A Neuroradiological Approach to Intracerebral Haemorrhage | Dr. Nadun Vithanage

追加: 2026-05-27

[00:00:03]So u lecture today is is systematic neurological approach for intracellular hemorrhage. So the lecture uh today the lecture will be discussing mainly on the intraaxial hemorrhages uh that is mainly the paranka. So I won't be dealing with the extraaxial hemorrhages like you know subaractid extra subdural this is mainly about intraarimal hemorrhage. So before moving on to the lecture we will do some cases with daily encounter. So the first case uh 60 year old patient with longstanding hypertension presenting it the neurological deficit. So as we always do we do CT nontra CT head for these patients. So there's a abnormality in the left lentififor nucleus. So you can try in your head like you know what is the possible diagnosis here. So there's a hemorrhage in the length for nucleus. There's my edma around it.

[00:01:03]That's the main abnormality in the CT.

[00:01:05]So you can you know and I will be discussing these cases in the later of my lecture. So you can try if you know you can tell the answer yeah that's fine. So just think in your head then. Uh so the next one 75 year old a normal tensue patient with severe headache and again the we did the CT head. So there's this right temporal and parietal in hemorrhage with some medema around it. So this patient with this history we proceed to MRI directly. So this one we did the MRI. This is the susceptibility weighted imaging. So you see this abnormality in the within the cell side there's hemosine staining here and in another image there is multiple micro hemorrhages which is basically cortical and fl showing small vessel disease again this is you know these pictures you can diagnose this case uh so you can you know work it out anyway I will discuss in this case as well the third one is a young patient it's a female with severe headache and seizure Again we see a left temporal lobe hemorrhage and this is actually pre and postcontrast images. So because of the non-contrast we proceed to a postcontrast image. Uh so this is a hemorrhage here and you see some linear density along the posterior fossa and uh we did this CT it's a postcontrast if I say the correct imaging you know the diagnosis so I won't say the correct imaging but it's a postcontrast CT so can work it out the diagnosis here as well yeah so next one we don't know the history of this patient actually patient was found unconscious uh respective uh found unconscious by the side of the road. So there is with the CT there's bilateral frontal hemorrhages inferior frontal and uh this is a bond ending of this patient and again we can work it out the diagnosis from these two pictures. So point I want to make is like always the non-contra is the key for further imaging. Sometimes we can stop there at the non contrast city.

[00:03:24]Sometimes you need MRI, sometimes you need CT angog, sometimes you need a CTV.

[00:03:29]Okay, I'll discuss these cases at the end of my lecture. So you can work it out by the I know most of the you know the diagnosis. So objectives will be first to define what is the hemorrhage interparangal hemorrhage and the clinical presentation I won't touch you know I won't touch much and the second will be role of imaging basically to diagnose the hemorrhage and what are the key content you are looking at the report by reading the report why what are the key areas you need to look at and the third important one is the etology so the report should direct your ideology if not you need to direct for a further imaging that's the purpose of the report our radology report and uh then I will be discussing what are when to do further imaging that's basically look for underlying lesion so what are the features or what are the risk for underlying lesion we discuss that then final I will discuss the ethology of intracellular hemorrhage in a brief classification which is like primary or secondary Moving on to the first objective. So intracellular hemorrhage is the focal collection of blood within the paranka.

[00:04:43]I use this ventricular system also because sometimes it can rupture into the salsi or ventricular system. So but basically the definition is intraarankal hemorrhage. Clinical presentation is you know acute neurological deficit seizures coma loss of consciousness and uh yeah second objective role of imaging. So first of all important thing is you need to if you are going to comment about the hemorrhage you you have to confirm it is a non-contrast CT so you are not going to comment uh in a contrast image so you can't so you need to confirm it's uncontra CT and you have to know the mimics sometimes calcification is like difficult when when classification is difficult to like you know say it's a hemorrhage classification so so this is This is a contrast image in the right side. You can see there's lot of contrast in the within the brain. So you can't definitely say whether there or not. Sometimes if there's a lesion in the brain in a nontra in a contrast it will enhance. So you can't differentiate it whether it's a hemorrhage or a lesion. So this is a basically uncontrast CT head. So, so you can see the difference between uncontra anyway is there in the film also. So, this is basically non contrast. I will briefly introduce some anatomical regions which I which I need when I'm discussing the in the lecture. So, these are deep grime metal structures. So, this is the codate nucleus and this is the lentififor nucleus here and this is the talmer.

[00:06:24]Okay. So when you go down so these are called B bra structures. So usually the hypertensive hemorrhages happen in these locations. Okay. So uh so this again another side this is called this is the area of dented nucleus. I'll show you here around here the dented nucleus. So again a site for deep low deep hemorrhages. There's again a site for hypertension hypertensive hemorrhage. So these are classic site and the division of intraaranal hemorrhage is like loba versus deep. Okay. So loa hemorrhages usually have underlying cause. So that happen means like it is in the loes frontal lobe parietal lobe, oxipital lo temporal. So what is that? So moving on to the next part. So yeah know the mimics. So biggest mimic is the classification. sometimes really hard to like you know differentiate whether there's a classification or whether this is a hemorrhage. So there are features we need to look at to differentiate these two. So in the left there's a classification this is bilateral and this is fairly symmetrical and on the left you can see so in the right you can see a hemorrhage it's kind of irregular and always it has this kind of basogenic edma around it that's a key feature to differentiate and so so this is kind of a differentiation we can have with classification and hemorrhage usually a density of the classification is more than 100 okay the house the hemorrhage usually around 50 to 70 and calcifications are usually bilateral but it can be asymmetrical sometimes unilateral also but it's because it's because of that reason it's kind of not a good feature to differentiate and hemorrhage is usually unilateral and I think the most important features this edema so you need to look for edema because calcification won't cause edema Because when there's blood in the paranka, it usually elicit like you know voggenic edimma or cytoxy edma. So that is the key feature here. And fourth one yeah mass effect also there. So mass effect usually if it's a tiny it won't have a mass effect but it's a large hemorrhage usually it will have a mass effect and shape. Yeah it's usually small and well defined but in a hemorrhage it's usually irregular. And this last feature sometimes help because if you are not 100% sure we can always do a followup like within 24 hours usually calcification won't change but in hemorrhage it usually evolve and change in appearance. I will show you some cases. So this one yeah attenuation. So this is the left hemorrhage. So usually the density househ is around 60. So that is the normal density of a hemorrhage. But if you see this is a corlexus classification is usual classification the H isue value is around 200. So it's more than 100. So it's again a helpful feature. But sometimes the soft classification may know go to like 57 then it's become tricky. So I will show you a case here. So this one patient was presenting with right side upper and lower lip weakness acute turn state. So the clinician's question was uh this is ignore this one. is old in fact and but the symptoms are acute and clinician's question was whether this is a hemorrhage or a classification uh because he need to start treatment so but in the non test there was no acute infog basically clear there's no infark but this question was this this is a classification or not the answer for that is the classification can be as I But here in the coded nucleus if you see carefully there's no edema around this focus of calcification there's no edema that's a key feature and here there's another helpful feature for me as well but you know here there's a MCA d side so that also helpful view this is MCA D but point I want to make is there is classifications which can be asymmetrical okay so we need to consider that and you know we need to call this most likely classification minimize a clear feature for that. So this is another patient again uh this one uh patient had a uh again weakness I think this patient had a visual visual deficit acute tone set and uh again this one has this classification in the basal ganglia. This is actually bilateral but asymmetrical. So this is slightly larger in the left side and spin in the right side. So this is kind of a asymmetrical basic angle classification that is also common and this is this one again we did the repeat CT and repeat C is in fact in the left ox left oxipital lobe here but uh yeah so this one is stable so you won't change this repeat CT this again you can see the calcification it doesn't change any same so this again tells you stable over like 24 hours and this is a classification patient kind of this is a bilateral asymmetrical classification.

[00:11:52]Okay. So next one this is another case again patient this patient has actually represented seizures and what you see here is cortically based abnormality. Okay. So it's a diffused abnormality in the left side of the hemisphere and it's dense hyperdensity. So this is when you're looking at this is look like a hemorrhage right but the again the trick is if you look at it carefully there's no edema here right there's no edma around this classification or density there's nothing there's no mass effect okay so again this is a dense classification this patient has a sturge patient is st with classification so this is again a uh because for this much of hemorrhage patient should have you know mass effect and edema that nothing there. So again this one is a mica the classification is the biggest mimica for hemorrhage.

[00:12:50]Yeah. So another point I want to highlight this is other confusion confusing uh only in the CT. So the corlexus calcification okay so when you look at the calcification here you can see this denser calcification but usually intravental hemorrhages usually lay on the posterior horns. it won't be like hanging like this. So if you want to you know if you are in a doubt look at the tempor oxipital holes. So the blood will because we do the CT on super posture. So blood will go to the dependent part of the brain. So this is the this is the intraventrical hemorrhage and this is the calcification. So any query like in any situation go for the posterior ones to look at hemorrhages. So that is the differentiating points here. Okay. So yeah so important content of the report that the clinician should look at intraventricle he extension if there's intraventricular extension that means it's coming to a lower resistant point so it will be the bleeding will be more because it won't tampon by the surrounding paranka so the you know the patient's problem will be bad and if there's inflameical extension then look for hydroapalis there is yes you or high risk of hydrographing the patient with intraventicular hemorrhage. And the third point with the hematis in the posterior fossa again there's a risk of you know brain herniation hydro because posterior for is a confined space. So you have to look for that and this is a CT sign actually this is a CT angographic sign or spot sign where we see a contrast enhancement within the throat. Okay. So that tells you there's active bleeding at the time of the CT angography. Okay. So that is again a poor prognostic sign and uh yeah so that means we need to follow this patient you know do the CT head like 24 to 48 hours to look for expansion of the clot and most important thing is we have to look for possible eiology and it should be directed on the report as well. So what is the ideology? So if you see a hemorrhage like this uh you need to think of we we usually think about the cause and if you can't you know conclude the cause we have to go for next kind of imaging okay so the question is when to do imaging and what is the imaging modality be used it is directed by the nonra series that's the most helpful clue to tell what you should do and the clinical picture so this question comes you know what to when to stop the imaging and when to do imaging. So there are this there are few articles published to look for this risk for underlying cause that's that's the issue we have you know we we see a hemorrhage okay always the clinician has this question whether there underlying lesion so there are some factors that you know direct you to underlying cause is this kind of low risk factors so low risk factors is in this this group there's a less chance for underlying cause is like 1 to 5%. The age of the patient is important. Age is if the age is more than 50. The risk of underlying cause is less. And the history of hypertension. If the patient has hypertension, the deploation of hemorrhage and their CT size of small vessel disease in this four setting we can safely say is most likely due to hypertension. Okay. So but there intermediate risk is like combination of high and low risk factors. I will discuss the high risk factors. So there are five high risk factors. Younger age if the patient is less than 550 and there's no history of hypertension and the low and there's no CD sign of smaller lease and prior malignancy. If these features are there if at least one feature is there we need to go for further imaging.

[00:16:57]Okay. So and combination like you know if the the patient has low and high risk factors again we need to go for further imaging further imaging and the low risk factors actually the eyes know if this patient has you know patient is hypertension the B is in the lentifor nucleus oralamus and there small vessel disease we can safely say this is most likely hypertensive related and you can stop imaging but if you have this highly sweetness We need to decide what to do. CT angog, CT venoggram or MRI. These are the three arms we have but this is directed by the nonas findings. Okay. So I move to the next part of the lecture.

[00:17:43]This is underlying ethology. So I will be discussing uh with the classification and what we do what what we do in this uh in this kind of ideology. So intracerable hemorrhage has this classification kind of basic classification primary versus secondary.

[00:18:03]So primary interal hemorrhage usually happens with the disease of the vessel vessel itself. Secondary interal hemorrhage usually has a cause for him like basically they have a cause like a tumor vular malfformation betas there some underlying cause.

[00:18:24]Yeah. So this is the basic classification. So primary usually chronic hypertension or cerebral aminoid angopathy. Secondary usually due to tumors, vascular malfformation, uh culative disorders, cerebral venus sinus trombos and trauma. So there are these are five but there are many more causes for secondary hemorrhages but I will outline these five features for now. So primary if I go to the primary so the hypertensive hemorrhage is the most common cause for in fact the intracellular hemorrhage usually his age is roughly around 50s the common and patient has long standed long-standing hypertension locations usually basal ganglia brain stem and cortex the cortex still hyperac can be happening cortex it's roughly around 10% but still can happen So these are the common findings of you know patients with hypertensive hemorrhage common sight. So this is a right length for nucleus hemorrhage.

[00:19:28]The key feature is look for this edema.

[00:19:31]This edema is slightly like you know it's not like disproportionate. It's actually like you know mild edema around the clot. If this has underlying lesion the edema should be extensive. So you think like you know if this is a facility with the hemorrhage if you see a large area of edema there should be underlying lesion most likely if the edema is less for example this kind of marginal edema is most likely hyper hemorrhage because if there's underlying lesion then basogenic edma should be like you know longstanding right not like you know acute so this is a pontine hemorrhage again and this is a talamic hemorrhage and this is a hemorrhage in the dented nucleus. So there are this is the classic site for hypertensive hemorrhages.

[00:20:18]So this is a MRI finding of a hypertensive microgra. So these are basically concentrated on the phalamus based ganglia in the deep glary structures.

[00:20:31]The cortex is fairly clear nothing in the cortex. So this tells you this is most likely hypertensive hemorrhage.

[00:20:39]Yeah I will discuss few complicating cases. So uh so this one again patient presenting with acute neurological deficit. So what do you see here is the large lenififor nucleus hemorrhage. So the point here is can you see a hemorrhage in the there's a small hemorrhage in the uh left sylvian fisher. Okay. So the left left sylvian fer hemorrhage and a leftform nucleus hemorrhage. What has happened here is that lentifor nucleus hemorrhage has ruptured into the silian fish because it won't go other way because the ventricular or the circle in the svin fish has cf right it's a low pressure system so there highly unlike to you know rupture this blood come into the paranka because parank is a kind of a high resistance system it has it has a temponoid effect and so what has happened is it has ruptured into the ventricular system or silver fish. So for these cases we don't need actually CT angograph because we can safely if the patient has hypertension we can safely say this most likely a hypertensive hemorrhage which has ruptured into the celian fion and so anyway we did the angog also in this patient uh with the clinical inquiry so can see the clear can see the clear MCA here just there's no anorism so we can see the aneurysm there's no anorism here in the Middle cable art is clear and uh that is that. So next case again it's a complicating case. So this one what has happened is there's a right calamic hemorrhage which has ruptured into the third ventricle. So it has patient has hydroalis because of the intraventricular hemorrhage. So this is these are still hypotensive hemorrhages. it does complicating with uh intraventicular is ruptured in the ventricular system. Okay. So, so the poor prognostic signs for hypertensive hemorrhages are intraventricular extension and if they have variable density within the clot it says there's active bleeding okay and the irregularity of the bleeding and spot sign which has which I discussed earlier. So the second primary cause for hemorrhage is the cerebral amoid angopathy. Okay. So pathology is just you know there deposion of beta amoid in the vessel which the vessel become fragile and prone to rupture. Okay. So the most common cause of lower hemorrhage in elderly and it never happen in basal ganglia talami brain that's a hallmark of this process. So it won't happen in the perforate art and there are some other features I will discuss with the image. So in amoid what happen is there usually patient will have loa hemorrhage. So this is the loba hemorrhage this is a site of a loa hemorrhage and they will have kind of a chronic subaroid hemorrhages. So they will present as a convexity subaragnoid hemorrhage and it will evolve sometimes when you do MRI I showed you in the you know initial part of the lecture there superficial cerosis. So there will be hemosine depression along the south side. So again another feature of amloid and they will have cortical micro beads.

[00:24:05]So these are tiny micro beads in the cortex and they will also have this small vessel disease also. So I will show you CT. So this one again a lower hemorrhage again can you appreciate the edema is really less here. So it's really unlike to have underlying tumor here because if it is a glyoma metacy it will have no disproportionate edema. So this is basically just a marginal edema and it has ruptured into the subdural space here. So there are subdural blood also and yeah these are the MR findings.

[00:24:37]So you can see the cortical cerosis.

[00:24:39]This is the hemos straining along the site. There are multiple these are micro hemorrhages. This is the small cell disease. So these are hallmark features of cerebral aminoid angopathy which is common in elderly and yeah secondary interable co hemorrhages there are number of causes so I will be discussing with this with some few cases and first one this one is 65 year old sos hemiplasia and uh so we did the CT CD you can see a hemorrhage again left frontal hemorrhage but if you can remember the previous images the edema is disproportionate right so there's lot of edema in the right left left frontal left frontal lobe and the hemorrhage is tiny so this is a no differentiating feature for we have we need to suspect underlying mass here because the EDMI is disproportionate compared to the hemorrhage so a few images so you can see again this is extending into the ventricle and there's some intraventricular blood and we straight away we went for MRI in this patient because we suspected underlying mass. So again we see this edema which is uh larger compared to the bleed and one point I want to say can you see a fluid level here there a can see some you know level here so again a feature of underlying lesion because there should be a cystic component to be like that you know to form a fluid level okay so here also we can see this fluid level and yeah so this is so extensive see the edema when you to the MRI it's much more excessive just edema even I think there's another lesion here so this is the postcontrast images so I'll be showing the eneasement of the lesion so this is a patient with gloma actually multif focal gloma so yeah so the tumors usually hemorrhage is common in gloma and metastasis hemorrhagic metastasis suspicious cities features edema which is disproportionate to the size of the bleed and the heterogenicity And second third is a mass effect. If he has you know mass effect which is again disproportion the size of the hemorrhage is again concerning and this level fluid levels and in these patients guide is to can directly go for MRI. If MR is not available we can go for a CT contrast contrast CT. Okay. The next case it's a 20 year old male presenting presenting with acute headache. So what do you see here? Again is a right frontal hemorrhage. Here again we don't see much edema right. So edema is as I said edema is common in tumors you know glomomasis again there's no edema but the age is 20 right. So you can't be expecting hypertensive or you know amoid in this patient. So there should be underlying leion. If I go to that risk category if is less than 45 we need imaging. So this one and interestingly you can see some you know added density here in the white matter. So this is white matter there are some few densities in the white matter and we in this patient actually we suspect AV malfformation we did the CT andography. So this is a CT and finding so there a arterous malfformation in the right frontal lobe around the site of you know that abnormality I was say and so yeah so this one yeah that's that's the direction. So the CT will direct you to what to do like you know in this patient with this clinical setting with hemorrhage we did a CT angog not the venograph. Okay. So in that then the direction is for cerebral DSA and it could be diagnostic as well as theraputic and next case this one is a 30y old female with seizures.

[00:28:29]Yeah again this is a kind of a well definfined lesion right. So it's a well definfined leion. EDMI is not that you know disproportionate. It's like you know we can uh it is appropriate for this kind of a hemorrhage and this is hypert and this one actually we then for straight away going for MRI for a particular reason because it's kind and having that appearance so we initially we queried a cavanoma so this is the look of a cavanoma in the MRI so yeah so this is a cavanoma again in the nontra look like a hemorrhage but it's kind of a intermittent chronic hemorrhage but the condition will look like dense but it's different from the hemorrhage density actually slightly different from the uh acute hemorrhage it's kind of less yeah this is again a case we recently encountered so this one we have a midbrain abnormality so there's a midbrain hyperdensity it kind of heterogeneous and it has this high density areas but there's no much mass effective uh No much edema. This one we did a CT angog thinking could be a malfformation in the midbrain but there was no abnormal vessel. There's no much enhancement also. This is intrinsic uh hyper density but there's no much enhancement there slight enhancement. Then this one because there is no vascular malfformation then we were thinking about again a brain stem cabinoma.

[00:30:03]So we did a MRI again for this patient.

[00:30:06]This one again we see a classic appearance of a cabinoma in the midbrain. Okay. So it's kind of a companion case for last one. So we have this lesion.

[00:30:18]So this one can see the cabinoma in the midbrain. It's the largest one. So this one usually the cabonomomas again we see commonly usually CT andogram is negative and DS also negative. And so basically we need to follow this up. You know patient will have recurrent hemorrhages.

[00:30:36]This location we can't do anything. So we need to follow them up. Next case 60 left sideed weakness. It's a soset history. So what we see again we see a right parietital occipital hemorrhage and you see a lot of edema here right?

[00:30:53]So you see lot of EDM is like a thinking of a mass there lot of EDMI around but the EDMI classic for not like a basogenic ed cytotoxic edma so you invol gray and white matter so yeah so this is hemorrhage but it's usually basically it's cytoxicma when you see cytoxicma the concern is for infa so and it actually confined to Miller vascular territory. So this is a hemorrhagic infact with hemorrhagic transformation. So other concern we have you know they can present it as a hemorrhage but there's underlying infog.

[00:31:34]So this is not a gloma because it's confined to the particular vascular territory and it has a cytoic blame have a vogenic rather than a cytoxic.

[00:31:45]Yeah. So this is a feature of hemorrhagic transformation of infar. The next case, so this one is a young female with oral contraceptive pills presenting with severe headache for 3 days with seizures. So what you see again here is the right temporal or oxipital hemorrhage and you see a particular sign here. So you see the these are sinuses.

[00:32:10]So this sinus is dense, right? So if you see this is opioid sinus is very dense compared to the rest of the sinuses. So then what we did here was we go for went for a CT vinograph. So we are suspected with this history and with this sign of you know dense vein we suspected a venus sinosis. So we directed for we went for a CT minogram you see that fill in defect in the empty delta sign we call in the superior selis sign. So we pen sinus is not filling. So uh yeah so this is empty for empty data sign. So this is Venus sinus thrombosis important to like you know look in this nonra CT look for the hypodense vein. So if you see the hypertense vein in the clinical correct clinical setting we can do CTV.

[00:33:02]Yeah. So this next one. So this patient found unconscious at the side of the road. So there is this we see a right frontal or inferior frontal hemorrhages there multiple hemorrhages and uh when you put the bone window there's fracture you know see there's a fracture here it's a tiny fracture in the left oxy lo so again mimica of like you know hemorrhage trauma can cause hemorrhage okay so but there are classic location for traumatic hemorrhages usually they happen in the inferior frontal anterior temporal region so that is the commonest location. So if you see hemorrhages in those locations, you need to look for the bone window. If you see the bone, if there are fractures and scalp injuries, then we can conclude it from a likely traumatic and you can stop there and we can ask again the history from the patient as well because sometimes the patient won't tell the correct history.

[00:33:58]So we can ask on the relative and you know conclude this is most likely traumatic injuries because those sites are classic. So you know normal hypertensive images won't happen usually it won't happen on that side and if there fractures and it is more uh we can clearly say it's a so this is again a traumatic contusions so again these are classic site so this is happen in the left anterior temporal region as well as in the uh inferior frontal regions bilateral injuries.

[00:34:33]So those are hemorrhagic contusions. So we you look at the CT uh bone window you can see the fracture this fracture in the uh left frontal frontal bone.

[00:34:49]So this is the fracture line here. So there's a fracture in the left frontal lobe. So this is the uh subsequent injuries to the brain.

[00:34:58]So yeah. So trauma. Yeah. most common location is anterior and inferior frontal and anterior temporal. Then you have to look for scalp injuries and skull fractures. Yeah. So yeah, it's come to the end of the lecture. Uh so yeah, so I will go back to the questions and now you know just the same thing. So 60 year old patient long-standing hypertension. So this is most likely a just a hypertensive hemorrhage in theform nucleus. Okay. So this one again this is cerebral amodopathy in a 75 year old no mensive patient is severe headache. So these are the classic signs I described. Third one this is a what do you think this is?

[00:35:45]So this is a venog. So this is the left temporal hemorrhage and this is linear struct is the dense left transverse sinus. So this is the dense vein. So this is the clot. So when you do the CT venoggram you see the fill in defect on the left trans sinus non opacified left transis this is the case of venus sinus thrombosis this one you see the classic site for contusions right so this is hemorrhagic contusion in the inferior frontal lobe bilateral and you see the fracture here the oxipital lo fracture this is the contraco injury Yeah, summary like you know I want to say is like you know non contrast CD is the key. So you need to look at the non-contradity before concluding anything and the further imaging sometimes we can stop at the non-contra CT and then you need to direct with the direction of the non-contradity you decide what to do like you know maybe CT andog CT we need more MRI and yeah that is the key actually and the edema it's the most important thing you have to look for edema the edema is different from like you know from hyperase from the underlying loma so it's a again a key feature edma Look for edema.

[00:37:03]>> Yeah. Any questions?

[00:37:06]>> Yeah.

[00:37:34]Just a blood clot at the house and the house will differentiate from >> Yeah.

[00:37:44]>> If you just have a blood clot in the NCA.

[00:37:49]>> Yeah. Can the house unit differentiate with this classification nowadays? Yeah, the the problem here comes like when the you know the classification is this MC is kind of a 2 mm 3 mm artery right so if there's a classification there usually you can't can measure it but it's hard but you know the classification density usually when you put the planes three planes the classification is usually eccentric and it has a different appearance to the clo so you can easily differentiate from the classification sometimes it's hard in the cavernous segment because cavernous segment sometimes is densely calcified it but still we can say you know it's kind of density is different but I won't go by the density household density but calcification as you know that appearance of a eccentric calcification and other point is like MCA densely will continue calcification won't continue like that the dense clo is continuing so it's a key feature and you if you put the three place we can safely say there's a clo classification sometimes it's hard in film but you know we can say in the uh three planes when you put the three planes.

[00:38:58]>> Thank you.

[00:39:06]Why did you say digital subraction is therapeutic? Yeah because yeah it's a AVM you know if you say we have diagnosed AVM in angog you know then the referral to the D and you know it can you know can treat that as diagnostic as at the time we can treat that lesion also because you know we can have the intervention can basically treat the lesion in the vascular Yeah, it's a good question. So, I will go back to Yeah. So, so if you take this image this one, so you see in non-contrastity we can see the gray first point is we can see the gray and white materiality even. So if you go back a normal CT uh this one so if you see this one so can you see you know there's a slight difference between white and gray matter so this white area is the gray matter okay so if you come to more medially this is slightly darker so this is the white matter so we can see differentiation if you if you Change the windows we can see it more. But in here also we can say this is if you come to here this is more whiter right? So that is gray matter. If you go more middle this is white matter is more like you know darker. So in vogenic edma what happen is the cortex will be intact you know cortex the brightness will be there but there will be more darkness in the white matter.

[00:40:59]That's that's just a vogenic edema.

[00:41:02]Okay. In the cytoicite it affect both V and white matter that's so if I show that infog now so this one so you lose this this is the gray matter you see this is whiter right so this is kind of dark this is the white matter so here you lose that marking so there's no gray white demarcation so this is cytoroxy edma in vasogenic edema I'll show you another Uh yeah. So this one can you see here? You see the gray matter is okay right? So this is only in the white matter mostly in the white matter. The gray matter this whiteness is intact but the white matter is more pronounced and is more darker. So this is basogenic edema. The S friendship.