signs here. This shows a chronic subdural hematoma. And we can also see that there's new acute blood layering posteriorly. So this is an acute on chronic subdural hematoma in a patient with multiple falls. I know that those mass effect was shift of midline structures here and the face mint of the salsa on the right side. This is a tricky cases. There's a lot going on. Where is the blood located? We've got a large left sided intraparenchymal hemorrhage. It involves the left frontal parietal lobe and extends in fear really to involve the temporal lobe. And we've got a lot of blood in the ventricles too. You can see blood in the lateral ventricles and in the fourth ventricle lower down. This is a combination of injure parenchymal hemorrhage, which is decompressed into the ventricles. So there's also subarachnoid hemorrhage. There is mass effect with circle effacement and there's some hydrocephalus as these ventricles are more dilated than normal. There's so much blood in the ventricles that it interferes with the normal re absorption of CSF at the parathyroid granulations. What's the diagnosis in this elderly patient? With confusion? Any tax eah. Uh Well, there's multiple high density lesions all over the brain here. So these are consistent with metastases, the most likely sites of primary disease causing brain mets in the lungs, kidneys, breasts, melanoma, and colorectal cancers. What is this lesion? This case shows subcutaneous right frontal swelling underneath that there's an egg shaped hyperdensity in keeping with a sub extradural hematoma and there's also a small inch prank more hematoma. So what else do we need to look for? In this case, we want to look at our bone windows as extradural hematoma is often associated with an adjacent skull fracture. We can now see the fracture of the right frontal plane which has caused the bleed. This one was taken after a bike versus car road traffic collision. We can see air inside the skull, pneumocephalus with an egg shaped extradural hematoma. And when we check our phone windows, we can see small Oculus of pneumocephalus and we can see the skull fracture adjacent to our extradural human doma. It looks small on this one slice. But if we do a CT recon, we can see it's quite extensive. Yeah. So what kind of study is this one? This is a post contrast ct brain. So we gave the patient contrast and took the scan two minutes later. And how would you go about describing this lesion? So hopefully, rather than panicking, you could remember the systematic method to describe a lesion. So in the left frontal lobe, there is an approximately five centimeter, a rounded lesion which is uniformly low density internally with a well defined thin rim enhancement. And there is a Dema surrounding the anterior medial aspect of the lesion and it's producing some mass effect with the face mint of the left complexity, Celsi but relatively little midline shift. The mass effect is less than we would expect given the size of the lesion. So what are the differentials? This could be an abscess or it could be a metastasis or it could be a primary brain tumor. There's only one legion, it'll be hard to differentiate them based purely on CT. So we're often led by the clinical history and we may need to do MRI have for further work up in this case. What kind of study do we call this? Well, this is a CT intracranial angiogram. This one is done in the arterial phase, but you can see a little bit of contrast in the venous sinuses at the back of the head. So what's the pathology on this study? We can see two aneurysms here arising from the right M C A in the Sylvian fissure and the terminal left internal carotid artery. These will likely need treatment by endovascular coiling as they're high risk of hemorrhage. What's the abnormality on this CT this one we've seen before, this is the dense maca sign. This is an early sign of thrombus in this vessel. Remember thrombus clotted blood and acute clotted blood is bright on a CT scan. There's no point faffing around with an MRI here. This patient needs urgent thrombolysis. So I'm going to call for them back to me. You're clinically appropriate. So what's this sign called? This is the starfish sign and the high density represents acute blood. Where is the high density? It's in the basil systems. So it's underneath the brain. And this bit at the center of the star of this is the super seller system because it lies superior to the seller Ter Sica where the pituitary gland lives and at the bottom of the star, there is more blood around this mickey mouse ears structure. This is blood in the basal system surrounding the mid brain. So what kind of bleed is this? This is acute subarachnoid hemorrhage. So this is the last question using the system that we've been through. How should we describe this lesion to someone over the phone. So we can say something like this. This is an unhand ct head and in the left basal ganglia, there is a three centimeter lesion which is a star shaped, it is hyperdense throughout with a well defined outline. There is faint rim of low density adama surrounding the lesion but no significant mass effect is seen and no similar hyperdensity is seen elsewhere in the brain such as in the ventricles. This is in keeping with an acute into prank mo hematoma. Remember you can use this method to describe any kind of lesion in radiology and it can really help you to sound more confident. So, thank you very much for attending and listening. Lots of these cases were borrowed from Radio Pedia and my colleagues at Southampton. So thanks to all of them and thanks to Acid and the SRT committees for arranging these talks. I hope they've been useful for you all. Uh And I'll be happy to answer any questions if you have time or you're welcome to contact me on Twitter or via email. Hi, everyone. I'm Sasko. I'm just taking over from Gillian in terms of hosting this webinar. Thank you so much for that talk, Cameron, that was really, really helpful. I've definitely got so many notes from that as well. Um Oh, I think I can just see a question popping up. Oh, we've just got a nice statement from someone say it was a great talk. So thank you for that. Um, I think we'll just have a five minute break now if that's okay. Obviously, if anyone's got any questions, I don't know if Cameron can hang around just in case anything crops up, but we'll just have a quick five minute break and then we'll go on to the next talk by Sandra if that's okay.