 And welcome to Noon Conference hosted by MRI Online. Noon Conference connects the global radiology community through free, live educational webinars that are accessible for all and is an opportunity to learn alongside top radiologists from around the world. We encourage you to ask questions and share ideas to help the community learn and grow. You can access the recording of today's conference and previous Noon conferences by creating a free MRI online account. Today, we are honored to welcome Dr. David Yusam for a case review entitled Sino-Nazel Case Review, Vitamin C and D. Dr. Yusam is a neuro radiologist and professor of radiology at the Johns Hopkins University School of Medicine. He's the author of more than 350 scientific papers and several popular books in radiology, including Neuro Radiology, The Requisites and is a series editor of the case review series. He has served as the president of ASNR and was awarded the Outstanding Educator Award from the RSNA. We are grateful to Dr. Yusam for her support of MRI online and for serving as our neuroimaging sub-specialty advisor. At the end of the case review, please join him in a Q&A session where he'll address questions you may have on today's topic and please remember to use that Q&A feature to submit your questions so we can get to as many as we can before our time is up. With that, we're ready to begin today's case review. Dr. Yusam, take it from here. Thank you very much. So today we are going to go through some multiple-choice questions on synonazel imaging unknown cases. I'd like to have as much participation as I can from the standpoint of the polling and the multiple-choice answers and we'll see how you do. So let's get going. Just as a reminder, my mnemonic vitamin C and D refers to vascular infectious traumatic acquired metabolic idiopathic neoplastic congenital and drugs. And those are the general categories of disease that we see across the full spectrum of pathology in the body. And in the synonazel cavity, obviously, it's going to be dominated by infectious etiologies, inflammatory etiologies and neoplastic etiologies. So let's begin. And my disclosures, I do have several books published by Elsevier for which I receive royalties. I do medical-legal expert witness work and I am one of the consultants and speakers for MRI online or Medallity. And yes, the fifth edition of neurobiology, the core requisites is coming out in March. So go to the Elsevier site or Amazon, wherever you want. All right, here's our first case. So what we got here is the sagittal T1-weighted MR the axial T2-weighted MR, a post-gadolinium enhanced scan here. And this is the flare scan. So T1 axial T2 flare and post-gadolinium, this is with fat suppression, T1-weighted scan. So what is the most likely diagnosis given these imaging findings? Do you think this is most likely a squamous cell carcinoma? A mucus retention cyst, allergic fungal sinusitis, inverted papilloma or a schnindarian polyp? So looking at the pathology that's being demonstrated, what do you think the most likely diagnosis is? If you think it's squamous cell carcinoma, answer number one. If you think it's a mucus retention cyst, answer number two. If you think it's allergic fungal sinusitis, answer number three. For inverted papilloma, you're going to put number four and for a schnindarian polyp, put number five. So we've got about 200 people on board and we're going to see what the audience recommends. So let's share results. And it looks like 68% of the people answered allergic fungal sinusitis and indeed that is the correct answer. You notice that on the T1-weighted scan we have areas within the paranasal sinuses that are bright on T1 as well as dark on T1. On T2, the predominant abnormality here is dark on T2 as well as flare. In fact, you might think that this is aerated sinus just looking at the T2. And then we get to the post-GAD T1 and we see, no, that's not aeration. That's very inspecated secretions or allergic fungal musin that is causing the very low signal on the T2-weighted scan and you see also that the ethmoid sinus is opacified. So remember that the signal intensity of the secretions in the paranasal sinuses is dependent in part on the protein concentration. And this was beautiful work that was done by the late Peter Somme in the 1980s in which he aspirated, he actually got the anti-doctors to aspirate sinus secretions and then measure the protein concentration. And what he showed was that this is signal intensity, this is the T1 and this is the T2. When you have low protein concentration, effectively just fluid, it's gonna be dark on T1 and bright on T2. However, as the protein concentration increases, you notice the first thing that happens is that the T1 becomes bright. This is the iso-intense line here that becomes bright. So you have a period where it's bright on T1 and bright on T2. But as those secretions get more and more musinous and less watery, you come to a point where it's bright on T1, but now it's dark on T2. And when it becomes a concretion, effectively like a calcification, it's dark on T1 and T2. So these are the graphs that you should know about protein concentration. This also will pertain to things like craniopharyngeomas or pineal region cysts or other things that have high protein content like colloid cysts, for example. The things that are hyper dense on CT, but dark on T2 include blood products. It's just like that. Hyperproteinaceous secretions, fungus. You may see that with osteomas or odontogenic lesions and indeed melanin, which may be bright on T1 and dark on T2 from the melanin is often hyper dense on CT in part, maybe because it may be hemorrhagic as well. So this was a case of allergic fungalsinousias, which is not an aggressive, invasive type of fungalsinousias. Remember that we have five different varieties. We have our non-invasive fungus ball or mysotoma. It's usually in the maxillary sinus. We have our non-invasive allergic fungalsinousias with the eosinophilia and the musin. We have the acute invasive fungalsinousias. Those are usually the patients who have diabetic ketoacidosis at presentation and are immune compromised and they may have mucor or aspergillus. Then we have the chronic invasive sinusias, longstanding patients who have chronic rhinocinousias. And then this unusual chronic granulominox invasive fungalsinousias that is not usually seen in America, but more commonly in Africa or Southeast Asia. Here's another example on CT of a patient who had allergic fungalsinousias and you see the hyper density to those secretions and there is some bony dehiscence because of effectively like polyps, it's remodeling the bone. The five criteria for allergic fungalsinousias type one, hypersensitivity, often seen with the eosinophilia, nasal polyposis, CT findings of pacification, eosinophilic musin and a positive fungal stain without demonstration of invasion. Here on the other hand on a MRI with bright on T1, this is turned out to be a mysotoma fungus ball in the right maxillary entromo pacifying it. This was one of the cases that I saw back when I was a resident in which the patient had severe fungal invasive sinusitis with mucormicosis. And what you're seeing on this post-gadolinium T1-wayed scan is opacification of the right cavernous sinus but absence of opacification in the left cavernous sinus. If you look at the carotid artery here faintly seen, it's narrower than the normal right side. It's got a little irregular margin. So this patient had fungal sinusitis with invasion of the cavernous sinus and thrombosis of the cavernous sinus associated with vasculitis. And the next scan showed MCA infarction secondary to the left internal carotid artery vasculitis from the invasive mucormicosis. All right, next case, case number two, let's move on. Here's the CT scan axial original data, sagittal reconstruction, MR T1 post-gad, MR axial T1 post-gad. So I'll give you a moment to look over the case. CT and MR with GAD. Most likely diagnosis for this entity, is this a mucosial? Is this putt-puffy tumor? Is this a dermoid? Is this nasal glioma? Or is this a sebaceous cyst? So the most likely diagnosis here, if you think it's a mucosial, answer number one, if you think it's putt-puffy tumor, number two, if you think it's a dermoid, answer number three, if you think it's nasal glioma, number four, or a sebaceous cyst, number five. So let's see how the audience is doing here. And I think we can end the poll because there's an overwhelming, let's share that results, overwhelming support for putt-puffy tumor, and that is indeed correct. You have a patient who has a frontal sinusitis with opacification. There's a little divot here out of the frontal sinus where the infection has entered the soft tissues of the forehead. And obviously this putt-puffy tumor was thought to initially be a tumor because it was presenting as a soft tissue mass under the skin. And the, let me give you a little history here. All right, putt-puffy tumor, forehead edema resulting from osteomyelitis of the frontal bone associated with a subperiosteux abscess, first described by Sir Percival Putt in 1768. Let me tell you, they did not have CT scans back then. That's why he thought it was a tumor rather than the spread of infection from the frontal sinus. And then obviously when he went to cut it open and got that purulent stuff coming out. So you have rhubor, tumor, calor, and doler. So redness, swelling, warmth, and the tumor in this case is the observable swelling of the forehead rather than to any neoplasm. And it's a complication of frontal sinusitis. So putt-puffy tumor. We often call it putt-puffy tumor but the gentleman's name was Sir Percival Putt. Frontal sinusitis is an entity that may be associated with the infection going superficially and creating a putt-puffy tumor but it could actually also extend intracranially where you may have an epidural abscess developed from the infected frontal sinusitis. You see that here. If this collection dissects the sinus off of the periosteum of the frontal bone it may actually cross the midline. And any collection that's crossing the midline we assume is going to be an epidural abscess or epidural hematoma as the case may be with trauma. So you may also see findings of meningitis. So look at the flare scan, look at the CSF. Is the CSF still suppressed on the flare scan? Or if it's not suppressed that might imply that there is meningitis associated with it. Obviously with this type of proximity to the superior sagittal sinus you may get sinus thrombosis and then have a superimposed venous infarction on top of the infection on top of the sinusitis, for example. Okay, we're moving on to the next case. This patient had previously had a medial antrostomy for inflammatory disease. And what you're seeing is the, this is the sagittal cis T2-weighted scan. This is the post-gadolinium T1-weighted scan. This is the axial T2-weighted scan. And you can see that we're going through this abnormality. And then this is the ADC map of the lesion. So patient who had previously had surgery and you can see that the lesion in question here that we're looking at is this area here. The most ominous feature of this lesion is what? Is it the dark signal on T2-weighted imaging? Is it the fact that it enhances? Is it the low ADC? Is it the eroded bone? Or is it being bright on T2-weighted scan? So on the imaging features of this lesion which one kind of bothers you most? Is it the dark signal on T2-weighted imaging? Is it the presence of enhancing tissue? Is it low on ADC? Is it eroded bone? Or is it bright on the T2-weighted scan? Which of these is the most ominous feature of this lesion? All right, T2 post-gad T2-axial ADC map. All right, we've got over a hundred responses. So let's see what people said. Okay, so the answer to the question by the group is low ADC and I would agree with that. The reason why I would agree with that is dark one T2, as you know, we just saw a case of allergic fungal sinusitis that can occur with insipid secretions. It can occur with fungal sinusitis. It can occur with osteomas. I gave you all of those differential diagnosis. Enhancement, so enhancement is important and solid enhancement is gonna be a pretty good indicator that this is neoplastic as opposed to an inflammatory process. So the fact that this tissue shows enhancement is an ominous finding. Low ADC, yes. However, remember that just as epidermoids may have low ADC and it's not necessarily because of hypercellular tumors in part because of the concentration of protein or the content of the lesion, you may see insipid secretions and things with high protein that will have restricted diffusion. You wrote a bone, definitely, but a lot of benign tumor, benign conditions, including mucosials, including polyps, including osteomas, those things can erode the bone and yet be a benign condition. Right on T2, usually that's reassuring. So that would be the least. So given all of these findings, what do you think the most likely diagnosis here is? Is this a squamous cell carcinoma? Is this an inverted papilloma? Is this melanoma? Is it lymphoma or is it fungus? So our lesion is here, relatively dark on the T2, showing contrast enhancement. Dark on T2, a little bit of obstructed secretions and low on ADC map. What do you think the most likely diagnosis is? Is it squamous cell carcinoma? Is it an inverted papilloma? Is it melanoma? Is it lymphoma or fungus? So number one for squamous cell carcinoma, number two for inverted papilloma, three for melanoma, four for lymphoma, and five that there's a fungus among us. See what people say here. So let's share some results and we have a mixture of different suggestions, including squamous cell carcinoma, lymphoma, inverted papilloma, not so much melanoma, not so much fungus. So I think that's reasonable. All three, the squamous cell carcinoma, inverted papilloma, and lymphoma may look this way. If you're going with the most likely diagnosis by the numbers, the most likely cancer of the paranasal sinuses is squamous cell carcinoma. So that would be the best diagnosis here. It's not a particularly good location for an inverted papilloma, which usually occurs along the common wall between the maxillary sinus and the nasal cavity or along the septum perusum. This area, which is effectively in the ethmoid sinus, is not the best location for an inverted papilloma, not classic. So our answers are low ADC and squamous cell carcinoma by numbers. It looks like there's some, I got some chat things. Let's see, no, not for me. Okay, no questions at the moment. Question and answer. What is a Schneiderian polyps? Schneiderian polyps are types of polyps that are included with inverted papilloma and it refers to the histopathologic features. And I'll move forward as they ask you about the next answers. All right, so here is a graph that you see from head and neck surgery and oncology, Justin Shaw, who's from Memorial Sloan Kettering. And he knows that the most common of the cancers of the nasal cavity and perinatal sinuses is indeed squamous cell carcinoma. And then we have this kind of other category, which are undifferentiated cancers. We have melanoma, which is the pink here, minor cell, very gland tumors, et cetera. And the synonasal undifferentiated carcinoma, one of the more aggressive of the synonasal cancers, all of these kind of look alike, except for melanoma, which hopefully you'll see as bright on T1 if it has enough melanin content within it. Ecession neuroblastomas are the ones that are usually in the upper nasal cavity and ethmoid sinus and cribiform plate that grow most frequently, intracranially and the characteristic feature of that is the peripheral cyst associated with the esthizio. That happens with other cancers, but the highest rate is with esthizio neuroblastomas or what we sometimes use the term olfactory neuroblastomas. Here's the 80% rule. 80% of sinus cancers occur in the maxillary entrum of those 80% to squamous cell carcinoma of those 80% to road bone and 80% have a history of chronic sinusitis. Moving on. Next case, CT scan axial raw data coronal reconstruction. Least likely diagnosis. Number one, granulominoce polyangiitis. Number two, fungal sinusitis. Number three, cocaine abuser. Number four, syphilis. Number five, plebsiola. So for this imaging finding that you're seeing, what is the least likely diagnosis? If you think it's granulominoce polyangiitis, GPA, number one, if you think it's fungal sinusitis, but number two, if you think it's cocaine abuser, but number three, if you think it's syphilis, but number four, and if you think it's plebsiola, put number five. So let's share the results and the correct answer here is fungal sinusitis, which I guess is the second most common answer here. Cupsiola is one of the bacteria that will collapse your nasal septum. So the finding here is nasal septal perforation and erosion and you have all that soft tissue. So in yesteryear, we would often use the term wagoners, but now we're using granulominoce polyangiitis. That's a pretty frequent cause of demonstration of sinus involvement by wagoners. Fungal sinusitis doesn't often cause septal perforation. Cocaine abuser in East Baltimore at Johns Hopkins is probably the most common thing and we probably have around a 10 to 20% rate of patients that you're reading their trauma head CT or motor vehicle collision and you see nasal septal perforation. So cocaine or other drugs, syphilis, saddle nose deformity associated with syphilis and leprosy, those are known causes as well. So the correct answer was fungal sinusitis. This is another one of the entities that can lead to a granulominoce sinusitis as well as inflammation in the orbit. So wagoners also may have inflammation in the orbit associated with a nasal septal perforation. When you put those two together, you will come up with the granulomis polyangiitis as well as sarcoidosis as another of the ideologies. It can occur after trauma. It can occur with a nasal septal hematoma that erodes the bone. So there's lots of differential diagnosis for nasal septal perforation. Here I have a relatively large listing. Remember, I talk about vitamin C and D, vascular infectious traumatic acquired metabolic adiabatic neoplastic and drug. And here we have our trauma causes. We have an inflammatory causes, lots of those collagen vascular disease, infectious causes, syphilis, et cetera. You notice that Cubsiel is not listed here, but it is one, it does mention fungal, but that's the aggressive fungal infections. Neoplasms, carcinoma, T cell lymphomas, and then all these toxic ideologies. All right, I want to make a point here that on this case, you saw that there was some dehiscence along the laminate paparacea. And when I am reading a sinus CT where I know the patient is going to surgery or is about or has gone to surgery, there's four critical areas of dehiscence that you might want to look at and put in your reports. The four critical areas of the dehiscence are the laminate paparacea as you see here along the medial orbital wall because if it's dehiscent and the surgeon is going in to clean up that ethmoid sinus, there is that possibility that they would perforate into the orbit and lead to an orbital hematoma. The second is the cribiform plate. Here you see a defect in the cribiform plate. In fact, this patient actually has a meningocial that's extending intracranially. So post-op, if they take down the middle turbinate, remember that the middle turbinate has a connection to the cribiform plate as well as to the lateral orbital wall. And if they're removing the middle turbinate, there's a chance that in that removal, they lead to a cribiform plate or a laminate paparacea, basal lamella injury to the medial orbital wall or the skull base. And that potentially could be a source of CSF leakage, but it also, if it's dehiscent, could lead to the next time they operate potential intracranial perforation. The optic nerve and canal. It's interesting how often you will see that the optic nerve at the optic canal has no bone around it in the sphenoid sinus and or posterior f-moid region, depending upon whether you have an anode cell. So I often will comment on the dehiscence of the wall of the optic nerve if they are contemplating sphenoidal surgery. And more and more, that's usually associated with cell tumors or pituitary adenoma resection, for example. And then finally, the carotid canal. So here we have the dehiscent carotid canal. You can see the enhancing carotid artery. There's no bone overlying it. Again, at our institution, they will do a 3D reconstruct, 3D dataset of the perinazole sinuses prior to pituitary adenoma surgery because they want to know where the carotid arteries are with the potential for injury if they're doing an endoscopic removal of the pituitary adenoma. So they want to see the walls of the carotid arteries and actually then also the tumors relationship to the carotid artery. So these are the four things you might want to think about adding to your report when you look at a sinus case that's either about to be operated on or has previously been operated. Okay, let's move on. Next case, most likely diagnosis. CT scan, axial and coronal reconstruction. Most likely diagnosis. Is this most likely an antrocoenal polyp? Is this most likely a mucus retention cyst? Is this most likely allergic fungal sinusitis? Is it inverted papilloma? Or is it the old Schneiderian polyp once again? So if you think it's an antrocoenal polyp, you'll put number one. If you think it's a mucus retention cyst, you'll put number two. If you think it's allergic fungal sinusitis, number three. If you think it's an inverted papilloma, put number four. And if you think it's a Schneiderian polyp, put number five. All right, tricky case. So most people put antrocoenal polyp and that is not the correct answer, although this looks exactly like an antrocoenal polyp. So why is this not an antrocoenal polyp? The density of this lesion is what should give you pause that this is not like a typical pups. Pups generally are lower density on the CT scan. They may even be fluid density. Remember that mucus retention cysts and pups of the maxillary antrum often are very liquidy and low density. The key here to this case was that this looks like hyperdense. Here's the mucosa here, peripherally that is less dense. This was histopathologically an inverted papilloma. So that was the second most common answer. So very good to those people. The antrocoenal pop, as you see here, more likely to be a low density lesion, but it does go through the ostium of the maxillary sinus. Usually we say it's the inferior ostium or the accessory ostium, but it does then project into the nasal cavity. That's sort of the coenal portion of it. And then it can even project back into the nasopharyngeal airway posteriorly. So from here, it may project posteriorly as a nasopharyngeal soft tissue mass. In this case, again, look for a lower density to suggest it's antrocoenal pop as opposed to the inverted papilloma. Here is an inverted papilloma. As I mentioned, it usually forms along the common wall of the maxillary antrum and the nasal cavity. And from there, it can grow into the maxillary sinus or into the nasal cavity or both. Here you see a little bit more growth into the nasal cavity than into the maxillary antrum. It will show solid enhancement, not peripheral enhancement. Peripheral enhancement, more common with the antrocoenal pop, not solid enhancement. And you can see that intermediate signal intensity on the T2-wayed scan. There are two features of inverted papilloma that we say are relatively pathognemonic to suggest that specific diagnosis. One is this little bony bar upon which the tumor may be fixed. So if you see that hyperostatic bone and the tumor seems to be centered around that hyperostatic area, that would be an indicator for an inverted papilloma. Again, usually the common wall between the maxillary antrum and the nasal cavity or along the midline nasal septum. The other feature that we say is relatively pathognemonic for a inverted papilloma is this cerebral form look to it. It has almost a look like gyri and sulci within it that you see here or gray and white matter. And you can see the enhancement as you see here. Maybe this is the cortex and this is the underlying white matter. That imaging pattern is more typical of inverted papilloma than anything else. Now that said, we always worry with inverted papilloma because there is that high rate of concurrence of squamous cell carcinoma at about 15%. So these tumors are resected in their entirety and with a margin because of the worry that there may be underlying squamous cell carcinoma. Unfortunately, the squamous cell carcinoma has the same relative imaging features as that of the inverted papilloma. So it's not as if you can look at this and say, oh, this is, you know, this one has squamous cell versus this one that does not. Okay, next case, question six, most likely diagnosis. So we have axial CT and a coronal CT. You see that contrast was administered here. What do we got here? Do we have orbital cellulitis, peri orbital cellulitis, host septal cellulitis, subperiosteal abscess or none of the above? So this case, what are we looking at? Are we looking at orbital cellulitis? Are we looking at peri orbital cellulitis? Are we looking at host septal cellulitis? Are we looking at a subperiosteal abscess or none of the above? So we're moving right along here. All right, let's see. So 66% of people put subperiosteal abscess and that is the correct answer. Let's go back to the original images. So most of the cases of inflammation of the orbit occur secondary to things around the lids, bites or lacrimal problems, et cetera, cellulitic things in the forehead, et cetera and sinusitis. And with sinusitis, it's most commonly the ethmoid sinus that has that ability to spread to the orbit. Why is that so? You see this a lot with kids because there are areas of dehiscence along the lateral wall of the ethmoid sinus. And even in adults it occurs and if you think of the lamina paparacea, the medial orbital wall of the orbit being that thin that we would call it paparacea, paper thin, you might expect that along those channels that have vessels going into it that you might have a root for spread from ethmoid sinusitis to the orbit. Additionally, remember that we have the anterior ethmoid artery and the posterior ethmoid artery that go between the orbit and the ethmoid sinus through those areas of vascular channels that communicate between the sinus and the orbit. So here we have this collection and you notice that it's displacing the medial rectus muscle. The superior oblique muscle is enlarged compared to the normal superior oblique muscle and we have this low density collection here and that is accounting for here. This is probably the medial rectus muscle and this is the collection. With these collections, we call them subperiosteal abscesses even if we do not see peripheral enhancement. So this is one of the locations that we would, you still use the term abscess even though on the post-contrast scan you don't see a walled off collection with peripheral enhancement. Most of the time nowadays, these lesions are treated with intravenous antibiotics and close observation in the hospital and if it does not quickly resolve then they usually are going to treat the sinus disease endoscopically and try to address the primary infection that's causing this problem with the sinus disease. When I was a resident and before endoscopic sinus surgery was so popular they would go needily along here under the periosteum and try to drain these surgically but this is no longer primarily a surgical orbital procedure. It's let's give high dose intravenous antibiotics see how the patient does if they improve continuing them as an outpatient on oral antibiotics if they don't improve rapidly then consider endoscopic sinus surgery to reduce the infection in the ethmoid science. Generally the ENT docs don't like operating when there's active acute sinusitis because of the potential for spread by virtue of their surgical procedure. Okay, so this was a subperiosteum abscess. Note that post septal cellulitis and orbital cellulitis are the same entity, the inflammation that gets into the orbit. Here's an example post septal cellulitis on the left side with infiltration of the orbital fat. You notice that the orbital fat on the left side is more dense than the orbital fat on the right side. There's all kinds of episcleritis that's happening here as well. Here's a collection that you see superior superior osteolabscess and this orbital septum all the diagrams always show it on a sagittal scan. What we usually want to see it is in an axial plane and this is the demonstration of the orbital septum in this case inflammation of the orbital septum still called periorbital cellulitis. Here we have the collection of the subperiosteum abscess in the, from the ethmoid sinusitis but here's the normal septal tissues that you see here and here, orbital septum. There is a classification for the degrees of orbital infection. We have the channeler classification. Number one is preceptal cellulitis. What we call the periorbital cellulitis, post septal cellulitis or orbital cellulitis, a subperiosteum abscess. So this was a case of grade three channeler classification. Four is actual orbital abscess where the lesion is in the intraconal space, for example. And then as an example of that mucormicosis case, we have cavernous sinus inflammation and dorthrumboflavitis. So I'm just going to refer to the question here. In your practice, do you proceed to MR with contrast for cases of suspected inverted papillomal on unenhanced CT or inject contrast on CT? We're going with MRI mainly because there is that potential for perinoral spread of tumor back through the teragopalatine fossa, as well as intracranial spread. And both of those are much better seen on post-gad MR than with CT. So it's pretty rare for us to do a contrast enhanced CT for neoplasms or for suspected intracranial spread of an infection. Can you have orbital subperiosteum abscess without concurrent orbital cellulitis? In general, what you see is the infiltration and edema of the intraconal fat associated with the subperiosteum abscess. So most of the time you get this infiltration of the fat. So it is with concurrent orbital cellulitis, but with the Chandler classification, we would call it RAID 3. Moving on to the next case. Here we have cis imaging, T2-weighted high-resolution imaging. This is the traditional coronal T2-weighted scan. Post-gad T1 sagittal scan, the axial T2-weighted imaging, and a post-gad axial scan. So here we have a child. And we have T2-weighted imaging high-resolution as well as post-gad O&M scans. What term should not be used for this lesion? It should not be used. Sensipital cephalosil, sphenoethmoidal cephalosil, meningocil, basal cephalosil, or none of the above, they're all good. So which of these is the inappropriate term for this lesion? Would it be sensipital cephalosil, sphenoethmoidal cephalosil, meningocil, basal cephalosil, or none of the above, they all apply to this lesion. OK, so for this case, the key here is the difference between sensipital and basal. And the distinction is that the basal cephalosils, obviously, base of the skull, are generally invisible to the naked eye, to observation externally. Sensipital cephalosils are ones that protrude beyond the skull, such that you see them like the pot-to-puffy tumor in the forehead, et cetera. And those are usually nasoethmoidal cephalosils that will project through the frame and cecum or other pathways and project as a visible to the naked eye lesion. So that's sensipital as opposed to basal, where it's invisible to you. So the correct answer here is that this is not a sensipital. No one would be able to tell what's going on, despite the huge size of this lesion. And this was indeed a congenital cephalosil. Now, the term cephalosil is kind of indistinct, let's say. Usually, we want to know whether the cephalosil contains meninges and fluid and or brain tissue. So depending upon whether you think this is purely meninges and fluid, you might use the term meningosil. If you think that there is indeed brain tissue gray matter that's permeating through as well, you would use the term encephalosil. And if it's both the meninges, the fluid, and the brain tissue, we would use the term meningoencephalosil. The sloppy term or the lazy term would just be a cephalosil, in which you're not making that distinction. Now, let me just see whether I can go with it. Answer in the chat. Do you think that this cephalosil is congenital? If you think it's a congenital lesion, please answer yes in the chat. If you think that it no, it's developmental or secondary to operative or trauma or other defect in the skull base, you would answer no. So just in the chat, you think this is congenital? Say yes. If you think no, this is developmental or post-op or other cause, say no. So I'm looking in the chat and there's a lot of yeses. And that is indeed the correct answer. And one of the reasons why you know it's the correct answer is you may have noticed that there's missing portions of the spleenium of the corpus colosum and the rostrum of the corpus colosum, identifying other congenital lesions that would suggest that this is a congenital encephalosil. Here is that CT scan where I was saying that there was absence of the cribriform plate. And look at this. Same patient. Grain tissue and fluid and meninges assumed to be present meningo encephalosil through the cribriform plate. This was a post-op patient who had a defect in the cribriform plate. This is a different patient. T1 weighted scan. Notice the puckering of the brain tissue towards this gap in the cribriform plate. Post-caterinium, a little bit of an enhancement of inflammatory change. This is actually the collection here and here. And where the collection is in the brain tissue is you don't see the enhancement. So cephalosiles are a potential cause of CSF rhinorrhea. And as you see here, congenital, most common occipital associate with potentially our RNA-QRE3 malformations. Post-op, post-trauma. Sometimes idiopathic intracranial hypertension or pseudotumor cerebrine may be associated with cephalosiles and meningoceles. That's why we look at the Meckles cave region to see where that's associated. And some tumors also may cause CSF rhinorrhea and or cephalosil. Okay, next case. CT scan, we have a coronary reconstruction from the axial data and here's the axial scan. Most likely diagnosis here, is this amicus seal? Is this amicus retention cyst? Is it silent sinus syndrome? Is it a hypoplastic maxillary antrim? Or is it a pollen? So given question number eight is, is this amicus seal? If so, answer number one. If you think it's amicus retention cyst, we're gonna answer number two. If you think it's a silent sinus syndrome, number three. Number four for hypoplastic maxillary sinus and number five, a pollen. So obviously the abnormality is in the left maxillary sinus. So, let's see how the audience did on this case. All right, so 73% of y'all went with silent sinus syndrome and that is indeed the correct answer. Why is this not a just a hypoplastic maxillary sinus? Well, the imaging findings that you note, no doubt is the puckering inward of the posterior lateral wall of the maxillary sinus associated with the proliferation of the fat and usually the floor of the orbit, the ypsilateral is depressed and the common clinical finding here is enophalmos because everything's getting sucked in and the globe actually becomes more inwardly displaced as the sinus is progressively decreasing in volume. So this is a source of enophalmos and the chronic sinusitis. This on the other hand is a patient who has a hypoplastic maxillary entrum. You notice in this case that the walls of the maxillary bone are actually thickened associated with that hypoplastic maxillary entrum and the floor of the orbit is not depressed. Here's another hypoplastic left maxillary entrum. Although this is bone window, you see that there's no proliferation of the fat that is associated with silent sinus syndrome. So silent sinus syndrome, usually you see complete opacification of the maxillary entrum. This was a little bit unusual in that it wasn't completely opacified and we call it also the adelectatic sinus as it kind of collapses on itself. And this is a manifestation of a chronic sinusitis with reduced pressure leading to the walls collapsing inward and compensatory enlargement of the perianthral fat. So silent sinus syndrome, usually with an opacified sinus. Okay, we're gonna end on this one. It's sort of a classic case and I wanted to show it in the session. Saddle T1 weight scan. This is a MRA that was performed because of the suspicion of an aneurysm and this is a T2 way. This is actually a haste image because the patient was moving all over the place. But Saddle T1, MRA and haste image. Is this most likely a mucosil? Is it a thrombost aneurysm? Is it a schwannoma? Is it an epidermoid or is it none of the above? So this lesion that we're seeing here is this most likely a mucosil? A thrombost aneurysm? A schwannoma, an epidermoid or none of the above? Final case. So this is a Petrus Apex case and the Petrus Apex is very much like the paranasal sinuses. So I thought it was okay for me to put it in here than a sinonasal talk. And the Petrus Apex may be pneumatized, it may not be pneumatized. When it's pneumatized, it has the potential for Petrus apocytus for Petrus Apex mucosils and for an inflammatory reaction from bleeding that leads to a giant cell reaction and what we will call a cholesterol granuloma. So the correct answer here is none of the above. This is an example of a cholesterol granuloma which is typically bright on T1 and maybe bright or dark on T2 depending upon the protein slash blood slash cholesterol content of it. You see here on the T1, it's in the Petrus Apex. It expands the Petrus Apex. So you see that here. The differential diagnosis is all of these. A mucosial of the Petrus Apex could look just like this as well and it's in the differential diagnosis but cholesterol granulomas are much more common and they're more heterogeneous particularly on T2-A and scanning. Most of the time with mucosils it's uniform signal intensity throughout the mucosil. Here you've got a little bright area, you got a little dark area, you got a little peripheral rim here of black. Is that hemaciterin or is that the bone? That's pretty typical of a cholesterol granuloma and not so much a mucosil. The reason why we have the MRA is to exclude a thrombost aneurysm because your Petrus carotid artery courses right by here and if you have a partially thrombost aneurysm you could have signal intensity that looks like blood products that will simulate a cholesterol granuloma in this case bright on T1 and it may be any signal intensity on the T2. Remember that thrombost aneurysms may have that same layering effect laminated appearance that you can see with a cholesterol granuloma and therefore could simulate that as well. Not like going to be a schwannoma not in the Petrus apex epidermoid. So that's fair, right? Because they may be bright on T1s the so-called white epidermoids. Most of them are dark on T1 and look kind of like dirty CSF on the flare. Most of them, however, are very bright on the T2. So this signal intensity would argue against an epidermoid of the Petrus apex. Epidermoids can occur anywhere in these bones. So it's fair. Again, we would hopefully have a diffusion weight scan which might help us. Remember, however, that diffusion weight scans in the presence of hemorrhage get very confusing to interpret because it looks bright and it may look like it has dark ADC but it's really not. It's, you know, blood products can do that. So in this case, the correct answer was none of the above because this was a cholesterol granuloma of the Petrus apex. So at this juncture, I'm happy to answer any and all questions about synonasal imaging. I will put in a couple of plugs if you don't mind and that is on our MRI online modality website. You have a case bank of 100 brain, 100 spine and 100 head and neck cases with multiple choice questions that I've created as part of a effort to have MRI online as one of your sites that you go to for case review, for board review. So if you, you know, are a little shaky in your neural, come see me at Johns Hopkins or alternatively go to MRI online and they have a material there and they are building a larger and larger case bank with multiple choice questions to simulate the boards. And that's probably gonna be appropriate for the next couple of years until we return to the oral board format with HOTC. So I'm gonna go to the Q and A and see whether there are any questions for me. Okay, questions, excellent question. Can susceptibility imaging help in the diagnosis of cholesterol granuloma? So most of the time, the blood products or the brightness is bright on T1 and bright on T1 is methemoglobin and methemoglobin does not have proton relaxation enhancement unless it's in the extracellular form. So remember that in order to see susceptibility artifact you have to have a difference on the signal intensity or the iron content inside the cell versus outside the cell or inside the brain versus in the extracellular space. So if the blood products are bright on T1 and bright on T2, that's the extracellular methemoglobin phase where you have proton-electron-dipodipodipole interaction but you do not have proton relaxation enhancement which is the T2 shortening effect. So just a quick review of hemorrhage. Methemoglobin has proton-electron-dipodipole interaction which leads to T1 shortening which makes it bright on a T1 way it's scan. Having blood intracellular and not extracellular leads to a bar-magnet effect of the difference in charge between in the cell versus outside the cell which leads to proton relaxation enhancement which leads to T2 shortening. Once you have cellular lysis and it's extracellular methemoglobin you no longer have proton relaxation enhancement it's no longer dark on T2 and that's why it is bright on T2 from water content. So a little digression there into hemorrhage but appropriate. Hey, what do circle of Lewis and your background stand for? C-O-W, circle of Lewis I think and that was the M-R-A. I think it's the picture of your cows behind you. Dr. Wilson. My cows behind me, people want to know about my cows. Those are bulls and this is my Picasso lithograph and if you want to read about it you can look up Picasso's bulls but effectively what I've interpreted as to be is that this is the progression of Picasso's artwork going from initially charcoal drawings to realism and then he converts to cubism over the course of time. This is more cubism and then if you look over here he got really minimalistic at the end and he just did line drawings. So this is sort of the history of Picasso's interpretation and how he drew bulls and this is Picasso's signature right here. Okay, what to the cow in the background? Please could you explain the features the surgeon needs to know in our Sino nasal CT reports? Okay, so as I said, most of the time that the surgeon needs to know whether or not there are any areas of dehiscence. The endoscopic science surgery nowadays is basically a medial antrostomy with removal of the young snake process and a potential ethmoidectomy, the vast majority of the surgeries. They will sometimes go into the sphenoethymoidal recess and relieve obstruction for the sphenoid science and posterior ethmoid sciences. So that said, the main thing are the areas of dehiscence around the ethmoid sinus that potentially could be the cribiform plate, superiorly and the laminate paparacea. Laterally, it's only if they're going into the sphenoethymoidal recesses that you would worry about those dehiscence in the carotid artery of the optic nerve. Now, the other things that they want to know is if the unxinate process opposed or attached to the orbital floor or medial orbital wall, there are times when that occurs and if they're going to remove that unxinate process and do the medial antrostomy and they rip that unxinate process and pull on it, then they're pulling on the orbital floor or the medial orbital wall and you can have that dehiscence and then bleeding into the orbit and the orbital hematoma. So they want to know about the unxinate process, whether it's just hanging free as it does 90% of time or is it bending over to the orbital floor or even to the medial orbital wall of the laminate paparacea. So those are the main things they want to know. Please explain question two again. Oh my God. Ashley, can you go back to question two? I don't remember which one that was. Okay, well, she's doing that. Are there any particular aspects of the bone involvement in synonazepathology that are specific or should guide our diagnosis? So I mentioned that that bony bar is a pretty typical finding of the patients who have inverted papilloma. Clearly if you have a popcorn calcification-like involvement of the bone, then you're talking about the chondroid lesions. Remember that the nasal septum is mostly cartilage and therefore you have incondromas, you have chondrosarcomas, you have benign chondroid lesions of the nasal septum that can occur and will point to a specific diagnosis. From the standpoint of other sarcomas, osteosarcomas or Ewing sarcoma, no specific imaging features in that situation. The other pathology that is typically a diagnosis you can make is brighton T1 and an aggressive lesion and the synonazyl cavity, we're gonna go with melanoma. Intracranial lesion with a system around the periphery, we're gonna go strongly with olfactory neuroblastoma or esthesion neuroblastoma. All the other ones, the snucks and the other undifferentiated carcinomas and adenocarcinomas, not so much. Perinural spread, we're gonna go with adenoid cystic carcinoma as the salivary gland lesion that can occur in the synonazyl cavity that has the highest rate of perinural spread, particularly into the pterigopalatine fossa. So for that, if I see perinural spread into the pterigopalatine fossa and start following the fifth cranial nerve, I'm gonna suggest that this could be adenoid cystic carcinoma with perinural spread. Lymphoma, usually more of a homogeneous lesion rather than the squamous cell carcinoma, kind of bland, that would help. Can you please explain how to differentiate superorbital ethmoid air cells from frontal becomes very confusing at times? I usually am able to kind of make that distinction based on usually the sagittal reconstruction that you can see the communication of the air cells with the ethmoid going above the orbit. Same thing is true with the anode cell. So I refer to the anode cell, which is an ethmoid air cell that actually extends superior to and sometimes even posterior to the sphenoid size, much better seen on the sagyl scan. For all those of you who have these questions and would like a little bit more definition, I did create a sinus nasal mastery course. It's between two and three hours, gets into more of the inflammatory disease and the sinusitis and the osteomatial complex, et cetera, with examples of all of these different types of cells, the howler cell, which is the maxillol ethmoidal cell below the orbit and the named cells, so to speak, and how to distinguish them. Most of the time, the surgeons nowadays are doing a relatively minimalistic surgery. They're just trying to open the osteomatial unit. So the unxinate process is taken down that allows the infundibulum and the middle myatus to drain more easily. Sometimes they're doing the partial ethmoidectomy, not all the time, and they're just trying to open the channels. Same thing with the frontal ethmoidal recess. They're just trying to open that up for frontal sinus so it would drain properly because what they found is the more they operate and the more they take out, the more likely you've screwed up the mucociliary clearance that normally pushes the mucus in the appropriate location back in the back of the throat and then we go and we swallow it down. So that's actually the best way, in a natural way that mucociliary clearance goes. It passes it back to the pharynx for us to swallow it down. If you do too much of this operation and you ruin all the cilia and everything, then it's all distorted and you have chronic sinusitis because it's not draining properly. So a little bit more minimalistic about functional and endoscopic sinus surgery these days. Please can you explain exactly what we have to look for anterior ethmoidal artery in our report? So I don't even report on the anterior ethmoidal artery. Anyone who's doing sinus surgery endoscopically should be able to identify the anterior and posterior ethmoidal air communications. It's that little triangular thing that you see. Again, I did describe this in my mastery series course. It's the little triangular opening to the ethmoid air cells that you will see on the coronal CT scan. That is the potential source of an orbital hematoma if they nail it. But orbital hematomas are incredibly uncommon nowadays with endoscopic sinus surgery. Everyone knows the anatomy. They do 3D to guide them most often. And so they know where the carotid artery is, the optic nerve, the anterior ethmoidal artery. So it's pretty rare to nail that. Please can you have to, okay. Question number two. What was question number two? Dr. Lee, something that was about potpuffy tumor. Oh, potpuffy tumor. So potpuffy tumor, as you saw in that specific case, you saw a defect that was in the frontal sinus leading to the scalp. And it was a large inflammatory process, not a tumor that occurs in the scalp and it presents as a soft tissue mass in the frontal region. And most commonly from frontal sinusitis, when you have potpuffy tumor, you always have to worry about potential intracranial complications which would include a meningitis, a sinus thrombosis, and an epidural abscess. I think that's it. Dr. Yusam? Yeah, I think so. Well, thank you so much for the case review and for answering all those questions you got. We appreciate it. My pleasure. Any other? And go ahead. Any other announcements? Yes, this is also the official kickoff of our new webinar series, Case Crunch Rapid Review, which are one-hour rapid-fire case reviews taking place between February and April. So if you're studying for the boards or you like case reviews like this, you can register for this series at the link provided in the chat. Hope to see you at those case reviews. Be sure to join us next week on Thursday, February 29th at 12 p.m. Eastern where Dr. Elizabeth Arlio will deliver a lecture entitled In Preparation for Women's History Month, Screening Memography Saves Lives. This lecture is co-sponsored with AWR and you can register for that at mrionline.com and follow us on social media for updates on future new conferences. Thanks again. Thank you, Dr. Yusam. Thank you everybody. Thank you everybody for attending and have a great day. Thank you, you too.