 Okay, we're finished with trauma now. Let's talk a bit about mixed hearing loss because there are only a few diagnoses that cause true mixed hearing loss. Certainly you can have two different diagnoses, one causing sensor neural and one causing conductive hearing loss, but in true mixed hearing loss, it is a very limited differential diagnosis. The first thing we want to talk about here is otosclerosis. Otosclerosis is the most famous thing that causes a mixed hearing loss. It has a cochlear and a finestral form and I'll show you examples of both of those, but there are several mimics of otosclerosis that we need to keep in mind when we are in the setting of mixed hearing loss. One is otosophilus, which has become so rare that it is almost never seen, but the other two are Padgett's disease and fibrous dysplasia and if we are careful, we will be able to distinguish these radiologically. Here's our first example of otosclerosis. You must look very carefully for otosclerosis because it's often very, very subtle. When you hear the history mixed hearing loss, that's your cue. That is going to remind you to look very carefully in this one particular location, this triangle of bone between the vestibule and the cochlea. That triangle of bone is the region where the normal structure, the fistula antifinestrum, lives. Now we can't see the fistula antifinestrum, but we know it lives there, so we call this the region of the fistula antifinestrum and that is where the finestral form of otosclerosis is. This piece of bone, right here, this triangle of bone should be exactly the same density as the rest of the otocapsal and you see here that it is too lucent. That is otosclerosis. Some radiologists like to use the term otospungiosis here, but I've found that the surgeons don't care for that term. Here's another example of finestral otosclerosis and again, to show how subtle this is, it's this triangle of bone right here should be just as dense. There's another example, finestral form. Now there's another, later form of otosclerosis. This is cochlear otosclerosis and in this case, it's a more severe disease. You see a halo of lucency all the way around the cochlea. You can see it in the coronal plane here. If you see it on MRI, there is abnormal enhancement all the way around the periphery of the otocapsal. This is the more severe, the more advanced cochlear form of otosclerosis. Now, there's a couple things that can look a lot like otosclerosis and can cause lucency in the inner ear, but we don't want a mistake for otosclerosis because we see them in the setting of mixed hearing loss. If you look carefully, that triangle of bone, the region of the fissula antifinestrum is too lucent in this case, but so is everything else. And that is our clue that we're dealing here with Padgett's disease and not just otosclerosis. Fibrous dysplasia is another lesion that can cause a lucency surrounding the otocapsal in something this extensive. I don't think anyone would be fooled. You've got all these areas of ground glass, classic fibrous dysplasia. Fibrous dysplasia usually spares the otocapsal and so this is a good clue, but this can also cause mixed hearing loss and we'll be on our differential diagnosis. Okay, let me speak specifically about one particular diagnosis, superior semi-circular canal dehiscence. Superior semi-circular canal dehiscence presents with a symptom called Tulio's Phenomenon. Tulio's Phenomenon is dizziness in response to a loud noise. So for example, someone will walk into a party and suddenly get dizzy or a truck driver might say, when I walk down this side of my truck, I get dizzy but this side I'm fine and it's which ear is closest to the engine. It's causing the noise, causing the dizziness. Tulio's Phenomenon used to be associated with otociphalus but as otociphalus has diminished in frequency, we've started to associate it more with superior semi-circular canal dehiscence. So what's superior semi-circular canal dehiscence? That's when there is a hole in the bony covering that's normally covers the superior semi-circular canal. So pressure can go from the semi-circular canals into the cranial vault. And there can be transmission of pulsation between the inner ear and the intracranial vault. This is called a third window phenomenon. We should only have two windows. We should have a round window and an oval window into the inner ear. And the reason you have a round window is that when you press on the oval window with the stapes, the round window allows that fluid to shift. It's a carefully orchestrated scheme that allows this fluid to shift in one window and come out the other. If you add a third window on that superior semi-circular canal, it's all messed up. And those vibrations, instead of a nice neat shifting of fluid instead, the fluid comes out here, it doesn't shift right, and the whole system is messed up. So it's that third window phenomenon that allows this to happen. Now many people have advocated for the planes of Stenver and Pauschel as a way of carefully looking for superior semi-circular canal dehiscence and I'll show you what it looks like in those planes. The reason we need separate planes of imaging is it can be very near, a very near thing whether the superior semi-circular canal is intact or not on an axial image. So we need some help from reformatted images. So we are gonna take reformatted images along the superior semi-circular canal and perpendicular to the superior semi-circular canal. The ones that are perpendicular are the plane of Stenver and the ones that are along the superior semi-circular canal is the plane of Pauschel. So here's what it looks like in the plane of Stenver. This is a normal superior semi-circular canal, a nice bony covering on top of it. This one, dehiscence semi-circular canal, you can see there's no bony covering on the top of the canal. Plane of Pauschel, same idea. Here is a nice bony covering over the superior semi-circular canal and here there is a gap over the top of the superior semi-circular canal. But now I'm gonna let you in on a secret, you don't need the planes of Stenver and Pauschel. Your basic everyday coronal reformat is perfectly good for this diagnosis. It performs just as well as the planes of Stenver and Pauschel. They are fun to play with, but they don't improve your diagnostic accuracy. So if you don't like looking at that many images, this will do just fine. You can see the intact bone over the semi-circular canal on this coronal and the dehiscent bone over the semi-circular canal on that side. There are no classic imaging findings for Meniere's disease, also called idiopathic endolymphatic hydrops. What's happening here in this disease is that the endolymphatic cavity in the center of the membranous labyrinth is expanding at the expense of the surrounding perilymphatic cavity. And so this disrupts the normal fluid dynamics in the membranous labyrinth. So how can you tell the difference between the endolymphatic cavity and the perilymphatic cavity? You have to distinguish between them to note that one is enlarged at the expense of the other. Well, one way you can do this is you can put a needle through the tympanic membrane and inject some dilute gadolinium and then wait for 24 hours. And it turns out that the perilymph preferentially takes up the gadolinium and you can see this on 3D flare sequences. These produce beautiful images. They are very high specificity. You can definitely identify patients with Meniere's disease. But to wait 24 hours and then re-image is very inconvenient for patients and it's an invasive test. You have to put a needle through the tympanic membrane. If you don't like that, you can do something that's not quite as nice but still very useful and that's delayed post-contrast imaging. If you give intravenous contrast and wait four hours, again, the perilymph preferentially takes up that gadolinium and you can do high-resolution flare imaging and you can get good images. They're not as nice as the tympanic injection and they have moderate specificity. This is only moderately inconvenient because you're waiting for four hours. Still not very convenient. There's one other option. The other option is your usual SSFP or KISS or Fiesta sequences. This is part of every single examination of the interviewer that you already do. You're already doing this every single time. Now, if you use this, it has the lowest specificity. They aren't as pretty pictures. You're not as certain of your diagnosis but it's very convenient because you're already doing it on all of your patients and you can go back to patients that you've already looked at and look again. Let me show you an example of what we are looking for in endolymphatic hydrops here. Notice, if you look very carefully, that in this high, even though there's high T2 signal throughout the entire inner ear here, there's a small stripe of slightly darker T2 signal down the center. That is the endolymphatic cavity and the perilymphatic cavity is around it and normally it is just a very thin stripe like we see here. Very small amounts of endolymphatic fluid. If that endolymphatic cavity expands and more than about one-third of the vestibule has endolymph in it and now you can see how much larger the endolymph is here compared to here at the expense of the perilymph, that is suggestive of many users. Not diagnostic. It's not as good quality as these contrast images. It's not diagnostic but you can suggest the diagnosis and the patient may go on to more confirmatory clinical testing.