 All right, it's just now about 12 o'clock. I see the numbers still rising, so we wanna give everyone a second to kind of keep joining. Just wanted to start off with a hello and welcome to the fourth of many live-streamed noon conferences hosted by MRI online. In our response to the changes happening around the world right now with the shutting down of all in-person events, we've decided to provide free noon lectures to all radiologists worldwide. Today, we are joined by Dr. David Usum. He is a professor of radiology, vice chairman and associate dean at Johns Hopkins. He has published over 300 scientific papers, author of Neuro Radiology, The Requisite, the Case Review Series in Radiology Business Practice, How to Succeed. He is the former president of the ASNR, and I just wanted to welcome him. I also wanna give a little heads up that we will be using the polling feature during this noon conference. So be aware that those are gonna be popping up. Also, I wanted to direct to your Q&A to the section in Zoom. We will have some time at the end of this hour to answer as many as we can. That being said, thanks so much for joining us, Dr. Usum. I'll let you take it from here. Thank you very much. It's a pleasure to be here and I wanna thank the MRI online team for inviting me. Everyone out there, please be safe. Follow your public health guidelines. But in the meantime, let's get going. So some of you may not realize that I've moved to Colorado. I'm still working for Johns Hopkins, but I'm out here in a beautiful evergreen Colorado and I'm gonna allow you to see the view that I have each morning of the great Rocky Mountains. And unfortunately, I'm gonna be silhouetted out here. But I thought that you could see the view that I have each day from my bedroom and to show you that I really made the switch. There you go. How about that? A little kerchief. And now I'm really a true Colorado. So let's get going with the seminar. I'll just turn on the lights so you can, every once in a while, you'll be able to see my face. Okay. So today we're gonna be talking about imaging of the temporal lobe and temporal lobe lesions. And the vast majority of patients with temporal lobe abnormalities will present with epilepsy. Now we were gonna be talking about temporal lobe epilepsy which occurs in 1% of the world's population. About 20 to 40% of them are refractory to medical management and therefore are considered for surgical treatment. So focal onset of seizures will occur in about 60% of these patients. So we're gonna be talking about evaluation of temporal lobe epilepsy. Most of you know I use an amonic to keep my mind open to different possibilities in a differential diagnosis. That mnemonic is vitamin C and D and we will be dealing with vascular infectious, I won't talk a little bit about, I won't talk very much about trauma but clearly the temporal lobes are susceptible to trauma. Metabolic acquired, metabolic, idiopathic, neoplastic congenital and drugs. And so these are going to be some of the categories of lesions that we will be describing as part of this seminar. Let's start off and see how we do with doing polling on our Zoom session. So you do have that polling function. And I'll ask the first question. For the evaluation of patients with temporal lobe epilepsy, what is the most useful poll sequence? Is it number one, axial flare imaging? Number two, coronal T2 weighted scans? Number three, coronal flare imaging? Number four, coronal T1 weighted scans? Or number five, post-gadolinium axial scans? So go ahead and select and answer and then hit the submit button. And we will collate the answers from the approximately 600 people that are currently registered for the course. So after a little bit of a pause to allow you to think about that, we'll now look at the results of that polling. So the highest group is number three for coronal flare imaging. And that is a very important post sequence. However, I'm going to talk to you about the correct answer, which for mesiotemporal sclerosis is going to be coronal T1 weighted scans. So we'll move to the next slide. Thank you, Paul. So what poll sequences do we use for the evaluation of patients with temporal lobe epilepsy? There are specific sequences that are recommended for that and that includes thin section coronal T2 weighted scans, volumetric MP rage T1 weighted scans. Most people do something along the lines of phase sensitive inversion recovery in order to maximize the gray-white differentiation, although as you can see with the MP rage, we're doing pretty well with that. And then as many of you answered the question, coronal flare imaging also is important for looking at the signaling tendency of the hippocampus. If we're looking at other ideologies for temporal lobe regions in a patient who may be an adult or for other aspects, we will be doing diffusion weighted imaging, susceptibility weighted imaging, look for blood products, particularly post trauma, as well as post-gadolinium scans to supplement the T1 weighted scans. And those may be in any plane, usually using a three-dimensional MP rage or volumetric T1 weighted sequence. Okay, so next question is the most common cause of temporal lobe epilepsy is what? Is it number one, mesiotemporal sclerosis? Number two, tumors. Number three, cavernomas. Number four, strokes. Or number five, cortical dysplasia. So once again, we'd like you to answer the poll, submit your answer, and then we will present the group answers in just a moment. So the options are mesiotemporal sclerosis, tumor, cavernomas, strokes, or cortical dysplasia for the most common cause of temporal lobe epilepsy. So let's see the results. Okay, so 59% of people put in mesiotemporal sclerosis and in fact that is the correct answer. And that can be defined in pathology or surgical specimens as well as clinically. So once again, when we think about mesiotemporal sclerosis, one of the few cases where the eye of idiopathic is the most common diagnosis. So we have the mnemonic of vitamin C and D with vascular infectious traumatic acquired metabolic idiopathic neoplasic and general and drugs. And of these, we usually put mesiotemporal sclerosis in the idiopathic group. That said, most people with mesiotemporal sclerosis have a prior history of febrile seizures as an infant. And so it's a little bit of a curiosity why the insult which occurs in infancy doesn't present until young adulthood with the temporal lobe seizure disorder. It has something to do with scarring and the susceptibility to seizures. So at neuropathology, when the surgeons take out the temporal lobe for evaluation after doing their either deep brain electrode to identify the focus of the seizure disorder and they do the temporal lobeectomy. We find mesiotemporal sclerosis in, as you can see, 35 to 49% neoplasms less likely. And unfortunately, as you see down below, a normal path is not unusual in patients who have had a temporal lobectomy even with the normal neuropathology however, 80% of the patients still get relief of their seizures. So it may be that such a small focus that's missed might be a sampling error in neuropathology. I like to show this video for you and it's important that you try to be, look as carefully as possible at the video and tell me afterwards what you see and what abnormalities you know. So here we go with the video. I hope the sound is good enough. Precisely 3.34 this afternoon was brutally blood-slicely at a time that this dastardly deed took the master bedroom by petunias in the bathroom. Well, the fascinating thing about this video is it's about power of observation but I think this is the funny part about this video was made by the mayor of London for a transport to inform motorists to look out for cyclists. That was a wonderful video and unfortunately for mesiotemporal sclerosis the findings are relatively subtle. I don't know whether any of you picked up that I changed my hat. So there we go. And we're looking at the hippocampal structures including the dentate nucleus, the corneum amunus which is thought to be one of the more susceptible areas of for seizure disorder and mesiotemporal sclerosis and portions of the sebiculum and the parahippocampal gyrus. These cells within the hippocampus are very sensitive to hypoxia and again it's thought that potentially at the time of a febrile seizure by an infant there could be damage to the CA2 region which leads to scarring which leads to in young adulthood the seizure disorder. Now this may be manifested in different ways. You can see high signal intensity as some people suggested in the hippocampus on the flare scans as one of the manifestations. However, this is actually not such a reliable finding. The reason why we use the phase sensitive inversion recovery sequence is because it is very nice in demonstrating the gray matter of the hippocampus outlined by the white matter around it and by the temporal horn of the lateral ventricle. So here again we see the difference in the volume of the hippocampus on the left side compared with the right side and the decreased volume is what we see in patients who have mesotemporal sclerosis effectively it's scarred down. So of the findings in temporal lobe epilepsy which is most valuable? Is it the signal intensity of the hippocampus? Is it the size of the hippocampus? Is it the loss of the normal internal architecture of the gray and white matter? Is it the size of the mammary body or the fornix? Or would it be none of the above? Which is the most valuable finding on MRI for patients who have mesotemporal sclerosis? Is it the signal intensity of the hippocampus, the size of the hippocampus, the loss of internal architecture, the mammary body or fornoceal size or none of the above? So go ahead and submit your answers and we'll see what people are saying. I'll give you a quick shot, smile. So Paul, can we see the results of the polling? Well, the correct answer is the size of the hippocampus. So hippocampal volume size can be assessed on T2 weighted scans or on your MP rage or whatever 3D volumetric sequence you use. And as you can see here, the left hippocampus is smaller than the right hippocampus. I just wanna reflect back on a trip I took to Hessefe, Brazil. So, obrigado to all my friends who are there from Brazil. And I was taken from at Hessefe by Fatima Argo and she took me to Porto de Garinas to the hippocampal or the seahorse colony in Porto de Garinas. And obviously the hippocampus refers to the seahorse tail with regard to that curving nature of the hippocampus. And here I got the temporary tattoo, I must admit. And after a while it did atrophy so mesiotemporal sclerosis hippocampal volume loss. Thank you Fatima. So mesotemporal sclerosis, if you look at the imaging findings, the size of the hippocampus is the imaging finding that is most accurate at 80 to 90% signal intensity, which obviously we see on the coronal flare scan is valuable but it's not as valuable as doing volumetric analysis of the hippocampal size. Loss of internal architecture, when it's present, it's very specific but not too accurate as well. Mammillary body, I have an extra M on the mammillary body, foreign seal side, et cetera. The only issue is that in about 10 to 15% of patients you will see bilateral mesiotemporal sclerosis in which case the size of the hippocampus comparing right to left may not be as reliable. So here again, another patient looking at the left or right size, in this case on serial T2-wayed scans we see the very high signal intensity in the right hippocampus indicative of the signal intensity changes that may be evident either on T2-wayed scan or on the flare scan, but usually not seen on your T1-wayed scan. If you do MR spectroscopy, you may see some diminution in the NAA peak associated with the side of the mesiotemporal sclerosis thought to be due to neuronal loss. Let's talk about advanced imaging techniques. So we have our standard pulse sequences that we use. What about post-processing? What is the most valuable advanced imaging technique for temporal lobe apilepizies, specifically for mesotemporal sclerosis? Would that be MR spectroscopy, diffusion tensor imaging, volumetry, functional MRI, or perfusion-wayed imaging? So if we are going to do some post-processing evaluation, which is most valuable? Would it be MR spectroscopy, diffusion tensor imaging, volumetry, functional MRI, or perfusion-wayed imaging? Good, so volumetry is the correct answer and that's why the MP rage sequence of 3D T1-wayed scan is the most valuable because looking at the volume of the temporal lobes is very useful. And I am not here to recommend any particular biometric analysis tool that you use. It happens that at Hopkins, we use NeuroQuant and it has a very nice and slick interface. It shows you the percentile of the left and right hippocampus individually to determine whether or not there's been volume loss as well as an asymmetry index between the two. Now here's an interesting feature, which I was unaware of until I learned about NeuroQuant and that is that you might think that the left hippocampus and left temporal lobe because of the dominance in language, et cetera, would be the larger of the two hippocampi. But in point of fact, the right is the one that has about three to 8% larger volume in most humans even if they're right handed. But anyway, what you're seeing on this analysis is that this patient's hippocampal volume is below the fifth percentile and therefore abnormal. The right hippocampal is right on the 50th percentile and this is very nice and slick software. If you have bilateral mesiotemporal sclerosis, you would find that the volumes would be decreased on both sides. So even though you might look side to side and say, oh, they look like they're pretty symmetrical, it will show you the overall percentile compared to normal controls. And you can see how well they do with regard to the segmentation. It's a program that can segment out gray matter and white matter as well as the ventricles. But as you see in the yellow, yellowish green color, that's doing a very good job on the hippocampal segmentation. And it can show you the analysis of the other structures of the brain. And we also use this in some patients where we have being evaluated for mild cognitive impairment for the issue about whether or not they have Alzheimer's disease. So here you can see the overall left hippocampal volume 2.76, the right hippocampal volume 3.08. And it gives you the asymmetry index. So when volumetry is compared with visual analysis, we find that volumetry is more accurate in most cases than the radiologists, the neuro radiologists doing visual analysis. Now the radiologist is going to be looking at signal intensity changes, maybe mammillary body size and loss of creation and loss of normal architecture. All the volumetry program does is measure the volume. And nonetheless, the automatic volumetry can detect atrophy at a very high rate, 95%. If you add in T2 relaxometry, you get increased accuracy even more. We did a study at Hopkins where we looked at our patients who had mesiotemporal sclerosis proven pathologically. And we compared pure neural quant comparing one side to the next versus all of the tools that the neuro radiologists had. And as you can see, neuroquant was more accurate at 79.4% than the neuro radiologists who was, which were a group of us accurate at around 75%. So even when you have patients to have a discrepancy between the neuro radiologists and neuroquant, in other words, the neuro radiologists says it's the left side, neuroquant says it's the right side that has mesiotemporal sclerosis. Out of that, neuroquant was again more accurate than the neuro radiologists at Johns Hopkins. So either send it to neuroquant or send your studies to a radiologist besides those at Johns Hopkins. Deezing. Okay, so what are the other findings? So one of the other findings that we look for is the cremated margin of the hippocampus. And as you can see on the normal side, on the left image, you have this kind of Ripley effect of the superior surface of the hippocampus. And when it gets smoothed out in this abnormal side, that's one of the subtle imaging findings that a neuro radiologist would pick up that obviously something like neuroquant would not. So we've talked a lot about the hippocampus and mesiotemporal sclerosis because that is the most common temporal epilepsy etiology, it's idiopathic. Let's move from the hippocampus and just look at some of the ancillary findings of mesiotemporal sclerosis, which I mentioned previously. They include loss of volume in the ipsilateral fornix and loss of volume in the ipsilateral mammary body. Those are secondary findings, usually when you have a pretty gross case of mesiotemporal sclerosis, but if you're wavering one side versus the other or you're not sure whether it's significant or not and you don't have a volumetric analysis program, that's, you can use the fornix or the mammary body. And here's just another example. In the coronal plane, since we're mostly looking in the coronal plane for mesiotemporal sclerosis, we see the reduction in the size of the left mammary body, the left fornix co-column. And you can see here that the volume of the gray matter of the hippocampus on the left side is reduced compared to the right side. Okay, let's move on from mesiotemporal sclerosis to other ideologies. What is the most sensitive part of the brain to ischemia? So we have a patient who may undergo anoxic ischemic injury. Which part of the brain is most sensitive? Is that the thalamus? Is it the periorolandic region? Is it the dentate nucleus? Is it the globus pallidus? Or is it the amens horn of the hippocampus? So were we to experience an anoxic ischemic injury? Where would the most likely area of abnormality be located? The thalamus, the periorolandic region, the dentate nucleus, globus pallidus, or amens horn? So let's see what the audience thought about that. So the correct answer is amens horn, although globus pallidus is probably the next most sensitive. In certain neonatal groups, you may see periorolandic areas of ischemic injury as well, but most people would say amens horn of the hippocampus, which is again that portion here in the superior surface of the hippocampus. So here unfortunately as a patient, thank yous. So people, I guess they went with number four, which was amens horn. So here we have a patient who attempted suicide by locking themselves in the garage, turning their car on. As you can see in these coronal images, there is abnormal signal intensity bilaterally in the hippocampal amens horn region. The globus pallidus is spared. However, when we look on the diffusion weighted scan, you again see hippocampal abnormality on the DWI corresponding to reduced ADC, and nothing that's evident in the globus pallidus. So some patients with carbon monoxide poisoning will show predominantly globus pallidus abnormality. Some will show hippocampal abnormality, and some also will show even occipital lobe abnormalities. But hippocampus is one of the areas for anoxic ischemic injury. So let's go on to a different case. So this is an unknown case, where we'll be pulling the audience. Here's the T1 weighted scan on your left, saddle T1 weighted scan, and the axial T2 weighted scan on the right. And obviously the abnormalities in the right temporal lobe. DWI and post-gadwin even hand scan. Give you a moment to look at that, and let's see how you did. What do you think the best diagnosis is? Is this a hemorrhagic neoplasm? Is it a hemorrhagic stroke? Is it an arterial venous malformation in that bled? Is it a cavernoma in that bled, or none of the above? So looking at DWI, the T2, the saddle T1, and the post-gad T1, which is the best diagnosis? Is this a hemorrhagic neoplasm, a hemorrhagic stroke, an AVM bleed, or a cavernoma that has bled? So go ahead and vote and submit your answers. And I'll give you a little shot of the entire background there, and very nice hills of Evergreen, Colorado. Okay, so 42% said hemorrhagic neoplasm, 22% said hemorrhagic stroke, 3% AVM, 15% cavernoma, and none of the above. So I'm just gonna go back here, I think I'm gonna go backwards, and point out one finding that some of you may not have picked up, and that was the absence of enhancement in the transverse sinus. So this is indeed a venous infarct. So venous infarcts have a high rate of being hemorrhagic. They will show edema and their curiosity, because sometimes they do show nice restricted diffusion. In this particular case, the DWI wasn't all that useful because there was so much hemorrhage associated with the lesion if we had done an SWI that you would have seen that blooming in effect. But clearly on the MRV, we've lost that transverse sigmoin and jugular vein on the right side. And this was a hemorrhagic stroke from sinus thrombosis. So venous infarctions, variable DWI findings, sometimes positive, sometimes not, oftentimes hemorrhagic, we usually say 75% hemorrhagic, maybe due to the cerebral veins or to the transverse sinus and the temporal lobe for temporal lobe abnormalities and lesions. So as I said, venous infarctions usually have some element of hemorrhage about 73%. It's usually associated with sinus thrombosis, although you can't have cortical vein thrombosis. And as I stated previously, the vein of labé would be what we would be worried about or deep middle cerebral vein for temporal lobe abnormalities. And most of the time, you will see this on non-contrast CT as a hemorrhagic infarction. Okay, with regard to sinus thrombosis, here's a question. Which of these findings will be unusual in patients who have sinus thrombosis? Is it number one, papillodema, number two, hydrocephalus, number three, increased intracranial pressure, number four, headaches, or number five, tautomyoclonus. So Paul, if we can pull the audience, the choices are number one, papillodema, number two, hydrocephalus, number three, increased intracranial pressure, number four, headaches, or five, tautomyoclonus. Which one of these is unusual with sinus thrombosis? So let's see what the audience said. The correct answer is pautomyoclonus. That's something that we see with hypertrophic olivary degeneration, not with sinus thrombosis. So the correct answer was pautomyoclonus. Papillodema, hydrocephalus, increased intracranial pressure, headaches, et cetera. Those are all part of the clinical spectrum of sinus thrombosis. Okay, just a quick check and make sure that everyone's paying attention. Where is Waldo? Paul, if we can remove the polling results. Where is Waldo in this picture? So I'm gonna give you a 10 seconds to find Waldo. Again, trying to increase your perceptual skills. One, two, three, four, five, six, seven, eight, nine, 10. If you found Waldo, congratulations. Where is Waldo? Oh, right down there in the corner. There's your mesiotemporal sclerosis binding Waldo. Thank you. Okay, next case. These are two separate cases. This is the coronal T2 weighted scan and this is the gradient echo scan and post-gad scan. Two different cases, both cases having temporal lobe abnormality. So consider that and let's go on. We're in the, so which diagnosis for the right temporal lobe and which for the left temporal lobe? So your choices are, I think I might have changed this, but the choices are left cavernoma, right cavernoma, left cavernoma, right developmental venous anomaly, left cavernoma, right cavernoma and right DVA. Number four, left DVA, left cavernoma and right DVA and number five, left DVA, right cavernoma. So which of these is the correct answer? So obviously we're in the vascular category here when we're talking about our vitamin C and D mnemonic. We have vascular infectious traumatic acquired metabolic neuropathic neoplastic congenital and drugs. And so the audience, the most common answer is left cavernoma, right cavernoma and DVA. And that's correct. So here is the left cavernoma surrounded by hemocidrin. On the right temporal lobe, you see both that sort of spray medusa look of a developmental venous anomaly, also known as venous angioma for some people. And you also are seeing these two darker areas. Now they could be unusual bleeds in a developmental venous anomaly. That's really rare, but more likely those represent cavernomas that may be associated with DVA and Bill Dillon has done the most work in evaluating patients with DVAs and says that around 15 to 20% of cavernomas have associated developmental venous anomalies or venous angiomas. So nicely done. This was an interesting case. Again, we're in the vascular category. This was an interesting case in which the resident who read it talked about the presence of an aneurysm or pseudo-aneurysm on the MRA. And what one is seeing on this MRA is what's called T1 shine through. You know about T2 shine through with diffusion weighted scans. In this case, it's T1 shine through. You know what? I'm gonna try to use my pen. Let's see where that works. Ah, okay. So that bright area there is a hemorrhage associated with a cavernoma. This is a cavernoma of the right temporal lobe which demonstrated metahemoglobin. This metahemoglobin is shining through on the MRA and looking like an aneurysm. It is not an aneurysm. It's just T1 shine through in an MRA. The MRA was actually normal with a little bit of atherosclerotic change. So this is a cavernoma which bled and has metahemoglobin. It's actually intracellular metahemoglobin because it's dark on T2 weighted scan. And in the right temporal lobe as a source of this patient's temporal lobe epilepsy. So now I've got to get off of my, and go back to the mouse. Okay. I'm gonna move this stuff. Sorry. So how about this next case? So this is a patient who was in status epilepticus. You're seeing the T2 weighted scan and the flare scan. And let's go to ask the question. While you answer the question, I'm gonna be removing the lines I made. So the best diagnosis is at middle cerebral artery distribution stroke, herpes encephalitis, ganglio glioma, acute disseminated encephalomyelitis, or none of the buts. So the best diagnosis, MCA stroke, herpes encephalitis, ganglio glioma, ADEM, or none of the above. Let me see where I can get rid of this. Undo, no, that's not helping me. Let me go clear. That's not helping either. All right, well, back to the mouse. So the correct answer, I missed that, okay, was none of the above actually. This is not an MCA stroke. It's a child who has rasmusans encephalitis. So the correct answer was actually none of the above. How do we know that this is rasmusans encephalitis and not the other diagnoses? Well, as you can see, the left hemisphere overall is smaller in size than the right hemisphere, as indicated by the enlargement of the lateral ventricular system on the left side. You also see the abnormal signal intensity, obviously, in the base of ganglia region, but this is not wholly within the middle cerebral artery distribution, and the whole hemispheric loss of volume is what makes the diagnosis of rasmusans encephalitis. The etiology for rasmusans encephalitis, as far as a pathogen, people don't know. It's the, whatever the microbe is, people just don't know at this point. It is a source of persistent intractable seizures and status epilepticus. It usually occurs in a pediatric age group, which argue against this being middle cerebral artery stroke. And the treatment is usually hemisperectomy, and sometimes that's sparing the base of ganglia so that way they maintain some motor control. But since these patients are usually in persistent status epilepticus, the family will accept the fact that the patient has weakness and will ask for the hemisperectomy. And the surgeon who has done the most hemisperectomies for rasmusans encephalitis in this country is our current HUD secretary, and that's Ben Carson. Okay, by contrast, here's an example of herpes. So usually we say that herpes is bilateral. It usually affects the peri-insular region. And one of the other imaging findings that helps us is when we see bright signal intensity in the singulum of the brain, either usually bi-ratherally, again, hemorrhage occurs in about 30% of cases with herpes. And these patients overwhelmingly have a fever. So herpes encephalitis and bi-ratheral involvement, singulum involvement would be the key as opposed to that case of rasmusans encephalitis. Okay, let's move to the next case. So we're in the infectious category. So we're doing vascular infectious traumatic acquired metabolic adiabatic neoplasic congenital and drugs. We did the idiopathic. We're doing vascular. Now we're in infectious. We did herpes encephalitis. We did rasmusans encephalitis. What about this case? Well, this is a really interesting case from the standpoint of presenting in Baltimore because we usually don't see this very much. This is a patient who has a live cystocircus. And what you're seeing is the little scorex of the live cystocircus and the surrounding edema and peripheral enhancement associated with on the flare scan and the post-gad T1 way of scan. It was important that the surgeon removed this with a cuff of normal tissue around it. You don't wanna pop into this cavity because then you may be shedding cystocircus into the subarachnoid space. And we know that that in and of itself is can lead to hydrocephalus and problems down the road. So this was a surgical specimen with the removal of the cystocircus. Okay, let's move to the next case. This is one of our unknown cases. Here we have a axial flare scan, DWI B1000 scan and the ADC map. So think about this because we have our next question and I'm gonna go to the question. So what is the best diagnosis for this case? Would this be an arterial stroke? Would it be an abscess? Would it be a metastasis? Would I be fooling you with another venous infarction with hemorrhage? Or is it a hypertensive bleed? And while I do this, if Ashley or Paul know how to get rid of my little scribble there, you can take it out for my computer screen. In the meantime, we've got this. Dr. Newsom, there should be an eraser tool in the same area where you grab the pen tool. That might help remove those circles. Let me see, I got eraser. Let's see whether that works. Thank you, sir. All right, moving on. So let's see what people said. Was this an arterial stroke and abscess? Okay, so 78%, give yourself a gold star. Indeed, as we know, abscesses may be bright on the DWI. They often are bright on the DWI and they show reduced ADC. In this location, I would be concerned about two things. Is it hematogenous? Or I'd like to see the temporal bone because sometimes you have infections of the otomastoiditis of the temporal bone, which may lead to intracranial abscesses. And in fact, sometimes you get septic thrombophobitis of the sigmoid science or transfer science associated with coalescent mastoiditis, for example, that can lead to a septic infarct, which would be the other thing in the differential diagnosis. This was an abscess. All right, I gotta get back to my nails. Yeah, okay. All right, next case. Here's another unknown case. We have a CT scan, again, temporal obligeans. You can see the patient's got fiducials on the outside of their head because the surgeon is going to remove this mass. Let's see what the question is. The most common temporal lobe mass to calcify is what? Would that be number one, algodendroglioma, number two, astrocytoma, number three, disembryoplastic neuroactodermotumor, number four, the DIG, the desmoplastic infantile ganglio-glioma, or number five, pleomorphic xanthoastrocytoma. You understand why we use D-net DIG and PXA instead, okay? So, disembryoplastic neuroactodermotumor, desmoplastic infantile ganglio-glioma, or pleomorphic xanthoastrocytoma, or oligo or astro. So, indeed, the correct answer is algodendroglioma. This is a tumor that frequents the frontal lobe and the temporal lobe, usually affects the cortical margin, and therefore is more likely to induce seizures. And in point of fact, this case was not algodendroglioma. This ended up being a parenchymal appendemoma. Now, appendemomas are interesting because in the posterior fossa, appendemomas usually occur within the ventricle as an intraventricular region that we see going outside the fourth ventricle and into the foraminal of lusca and majendi. But in the supertentorial compartment, appendemomas usually are parenchymal in their location. So this was a parenchymal appendemoma, not an algodendroglioma, but the correct answer to the question is an algodendroglioma, particularly in adults. All right, we have another case here. This is a patient who has a peripheral lesion. It's in the posterior portion of the temporal lobe at its junction with the occipital lobe. And you can see the interesting pattern of heterogeneous contrast enhancement. So what would be the best diagnosis? While you look over the options of ganglio-glioma astrocytoma, algodendroglioma, metastasis, or none above, I'm gonna switch to my other cowboy hat from Colorado. How do you like that one? There you go. Plenty of sweat to eat your heart out, right? Okay, so let's see what the audience said while I was doing my different costume changes. Ganglio-glioma is the correct answer and 52% of you said the correct answer. Metastasis is not really the pattern of enhancement to be unusual. There's not that much edema associated with it. Whereas a ganglio-glioma in an adult would be a good answer for this unknown case. This is a patient who has pleomorphic xanthalastrocytoma. You see the relatively subtle abnormality on the flare scan in the left medial temporal lobe, as well as some contrast enhancement that's on the periphery of the lesion. And that is typical of the PXA. The PXA is a tumor, the pleomorphic xanthalastrocytoma is a tumor that has a mean age of presentation of 14 years, usually presents with seizure. And it may involve both the cortical portion of the brain as well as having a meningeal contrast enhancing nodule. And there is an element of cystic change that can occur. So here are two different patients with PXAs. On your left one case and then up and down here on the right, another case. You notice that the case has cystic components, both interparenchymaline here it's extending outward but also has a peripheral contrast enhancing nodule which may extend to the meninges. That is a little bit better seen here on this patient who has both a cystic component as well as a solidly enhancing component and the solidly enhancing component goes all the way out to the periphery and may show a small dural tail, not as we'll demonstrate in this particular case. Okay, so when we look at tumors since we're now we've done vascular infectious we're skipping to the neoplastic category. Which one of these tumors has the youngest age at presentation? Would it be the desmoplastic infantile ganglia glioma, atypical teratoid rabdoid tumor, disembryo-plastic neuroectodermal tumor, pleomorphic xanthylastrocytoma or glioblastoma. So between all of these, which one presents at the youngest age? Dig ATRT Dnet, PXA or GBM. So your answer is ATRT and that is the second youngest lesion. Infantile should have been the giveaway on the dig. So here we have the ages at onset, usually with kids, dig ATRT Dnet but the dig is that infantile, the ATRT is young childhood, young adulthood, ganglia glioma and the PXA we already saw that at 14 years of age mean for PXA. In the adults we usually think about astrocytomas and algodendrogliomas and obviously glioblastoma. So the dig, the dig will present in the first or second year of life. It usually has cystic and solid components and it too may have a meningio attachment which will show contrast enhancement. There is a variant of this called the desmoplastic infantile astrocytoma and this is a tumor that is a little less cystic than the dig and it occurs in a little bit older age group. Both of these are benign tumors that are WHO grade one and as you can see, they occur in the temporal lobes but also the frontal lobes. Here you have a good example of a child with a dig, it has cystic components related with C, has solid components seen on the arrow and with the white arrows you can see the extension of the dig going to the meninges and having a little bit of a dural tail along the lateral aspect at the lower aspect of that cystic lesion on the right side. Contrast that with the ATRT. Now the ATRTs are ugly looking lesions, they usually are very large at presentation, greater than five centimeters, typical age two to four years of age, so a little bit older than the dig. I guess we would also consider a teratoma as something that might even be younger than the dig, so I'd probably go teratoma, dig, ATRT and then get into our PXAs and D nets. But this lesion has hemorrhage, it's got irregularity, it's got funny enhancements, it's got necrosis associated with it. These are really large lesions and quite ugly. As you can see, I said two to four years of age, 1.6 year median cerebellum, cerebrum and they don't respond as well to chemotherapy as opposed to the medulla blastoma. You can have ATRTs in adults and that's probably why the mean age gets skewed a little bit higher than the digs and that mean age can be 32 in the adult ATRT. They look similarly in that it's a necrotic lesion with or without calcification, usually enhancing and usually quite large in size. So when we think about the neoplastic category, we've gone over some of this, cystic components, ganglion glioma, juvenile polycytic astrocytomas, D net, we'll talk about shortly, PXAs and digs, cortical involvement, usually ganglion glioma, D nets, PXAs and digs and calcification, most commonly oligodendroglioma. So to review, which one of the combinations of tumors has a, often a mural nodules, sometimes with a meningio attachment, would that be PXAs and digs, PXAs and ganglion gliomas, digs and D nets, D nets and ganglion gliomas or ATRT and digs, which ones are the ones that characteristically have a mural nodule that may extend to the meninges and show a little bit of a durable tail? Does that see how well people paid attention to me? So 53% of you are either speaking English or not understanding my, they correct answers, PXAs and digs. They have a mural nodule that sometimes attaches to the meninges and they see a durable tail associated with it. Thank you for that. Dr. Yusin? Yes. We've got about one minute left. Okay, so I'll cruise through this. I'll just point out with D nets may have a bubbly region to the, to it and may have associated cortical dysplasias. And the other reason that can have cortical dysplasia associated with it is the ganglion glioma. And here you see a ganglion glioma cystic out in the cortex with an abnormal cortical feature to it. So I will end with one more question if I could on limbic encephalitis. This patient has a perineoplastic syndrome and let's ask the poll this final question. Let's ask the attendees this final polling question. The names of perineoplastic syndrome antigens do not include they include all of them except one. Is it yo, re, jo, hue or trot? Which one of these is not a perineoplastic syndrome antigen? Is it yo, re, jo, hue or trot? So this is not a joke. It's true. Let's see what people say. Yo, re, jo, hue or trot? All right, so we got pretty much all across the board. Actually, the correct answer is jo. All the others are names of perineoplastic syndrome antigens. Not jo, but yo, re, hue, trot. And various of these that affect the neurons can lead to a perineoplastic limbic encephalitis. So I'm gonna move to my recap slide here and say when in doubt consult vitamin C and D. There are vascular lesions that affect just traumatic idiopathic neoplasic and congenital lesions that are bound in the temporal lobe. That's your differential diagnosis. Understanding that mesiotemporal sclerosis is the most common cause of temporal lobe epilepsy. And the most reliable finding is the decrease in the size of the hippocampus, which is why we resort toward to AI and do some hippocampal volumetry. With regard to infectious, think about herpes. That's probably the most common temporal lobe infection. Although look at the temporal bone to see whether there's direct spread. The neoplasms can be separated on the basis of age. We talked about DIGs and ATRTs as very young in age. And then we have the young adult and teenage with the PXAs and DNATs. But you can also find cysts and calcification and whether or not it's involving the cortex or not and the presence of enhancement. Finally, we always have to think about a stroke and that's in the adult population. Trauma with the temporal lobe banging up against the greater wing of the sphenoid and being therefore a source of hemorrhage and epilepsy in the future. And what I didn't get to were the congenital lesions which are your congenital disclosures, cortical disclosures, which may be the source of the seizure as well. So at this juncture, I'd like to stop and try to go to the chats and see, let me see the question and answer and see whether there are any questions that I can answer for you. Ashley, are you with me? I'm here, Dr. Yusman. So I've got your few answers open in your question and answer box. I can read those for you if that would help. Okay. So one of the earlier questions was about the GBM being congenital and they wanna know why that was not the answer. I think that was in reference to an earlier question. Why, I think it was the neonate question perhaps. Okay. So it's pretty uncommon to see high grade neoplasms in the, as a congenital finding or as in an infant. They do occur, it's much less common than your low grade astrocyte tomas, particularly when you think about, for example, the brainstem gliomas or patients who have neurofibromatosis with hyalocytic astrocyte tomas. So I wouldn't go to GBM in a congenital or any child. If I see a tumor that looks really aggressive like a GBM, I'm gonna look again at the age, but I'm more likely to think about it as something like an ATRT or potentially a, you know, a more aggressive looking lesion such as some of the D nets. Although they're benign, they have cystic components that can sometimes look like it would be necrotic. Okay. And at the end, would you please throw more light on specific mesotemporal sclerosis features? Okay. So this is a good question for a multiple choice question. If you're asked at the boards. So as I said, the most reliable is going to be the volumetric change in the hippocampus. Number two is going to be the flare signal abnormality on coronal imaging showing bright signal in the hippocampus. Number four would be loss of the normal gray white differentiation. So we see blurring of gray white. That would be another of the findings. Loss of the cremated superior margin of the hippocampus. So it looks more flattened and rounded is another of the findings. Ipsilateral mammillary body atrophy. Another of the findings, Ipsilateral. Fornaceal column atrophy. Another of the findings. Those would be some of the more reliable of the imaging findings of mesotemporal sclerosis. I see a question, it's, is 3T MRI required for the evaluation of the temporal lobe? So no, the Norquan software will work on 1.5T as well as 3T. You don't require a 3 Tesla scanner for that. That said, it is a subtle finding for hippocampus sclerosis if you don't have a volumetric analysis package. And therefore it's useful to have that kind of high resolution with 3T that you can do thin section imaging. And the other value that 3T would have would be for the detection of susceptibility in things like cavernomas or any hemorrhagic lesion or post-traumatic injury. I could keep scrolling down, Paul, and answer the questions as they come. Why not the right temporal lobe abscess can be a venous stroke? So I would say that the main problem with that case being, not being a venous stroke was the shape. It was just a little to what we would say geographic. It was a little too rounded. And if you see peripheral enhancement in a round lesion with restricted diffusion, I'm much more likely to go with an abscess than with a venous impart. Could that diffusion weighted abnormality actually have represented hemorrhagic material? It could have. That's a possibility. And sometimes we get fooled with hemorrhage on DWI versus abscess. But I would say that relatively smooth margins, peripheral enhancement will go for an abscess. There's also this double rim sign that you can see with susceptibility weighted imaging that also suggests an abscess over things like tumors. What's the differential diagnosis for lesions in the ponds in a child under 10 years old? This reason showing hemorrhage and calcification as well as restricted diffusion. So we're talking hemorrhage and calcification in a lesion in the ponds. I would worry about something like a cavernoma that can calcify it would show hemorrhage, restricted diffusion, not so much except if you're getting fooled by hemorrhage. But since this is a talk about temporal lobe and not the ponds, I'll pass on the rest of that. What is the effect of steroids on glioma? Do they not enhance after steroids? So it's true that use of steroids will decrease the contrast enhancement associated with anioplasms as well as other ideologies that may show contrast enhancement. So we always need to know that. In fact, for the reno criteria of brain tumors, being on steroids is one of the potential exclusionary factors that lead us to have more difficulty in predicting whether or not there's a tumor response or whether it's a pseudo progression or whatnot. So it is something that you wanna look in the medical record for. How do you distinguish a glioblastoma from an abscess? So there's lots of different characteristics. Usually that homogeneous restricted diffusion as opposed to heterogeneous restricted diffusion is more common within abscess. We look at the wall of the abscess. Generally we say that the wall, the outer wall of an abscess is smooth, whereas the inner wall of the abscess is regular with glioblastomas because it's growing out from the necrotic portion. The wall is more regular on the outer portion of the necrotic area with a GBM. You can also use that susceptibility double rim sign where you see the right signal intensity. And that is usually an indicative of the oxidative process of the bacteria as they're undergoing the respiratory burst, for example. So that's another way. And usually glioblastomas are much more infiltrative. Next question, is there a decrease in size of bilateral hippocampus? Then how do we define mesotemporal cirrhosis? So bilateral hippocampus, bilateral mesotemporal cirrhosis will result in reduction in both sides of the hippocampus. That is a problem for us. For that, again, I would look at the absolute volume analysis using a volumetric software such as Norquan. So if Norquan shows both hippocampi below the fifth percentile compared to normal controls, then we might suggest mesotemporal cirrhosis. Hopefully you have good clinicians who are doing the EEGs and determining which side is the side that they suspect of the seizure focus. But it can be difficult, and that is one of the potential pitfalls. I didn't mention calvaryl changes for tumors, not so important. My bad. So some of those slow-growing tumors, particularly ganglia gliomas, in fact, the ganglia glioma that had cortical dysplasia that I showed, if you go back in the slides, actually did have some calvaryl remodeling. And some of those slow-growing grade one tumors will lead to calvaryl changes. They don't, you know, if I see calvaryl changes in an adult, I'm more likely to wonder whether this is an extra axial lesion such as a meningioma that's causing hyperostosis, et cetera. So a good point. Thank you for the anonymous attendee. Would there be a difference between clinical presentation between a degenerative illness like any dementia and ADF-TD and a space-activating lesion in these areas? Yeah, that's true. And usually patients with Alzheimer's front to temper of dementia don't present with seizure disorder as opposed to lesions that are inducing edema are more likely to cause a seizure focus. And obviously, you know, a space-activating lesion is not likely to cause dementia in the acute setting more. So that would be two different clinical settings. Regarding tumors, some are too similar radiologically. To which extent is radiology important in giving a diagnosis? So I'm, you know, I like the intellectual gymnastics of predicting tumor histology. In the end, the neuropathologist is most helpful here and I can guess and guess and guess and be wrong. So, but I do think that number one, looking at the age, number two, is it cortical or is it deep? You know, the glioblastomas are not going to be cortical lesions. Is there calcification? Is there cystic change? Calcification, I'm going to go with the oligo. I might throw in the appended moment. Cystic change, much more likely to go with the pyrocytic astrocytoma or PXA, or the D-net, for example, has that kind of mulberry, multiple cystic areas. That would be helpful. Absence of contrast enhancement would be helpful. I'm more likely to go with the low-grade astrocytoma in that situation. And oligos don't, you know, I think the number is around 20% of oligos enhance and 80% do not. Space-occupying region need temporal orbit. Yes. I think we're going to have to, we're going to have to cut you off there. We're a little past the one o'clock mark. All right, let me, I have one more cat change. All right, I'm ready. So thank you for your attention. It was a lot of fun. And I hope that you learned something and remember vitamin C and D. The shot of Colorado. Back around, there we go. All right, Dr. Yusam, thank you so much for your time and your many hats today. And thanks to all of you for participating in our noon conference. Reminder, this conference will be made available on demand in the next 24 hours. Tomorrow, please join us at 12 p.m. Eastern Standard Time. We'll have Dr. Mikesh Parasignani with us. He will be talking on the role of MRI and imaging of rectal cancer. Please visit MRIonline.com to sign up for future noon conferences. Thanks so much, Dr. Yusam. Thank you.