 Hello everyone and welcome to this prelude for the upcoming monsoon edition of the 20th MRI teaching course. As we all know, this is one of the much awaited annual conferences. This is the 20th year and this is a conference where we cover everything from basics to advances in MRI. And last year we shifted from the on-site pattern to the online platform, which gave us a lot of opportunity to expand and a lot of flexibility as well. So though there were issues and a lot of new challenges with the ongoing pandemic, we have with us this online platform giving us the flexibility to learn at our own pace and at our own space. So this year also the 20th MRI teaching course will be a comprehensive course and we are happy to inform that we have expanded it from a three-day format to even better five-day format. And we are also having preludes in between as we understand that MRI is a vast topic in itself and it takes years to understand and gain the knowledge. But to cover the topics in these few days is really difficult. Therefore, the physics part of it and anatomy we have kept as separate sessions two days. 7th of August we'll have the sessions dealing with the physics topics, specifically directed to our residents who have just joined ideology. We'll have basics and advances in MR sequences. We'll learn about MR artifacts. We'll learn about MRI safety, MRI coils, which are used 3 Tesla, 1.5 Tesla, the differences, etc. This will be on 7th of August Saturday evening. The second day will be a detailed MRI anatomy which will be on Sunday 8th of August and here we are going to cover the basics of neuro and MSK anatomy. As we know that before we start understanding the pathologies, we should understand the anatomy because that is how we are going to learn to identify the difficult cases in our practice. We'll have a short focus session on anatomy like anatomy of mid-sage brain, anatomy of CSF spaces, cranial nerves anatomy, neurovascular anatomy and then we'll have it followed by anatomy of knee, shoulder, ankle, elbow and wrist joints. We'll have our expert team dealing with these topics including our mentor Dr. Deepak Patkarsar and Dr. Malini Lavande who everyone knows whoever is dealing with MSK imaging. Then Dr. Divyata, Dr. Ravi Thapar, Dr. Amit Chaudhary, Dr. Gayathri, Dr. Harshad and many more. Next day will be a full day session on neuroimaging topics which will cover everything including infections, including neurodegenerative spectrum including everything like COVID-19, mucormycoses, then updates on brain tumours, pediatric and adults, updates on advances like perfusion, DTI spectroscopy and also something like cellar, paracellar areas or vital pathologies and stroke and update. With this we'll move to the next session which will be completely dedicated to MSK topics and there we'll have everything beyond anatomy because anatomy we'll already see on 8th of August. So this session will deal with the detailed MRI in knee, shoulder, ankle, wrist in approach to tumour like lesions in soft tissues as well as in osteo structures and followed by some advances like peripheral neuropathies, cartilage imaging etc. And then we'll have a complete day on body imaging topics which will cover basics of cardiac imaging basics of breast imaging using MRI. Then we'll have sessions on liver lesions covering benign liver pathologies, then the chronic liver disease, how to report and then how to identify and report as per the lyrads. Then we'll go to session on pyrads as well that is multi-parametric MRI of prostate. We'll have sessions which will be focused on gynec malignancies and some sessions on MRI defecography, enterography like techniques. So hopefully with this course we offer you whatever best can be made in a short day conference on MRI and all these topics are online so you can attend as per your flexible schedule at your own space and these will also be provided after the course gets over for at least a month. We have an honour to have with us the international faculty members as well as they acknowledged and also came forward to support us to this noble cause of teaching and spreading education. So we have Dr. Jain Narang, Dr. Ashish Chawla on board, Dr. Vinil Shah, Dr. Ankit Tandon, Dr. Manjiri Dige, Kaurang Shah sir, Asim Lahiri, Dr. Jim Voo, Dr. Kidar Jambekar, Dr. Rajan Jain and Dr. Raj Kidar as well as many more additions. And as always the most important part of any conference are our delegates so we require your support and we call for submissions for papers and posters if possible related to MRI topics and the last date of submission is 1st of August. Guidelines are very simple. You have to send us in a PPT format consisting of 15 to 20 slides. Last slide should consist of references and the file size should be 10 MB or less. So you can mail the paper and your posters to this mail ID of IRmasterclass at gmail.com. We are thankful to our educational partners, Care Stream, Sanrat Bears and also to the organizing committee members for their efforts and timely contributions. Dr. Sanjeev Mani sir, Dr. Deepak Patkar sir, Dr. Jignesh Thakkar, Dr. Shalyendra Singh, myself, Dr. Mitusha Verma, my colleague Dr. Kauria Hoja and the support behind everything. Mrs. Mamta Patkar ma'am and Amit Poonkar sir for the relentless technical support. So with this let's go ahead to the first topic of this prelude which is MRI imaging in Kolan Jio Karsinoma and for this we have with us Dr. Ashish Chawla who started his career in ideology from the city of Mumbai but soon he developed a lot of new avenues and then he did fellowship in abdominal radiology from University of Colorado USA, a fellowship in cardiothoracic radiology again from University of Colorado and he has several textbook chapters to his credits and published around 80 articles. He has been senior consultant at Department of Diagnostic Radiology Kutepua Hospital Singapore and he is also Diplomat of American Board of Radiology. So we are thankful to you sir for sharing your knowledge and for your time and contribution. Let's begin with the first session of the day. Dr. Ashish Chawla, then I am going to speak about MRI imaging of Kolan Jio Karsinoma. So I will discuss the imaging spectrum differential diagnosis of Kolan Jio Karsinoma and the limitation of imaging of biliary structures. Kolan Jio Karsinoma is the most common primary biliary tract malignancy, its second most common primary hepatic tumor after hepatocellular karsinoma. Seen worldwide, most common is not Thailand where it is due to association with liver flukes infection and it is seen twice more frequently in males compared to the. So these are the risk factors of Kolan Jio Karsinoma genesis, parasitic infection as the liver flukes I just talked about. Primary is Kolan Jio Jio, Koleletiasis, biliary disorders like Kolelocal cyst, hepatitis B, hepatitis C and cirrhosis as well as lifestyle related risk factors. I will go into the details of Kolan Jio Karsinoma genesis. So these slides will be there in your PDF. Hepatitis B, hepatitis C and liver cirrhosis, they are common risk factors for developing Kolan Jio Karsinoma and hepatocelular karsinoma. So be aware of that. Many times clinician wants to answer whether the patient with cirrhosis has Kolan Jio Karsinoma or hepatocelular karsinoma. So that's the rule of the radiology. So coming to the anatomical classification, the Koleletia karsinoma can be divided into periferal intra-hepatic Koleletia karsinoma, hyalur intra-hepatic Koleletia karsinoma extending from the insertion of the cystic duct to the second-order bile duct and then the extra-hepatic Koleletia karsinoma as shown in this illustration. More important for us is to know the morphological classification of Koleletia karsinoma. These can be divided into mass forming Koleletia karsinoma. So the mass forming Koleletia karsinoma, they tend to invade into the liver parenchyma. They tend to obitrate the partial vein without invading into it. Whereas the second type, periductal infiltrating type, they tend to grow out of the bile duct, so they usually present with long structures and dilatation. The third type, the intra-veclo-type, it grows into the duct as a papillary mass expanding the bile duct. This one has the best prognosis. Why the morphology is important, because it decides the tumor's behavior, surgical approach, clinical outcome. Overall, prognosis of the patient is decided by the morphology. Workup of the patient, biochemical workup, serum C199 information is quite useful in differentiating the Koleletia karsinoma from hepatocelular karsinoma inside that the patient with Koleletia karsinoma can go either way, either Koleletia karsinogenesis or they can develop hepatocelular karsinoma. But be careful, patient with benign biliria disease can also have high C199. So the mass forming Koleletia karsinoma, usually they are irregular mass, lobular mass with well defined margin. In the periphery of the tumor, they are abundant tumor cells. In the central area, there are necrosis, fibrosis, and myosin, high point test on T1 and heterogeneously bright on T2A2DV. Enhancement pattern is quite characteristic. In the arterial phase, they show peripheral same range of enhancement with progressive stature petal enhancement in the subsequent phases. In the delayed phase, there is more intense enhancement. They are predominantly hyper intense on the epitopillary phase. And I'll talk more about it, some interesting signs on the epitopillary phase. The insular features are quite useful sometime in differential diagnosis. As I mentioned, the Koleletia karsinoma tend to encase the porcelain instead of invading as a tumor thrombus. They may be associated biliritalitation, low bariprophy, capsule attraction and some other ansularity. This is very interesting sign, cloud sign. This is seen in patients with the Koleletia karsinoma in the epitopillary phase. So the central area of the tumor is bright in epitopillary phase and the peripheral is hyper intense. That is for cloud sign. Here is an example of a cloud sign which we reported in this journal. But this is not specific for Koleletia karsinoma. It can be seen in metastasis from the muciness tumors. Another sign is the target sign which is more specific sign of Koleletia karsinoma. So in the high V value diffusion major images, there is bright signal here because of the tumor cells. In the central area there is dark signal because of the fibrosis or necrosis. This is seen only in the high V value images. This is quite useful sign practically to differentiate small epitopillary karsinoma from the Koleletia karsinoma. So this is seen in the Koleletia karsinoma. So in the first case here, T2 facet images show a heterogeneous mass on the in the in the level and it shows heterogeneous T2 bright signal. The central area is more bright. The periphery is not so bright. In the high V value images and ADC images clearly there is a cloud sign. So there is darkness only in the periphery of the tumor and in the central area is more of a T2 shantra effect. So this is sorry it's a target sign is present. It's hypo the tumor is hyper intense on T1 white images. In the actual phase classical peripheral rim like enhancement and in the venous phase and 3 minute and 5 minute delay phase there is progressive enhancement. See the enhancement in this area becomes more dense with the time lapses in the habitability phase. What we are seeing is classical cloud sign. So this is how a Koleletia karsinoma looks like classical Koleletia karsinoma and everything specific is present about it in the Koleletia karsinoma. Sometimes even a single image is quite diagnostic of Koleletia karsinoma. So I'm showing that this is a patient who has a mass which is showing heterogeneous enhancement. There is peripheral interaction. There is attenuation of the portal vein. It's not invaded. See there is compression of the portal vein. There is associated peripheral ductal dilatation. So one image quite confidently I can say that this is probably most likely Koleletia karsinoma. Another example 58 year old man with hepatitis B and cirrhosis CT scans shows in the portal venous phase a mass here. So the question again whether this is Koleletia karsinoma or hepatocellular karsinoma. MR shows a lot of light on this case. Let's see that MR of this patient. So on T2 fat sat images the mass is heterogeneous, mildly bright on the periphery and dark on the center and on the diffusion weighted images is bright. I'm not showing the ADC because of the lack of space on my slide but it was dark on ADC so there is restricted diffusion. Look at this component of the mass it is extending into a tubular structure whether it's a portal vein or it is a duct. So see that it's bright, it's the same as some primary mass. On T1 weighted images this mass is enhanced. In the arterial phase there is barely any enhancement in the mass but there is some very mild enhancement in the mass. In the venous phase and the delayed phases there is progressive and more tensile enhancement in the mass as well as this component which is actually here. So this is actually here there is an ancillary feature here, the duct is dilated here and there is capsule retraction. Happy to be able to face the mass washes out and if you move more cordially slices then this component which we were analyzing is not going into the portal vein as the portal vein is here on this side and the mass is here and it's actually extending into the right duct. So all these features are favoring the diagnosis of cholinchocarsinoma. So quite comfortably I can tell my clinician that this is not epitoma, this is cholinchocarsinoma. Differential diagnosis as I said in the clinical practice is quite is a common query how to differentiate cholinchocarsinoma from hepatocerocarsinoma so in my, this is the chart I got it in my experience this presence of fat is quite useful when the fat is present is more likely hepatocerocarsinoma because I have not seen fat really cholinchocarsinomas in the literature they have described though then the capsule in the delayed phase is seen in cholinchocarsinoma, in the hepatocerocarsinoma and not in the cholinchocarsinoma. Diffusion with images as I mentioned is they can be target like appearance which when it presents is quite useful. Portal vein involvement is typically in hepatocerocarsinoma there is tumor thrombus whereas in cholinchocarsinoma there is encasement of the portal vein other than tumor extension then the duct may be dilated in cholinchocarsinoma whereas in only large beta-cellocarsinoma ducts are dilated. Another example a 54 year old man with hepatitis B again the question is same whether this is hepatoma or cholinchocarsinoma MRI let us see the MRI what it shows so on MRI this lesion is mildly bright but quite well demarcated on G2 fat side images. There is a lot of information in the G1 major images so in the out of phase image the tumor looks more darker that is signal loss suggesting that there is fat inside the mass and this is bright on the value images and I am not showing the diffusion but it was dark on diffusion so there was presence of diffusion and in the out of phase there is very mild enhancement compared to the unenhanced white images not the typical enhancement pattern of hepatocerocarsinoma but what is interesting is that in the 3 minute delay phase and the hepatocular phase there is a very subtle capsule formation so we have 2 evidence to work hepatocerocarsinoma and then the further evidence comes from the biomedical work of the patient the patient alpha fetal protein level was more than 400 where as the CA19 was not high so comfortably again we gave a diagnosis of hepatocerocarsinoma this tumor was reflected and the final diagnosis was well differentiated hepatocerocarsinoma A real differential diagnosis of mass homicollinchocarsinoma is hemangioma not the classical hemangioma but the sclerosin hemangioma the classical hemangioma typically has peripheral nodal enhancement in the arterial phase and which moves sensibly whereas in the sclerosin hemangioma the same findings are present but they are delayed so in the arterial phase there is nothing but in the venous phase there is peripheral nodal enhancement and in the even in the quite late phase there may not be complete filling up of the tumor of the hemangioma because of the fibrosis element present in the center of the hemangioma so in the clinical practice again it becomes sometimes difficult these keys are helpful the hemangioma they don't show any restricted diffusion the diabetics are never dilated in the presence of hemangioma epilopilatesase is not that useful so an example here 41 year old man with incidental lesion and inlavor on the ultrasound in the CT scan single phase photovine phase shows there is a lesion with the heterogeneous enhancement in the periphery of the right lobe of liver amount was done for this patient on fat fat titiated images the lesion is heterogeneous on a slightly bright in the periphery but dark in the center in phase out phase at least confirmed there is no fat so unlikely hepatocellular carcinoma no clue for hepatocellular carcinoma there is no restricted diffusion quite useful evidence and in the actual phase there is no enhancement in the venous phase there is peripheral mild enhancement in the delayed phase there is centripetal moving off contrast and finally in the tamiya delayed phase the lesion completely enhancing in the hepatocellular phase there is some nodular patchy enhancement in this patient so again it's more favoring the sclerotic hematoma because there is no restricted diffusion and there is delayed sort of if you enhancement is slightly delayed compared to the classical hematoma but in the clinical practice the decision making it become difficult to call a sclerotic hematoma a sclerotic hematoma it's usually a hindsight diagnosis in my clinical practice so we suggested biopsy no biopsy was performed in this patient but this remains stable over nine years when I was following this patient almost same as the appearance so because it's true at that this is probably a case of sclerotic hematoma definitely collineal carcinoma is out of question and there is no ancillary feature of like the absolute interaction or peridactyl dilatation in this case to suggest as collineal carcinoma so comprehensive evaluation is important in such a case this is an interesting case recently encountered but we have few more cases like that a 51 year old man with sigmoid mucus melignancy operated a couple of years back so this patient had undergone a CT scan that showed multiple masses in the level e.g. MR for further evaluation so on T2 fact set images there are at least two masses in the level one here and one here they are mildly bright but not exactly T2 bright but they have a margin quite well demarcated there is restricted diffusion and if you carefully evaluate the diffusion it is the target sign the target sign is present there is restricted diffusion in the perisary of the mass and in the central area it is more of a G2 shine through on an as wide high point turns and look at the venous faces and the three minute delay and there is progressive enhancement in both the masses serious air and in the epitome phase classical cloud sign so we knew from the history that patient has a mucus in the history of colon jocob mucus in a sigmoid mass so these are probably metastasis and the clinician also knew that this is metastasis but we have to give a differential diagnosis that may be the semi-g-focal colon jocob radiological differential diagnosis but final diagnosis was confirmed as mucus in a metastasis so learning point is that the mucus in a metastasis is very differentiated radiological from colon jocob sinoma but that usually this is not a question because you always have a history of a mucus in a melignancy in breast or colorectal cancer in such patients or with metastasis move on to the peridectal infiltrated colon jocob sinoma they arrive between the second ordered bile duct in the discussion of the cystic duct they spread along the bile duct so but in practice a combination of peridectal infiltrative and mass forming tumor is more common so they usually the MR feature is of peridectal thickening which is high point chance on T1 that shows progressive enhancement typical signature imaging features colon jocob sinoma high point chance on T T2 radiative images they are usually associated with ductal dilatation and ductal narrowing that actually draw your attention towards the mass the presence of ductal dilatation and the most important in practice is the presence of restricted diffusion in the peridectal thickening that makes our confidence high to call it a melignant structure so here is an example of a patient 52 year old man presented with sepsis and abnormally function test and this is how they usually present so on the CT scan, single phase, photovenous phase there is just focal ductal dilatation nothing else focal ductal dilatation in the lab that photovenous is not trombose but it's it's compressed, it's narrowing caliber it's invaded by the mass so the MRI was done for this patient for further evaluation on MRI there is ductal dilatation in the left side and the duct are not as bright as they should be they are very cloudy bright but they are bright, see here very difficult to make out most useful, restricted diffusion it was present, I'm not showing it in the ADC here because of the lack of space on my slide but there is bright signals here in the distributed images on the contrast phases there is periductal thickening and enhancement, see along the duct here involving a long segment of the duct typical example of periductal infiltrated by Collin Chukar Sonoma and this is how they usually present focal dilatation of the duct either segmental or lower some territorial, so the TECO message is one of the TECO messages to never ignore focal ductal dilatation if you see on CT do for workup on this patient so this patient came back six months later I have put up the initial CT and follow up CT side by side and you can realize six months later the mass is now quite obvious so initially it was a ductal, periductal infiltrating mass now it has become a combination of periductal infiltrating and mass forming Collin Chukar Sonoma this is usually the stage when we give the diagnosis confirm diagnosis of Collin Chukar Sonoma that is not good for the patient because by this time it's inoperable it's good to diagnose it's quite beneficial to diagnose the Collin Chukar Sonoma at this stage and that is possible confidently only by a combination of MR and ERCP as shown with this example so classkin tumor everybody knows about it this is the classification of classkin tumor difficult looks like complicated slide but the slide is more useful to understand the classification so in type 1 only the common hepatic duct is involved without involving the confluence in type 2 the confluence is also involved in type 3a the right duct is involved in the type 3b the left duct is involved the right duct is there and the type 4 is inoperable both the ductal systems are involved along with the hepatic duct so this classification is useful for prognostication and for guiding the cell so 56 year old man with elevated level function test and services there is a mass here in the high lung with ductal dilatation bilaterally the right duct as well as left duct on T2ase images that's showing restricted diffusion and in the contrast enhancement phases there is typical signature of Collin Chukar Sonoma enhancement no doubt this is a classkin tumor and the portrayal was created in this patient MRCP is quite useful in these patients in classifying into the PISMAT categories so in this patient the left duct is there involved and the main duct is involved so this becomes type 3b classkin tumor in this patient's surgery was not performed treatment was given and give the presence of mobility so this is how the classin tumor look like now we move on to a common scenario that we face in our clinical practice especially the extra hepatic bowel that stretcher I see it every twice or thrice in every here is an example classical cases 58 year old man joined this MRCP shows abrupt cut off of the dilated duct while actual ducts are dilated 3 minute delay phase shows that there is some tough of soft tissue enhancing at the level of cut off, axial post contract delayed images are useful showing that there is an eccentric soft tissue here nodule in the region of the structure quite well seen here so in this patient they have presence of two evidence to suggesting the presence of malignancy so you can comfortably call it colangiocarsinoma which is usually confirmed by MRCP so this was confirmed after we gave the diagnosis of colangiocarsinoma now we move on to the opposite category of the patient a 60 year old woman with recurrent biliary colic in this patient on MRCP you can see that the ducts are dilated there are pulse ducts then there is a stretcher post contract delayed images shows that there is a gradual tapering so the gradual narrowing that is not abrupt cut off on actual images there is no paeductal thickening what you are seeing here is calculus within the CBD there is no convincing paeductal thickening and there was no sufficient diffusion in this area so there is no evidence of malignancy probably benign but again radiologist should be careful calling a benign lesion a benign you never know cannot exclude because of colangiocarsinoma but you can give whatever you see you can describe and favour one diagnosis or other benign so in this case we call it probably benign but the patient underwent again this patient was stable for 4 years the MRCP was done and we concluded that there is nothing no malignancy in this patient so problem here the clinician asked whether the bioduct structure is benign or malignant so final diagnosis usually is with the ERCP we can suggest we can look for the evidence so the evidence for malignancy represents our paeductal thickening usually eccentric abrupt narrowing presence of restricted diffusion but the tumor tissue is so small it is very difficult to have a restricted diffusion in that area benign structure again it takes a lot of experience to call benign structure and it is better to leave the decision on the clinician you can just mention you report more evidence you are collecting towards either of the move on to the third type of colangiocarsinoma the intracutative colangiocarsinoma is usually present like a polyp as a papillary growth in the lumen of the bioduct and there is no parenchyma extension this one has the best prognosis because it does not invade the liver parenchyma in clinical practice you encounter them as a focal or diffuse ductal dilatation with or without papillary mass and sometimes as an intracutal cast like lesion with a mildly dilated duct they have the signature of colangiocarsinoma or that how it looks like so a classical example of ductal type on T2 health images there is a mass health mildly bright on T2 weighted images mildly bright on high B value diffuse animated images it was dark on ADC so there is restricted diffusion and classical signature enhancement of colangiocarsinoma progressive in the phases 3 minute delay phase shows that the mass is growing within the duct expanding the duct and there is upstream dilatation of the duct MRCP not the MRCP this is T2 probably his the mass is located in the duct so this is how the intracutal colangiocarsinoma looks like the MRCP was done in this patient and colangiocarsinoma was proven I couldn't follow this case because of the certain because the case notes were locked sometimes they can be seen on CT scan like in this case and in this case there is an enhancing mass in the CBT anti-anxious proven this has to be malignancy but in this case it came out as this plastic so there are few other pre-malignant lesion described in the literature very rare to pick up prospectively it's usually the benignity is the hindsight diagnosis for us radiologists clinical practice everything enhancing in the CBT is colangiocarsinoma and channel let's prove another voice I follow that rule coming to the conclusions we must be aware of the signature appearance of the colangiocarsinoma awareness about the differential diagnosis as I mentioned the mucinex metastasis from colorectocarsinoma we should always seek help from the clinical and lab data and the radiologists this is very important that you have high index of suspicion for colangiocarsinoma when you are assessing focal stretch intra-herpetic or extra-herpetic biliary structures don't leave the patient alone follow up with those cases if the clinician do VRCP brushing even if it's benign I will become an if you know the patient ask him to follow up maybe 6 months, 3 months and you may save some life Thank you sir for that wonderful session on imaging with MRI in cases of colangiocarsinoma few questions are coming in the chat box so we'll take the questions at the end of the second lecture and for the second talk we have with us Dr. Alok Jaju who is the program director of pediatric neuro radiology fellowship and also radiologist at Ann Robert at Chiluri Children's Hospital Chicago assistant professor at Northwestern University Feenberg School of Medicine and so we'll be taking us through various cases with interesting diagnosis and pediatric brain thank you sir and let's begin with the session my topic for today is case-based review of pediatric brain it's a very broad topic and it's difficult to do a comprehensive review of pediatric brain within 30 minutes so what I'm trying to do is show a couple cases from each of the major etiopathological groups these are less common diagnosis although these are not complete zebras these are conditions which you will encounter in your clinical practice and maybe on your exams and also all of these conditions have distinctive imaging features that can help you make a very confident diagnosis and does make a difference to the patient care so let's get started the first case is the eight-day old full-term neonate who presented the seizures so on the axial and coronal diffusion weighted images in the top row we see these multifocal areas of linear and ovoid diffusion restriction involving the deep and very ventricular white matter of both cerebral hemispheres there is involvement of the corpus callosum there may be mild hyperintensity within the deep nuclei including the globus validae and thalamus however otherwise there is no significant deep nuclei or brain stem involvement the T2 weighted images are essentially unremarkable partly because of the expected T2 hyperintensity in the white matter that this is related to incomplete myelination so what's the diagnosis here is it hypoxic ischemic injury is it involved error of metabolism is it related to some kind of infection or is it related to a thromboembolic phenomenon so this imaging appearance of these multifocal white matter involvement is characteristic of parico virus many go and supply it is hypoxic ischemic injury can have white matter involvement but the lesions are typically more confident in bone errors of metabolism have more specific patterns of involvement where they involve the deep nuclei and the brain stem more often and thromboembolism would be very unusual at this age and with this presentation so although this imaging shown here is fairly typical of human parico virus infection it's not entirely specific you could have the same pattern with otovirus and providers you can go to the another viral infection the important thing from our standpoint is to make a diagnosis of viral and supply it so that the appropriate treatment can be initiated this typically presents in neonates and infants with most of the cases diagnosed before the age of one month once the diagnosis is suspected confirmation is easy by a CSF PCR on imaging as we saw here diffusion weighted images are the most sensitive although these lesions can sometimes have associated pedicill hemorrhages of the gradient echo sequences an accurate diagnosis in this scenario can help avoid an extensive metabolic or vascular workup moving on to the next case it's a 15 month old child who presented with alderminal status a fever and a throat swab positive for better influenza virus on the axiom coronal T2 weighted MRI images we see these expansion areas of T2 hyper intensity involving bilateral thalamide and also there is involvement of some corona radiata and the white matter structures on the diffusion weighted images there is a restriction mainly along the periphery of the thalamic lesions with additional diffusion restriction in this plenium of corpus callosum in the periventricular white matter on the gradient echo images there is hemorrhage with the bilateral thalamide pre-contrast T1 weighted images demonstrating low signal within the thalamic lesions and the post-contrast T1 weighted images demonstrate this brim of peripheral enhancement amovilogram was performed which was deemed unremarkable so what's the diagnosis here is it related to straight sinus thrombosis is it a mitochondrial disorder like lila is it acute disseminated encephalomyelitis or ADEM or is it acute necrotizing encephalopathy so this imaging appearance is suggestive of acute necrotizing encephalopathy straight sinus thrombosis can have involvement of the thalamide but as we saw there amovilogram was negative mitochondrial disorders can have scattered in parts of the deep nuclear and the cortex ADEM can also have bilateral thalamic involvement but it does not have this degree of edema and necrosis and in this case we don't see any other white matter involvement any other significant white matter involvement acute necrotizing encephalopathy presents with these hemorrhage and peripherally deputant restricting and peripherally enhancing areas like we see in this case so this is a rare filament encephalopathy which has been described with different viral infections typically with influenza, para-influenza and pro viruses however more recently a similar imaging appearance was described with COVID-19 although this is more common in children cases can be seen in adults in fact the cases of COVID-19 have been described in adults there is a genetic predisposition children who have this RANBPG gene mutation tend to have a predisposition for developing this condition in response to viral infection on imaging as we saw this is characterized by necrotic hemorrhagic lesions of bilateral thalamide and involve the putamen cerebral and cerebellar white matter as well as the brainstem next case is prenatal imaging with abnormal fetal ultrasound and MRI at 22 weeks of gestation so we have sagittal axial and coronal T2HIS images from a fetal MRI which shows this avoid relatively well defined mass-like lesion in the posterior aspect of the head mostly iso intense in T2 signal along the periphery but the central portion has this low T2 signal and corresponding high T1 signal which may suggest either blood products or calcifications so what's the diagnosis here if you're thinking in terms of a neoplasm pterotoma would be most likely in this age group if you're thinking in terms of vascular malformations venocalin malformation would be common at this age group if there's some kind of a dural sinus malformation or is it hemorrhage with an extra axial mass like in an x-ray let's look at some postnatal imaging before we come to the diagnosis so on the postnatal MRI we have this pre-contrast T1 weighted image which shows this heterogeneosity T1 hyper intense lesion in the posterior aspect of the of the cranium centered in the region of the torcular on the post-contrast T1 weighted images there is enhancement of the dural sinus around this heterogeneous lesion which is suggestive of large blood clot within the dilated torcular we also see gradient susceptibility and diffusion hyper intensity within the lesion like related to blood products here are some sine images which show that there is dilatation of the dural sinus with this large heterogeneous lesion presumably a blood clot which is centered in the region of torcular as we can see on this post-contrast images there is enhancement of the dural sinus around this partially filling blood clot in the region of the torcular so the diagnosis here is dural sinus malformation it's a rare kind of vascular malformation and which is different from the more common venochialin malformation so this is characterized by massive dilatation of the dural sinus typically the torcular although it can involve the sigmoid sinus or the or the jucular bulb dilated with neural AV shunting the AV shunting can be difficult to demonstrate on conventional MRI or MRA and often requires a catheter angiogram this condition is typically diagnosed in the prenatal or the early postnatal period the massively enlarged torcular is typically partially thrombosed the dp structures are normal which would distinguish it from the more common venochialin malformation the prognosis of the condition depends on the presence and degree of dural AV shunting the higher the degree of AV shunting the worse is the prognosis and worse is the degree of parenchyma changes and hydrocephal associated with this condition again these depending on the degree of AV shunting these lesions can spontaneously regress but more often they require embolization next case, case number 4 is a 7 day old female who presented with lethargy and poor feeding on the axial diffusion weighted images in the top row the metric areas of diffusion restriction in bilateral deep cerebellar white matter this would be the cerebellar peduncle the dorsal aspect of the brain stem extending into the thalamus, cocellums of the internal capsules, corona radii and the periorolandic white matter on the ADC map we see this correspondingly markedly low signal in these areas of the deep cerebellar white matter and the brain stem on the T2 weighted images there is mild hyper intensity and maybe intervention involving the dorsal brain stem and the thalamus so what's the diagnosis here in the 7 day old child is it an inborn error of metabolism is it related to basilar artery thrombosis is it an encephalitis or is it related to hypoglycemia so this pattern of involvement of the cerebellum brain stem and the corticospinal tract is very characteristic of maple syrupy ring disease so maple syrupy ring disease is an inborn error of branch amino acid metabolism it's typically diagnosed with newborn screen however if the diagnosis is not made in the time or if it's not intervened upon symptoms developed by the end of first week like we see in this case this characteristic pattern of edema involves the myelinated structures and it's because of the intramylin we call the myelin splitting edema these patients can also have a component of basogenic edema due to blood brain barrier breakdown but the more characteristic image in appearance is attributed to the intramylin edema and as we saw in this case we see marked deficient restriction oftentimes the ADC values are greater than 50% lower than the normal brain and it involves the myelinated parenchyma including the cerebellum white matter brain stem and the corticospinal tract the next case case number five is the 18 month old child who had a history of infantile spasms or vest syndrome who presented for an outpatient MRI with about 10 days of hyperkinetic movement so on the deficient weighted images we see these bilateral areas of deficient restriction within the thalamide also with some involvement of the midbrain that is involvement of the central tegment and tracts of the font and also the cerebellum white matter you can see the pattern of emollent of the deep nuclear and the brain stem on this coronal DWI image on the ADC map we see the corresponding low signal in bilateral thalamide and there is a mildly expansility to hyper intensity on the post contrast images there is more associated enhancement between these areas so what's the diagnosis here is it ADEM, is it some kind of a metabolic disease, is it related to a drug toxicity or is it related to osmotic demyelination so diagnosis in this case is vagabatrin associated reversible MRI changes so this child has history of infantile spasms and was being treated with vagabatrin ADEM can again have thalamic involvement but also there would be a history of viral predrome, prodrome and the child would be more symptomatic, metabolic disorders can have a similar pattern but again the child would be more symptomatic osmotic demyelination would present acutely with the history of electrolyte imbalances or some underlying conditions vagabatrin is a common drug which is used for treatment of features particularly infantile spasms and it can also be used for patients with tuberculosis with agabatransaminase inhibitors MRI changes are very common with treatment and seen in up to 22 to 32% of the patient and often with relatively mild or no clinical symptoms as we saw in this case this was outpatient MRI for relatively mild clinical symptoms this appearance is more common in children under 2 years of of age and the MRI findings the incidence of MRI findings is don't dependant. On MRI as we saw in this case there is symmetric diffusion restrictions between the deep nuclei, brain stream and the dentate nuclei and the findings are typically reversible over a few months and sometimes even with continued treatment. So the important point to note here is these characteristic MRI findings in a relatively asymptomatic infant with seizures should be considered as a drug history. Case number 6 is a 2 month old child who presented with a scalp lump in the midline parietal region. Initial ultrasound showed a hypoechoic lesion in the scalp with surrounding subcutaneous of tissue thickening. There was this hypoechoic crack which appears to extend intracranially and this is the color Doppler flow within the duval venous sinuses which appear patent. On the subsequent MRI imaging we see this elongated crack extending from the pineal system all the way up to this bone defect in the parietal bone and in the subcutaneous tissue there is this heterogeneous heterogeneous digital signal with some fluid signal proliferation of fat and some heterogeneous fibrotic change. On the post contrast images again we see this fluid field crack extending all the way up to the parietal bone defect and extracranially there is also this abnormality of the duval sinuses with this vertically oriented sinus which extends along the anterior aspect of that crack. On the m-orvenogram images we see this abnormally vertically oriented sinus which is related to abnormal orientation of the straight sinus and the persistent phylocein sinus and on this coronal projection we see this this kind of a filling defect in the in the supidus agital sinus which is related to focal fenestration of the supidus agital sinus from this fluid field crack by selecting it to extend to the parietal bone. So what's the diagnosis here? Is it an atrodic cephalosil? Is it a dermoid with intracranial crack? Is it a lymphatic malformation with intracranial extension? Or is it sinus pedocrinus? So this is the case of atrodic cephalosil. Dermoid can also have a subcutaneous mass with intracranial extension although they are they are more common in the occipital lobe and also they won't have these associated parenchyma changes. Lymphatic malformation can have underlying bone involvement but it's unusual to have an appearance like this. Sinus pedocrinus is dilated veins with intra and extrachranial communication and typically it would occur in this parietal location however they won't have the parenchyma changes as we see in this case. So atrodic parietal cephalosil is a rare kind of neural tube defect although it accounts for about 38-50% of all cephalosil. The subcutaneous lesion or the subcutaneous mass contains meninges and vestigial tissues sometimes neural and glial tissues but there is no prank animation of parenchyma. The characteristic imaging findings are this cigar shaped CSF cleft which extends from the midline in the pineal or the supracerebellum system up to the extrachranial lesion and also there is elevation or the spinning top appearance of the tentorium with an enlarged supracerebellum system. Also there is abnormalities of the dural venous sinuses with a vertically oriented sinus which can be related to the straight sinus or the persistent palcine sinus. This condition can also be associated with other intracranial abnormalities so be on the lookout for that like corpus callosum abnormalities, cortical malformations and ventriculum medley. Next case, case number 7 is a 4 day old child who presented with a prenatal diagnosis of severe hydrocephalus. So we have T1 and T2 weighted MR imaging which shows this severe ventriculum medley and also when you look at the brainstem there is hyperplasia of the brainstem particularly the form with this abnormal z-shaped or kinked appearance of the brainstem. The tectom is somewhat prominent but also the hyperplasia of the cerebellum will partially clue its procedure. On the axial images the cerebellum appears malformed with this lobular contours. The supratentorial brain parent can also appear abnormal with lack of sulcation giving the reason septic appearance and also when you look at the cortex it has this lobular lumpy bumpy appearance bilaterally. Again same findings on the coronal T2 weighted MR chain. Images through the orbits show these linear T2 hypointen cracks which extend from the posterior aspect of the lens all the way up to the fundus which is the residue of a phpv or a persistent hyperplastic primary vitreous. So what's the diagnosis here? Is it a congenital muscular dystrophy? Is it quarantine tegmental cap dysplasia? Is it congenital congenital or is it all sequelae to congenital CMB infection? This constellation of imaging findings is very characteristic of congenital muscular dystrophy spectrum. The prototype of which is the Walker Warburg syndrome which this patient had. So what is congenital muscular dystrophy syndrome? This is the spectrum of autosomal recessive muscular dystrophy syndromes some of them have names like pokoyama, muscle-like brain disease or Walker Warburg syndrome. The Walker Warburg tends to be the most severe of the muscular dystrophy spectrum. These are also called as alpha dystroglyconopathies because of the metabolic defect affecting the dystroglycan molecules which is found in multiple tissues including the muscle CNS and the ocular tissues. On imaging you may not be able to make the diagnosis of a specific subtype and you can call this a Walker Warburg phenotype or you can call it alpha dystroglyconopathy. The characteristic imaging features as we saw in this case include the king tenor hyperplastic brain stem, hyperplastic cerebellum with this plastic cerebellum perenchyma often with microsys. There are typically myelination defects. The subcutin-todial brain perenchyma demonstrates cobblestone lesion cephaly that is associated with choclorometallin. There can be corpus callus and dysgenesis and there are ocular anomalies like in our case we saw BHPV but it could also be associated with morninglorid disc anomaly. Next case, case number 8 is a 2-year-old child who presented with nuances seizure and a frontal lobe mass on outside hospital CT imaging. On this initial non-contrast head CT we see this hyperdense mass in the anterior and mid-lines strangling the calf cerebrae and involving lateral medial frontal lobes. On the subsequent MRI we see corresponding gradients of susceptibility in this region on the flare images there is subtle hyper intensity and expansion of the medial frontal cortex on both side of the calf. The diffusion weighted images are essentially normal. There may be some cortical technique but no diffusion restriction and this is post-contrast flare imaging and you can compare it to the pre-contrast flare imaging. There is some enhancement of the cortex and bilateral medial frontal lobes although most strikingly there is enhancement of the electromagnetic structures in the involved areas. And post-contrast flare imaging is a very useful technique especially for brain tumors and we have this whenever we give contrasts within the flare sequence post-contrast and I would strongly recommend you do that at least for the brain tumor patient. This is the post-contrast weighted imaging which again shows this ill-defined enhancement between the cortex and the leptomeningel. So what's the diagnosis here? Is it a meningioma? Is it meningio-angiomatosis? Is it an angiopericytoma? Or is it cavernoma? So this imaging appearance is suggestive of meningio-angiomatosis. Meningiomas are also extra-axial lesions but typically they don't have an infiltrative cortical component and the imangiopericytomas also tend to be more extra-axial. Cavernomas can have the hyperdensity like we saw on the CT here but they would typically have the popcorn appearance with more heterogeneous internal signal on deteriorated images. So what is meningio-angiomatosis? It's a rare benign lesion which is centered in the cortex is probably a hematomatosis lesion. This is common in frontal and temporal lobes and often presence with headache and seizures. 25% of these cases are associated with NF2 and the patients who have associated NF2 present early and can have multiple lesions. So although the mean age for diagnosis for meningio-angiomatosis is in early adulthood, the pediatric cases which you see are most commonly associated with NF2. It's a cortically-based, calcified lesion and enhancement is very common. On histopathological exam there is cortical infiltration with very vascular meningocinal proliferation and a lot of somomomobodies and these features can help distinguish it from other conditions like vascular malformation and meningio-angiomatosis may be suspected based on imaging. Next case and I think it's my last case is a 4-year-old child who presented this papillodema on the initial MR imaging on the axial and coronal T2 weighted images, we see this multi-pocal areas of rounded T2 hyper-intensity and it is almost just like changes throughout the cerebellar hemispheres as you can see here on the coronal images as well on the post-contrast imaging there is some leptomine engine enhancement corresponding to these areas but it's no prominently seen on the surface of the brain stem and extending all the way over the surface of this cervical spinal cord. We also did the spine imaging at the same time and the spinal cord again on the T2 weighted images shows these multiple areas of rounded T2 hyper-intensity and caustic lesion throughout this spinal cord and on the post-contrast imaging there is thick nodular leptomine engine enhancement throughout this spinal cord extending all the way to the conus medillaries and also along the cord like my9 and the tachyclasecterones. So what's the diagnosis here? Is it Cryptococcal meningitis? Is it Neurocystisocosis? Is it some kind of a disseminated tumor? Or is it related to neurocutaneous melanosis? So this is an example of a diffuse leptomeningial glionuronal tumor. Oftentimes at the initial presentation it can be confused with atypical infections like Neurocystisocosis or tuberculosis but the patient had no clinical findings of infection, no prior history and the CSF was negative for infections too. Neurocutaneous melanosis can also present with diffuse leptomeningial involvement of the brain and spine. However it typically does not have the T2 hyperintensive changes as we see here and also neurocutaneous melanosis has intrinsic T1 hyperintensive typically in the cerebellum and needle temporal lobes because of the melanin deposition. So what's diffuse leptomeningial glionuronal tumor? It's a newly defined tumor entity. It's a mixed neuronal clear tumor which was described by WHO in 2016. It's characterized by this diffuse leptomeningial enhancement with multifocal small cystic appearing lesions throughout the brain and spinal cord. So imaging appearance which we are seeing here is pretty characteristic of this diffuse leptomeningial glionuronal tumor although sometimes it can also present with focal masses particularly in the spinal cord. Like I said it can be confused with atypical infections so awareness of this disease entity can help you make a more accurate diagnosis and direct clinicians in the appropriate direction. So to summarize we saw a couple of examples of each of the different etiopathological groups in the infectious and telemetry category. We saw a parico virus meningo and cephalitis which presents with these characteristics linear and avoid diffusion restriction within the white matter. We saw acute necrotizing and cephalopathy which is a complication of viral infections and presents with very fulminan necrotic lesions in the thalamide. In the vascular category we saw neural sinus malformation which is an uncommon which is an uncommon kind of vascular malformation which is characterized by this massive aneurysmal dilatation of the tar filler with associated neural AV shunting. In the toxic metabolic category we saw maple therapeutic disease which has this characteristic pattern of involvement of the myelinated white matter demonstrating diffusion restriction and with presence early on in life. Then we saw vicar-battern associated changes. This is something which is fairly common in kids who are being treated with vicar-battern for seizures and this is typically not, these kids are typically not very symptomatic and the condition is reversible sometimes even the continuation of vicar-battern. In the congenital category we saw the parietal electrotic cephalosine where we have the CSFL tract which communicates with this small extra cranial soft tissue abnormality and can be associated with this abnormally oriented vertical neural venous sinus which all the congenital muscular dystrophy spectrum which is characterized by brainstem hypoplasia and this intracranial and ocular abnormalities. Lastly in the tumor category we saw meningio-angiomatosis which is this cortically based infiltrative mass with associated leptomeningial involvement and this also saw diffuse leptomeningial glural neuronal tumor which is newly described tumor entity which is characterized by disseminated disease in the brain and spine. So with that I thank you for your attention. If you have any questions please feel free to email me. So with this talk on pediatric cases and interesting diagnosis we come to an end of today's Prelude and this I request you once again to register for the upcoming MRI teaching course and I already mentioned it's a comprehensive 5 day course which we are going to be covering all the basics to advance topics related to MRI including physics including anatomy which will be on 7th and 8th of August. Registration links are shared in the chat box so you can take from there even on social media platforms we have shared the links one day we will have complete session on Neuro topics, second day will be complete MSK coverage and third day will be on body imaging topic. These lectures plus added Prelude sessions will be there so almost will be taking during these 4-5 days around 80 plus lecture topics we invite you to please submit your papers and post a presentation and be a part of the event. We are thankful to our educational partners Sanrat, Bayer's, Fugifilm and CareStream for their constant support. We are thankful to Viveer Imaging this is the entire organizing committee we are here to guide you through the registration process if you have any doubts or facing any issues during the same and there are many more conferences in line from Indian radiologist and we have options of wonderful discounts when you register for these in totality so please do visit our website to get the details we will have a Prelude session today evening again 7pm so if you wish to attend these topics you can rejoin today evening as well and there is a question in the chat box about the timing of injection during triple phase examination so we have received the answers from the expert that the best way is to go through bolus tracking approach only as we do in CD scan similarly we have bolus tracking softwares and sequences in MR and if possible with pressure injector otherwise most of the places we don't have pressure injectors for MR imaging so by bolus tracking we have to take acquire multi-phasic images where we should not miss the early arterial and late arterial phase and then aim to acquire the venous phase in both portal venous and delayed in cases of lesions like cholangio even the 10 minutes and delayed phases like 40 minutes delayed may be important so based upon the situation you can plan your MR phases and later on also take additional delays in two planes so with this we come to an end of this prelude and hope to see you all soon stay tuned next Sunday also we will have fresh prelude with two more topics of interest and let's meet for the main conference on 7th of August thank you all