0:01 [snorts] 0:08 What's up, ninja nerds? In this video today, we're going to be talking about brain tumors. Again, this is a part of our clinical medicine section. If you guys haven't already, continue to keep going back, watch these in order. So, before we talked about breast cancer. After that, we talked about lung cancer. And today, we're going to be talking about brain tumors. If you guys are really liking these videos, they make sense to you, please continue to support us by hitting the like button, commenting down the comment section, and please subscribing. Also, if you guys want, if you go down in the description box below, you go to our website, there's a link there that'll take you there where if you guys become a member, you can have access to notes, illustrations, quiz questions. We're developing exam prep courses, and there's so much more. So, go check it out. All right, without further ado, let's get into the pathofizz, my friends. All right, my friends. So, we're going to talk a little bit about brain tumors. When we talk about tumors, you got a big old goober hanging inside of the head. We got to know particularly, is it a primary tumor? So, in other words, did it originate from 0:56 some of the tissue that's already present in the brain? things like astroytes or oligodendrites or swan cells or did it arise from something else? But it's basically tissues that were in or very very near the actual central nervous system or did it start somewhere else somewhere else outside of the central nervous system and spread and broke across the bloodb brain barrier to get into the brain tissue and that's called brain metastasis. So there's two different types of tumors that patients can form. a primary brain tumor and believe it or not this is actually less common. So when you actually look at the percentages of tumors that are primary this is somewhere around approximately 30%. Right? And then with brain metastasis that could be somewhere around approximately the remainder so which is about 70%. So this is definitely going to be something that you want to be more aware of. brain metastasis when you ever you have a tumor inside of the brain which again can manifest in a bunch of different ways which we'll talk about or can be seen similarly on an image that metastasis may look something like a primary brain tumor. It's important to 1:58 remember that this came from somewhere else and we'll talk about that. Let's focus our attention though because this is going to be the portion where you can get tested on for the exam. Primary brain tumors, as I said, arise from gile tissue or neural tissue or something similar, but it arises from some tissue that's native to the actual central nervous system. The way that we like to organize it to make things easier and categorize it for us is we base it upon the relationship of the tumor to what's called the tentorum cerebelli. You're like, "Oh, no, dude. The anatomy." Yeah, I know. But it's actually very easy. So, imagine here you have these dural septa. The big one that most people know is the one that comes right here, right down your fissure, right? That longitudinal fissure. We have what's called the faulk cerebri. Well, we have another one right here. And it goes right between the cerebellum and actually kind of the occipital and parietal lobe area. And that's called the tentorum cerebell. So, it's this little like piece. You see this blue tissue that comes here? You have what's called the perryostial layer 2:59 of the duramatter, which is that baby blue color. And the one that breaks away and dips into that space is called the meningial layer, the dermat. That chunk right there going in between this part of the upper lobe and then the cerebellum. That's the tentorum cerebelli. So let's actually write this one right here. That's a tentorum cerebelli. And again, this is a coronal section. So if you imagine I'm taking a section like this and I'm slicing this off and you're looking at this the actual brain that way. This one is a sagittal section. So I'm taking a section like this and I'm looking at the brain when I take that piece off. this way. Again, look, here's the occipital lobe. Here's the cerebellum. You see that t that tissue fissuring right in there? That's again the tentorum cerebelli. So again, let's write this structure out. It's a false I mean it's a it's kind of a dural fold or dural septa and it's called the tentorum cerebelli and we just sometimes call it the tentorum. Now imagine there's actually a hole. So there's a tentorum 3:59 cerebella that comes like this from both sides, right? And so it creates a little hold called the tentorial notch. The tentorial notch is where sometimes parts of brain tissue when brain matter starts actually getting under pressure, it can squeeze through the tural notch. We'll talk about that later. But what I want you to imagine is this tentorum cerebelli separates the brain into two compartments. So what I mean is everything above the tentorum cerebelli is pretty straightforward. It's called let's actually do this in red. This is called the supra tentorial compartment. And then everything below the tentorum cerebelli. So these structures here is called the infractoral compartment. The reason why this is so nice is that whenever we actually have tumors, we can determine if that tumor is again present here. So if I have a tumor that's actually present inside of the cerebellum, what kind of tumor would I call that? I would call that an 5:00 infrontal tumor. If I have a tumor that's somewhere located up here in the frontal parietal loes or things like that, this is a superal tumor. That's really important. And the reason why this is important is superentorial tumors which we can find up here above the tentorum cerebelli are more associated with adults. So when I think about a super tintorial tumor I'm thinking about it's more likely and more common to see this in an adult patient. Whereas if I had a tumor here in the cerebellum or near the fourth ventricle or near the vermis here that infratorial tumor is most associated with pediatric patients. Do you see why this is an important epidemiological fact? So again tentorum cerebelli is your landmark above it superentorial that's where tumors occur in mo mainly adults. There's a few exceptions. And then infrinurum or that compartment if a tumor is there, it's an infrontatorial tumor that's associated with pediatric 6:00 patients. Now brain metastasis is interesting. So again, we use our landmark here. What's this landmark again? It's called the tentorum cerebelli. Let's just remind oursel of that. And again, the purpose of the tentorum cerebelli is really to be kind of like a it's really just imagine it imagine like a a fold that encloses uh veins. So it's supposed to protect some of the veins that are actually present there. Now this centurium cerebelli what's really important is with brain metastasis it's not just one location where the tumors occur. Brain metastasis is interesting. You can have a tumor that can occur here in the superentory. You can have another tumor that could still occur in the superentory. You could have another one that occurs here in the infrintorum. So, one of the interesting things about brain metastasis that makes it different is usually primary brain tumors are more solitary. You usually have one big 7:01 tumor. Brain metastasis is usually interesting in the fact where you can actually have so let's bring all these here there's one tumor there's two tumors there's three tumors so with this you can have multiple brain masses right whereas in primary it's often times more solitary now here I want you to remember this is not always the case just because a patient has brain metastasis they they can have just one tumor it's just the way that they're going to talk to you about on the exam is it's usually going to multiple brain masses and these brain masses can be both superentorial or infratorial. So here's what I want to add on to this. So with brain metastasis something that is important. So here we'll put important to remember so that way you think about this when it comes up on the exam. Usually this patient will have an underlying history of a primary cancer. But here's the big thing on imaging. Whenever these patients come in and they get imaging, if you see 8:01 usually multiple brain lesions, that's one thing, but they have a very characteristic location. All right, so again, multiple oops, I forgot an L here. Multiple brain lesions. But one more thing is also important that it occurs most commonly along the gray white junction. So usually the outer cerebral cortex is gray matter and then inside is white matter. Right at that junction is where we see those tumors. So they occur that's what's really characteristic occur at the gray white junction. And lastly what's important to remember is they can occur in both tentorum. In other words they can be infra or supra tentorial. They don't always follow that classic presentation. As we said, super tentorial tumors are usually adults. Infronttorial tumors are usually pediatrics. There's a few exceptions. These can occur in any and sometimes 9:01 both. They're usually along the grey wide junction and usually have multiple scattered lesions. Really important to remember. All right. Primary brain tumors. I want to dig into this a little bit because we talked about the tumors that can occur superily and infrinally. Let's talk about some specific characteristics. So, we talked about this one a lot. Let's talk about each individual one and get a good understanding because sometimes they can test you about this on the exam. Again, you may see it more in your step one MCQs, but it sometimes can come up relevant within the step two clinical vignettes. So, let's say we talk about superal tumors. Again, I want to highlight here that we say for the most part this is adult. There is two exceptions of where a patient can have a a tumor as an adult and it's not present in the superentory. I'll talk about them because they're in the infrinurum. Two exceptions. So we'll actually let's write that out here. Um two exceptions to this is going to be two tumors. One 10:03 is called a hemangio blasto and the other one is called a schwanoma. So we say heangio blasto and the other one is called a schwanoma. These can also occur in adults but they're actually in the infrinurum. So that's one little exception to think about but for the most part it's going to be these particular tumors. All right. So the most common malignant tumor, the scary tumor that's a primary brain tumor is what most people refer to as glyobblastoma multififor. It's a type four astrocyto. What happens with this one? Let's actually write this out. It has a precursor. So it has to start I told you brain they start from somewhere else. It spreads via the blood and it gets to the brain breaks across the bloodb brain barrier. These arise in the brain tissue. So some type of tissue in the brain had to become mutated and then 11:04 turn into a malignant cell. That cell that precursor is actually a astroite via the name. That's why we call this is a stage 4 astroytoma. So it actually arises from astroytes that develop mutations. Usually it's in the um isoccitrate dehydrogenase enzyme. What happens is location is key for a tumor. So you want to know location. So remember I told you super tentorial is going to be all of these but sometimes when we look at the image on the MRI or the CT scan we actually want to know where is it most characteristic of what what is the tumor most characteristic of and so location for glyopblastoma multififor is usually frontal or temporal loes but here's the thing let's say here I start off with a tumor here's my glyobblastoma multififor right all of a sudden I see this tumor here it's in the frontal temporal loes but here's what's characteristic you see this structure it's actually fibers that go across from communicate side to side. It's called the corpus colossum. This tumor can span across the corpus colossum. And what it 12:06 does is when it spans across the corpus colossum, it actually tries to give I'm not even kidding. They call it this a butterfly look. It's called a butterfly glyoma. So what we talk about locationwise is usually it's a tumor that when we see it, it spans across the corpus colosum. That's the big thing is it can move from one hemisphere to the other. So it spans the corpus colossum. And so this is one that's really really scary. It actually ring enhances and it looks I'm not even kidding. Has that butterfly. Let's actually write that out. Just so you know, it's called the butterfly. The butterfly glyoma. And we will talk about this when we get into the diagnostic section. So just hang in with me for that point. Now all right. Glyobblastoma multififor it's astroytes that started off normal mutated became a nasty tumor and then grew like this is a stage four this is a bad prognosis the most common malignant tumor in adults with that being said the most common 13:08 benign tumor it's usually benign there is chances of it being malignant but it's not always the case is a meningioma this is the most common benign uh tumor brain tumor superal tumor in adults with meniomas what happens is you see See the blue tissue here? That's called the arachnoid matter. Now the originally we said there was a dura matter but remember there's different layers to the meningis. There's dura then there's arachnoid then there's pia. We're going to represent this blue as being the arachnoid matter. I know we prior we talked about as being the dura but in this case I'm going to represent it as the arachnoid matter. There's cells in there that are actually called arachnoid cap cells. So the precursor cell is going to be what is it again? Come on, spit it back to me. Let's go. The arachnoid cap cells. It's called the arachnoid cap cells. Now, these cells were once normal. They decide to get all jacked up. And what happens is they mutate and they start to become abnormal. What they do is it usually 14:09 most common location. So remember this structure here, it's called the faulk cerebri. It loves to form right around that area. And so imagine here, I'm going to get rid of some of this tissue because it actually is what we call an extra axial tumor, meaning it occurs outside of the parankma. Isn't that crazy? So, [snorts] here I'm going to get rid of some of this brain tissue here. And what I'm going to do is I'm going to take this this tissue here and make it kind of bulgy. And usually it it kind of has somewhat of like a kind of a crescent shape to it sometimes. And it can really get these things can get super super big. I've seen some pretty large meniomas um in the neurocritical care. So now look at this thing. It's smooshing on brain tissue. That's a meningioma. And funny enough, they form these things which really anchor them down called dural tails. They really really hold it down. But it's basically a tumor that most often occurs within the um sides of the faulks. And so we say they're often times parasagittal. They can occur really anywhere, but the most common location is right on the side of the 15:09 faulk cerebra. So we call that parasagittal. So let's write that down. location of where it is most often seen [snorts] is the parasagittal region. All that means is on the side of the faulk cerebri. So it's usually a um alongside the faulk cerebri. All right. And all I want you guys to remember is we often say that is called parasagittal. All right. Cool. We got the meninge down. All right. spans corporal scosum GBM it's occurring within the parasagittal regions makes kind of a more of a crescent shape menioma most common malignant most common benign we go to these two these are less common but there's something to definitely consider this is called an igodendro now it kind of occurs in somewhat of a similar location as GBMs it's usually frontal loes it can actually be sometimes bilateral but most of the times what we see is we see a tumor that often times occurs 16:11 in the frontal loes [snorts] and it has a lot of heavy calcifications. One of the big differences is look at this. This one may have started in the frontal lobe. Does it cross the corpus colosum? No. That's really high yield to remember. But it's also important to remember what does it start from? Well, look at the name. This one may have been hard to understand. Glyobblasto, but I want you to remember it's a type of astroytoma. Astroytes alodendro. Take a second. Think about it. What type of gile cell could that be? Alodendroytes. So it arises from your oligo dendroytes. They become mutated. They get jacked up. They start to multiply and they occur where in the frontal loes just like you can with a GBM. Big difference here is this does not cross midline like the GBM does. That usually crosses midline. So, it's usually frontal loes, heavy amounts of calcifications, and also this one doesn't have that 17:12 significant degree of ring enhancement as GBMs do on MRI with contrast, which we'll talk about in the diagnostic section. But again, big thing does not cross. [snorts] No crossing of midline. All right, that's really important to remember. Does not cross midline like the GBM does. Pituitary adnoma cranophreniomas. These I like to group together because funny enough they tend to occur in the similar location. So let's start off with the pituitary adenoma. So with the pituitary adenoma, what I want you to know is this starts from specific cells. The most common type of adenoma is usually from lactoroes. So there's all these different types like you know you have the corticotroes you have the sematroes you have the thyrorroes all of those that produce hormones which type of cell usually develops a lot of them is the lactoroes and lactoroes make what 18:14 hormone come scream it out to me prolactin. [snorts] So often times when you get a pituitary adenoma the precursor if you will is going to be what it's going to be lactoroes. So, it's going to be often times it's going to be those lactoroes. Now, here's another really important thing. When these occur, they occur where? Well, they're right on the pituitary. It's usually around the anterior pituitary. So, location is we just like to call this, we like to say it's around the celotica. That's that anatomy term that we like. It's usually a cellar. We call this a cellar mass, meaning it's a mass. And we're going to represent this here again. It's a mass occurring in this little groove here. What is that? The celotica. It's a saddle. So that tumor is sitting in the saddle. And it's usually along the anterior pituitary. Cranoparangiomas. And they love you got to pay attention. Wake up. I know. I know you're tired. I 19:15 know. Believe me. I get it. But hang in with me for a second. Pay attention right now because this could be a test question for cranial freniomas. They also like to occur in this area. They occur again, they can kind of really get to decent sized and they can actually start to engulf. Let me actually do a different color. Let's do it just for the sake of it. Let's do it in like this pinkish color here. So I'm going to say cranopangiomas. They kind of get here and they can get a little bit above the pituitary. Right now here's the big term here. This tumor arises. It's a you know there's what's called the wraths pouch. There's a remnant of the Wrath keys pouch and this thing right here really starts to kind of get around the posterior pituitary and around the stalk and just mashes on that son of a gun. So this one I want you to remember precursor is going to be Wrath's pouch. Write this down. Keep it in your brain. It's the remnants of the Wrath geese pouch that sometimes they'll ask that. And this is a little 20:17 bit digging into your embryology locationwise. It's still in the celotica, but it can sometimes just get a little bit above that. So sometimes we actually consider it to be like a cellar or supracellar mass, but they're often times we kind of say they're very very difficult to completely distinguish and sometimes you need the tissue to really get to that. But we'll say that this is again going to be more of a supra seller mass, but they are relatively close in proximity. So what I want you to take away from this is primary brain tumors if it's above the tentorum cerebelli it's super tentorial. Those are mostly adults. Two little exceptions to consider just to add that into the brain space there. But the big ones GBM what do I want you to take away from it? Frontal loes crosses midline via corpus colosum. Alendentricoma frontal loes does not cross midline. Menioma is not even a part of the brain. This one it's actually important to remember this term. This is extra axial that means 21:19 that it does not actually arise from the brain parankma. So extraaxial where along the side the faulk cerebra parasagile pituitary and cranophreniomas near the celotica. If I said one is from lactoro you say pituitary adenoma. Most likely it's called a prolactinoma. And if I say it's coming from rakey's pouch remnants you would say cranoprrenioma. And we'll talk about this again, but remember Rathy's pouch, it's kind of derived from the nasoparangial mucosa and it kind of migrates backwards. That right there, there's remnants of it that actually occur and that's what causes that kind of cancer. All right, we now have an idea of location. So when we get imaging, we can kind of say, ooh, it's in this location. Does this it could be this one. Often times though, you got to get the tissue to make the definitive diagnosis. Let's say now I talk about tumors below the tentorium cerebelli. They're infratintorial. I told you that these were for adults. I 22:20 bet you could make some kind of assumption here, couldn't you? Let's make an assumption here. My red marker is starting to suck a little bit here. Let me switch it over. Switch it over to this bad boy. Infanttorial tumors are usually pediatrics. So, let's write that down. That's going to be something you see. Ooh, look. Look at that. Look how juicy that is. The pediatric population. All right. Now, with these again exceptions is the schwanoma and the hemangio blasto. These st can occur in the pediatric population. Don't get me wrong. Um but these again can also be in adults. So there's always like these fine-tuned exceptions but for the most part the biggest one is pyocitic medelblasto appendimoma and again these ones can also still be in the pediatric population but again these oftent times we see them a little bit more in the adults. Pyocitic astroytoma again below the tentorum cerebellic pyocitic this is 23:21 a tumor where usually precursor guess what it's the term astroytoma this is a a grade one so there's always grade one grade two grade three grade four so grade one is your pyocitic right grade four is glyobblastoal multififor so this one is actually the most common type of usually we would say benign um uh brain tumor in the pediatric population. Now, precursor here, it's actually pretty straightforward. It's within the name, thank goodness. But what's the precursor, my friends? It's astroytes. Now, I know you're probably like, "Zack, can I just really just say simply that these tumors that really when I talk about them, they're present specifically in just the infrinurum or the supertorium?" Yeah, you definitely can. But again, it's important to remember that when we talk about the location of these, we can have a little bit more specificity. We're going to be good clinicians. So location-wise, when we look at this tumor, it's often times more in the cerebellar lobes. And these can be 24:23 pretty like large and cystic appearing. So this right here is going to be where you would see your pyocyic astroytoma. So locationwise, it's usually going to be in the cerebellum. So it's usually within a cerebellar hemisphere. All right. Now my next one is medeloblasto. This is actually the most common malignant type of uh infratorial brain tumor in the pediatric population. Now precursor. This one actually has doesn't have a good name. You're like, "Oh, it comes from the medularary tissue, bro." No, it doesn't really come from the medularary tissue. For this one here, let me set up here for a second here. Um for melastoma what's really important to remember this one is this actually arises from neuroectomal cells. So let's actually talk about this one here. Here's my precursor cell. This one is actually from neuroctomal cells. So called neuroectomal cells and they're kind of like primitive 25:25 parts of it. But here's what I really want you to remember. When we talk about the medeloblastoma, the location is usually the big big one to remember here. So locationwise, it loves to occur. So here's your lobe of the cerebellum. Here's a lobe of the cerebellum. Guess what's right here? You have this middle part of the cerebellum. It's called the vermis. That's the most beloved location for these medular blastoomas. You know what's also really, really scary about melastoomas. And this is definitely a test question. So perk your ears up here a little bit right now. I want you to really really pay attention. So again, location is definitely going to be the vermis. So the cerebellar vermis. Here's what's really interesting. This tumor is super scary. And guess what it can do? The tumor can actually get really close to the fourth ventricle. It can seed into the fourth ventricle. If it gets into the fourth ventricle, where does that go? Fourth ventricle comes out. You have the superior apertures, the superior and medial apertures. And then it can also move downwards into the central canal. Where's the central canal move? down through your spinal cord all 26:26 the way down to the lumbar spine. This melasto is high risk for what's called drop metastases. I want to write that down. So, this one has a very high risk for what's called drop metastasis. So, meaning that this thing can spread. It can spread metast Oh, I said stasis twice, bros. Come on. Metastasis. So it has a very high risk of drop metastasis. All that means is that these tumor cells can get into this the actual fourth ventricle in the cerebral spinal fluid and can seed through the cerebral spinal fluid. Tell me that's not scary. So sometimes what you actually have to do is when a patient gets diagnosed with medal blasto you also have to do an MRI of their spine to make sure that the actual tumor hasn't spread to other parts of their spine via the from it doing the drop metastasis. But that's just a little factoid I wanted to tell you about. All right. appendimoma. With appendimomas, [clears throat] this one's actually kind of nice because 27:26 you think about appendimoma, that's the appendimal cells. Oh, boy. Oh, daddy. So, precursor cells here. This is the appendimal cells. So, if I got my appendimal cells, the one thing I want you to remember here is that these things really occur within the fourth ventricle. So they usually arise, it's a tumor that seeds itself within the fourth ventricle. So this one can also spread, believe it or not, via drop metastasis. It's just we see it more common with medulas for some reason. But locationwise is very key. So if I ever kind of like just popped quizzed and said, "All right, tumor that occurs in the ver medelastoma, tumor that occurs in the cerebellar lobe, pyocitic acroytoma, tumor that occurs in the fourth ventricle, you would say appendimoma." So that's a really important thing to be able to remember just like if I said hey tumor in the frontal lobe crosses corpus colossum GBM tumor in the frontal lobe does not cross the corpus colossum aloendricoma tumor that's actually located again within the um the extraaxial parasagile 28:29 region menioma tumors that are within the celotica pituitary adinoma or cranopioma right so you get the point of why that could actually be helpful so now we got this down the next one to think about here is a mangoblasto as heangobblastoomas can kind of be somewhat tough to differentiate from pyocitic acroyatomomas. We actually have to think about these a little bit but usually um I'm going to do this in a different color for a reason. These are actually going to be like from vascular tissue. So it originates from vascular tissue and it also likes to occur within the cerebellum. So within the loes of the cerebellum problem is heangoblasto can also occur other places. They can occur in the retina. You know where else pyloitic astroyeromas can co occur? They can occur in the optic nerve. That's one thing they can test you on. So pilot acidic athoma remember optic it can occur in the optic nerve. Optic glyomomas heangoblastto can occur in the cerebellum as well as the retina. But they also have other tumors associated with this is actually associated with what's called von hippolindow syndrome 29:31 which we'll talk about. But again precursor is the key thing. So if I said what where does it arise from? It's actually arising from a vascular tissue origin. So I just want you to remember it arises from vascular tissue. All right, but here's the big thing is again where would it be located in the infrontium and locationwise it's just usually in more within a lobe of the cerebellum. You're not going to find in the vermis you're not going to find it in the fourth ventricle. You're going to find it more within a lobe. All right. So usually this is going to be within the cerebellum itself. All right. This next one's really really important to remember. It's called a vestibular schwanoma. So schwanomomas these are cool these are often times associated with neurop fibromyitosis particularly type two which is a type of genetic syndrome but with neurop fibromytosis type two you can actually get bilateral vestibular schwanomomas schwanomomas are usually tumors that okay here we go so look here's their pawns right here's our pawns here's the cerebellum and here's the vermis the fourth ventricle the tumors usually occur right on the the junction of where 30:34 the cerebellum and ponds kind of eat. So we call this the cerebellar pontene angle or the cerebellar pontine angle. So let's actually write this down. So precursor Oh, I bet you like this one. What would the precursor cells be for this? This would be the Schwan cells. Yeah. So this is from our Schwan cells. So they become malignant. This is usually This is usually a benign tumor though. It's usually more of a benign tumor, but locationwise is really, really critical. Where is it going to be located? It's usually here at the cerebelloo pontine angle. So again, where is it? Cerebelloo pontine or pontine angle. This is a very very very important one to remember. Okay, so schwanomomas right there on the sides of the ponds where it joins with the cerebellum. Really important one. Last one's a funky one because you really 31:34 when you look at it pineal here's my tentorium cerebella. So some people be like, "Bro, Zack, come on. Look, here's my tentorum and all of these. Here was the tentorum, but it was below cuz we're all talking about cerebellum and near brain stem. All of these make sense." But then you look at pineal. The pineal gland is kind of within the area of the dianphylon. So you'd be like, how does that kind of fit? Well, really what kind of happens is we kind of consider this tumor when it originates from the pineal gland. It kind of dips down here in below the infrin uh below the tentorium cerebelli and compresses and kind of starts to move in through the tentorial notch to the midbrain. So that's really where the pineal starts is that again it starts from the pineal gland. I don't know I was writing that. So this is actually supposed to be precursor. So precursor this is going to be from the pineal gland. But the big thing here to remember is really when you think about 32:34 it, it originates in the dianphylon, but the tumor tends to spread just a little bit more into the dorsal midbrain, which is technically below the tentorum cerebelli. So when we talk about location, location, location again, the big thing to remember is we really consider this to be more of a dorsal midbrain tumor. So we say it's more of a dorsal midbrain especially lots of compression there. We'll talk about the characteristic features that suggest a dorsal midbrain tumor like a pinealoma like paranal syndrome. We got a lot here that we talked about my friends with tumors primary brain tumors less common but arise from tissue that's native to the CNS. Brain metastasis. These ones are usually coming from somewhere else outside the body and going to the brain tissue. Much more common superal tumors adults. I want you to think about the differential. GBM, aliodendrioma, menioma, cranophrenoma, pituitary adenoma, infratorial tumors more common 33:35 in pediatric patients. Pyocitic astroytoma, merolast, appendimoma, hemangioblastoma, schuanoma as well as the last one here pinealoma. When I from this tell you metastasis, it's usually not as much of a solitary tumor where primary tumors are more solitary. Metastasis, it's usually multiple lesions. They're scattered. They're diffuse. Gray white junction is really important, but they can occur in the superentory or the infronttorium or both. Now, let's move in really quickly to talking about the causes of metastasis and the causes of these tumors forming. We got tumors in the brain, right? You got these you got these honkers hanging out there. We got to understand again more particularly we're building our foundation, right? So I know it seems like Zach I feel like we're talking a lot about the introduction stuff. We are we're going to we're going to get some more of how this clinically applies, but we got to build our foundation. So when we talk about brain metastasis, we have to know where are these tumors coming from? Because as you kind of go in and you actually evaluate a patient who comes in 34:36 with clinical symptoms, things like headaches or focal neuro deficits or maybe they have papa edema or they're they're having nausea and vomiting and they have particular diplopia and I don't know just a bunch of different symptoms that scream that there's something in like structurally going on inside of the brain that would make you start getting imaging. Once you obtain that imaging then you would find oh this is a brain mass and you could use the things that we talked about to kind of think about it. But what I want you to think about is also if a patient's coming in and they have these symptoms, you get a bunch of different lesions on their MRI or their brain CT, you have to start thinking, okay, could this be metastasis? Look through their history. Do they have a history of a primary cancer that could have spread? Or if not, I got to go look and make sure that I rule out that primary cancer from the lungs or somewhere else. So where are those primary cancers most likely going to be that spread to the brain? So oftent times it's going to be most commonly a tumor that comes from the lung. So lung cancer by far is going to be the most common cause for brain 35:35 metastasis. And when I talk about these, I'd say with that caveat that it's most likely small cell lung cancer. You can see it in the non small cell, but again, it's going to be way more common in small cell lung cancer. The [snorts] next one's breast cancer. Again, when I talk about breast cancer, there's different types of breast cancer, but breast cancer usually when it's more likely the most common car uh type, which is invasive uh ductal carcinoma, right? The next one is renal cell carcinoma. Renal cell carcinoma is a really important one to remember. The other thing that's actually really important to remember that kind of sucks, it's really really sad with any of these tumors, right? If it occurs here originally, occurs here originally and it spreads These when they get to the brain, really all of these except for this one when I'm going to talk about this one next. When they get into the brain and they actually break across the bloodb brain barrier and they form that mass, they actually can cause hemorrhaging within that mass. And so you can actually get what's called hemorrhagic metastasis. So you can get bleeds in the brain, 36:36 especially from lung cancer, breast cancer, renal cell carcinoma. And the next one here is a particular type of skin cancer. This one is obviously the most malignant and scary type of skin cancer. It's not squamus. It's not basil cell. Yes, you got it. It is melanoma. Melanoma is that scary one that if it metastasizes to the brain, it can cause pretty nasty hemorrhagic metastasis. So, all of these can cause hemorrhagic metastasis. This one is actually I'd say one of the least common ones, but it is something to consider if a patient has underlying cancer of the uh large intestine or the rectum. So, colarctyl cancer is also another one that should come up. And also, we'll talk about this a little bit later, there's specific genetic syndromes that predispose certain patients to having brain tumors and colloctal tumors. We'll talk about it's called Turco syndrome. But when I talk about all of these, it's really important to remember that this is the most common, second most common. These right here, when they spread to the brain, they actually cause bleeding to 37:38 occur. So, hemorrhagic metastasis. This one less common, doesn't usually cause hemorrhagic metastasis. How do I remember these? Because a lot of times it's hard to remember all of these. Lots of bad stuff kills the cortex. L obviously for the lung. Bad is going to be for what? The breast. S is going to be skin. So I want you to think of skin. When you think of skin, you think of melanoma. When you K kills, think about kidney. And when you think about kidney, I'm going to abbreviate this renal cell carcinoma. When you think about C, you're going to think about what? Color rectal cancer. All right. So those are things I want you guys to be thinking about here as potential causes of something that spreads to the brain. Again, they occur here and then what happens is any of these tumors, what do they do? They take they get into the bloodstream and they spread and get into the brain. They break across that bloodb brain barrier. All right, let's get into the primary brain tumors. Okay, so we got the the the the meta metastatic causes down. What about primary brain 38:38 tumors? We don't really have a lot of good reasons as to why these dang things happen. A lot of the times one of the ways it's it's you know we as as clinicians I'm going to get on my soap box just for a second I promise when you when you do imaging and it comes with radiation you run the risk of potentially giving a patient there is that chance of cancer you're giving radiation that can damage DNA cause mutations and if those mutations don't get repaired properly you bring about the opportunity for this to transform into a malignant cell and cause cancer. So, when patients are getting frequent radiation, this I'm not even kidding. This could be things like just getting CT scans very frequently, getting um whole brain radiation therapy, any of these kinds of things right here, this can potentially stimulate this cell to undergo a mutation. So, it can stimulate, let's actually make this very, very clear here. It can stimulate a mutation. If you stimulate a mutation, you bring about the opportunity of this 39:38 normal glyial cell or some type of brain tissue of the CNS turning into a malignant cell. And this is when you can get tumors. All right, that's one reason. A lot of the times though, we don't really have a good reason. They had no exposure to ionizing radiation. It just happened. It's unfortunate. You got the crap end of the stick here. What happens is you have usually just like these progenitor cells. These are cells that can really become a specific type of gly cell. So here's our progenitor cell. If the progenitor cell for some reason develops a mutation, usually the most common mutation that you want to think about and test for is called the iso citrate dehydrogenase. And there's one and two. This mutation if it occurs it causes the progenitor cell to turn into a gile cell tumor which we call and we term a glyoma. So let's actually I'm going to make this blue line here so just so I can have some room. This is called a glyoma. 40:39 All right. Now if I have a glyoma the problem with this is that this glyoma can then decide do I want to become another type of tumor cell or another type of tumor cell. If this then develops another type of abnormality within the genetics and we call this abnormality a I know this is a lot trust me but it can be tested on. On chromosome number one you have that short arm. If that becomes mutated, you have a deletion. Plus on chromosome 19 on the long arm, if that becomes deleted, this can transform this glyoma. All right? If you develop this type of mutation here, this can transform this glyoma into a malignant oligodendrite. So this would then become what's called a oligo dendro glyoma. And now this thing can start replicating, replicating, replicating. and you get this brain mass that forms. All right? 41:40 If you don't get the one p 19 co-deilion, but you develop other weird mutations, maybe maybe it's in the TP 53, right? So the p-53, which is a tumor suppressor gene, maybe that becomes mutated. Whatever it may be, that mutates and it becomes a nasty cell, but there's no deletion. That's the key. No deletion present here. We'll even write this down just so we're super clear. One P. There's no one P 19 co-deion present. If that happens, this turns into what's called a astroytoma. So you get the point here. We can get brain masses from ionizing radiation exposure continuously or just sporadic mutations due to unfortunate genetics. Idh mutation can occur in both of these but an IDH mutation and a 1p19 QC code deletion suggests oligo dendro glyoma. 42:41 Really important to remember oftent times this helps us because these types of uh codeions and mutations tell us if a patient will respond well to a specific type of chemotherapy called teosolomide. All right, that's why I mentioned that. Another reason why these brain tumors can form inside the essential nervous system because of these gly cells just mutating not just because of radiation not just because of sporadic mutations but it could also be due to genetic predisposition from weird syndromes. One is called neurop fibromyitosis. There's a type one and type two. What I want you to know is that neurop fibromyitosis type one is often seen and it's associated with pyocitic astrocyto. Now that's one thing. Neurop fibromyitosis type two is often times associated with a couple of them. It can be associated with appendimomas. It can be associated with meniomas. And we'll write those down. So appendimomas, meningiomas. There's one really, really 43:44 important one. It's bilateral vestibular schwanomomas. That is what I want you to remember. So what I'm going to do is I'm going to kind of say that this is the important one to remember. Bop neurop fibromyitosis type two bilateral vestibular schwanomomas are the awesome thing that they can be tested on on the exam. Now one of the things about neurop fibromyitosis it can cause like weird neurop fibramomas to form. But one of the things that they'll test you on the exam that are often times associated with nerve fibromyitosis is skin lesions. And um I want to actually show you what they look like. These skin lesions are called cafe allett spots. They look a little bit like this. So whenever you see these kinds of spots, I want you to think about neurop fibromyitosis. And if I said type one pyocyic, if I said type two, I really want you to think about bilateral vestibular schwanoma. The other thing that's really important here is pyloitic astroytoma for type one usually, just 44:45 remember this, it's on the optic nerve. Remember I told you it can occur in the cerebellum. Where else it's going to occur? Optic nerve. If it's associated with nerve fibromyitosis type one, it is optic. So look for a patient who has weird skin lesions, cafe aliot spots and optic nerve compression, bilateral vestibular schwanoma. Think about cafe spots plus tumor that's located within the cerebellar pontine angles. Now that deserves a little time to talk about something. When we see a patient come in with this triad of symptoms, think about tuanomas. What is that? Well, one is they'll come in with what's called sensory neural deafness. That's one thing. Second thing that they'll come in with vertigo or balance problems. And the third thing that they can come in with is tonitis. So if a patient comes in with tonitis, which is ringing of the ears, if they come in with balance issues and if they come in with sensory neural deafness, 45:45 not and so there's conductive deafness and there's sensory neural deafness. We actually have to use what's called the Weber and Renee test to really determine that sensory neural deafness, vertigo, and tonitis really suggest a vestibular schwanoma. And if it's on both sides, it's associated with nerve fibromyitosis type two. If I said optic leoma and cathallet spots, you would think neurop fibromyitosis type one. All right, cool. The next one is turo syndrome. Now, I know I'm not even trying to be mean. This is usually someone that where they use like they use different tricks of thinking about a turban. There's brain tumors that are also associated with colloerectyl cancer. So there's two tumors which kind of go hand in hand. So usually patients can have like colorctyl polyps which put them at high risk for cancer, right? So it puts them at high risk for cancer and they can also have two different types of brain tumors that can be associated with these colctal polyps. Lots and lots of polyps. So they can have lots of polyps, lots of them that can be associated. can lead to 46:46 cancer. The other thing is that you have two different types of brain tumors which can be associated with this. One is called a glyobblastoma multififor or it could be a medelo blasto. The one that's often times more tested than not is going to be this medelo blastto. So you're going to think about a child who comes in with symptoms of infrarctoral tumors and who now has a ton of polyps in their intestines. There's actually different types of variants of Turo syndrome. There's the Lynch variant and that's associated with GBM. So that's actually due to a mismatch repair kind of problem. And so usually that can be associated with like colctal cancer, endometrial cancer, ovarian cancer, but also can be associated with GBMs. The FAP variant, which is the familial admitosis polyposis, they have tons and tons and I'm talking just tons of polyps in their colon at a young age. 20-year-old with hundreds upon hundreds of polyps in their colon plus a brain tumor like a medaltoma. This is the one to remember. 47:48 That's the one they'll test you on with turo syndrome to turo syndrome colarctal polyps and I mean tons of them plus a tumor in the um usually an infratorial compartment cerebelleris measurlast that's something to remember. All right multiple endocrine neoplasia type one this one is associated with three particular tumors. I know we talked about this in endocrine. you have men one that's the three Ps it's pituitary adenoma it's a parathyroid adenoma and it's a pancreatic tumor right so let's actually write those down so again we had them right here to remind us it's a pituitary adenoma right all right so you'd have a tumor right here it's a parathyroid adenoma and this is going to be associated with what hyperarathyroidism usually and then there's going to be a pancreatic tumor and usually this is associated with what's called zolinger Ellison syndrome releases tons of that gastrin that can cause peptic ulcers so pancreatic tumor when I talk about this is the three Ps. So remember the three Psuit, [clears throat] parathyroid, pancreatic. If I said MEN 2A, just to test your 48:48 knowledge a little bit, it's two P's and one M. So it's actually parathyroid tumors. They have fiochromosytoma and medularary thyroid cancer. And if it's men 2B, it's two M's and one P. And so for that, it's meillary thyroid cancer. It's a morphonoid body habitus and it's usually focytoma. All right, next one here, von Hippolinda syndrome. This one is actually really high yield. This is a mutation that occurs on chromosome number three and it's also associated with this type of triad. And usually what happens here is you get the tumor that's occurring due to vascular tissue origins inside here inside of the cerebellum, but it can also occur in the retina. So it can also occur in the retina. Which one's that one? Heangio blastoomas. So you can get a heangio blastto and again two locations because we're talking about brain tumors we really care about the one that's occurring inside of the brain but it can occur where else just to remind yourself let's draw where else could occur here in the retina. All right the other component here is what a 49:51 tumor here renal cell carcinoma. All right so renal cell carcinoma is also associated with this one. And then the last type of tumor here that can also be associated with this is you can sometimes get a tumor right here in the adrenal medadulla. What's that called? Fiochromosytoma. So you can get a focytoma in multi multiple integrated neoplasia. Right? But you can also have it here in von hippolinda syndrome. So fo chromosoy. So if I told you hey bilateral vibilwano you would say nervetosis type 2. If I said optic gloma, right, and I told you it's a pyocyic one, that would be nerve fibbrintosis type one because they're associated with the cafe alat spots. If I said, oh, this patient has potentially a ton of polyps and they're 20 years old and on top of that they have a tumor in their mid their uh their cerebellum. You would say this is turo syndrome. If I said that they have three different tumors, it's the three Ps. You think about men one. And if I told you that they have uh they're a young child and they have tumors inside of the retina and in their cerebellum, they also have renal cell carcinoma and 50:52 fiochromosytoma. we think about von hippo lindow syndrome my friends this covers really the causes and kind of gives us an important kind of understanding of how these really tumors form now that we've done this what I want to do is I want to say okay patient comes in they present with these symptoms how do I actually get to the point where I can then say let me move through think about these symptoms determine my diagnostic approach and then from there determine the proper treatments and one of those treatments is going to be getting imaging to figure out what does it fit in and maybe getting biopsy ies to figure out what is the tissue makeup and then thinking back to their history what could have caused this. So now that we've done that let's move now into the next step which is thinking about how they will present. All right so now we have a patient coming in they're presenting with classic findings of brain tumors. What would that be? Well there's a there's a triad but just because a patient comes in with a headache like don't just be like oh there's there's definitely a tumor up there. No there's there's specific ways that patients present a 51:48 headache could be a tension headache. It could be a migraine. It could be a cluster headache. It could be from a lot of different things. It doesn't mean that they got a big old tumor hanging out in their their cerebrum. So, you have to kind of think about this. There is specific red flags that may make you decide to get a image of a patient. So, if the patient says, "I got the the worst headache of my entire life. It's a thunderclap headache. Get an image." Another thing that may, it's not as like a great of a red flag, but it's something to consider is if a patient comes in with a headache, and that headache is usually it's worse in the morning. All right? So, it's worse in the A.M. Now, you can also get this in patients who have obstructive sleep apnea, but that's one particular thing. The reason why is is this headache is usually due to elevated intraanial pressure. And so, whenever they're laying flat and then they get up in the morning, that usually is one of the big reasons. oftentimes it gets a little bit better during the day is if they're upright and they're moving because it helps to move the cerebral spinal fluid and um I'm sorry the um venus blood out 52:46 of the brain. Another thing is that it's also associated with nausea and vomiting. So if they have vomiting right away in the morning, that's also concerning. So it's usually associated with nausea and vomiting in the early A.M. Those are things that should definitely concern you. The other triad that you want to be thinking about here, and this is what really if a patient comes in with a headache and they also have this, this is another reason to scan them, get an image of the brain, see if there's a structural lesion there. But it's focal neural deficits or focal neurological deficits. And these deficits really depend, so we're going to write this down. The type of deficit they have depends upon the tumor location. So it really just depends on tumor location and I actually want to talk just a little bit about that and really differentiating focal neuro deficits. If it's a superenatorial tumor or an infratorial tumor, but we'll come back back to that. If a patient comes in with headache and they also have weakness on on one side of their body, get an image, 53:48 right? That's really really important. Headache, weakness, visual defects, they can't appreciate one side of their body. they have loss of sensation, numbness, thing. Those are reasons to say, "Hey, I should probably get an image, make sure that there's not a brain leion going on, whether it's a stroke, whether it's a bleed, or whether it's a brain tumor." The next one here is also something that they like to hit on for the exam, and it's usually someone who comes in and they have just a complete change in personality and memory and executive function. That is really important. So, think about cognitive and behavioral changes. So, if someone's just acting completely different than their normal self, that may not just be that they're a, you know, a little bit of a, you know, a douche. It could be because they got a tumor somewhere in their temporal lobe or their their their frontal lobe that can determines a lot of their personality, their memory, their executive function, um, their determination of inhibiting inappropriate thoughts. And so this could indicate potentially uh maybe 54:50 there's a tumor that's embedding itself um in the frontal lobe or the uh the temporal lobe. All right? And that that may be the reason why. All right? Especially frontal lobe. So temporal lobe or frontal lobe. All right? So these are things to definitely be thinking about. If a patient comes up with a headache, think about the headache a little bit. Just because they have a headache doesn't mean that they have a brain tumor. All right? Not everybody has to go run into the ER. some types of focal neural deficits associated with a headache, you should definitely get imaging. And if they have these weird cognitive behavioral changes, guess what? If patients have differences in behavior, differences in memory, differences in personality, obviously work them up for things like delirium or an altered mental status. And often times that comes with a good thorough laboratory, but also imaging workup to make sure that you rule out structural brain lesions. And so that could be in the workup there. All right, let's say that the patient comes in with focal neural deficits. It's actually really important to think about could it be a super tentorial tumor before you get the image 55:46 or an infronttorial tumor. It's always good to try and localize lesions. So superal tumors, one of the big things to think about is what if I represent this in different colors. What if I had a tumor that's sitting here on the primary motor cortex? What would that potentially represent? Well, one thing it would do is I may have a patient come in with motor deficits or they may come in with weakness. Right? Right? So if it's sitting on the motor cortex compressing on the motor cortex or compressing on the cortical spinal tracts, they can end up with weakness. It may be on the you know contrlateral side of the body but there's weakness. If there's a tumor compressing here on the semataensory cortex or the sematensory association cortex that's controlling sensation that's controlling propriception that's controlling a stereognosis. So a lot of those things are are your propriception your sensation of self all of that. So that's really important that they could have sensory deficits. So if patient has a tumor that's causing a headache and they also have sensory deficits, that's also something to consider. And then the third is what if they have a 56:46 tumor that's either compressing here on the optic tract or that's compressing here and parts of the occipital lobe where the primary visual cortex is. If I got a tumor that's sitting right here in the primary visual cortex, that could be a big issue, right? because the primary visual cortex is the one where a lot of the visual field is moving. So that's really really important and this could cause field cuts. That's really important to remember. So do they have visual field cuts, right? Because if you have like a pituitary tumor um or a cranophrenioma pressing on this, this will cause what? Bilateral temporal hemianopia. But if it's compressing here, it'll cause contrlateral homous hemiopia. And then the fourth big thing that always tells us if there's some type of like cortical thing going on is usually if there is hemi neglect. This doesn't mean that the patient is being neglected or I don't know neglecting other people. All it tells me is that they're losing an appreciation of their their opposite side of where the lesion is. Usually 57:47 this occurs in the non-dominant hemisphere which is the right side for people. So if they have a brain tumor somewhere within that frontal parietal lobe area they may lose the ability to recognize or appreciate the opposite side of their body. You may touch their left arm and they don't even know it's there. You may ask them to move their leg and they move the opposite leg. You may tell them, hey, look over here, but they don't appreciate or see you on the opposite side of the body. So that's called hemi neglect. Now for infrarctoral tumors, it's also really important to remember if I got a big goober that's sitting here somewhere with inside of the cerebellum, the cerebellum controls a lot of my balance, a lot of my coordination, right? And so this obviously could present with things like atexia, right? That's one potential thing. Um, another thing is it may also cause um abnormalities within my finger to nose testing. What's that called? Dysmetria. So looking for dysmetria should be something that you would think about here. And even we do other testing. You know what's um when you have their patient do rapid alternating movements? What's that called? And if 58:49 they can't do it, it's kind of like it's it's improper kind of like rapid alternating movements. It's called disdoinesis. Right. The third thing here is you also want to consider if a tumor is somewhere near and compressing or near the vicinity of a lot of your cranial nerves. So imagine here I'll represent this in orange. Let's say here I have a bunch of different cranial nerves that are running out here. If I have a tumor that's either in that vicinity, right, and it's compressing on or I have a tumor right there. So let's say I have a tumor and it's compressing on some of these cranial nerves. What else could you get? Cranial nerve policies. So cranial nerve pausies are also really worthy of considering some type of thing going on. And then I think the last thing is besides atexia, you could also consider things like vertigo. Vertigo, usually central vertigo is something also to consider. Again, this is all usually due to interruptions within the cerebellum. [sighs and gasps] But these are the things I would want you guys to think about. So if a patient comes in with a headache and any of these symptoms, you 59:49 would think about could it be an infrontal tumor? If they come in with a headache and some of these symptoms, you think about a super tentorial tumor and then you would work them up from there. Let's now move in and say, okay, patient comes in, they're saying, I got a headache. It's really bad in the morning when I get up. As I move throughout the day, gets a little bit better. I do have some nausea, some vomiting associated with it, and I've noticed that I also have like some weakness on an affected side. Then you start thinking, okay, dude, I'm a little bit concerned for a structural lesion. Other things that may start making you think about something else is really really going on is do they have features that are associated with intraranial pressure that's really really high. We can't talk about intraraanial pressure unless you discuss the beloved Monroe Kelly doctrine and all that says is the skull is a fixed structure. It doesn't allow things to allow the skull to expand. Anything that's inside of the brain, whatever those components are, if it gets bigger, the skull will not expand. What are those three components? Well, I'm representing it here in kind of like a 1:00:42 little chart for kind of an easy way to remember this. Here is blood. This consists of arterial blood and venus blood. Here is brain matter. So, this is going to be brain tissue. All right. And then third here is CSF and blue. If we increase any of these components more than what they're supposed to be, they'll start compressing on those other structures and also it'll build up inside of the skull and the pressure will go up. So let's think about what happens in a brain tumor. If a brain tumor starts to occur, what happens is the brain tissue starts to get worse. All right? So here's what I'm going to say. Let's say that I decide to increase the brain tissue. I increase the brain. I'm sorry. Let's say I increase in this case the CSF. So if I increase the CSF, if I increase the CSF, the reason why that would happen is you have a tumor that's somewhere within the the central nervous system and it's compressing on your ventricular system. All right? As 1:01:43 it compresses on the ventricular system, let's say, for example, it's in the um cerebellum and it compresses on the fourth ventricle. You can't get CSF through the fourth ventricle. And so it backs up into the cerebra duct, backs up into the third ventricle, backs up into the later ventricles. And what happens? they balloon up and they get big. What's that term called when you obstruct the ventricular flow and the ventricles get big? It's called obstructive hydrophilis. Obstructive hydrophilis is definitely due to um in this case can happen in patients who have brain tumors. And this is going to do what? Well, think about it now. You increase this compartment that starts squishing on the brain and squishing on the vascular system. So you get less blood flow coming to the brain and you compress on the brain tissue. That's not a good thing. This right here is what increases a patient's intraraanial pressure. All right. Intraraanial pressure should normally be less than 20 millm of mercury. If the intraraanial pressure is greater than or 1:02:45 equal to 20 mm of mercury, we consider that to be pretty high. We don't want that. So that's something that we want to try to avoid. Another reason that patients with brain tumors develop high ICP is because you increase the brain tissue. You increase the amount of brain components. So if I increase the brain components and what I mean by that is a tumor. So now I have this tumor which is accompanying for it and guess what else happens when you get a tumor especially brain tumors. They secrete chemicals that break down the bloodb brain barrier, especially the tight junctions. And those are supposed to maintain a a controlled degree of permeability. If I break the tight junctions down, fluid leaks out from those vessels into this space around the tumor. And then you get edema. So vasogenic edema is another component here. Well, now I have more brain tissue that I than I want. And guess what it's doing? It's compressing on the blood supply coming in or out of the brain and it's compressing on my ventricular system so that I get less movement of 1:03:47 CSF. So this right here will also increase the patient's incraanial pressure because again that skull is not going to say oh increase in size for you. No, not unless you have a baby um who h still has those fontels which will allow for a little bit of stretching. So that's the concept here. So when a patient has an increased ICP that number gets above 20, it's usually due to hydrophilis or the tumor and the swelling around the tumor. Question is how will that usually present? Well, we already talked about one of them. If I got a tumor and that thing's compressing on the meninges, the meningis have lots of pain receptors here. Those pain receptors send signals to the trigeminal nerve and that triggers a headache. So headaches are often times very very characteristic. All right? And this is usually due to menial irritation from the tumor compressing. Second one is you can activate this purple structure here. You see this purple structure. If the pressure comes up enough that it starts to activate specific structures, especially this one in the medulla, that's called the emmetic center in the 1:04:48 medulla. The emmetic center in the medulla controls your um your emisis process, your vomiting process. And so guess what? That's associated with nausea and vomiting. This is very very common. All right. That's why when we talked about the classic symptoms, the classic tritis headache which is associated with nausea and vomiting and headaches usually in the morning. It's due to a high intraanial pressure. So the nausea and vomiting is due to what? It's due to um stimulation of what's called the cheotrigger zone or the center. So a medicic center which is located in the medulla. All right. The next thing that I also want you guys to think about is we can also have this tumor getting big enough and the pressure rises enough that it compresses on this structure. What is this structure that runs from the midbrain, the ponds, and the medulla? It controls your level of wakefulness and arousal. It's called the reticular formation. If I compress the reticular formation from high pressure, guess what that can do? That can lower your level of consciousness. So you can end up having 1:05:49 a declining a decreasing level of consciousness. So a decreasing level of consciousness. This can vary in how it presents. Often times the patient may start off as being just a little bit lethargic. They're a little tired, but they can wake them up. Then they can get a little bit worse where now, hey, I got to kind of like I got to move you around a little bit or yell at you. And so now you're at the point where it's like you're not really lethargic. Now you're like really somnant and it's hard to get you up. And then from there they can get even worse to where like man I got to really really stimulate them but they do wake up. So now they're kind of in an upunded state and then eventually I got to really really really move them and give painful stimuli to get them to wake up. So then they're in more of an a stuper and then eventually I can squeeze and do anything to them but they won't wake up and they become. So due to the worsening worsening intraraanial pressure you can move through that systemic process or that progression if you will. The next thing that can happen here is you see here if the pressure is big enough so you know um there's CSF 1:06:47 right so not only could it be because of pressure but also if you have a buildup in incraanial pressure you know there's fluid that's around this optic nerve sheath so you have what's called the optic nerve sheath and there's um there's cerebral spinal fluid there if the pressure inside of the brain is going up the cerebral spinal fluid it can kind of transmit that pressure around the optic nerve sheath and it can kind of squeeze down on the optic optic nerve. And if you squeeze down in the optic nerve, guess what drains the coming through this area? You're supposed to drain veins there. Can't drain the vein. And so what happens is you get a lot of venus congestion right here around the entry called the optic disc and it gets swollen. And these patients can experience something called papa edema. So papadeema. The next component here and this is the last one is if I have enough pressure, you see this nerve here. So watch this. Sometimes you can get enough pressure, enough shifting where it squeezes right there. So there's a nerve here. It's called the abdusen's nerve and it actually kind of comes from the ponds and it works. So let's actually uh move 1:07:48 this a little bit here because it's not technically where it should be. It should be right there. Just me being a little anal, but it should be in the ponds and it's going to move its way through here. You see this right here? This is called the clus. And then as it moves up the clus, it makes this turn. You see that little bone there? Whenever you actually have pressure that builds up, it smashes that nerve against the bone, the little pointy part part of the bone. And now that nerve when you compress it, you lose signals. Guess what this nerve is? This is the six cranial nerve. Guess what the six cranial nerve goes to? It goes to what's called the lateral rectus. And so now you don't have good signals running down the abducins nerve. And you inhibit the lateral rectus. And it's supposed to control your lateral gaze. What this does is this changes their ability to see objects as one entity and it causes double vision and so often times these patients get dipopia. So double vision that's really important to remember. All right. So again headache is due to menial irritation from pressure. Nausea 1:08:50 and vomiting is pressure on the center. Decreasing level of consciousness is comicular formation. Paplade edema is pressure that's being transmitted via the CSF and squeezing down in the optic nerve sheath causing blood to not drain from the retina especially around the optic disc. Paplade edema dipoplia or dipopia is whenever the abducence nerve because it runs up and it gets right on that sharp part it presses down and smashes on the nerve and the lateral rectus can't contract. Now this is not the cl this is not like how all patients present when they have intricate pressure. It may just be a headache. It could be nausea and vomiting. It could be they're a little bit more sleepy and harder to wake up. They could if you get a fundoscope and look at their their actual retin, oh yeah, the optic disc is pretty pretty enlarged. They may have double vision. But sometimes they may come in with very severe presentations like herniation of brain tissue where brain starts moving through spaces where it's got to find somewhere. If the skull won't expand, I'll find a hole and I'll shove myself through there. Not trying to be weird, but that's what it will do. 1:09:50 Let's now talk about that whenever there's herniation symptoms. All right. So now if a patient comes in again they have elevated intricraanial pressure you obviously want to watch out for things like we talked about headache nausea vomiting you want to watch out for again potentially is there any signs of papa demon fundoscopic exam that's definitely very concerning and is there any dipopia declining level of consciousness is really really important but when a patient starts presenting with the classic findings of what I mean the tellt tell sign that the pressure is up and the patient's at risk for herniation we use the Cushings triad from the exam. And so the Cushings triad basically looks at three factors. One is it looks at the heart rate, it looks at the blood pressure, and it looks at the breathing. And what we want to know about this is what's happening with the heart rate. Well, what happens is you end up is as the pressure builds up in the brain, you compress in the medulla. And the medulla is controlling a lot of your cardiac activity, especially cardiac acceleration. And so if you lose that cardiac acceleration, you lose 1:10:51 exttrinsic supply that helps to speed it up. And so unfortunately it will start to go down. Your body will try to compensate to increase the blood flow to the brain in that time frame. And what it'll do is it'll try to push your blood pressure up so you can still try to profuse the unfortunately very hurt and injured brain. And then on top of that, whenever we have compression of the medulla, guess what else is there? Your respiratory groups, your vententral, your dorsal respiratory groups, your pontine respiratory groups. All of these things control your breathing patterns and if a patient has compression of the brain stem your breathing patterns will be very very irregular and so that is what we get concerned about is having irregular breathing patterns. All right. So that's what I want you guys to be thinking about when we talk about pressure building up in the brain enough that it actually again skull won't expand. It's going to start popping through spaces or holes where it can find it. That's when we get worried about herniation. So there's a couple different syndromes I want you guys to be able to pick up. So whenever they talk in the exam, hey, if a patient has 1:11:50 subfausing herniation, what's the biggest thing to remember? They have contrateral hemiparesis or he you know, you know, hemiparesis or sometimes it could be contrlateral paralysis of the muscle. But what I really want you to understand is big big takeaway features, but I'm going to try to walk you through on how that actually happens. So subfausalian herniation, usually this is a superal tumor. Let's say I have a tumor sitting right here. It's in the frontal lobe, parietal lobe. And what happens is it pushes, it has a mass effect. So it pushes on structures that are nearby. There's one structure here. It's right this portion here, right next to the f. So you have the faulk cerebri, which is running right here. Right here is what's called the singulum. If it's getting mass effect from a nearby tumor, it actually tries to push. And what it does? It pushes this way. And so as it pushes this way, guess what happens? It'll try to herniate underneath the faulks, but what it does is it squishes everything in its path. What's right in the path here? It literally is running right here. What's that vessel? The anterior cerebral 1:12:52 artery. So when a patient develops subfalian herniation, the biggest concern is that the singulum moves under the faulks cerebri and compresses the anterior cerebral artery. And when you compress the anterior cerebral artery, what does the anterior cerebral artery do? Well, think about it. You have different zones, right? So, you have a zone technically, if I were to do, let's say I do this one in like blue, this is kind of like your anterior cerebral artery territory. And then here, if I did in red, this is going to be most of your middle cerebral artery territory. And then if I did this one, let's say in this like baby blue color, this is going to be most, and this actually, let's actually use a different color. Let's use orange. This would be your posterior cerebral artery territory, right? And so when a patient has comp like they have compression of the ACA, they can actually develop infarction. And so what actually ends up happening is you're going to get infuction of the frontal lobe. And so 1:13:52 this area will become compromised, the one I have in this blue color. So this area is going to become damaged. And again, it's going to be on the opposite side of where the tumor is. So now they're going to end up with a potential frontal lobe infarction. Now the frontal lobe or at least in that potential area you're going to have the motor cortex and the motor cortex if you think about the motor homunculus the motor homunculus always goes for the foot is going to be closest to the medial portion and then it goes you know maybe you got foot then you got the legs then you got the torso then you got the face all the way over here. So what area is going to be most predisposed? It's going to be the legs. And so your lower extremities tend to be the most affected structure. And so what happens is let's say here I have my corticospinal tracts that are going to be here from that frontal lobe. They're supposed to all kind of give me my corticospinal tracts that run here. They run through the internal capsule. They come down the midbrain, the ponds. They decate here at the medulla. They go to the spinal cord. And from here it's going to go to the 1:14:53 muscles and it's going to cause these muscles to contract. It's going to be the contrlateral muscle, right? Well, [snorts] if I end up causing infarction here, all of this gets injured and damaged. It loses the signals. I lose this signal. I lose the contraction of the muscle. And if I do that, that's how the patient experiences what's called contraateral hemaresis. And this is because they ended up having an infarction of that frontal lobe area here. [snorts] And that is again going to cause an infarction of the contrlateral side. But it will be on the same side as where that mass is. And this was the problem is the mass was here. It was exerting its mass effect. And that mass effect is what end up leading to the singulum herniating underneath the faulks and pushing on the anterior cerebral artery infarcting that tissue. That's what I want you to take away. So subscene herniation. The biggest feature here to take away is the muscles will be weak on the contrlateral side of where there was an infarction. But it's because the mass effect pushed 1:15:55 the singulum underneath it and compressed the anterior cerebral artery. All right, cool. Uncle herniation. With uncle herniation, what happens here is there's a tumor and it's usually going to be somewhere within the temporal lobe and it can be pretty big. Sometimes it can be a little higher, but if it's really really big, there's a lot of edema, there's a lot of swelling, then what can happen is again it'll exert its localized mass effect. But what happens if that mass effect is enough that when it pushes here, let's say this is the most medial portion of the temporal lobe. It's called the uncus. If that starts slipping here, you see there's the tentorum cerebelli, these little blue things that come inwards right here. If this thing slips over the tentorum cerebelli, what it'll start doing is imagine this. I'm going to squeeze on the midbrain. Now I'm going to push and mash on that midbrain. And as I mash on that midbrain, I'm going to get damage to a lot of different surrounding structures. So again, what happens in 1:16:55 this scenario is that the enkus moves through this notch. What is that space called between the tentorium cerebelli? The tentorial notch. So it moves through the tentorial notch. And when it does that, it compresses a couple different structures, but particularly it compresses the midbrain. With this being said, when it compresses the midbrain, there's a couple different structures that are important to the midbrain and then surrounding that area where the midbrain resides. One of those areas is it's going to cause compression of the PCA. So, it compresses the PCA, the posterior cerebral artery. So, that's actually So, you come up here, you got the verts, you got the basler, and then here's your PCA. If that thing herniates, it can compress on the PCA. Now, again, think about your territories. Here's my frontal lobe area where the ACA is going. This is frontal and sometimes even parietal, right? And then we'll go to the next part here which is going to be the MCA territory which is going to be like all this portion right here. And 1:17:55 then here we're going to have the PCA territory. Now the PCA territory, there's one really really critical area that actually gets hit here and that's near the occipital loes. Now if you hit near the occipital loes the problem with this is that you lose the primary visual cortex. And so what can happen here is you can actually get occipital or at least around that area you can get an occipital lobe infuction. Now if that happens let's take a second to think about why that would be absolutely terrible. [snorts] If that happens here that's where the primary visual cortex is. So think about this for a second. Let's say here I have my visual pathways, right? Let's say here I have a visual pathway right here. And that's going to be picking up information from the the medial visual fields or your nasal visual fields. And let's use pink as the other color here. This is going to be the medial hemi retina. This is going to pick up your temporal visual fields. Same thing. Here's the medial portion here. And then 1:18:56 we'll come over here and we'll say that again. This is going to be the temporal fields. So what happens is these pick up their visual information from here and this picks up visual information from here and then again this one picks up visual information from over in the medial field and this one picks up visual information from your medial fields. When that happens when they pick up that information they carry that down via their fibers. The lateral fibers never cross. They go to the lateral geniculate nucleus and then in the lateral geniculate nucleus they get sent outwards to the cortex via the optic radiations. Same thing for this one. It's going to go here. It's going to move out go to the lateral geniculate nucleus and then optic radiations are going to go to that primary visual cortex. The medial fibers these cross. So they go over here. They go to the latericulate nucleus and they come over the optic radiations. And then same thing, this one's going to move here and it's going to cross lateral 1:19:56 geniculate nucleus and then you're going to go to your optic radiations through the occipital lobe. So if you're noticing what's happening here, you're getting this information. Let's say that we infarcted this portion. So let's say this is the area that got destroyed because we infarcted that PCA territory. If you follow it back, it's going to give you the lateral fiber. So you're going to lose this field, right? And that's going to be so this field right here gone. We lost this field. So let's actually put some red axis here. This field is gone. Then we have to follow the medial fibers. So we're going to bring this one over here. Come over here and you lose this field over here. When you think about it, if you lose this visual field and you compare it and you look at this within the aspect of the patient's vision, we actually look at vision kind of a little bit like this as our visual fields. And then same thing here. What do you notice about their visual fields? This visual field and this visual field is preserved. But 1:20:58 these visual fields that are technically if you want to think about it on the right side there. So they're homonymous but it's going to be contrateral in that aspect. This is contraateral homonymous hemianopia. So that's one potential presentation that you want to watch out for here. It's called contraateral homonymous hemi anopia. And that's usually because of the PCA compression causing occipital lobe infaction. Now, the other thing that can happen when you compress the midbrain is when you compress the midbrain, there's a couple different structures here. Let's say that we have this one here, and this one is actually going to be the third nerve. So, you have the third cranial nerve, and we have this guy here, and we'll have this guy here. And it's associated with parasympathetic fibers. So, there's two different types of fibers. There's sematic fibers which are going to be going to the muscles the extraocular muscles and then there's parasympathetic fibers and these specifically go to the uh pupil they control the pupils and accommodation reflexes right and so it's really really 1:21:59 important to remember this if you have this herniating and smashing on the midbrain let's say that this is occurring here on the left side we're going to damage these so let's damage these if I damage these and this is all the cranial nerve three cranial nerve three nuclei I lose two pathways one is the motor pathway that is more sematic if you will and that controls the extraocular movement so it controls the EOM and I lose the pupil pathway which is the pathway that is going to control whether the pupil dilates or constricts that's going to be interfered with because again I'm compressing on these structures and I'm losing losing that supply. So if that happens, let's think about this. I lose the motor supply going to these muscles. And there's a bunch of different muscles. I'm going to just quickly list them for a second. This one will be the superior rectus. This one right here is going to be the um we're going to say in this example, 1:23:00 it's on the medial side of the eye. Medial rectus, inferior oblique, and inferior rectus. Superior rectus, inferior rectus are supposed to have specific jobs. Superior rectus elevates. Inferior rectus depresses and then you have the medial rectus that helps to adduct the eye, bring them inwards and then the inferior oblique does what? Well, it helps to elevate the eye, right? And it usually helps to move it. Now, here let's think about this. If I lost the cranial nerve 3 supplies all of these muscles, you're going to lose the ability to do what? To adduct the eye. you're going to lose the ability potentially to elevate the eye via the superior rectus. What muscles become completely unopposed. Now you end up with the lateral rectus being unopposed and you end up with the uh superior oblique being unopposed. The lateral rectus does what to the eye? Pull it out. What does the superior oblique do? Depresses it and then it causes it to go out. So what ends up 1:24:01 happening to the patient's eye is they end up with what's called a down and out presentation. So they end up with a down and out eye. And the reason why is because you lose the motor supply to which muscles? You lose the motor supply to the superior rectus, the medial rectus, the inferior oblique, and the inferior rectus. Which muscles are now unopposed? Lateral rectus pulls the eye out. Superior oblique is supposed to do what? It's supposed to naturally bring it down. So now that lateral rectus is going to pull it out and then that superior oblique is going to pull the eye down because they're completely unopposed. That's the concept I want you to remember. All right. The other thing is that we interfere the pupil pathway. So we also decrease the motor pathway and now we're going to decrease the pupil pathway. Now I told you that there's two parts of the cranial nerve three nuclei. One is there's sematic and the other one is the Edinger Westfall. So there's the sematic which controls the motor pathway and then there is the 1:25:03 Edinger Westfall nucleus and this is the parasympathetic pathway that goes to the pupil. If we interfere with that, we damage that. What is parasympathetic supposed to do? Do you guys know? Supposed to constrict the pupil. Supposed to constrict the pupil. You're going to lose the ability to constrict the pupil. Now what happens? The pupil starts dilating. So because of this you lose the ability to constrict the pupil. The pupil will dilate. So now you end up with a dilated pupil because again I don't want to go crazy through the physiology because this is supposed to be more of the clinical aspects. We've talked about this more in step one and more in our pathophys. But again if you injure the sematic fibers you lose the movements of superior inferior rectus inferior oblique and medial rectus. So then superior oblique and lateral rectus become unopposed. If you lose the parasympathetic supply to the pupil, it's supposed to constrict it. Now, it's going to be unopposed and it's going to dilate. So, these patients can have a dilated and pupil with a down andout movement. 1:26:04 And it's on the ipsyal side of where the herniation is. So, ipsyal, that's important to remember for down and out of the eye and dilated pupil. It's ipsilateral. One more thing for uncle herniation. There's three things so far. contrlateral hommonous hemopia from PCA infarction. Second thing is a down andout movement of the eye with the dilated pupil that is usually not going to be as well as responsive to light. And then lastly, they're going to have another problem. There's motor fibers that run through this way. So let's actually do this. Let's pick let's do orange. Let's say there's motor fibers that are supposed to be coming through this portion here called the cerebral podunkcle. And what they do is they run down here through the midbrain. They come down the pawns and then eventually they do what? They decisate at the pyramids in the medulla. They come downwards to the spinal cord. And then what do they do? They end up going to the muscles and causing contraction. But what side of the body is it on? Contrateral. 1:27:06 If I'm pressing on that side of the midbrain, what am I going to do? Damage that nerve. I damage the cortical spinal tracts as they move through the cerebra podunkcle. And if that does that, I don't send signals down to the contrlateral muscle. So, what's another potential presentation I'm going to put down here? Let's make some room here. This is going to be contrateral. We're going to really mash this in, guys. Contrateral hemi paresis. So, if I say patient has a tumor, they're starting to herniate. I say they have a down and out movement of the eye with a dilated pupil. they have loss of visual fields and it's usually on the same side. In other words, when I talk about this, it's like this visual field here for the the nasal portion on my left eye and it's going to be the what [snorts] the temporal field on the other eye. So, it's on that right side if you want to think about it, but it's opposite visual field. So contrateral homonymous hemopia 1:28:11 and then if I also say that they have contrateral hemiparesis you're going to say uncle herniation there's this weird phenomenon I want I'll talk about it more in the intraraanial pressure lecture but there's something called a kernahan's notch syndrome and kernahan's notch syndrome is basically whenever the pressure is so high that you smash the midbrain and then this other midbrain gets smashed against the tentorum and so you can actually end compressing the the cortical spinal tracts here. So the patient can actually get ipsilateral hemiparesis which is kind of weird but we won't go too far. I just want to keep it at that. So subfaling contrlateral hemiparesis boom done. That's the ACA infarction. Uncle herniation. Unkus herniates compresses the third nerve in the associated eding westfall. Dilated pupil non-reactive to light down and out movement compresses the PCA. Contrlateral hommonous hemopia compresses the cerebrauncle contrlateral hemiparesis. Now what? Let's move to the next one. The next one here is called central transentorial herniation. 1:29:11 This is essentially when a patient has so much swelling and usually it has to be kind of a symmetric pushing down. So I'll say that I have a tumor right here and a tumor right here. So it's usually whenever a patient has significant amounts of cerebral edema or they have like two big tumors and these tumors are causing kind of a I don't know I guess I would say use the term like a equal amount of downward or surrounding mass effect. As it does that this whole portion here which we're going to kind of like I'll do in a dotted line here. This is called the dianphylon. This is called the dianphylon. The dianephylon is going to get pressure from above. And what it's going to do is it's going to literally smash down through this space. What's that space called? The tentorial notch. And so what ends up happening is the dianphylon shifts downward through the tentorial notch. That's why we call it transentorial herniation. So what ends up happening in this patient is they end up having a dianphylon. Their dianphylon 1:30:12 pushes through the tentorial notch. And when it pushes through the tentorial notch, it literally squishes on the brain stem. And what that do is that's going to push on that's going to compress the upper portion of the brain stem. So it usually starts off as compressing the midbrain and then it progresses to compressing on the ponds and even the medulla in certain cases. But here's how I want you to think about this one. So with subfalene it was a structure moving over and compressing. With ankus it was the thing moving through the dental nod and compressing on the midbrain. This one it's an entire deep structures that are smashing down in the midbrain. I'm not even kidding. It's like imagine it like an accordion. Like I'm playing the mid the the brain stem like an accordion. I'm smashing this thing down. By doing that, you can actually smash this thing down so much. There's little vessels here. So, imagine I have a downward traction here on the brain stem. There's small little vessels, the little perforated vessels off the basel artery going into the ponds. These 1:31:13 things get shredded to bits and they cause like little hemorrhages to form inside of the ponds. And this is actually characteristic of central um transitory herniation. We call them direct hemorrhages. So these are called direct hemorrhages. And so that's something that you can kind of see due to like the destruction of these pontine perforator vessels. But one of the big things to remember for this one is you compress a bunch of different structures. So what I want you to know is pupil changes, motor changes, and brain stem reflexes that get affected here. In this scenario, we have pupil changes. First, if I have this thing smashing down, the first thing that it does is it smashes down on these sympathetic nerve fibers coming from the hypothalamus. So, sympathetic is supposed to do what? It's supposed to cause dilation of the pupil. And then here I have the Edinger Westfall nucleus. So, this is my Edinger Westfall, which is the parasympathetic fibers. This wants to cause constriction of the pupil. Right? What happens is when you get downward pressure the dianphylon that includes the 1:32:13 hypothalamus you compress the sympathetic fibers first and so if you compress the sympathetic fibers first what would be the first thing to happen you would lose the ability to dilate and so this is the first thing that happens so first thing that's going to happen is you'd lose the ability to dilate so if you can't dilate now you have all constriction what's going to happen to the pupil it's going to get small so what'll happen first is you're going to get small small and kind of like pinpoint pupils. So I say small pupils. Then what happens? That's the first thing. As the compression worsens, you then start squeezing and compressing on the edinger westfall nucleus, which is the parasympathetic fibers. And then you lose the ability to constrict. So if you lose the ability to constrict and the ability to dilate, then what happens? They stay the same size. They stay mid-p position. So then what happens is the pupils will then change to become mid-position and relatively fixed and fixed. So that's the first thing I want you to realize when you start seeing this. The second thing is motor changes. 1:33:16 So you guys remember there's a structure here called the red nucleus. And the red nucleus controls what's called your um your rubro spinal tracts. If you don't remember that go back watch our tracks video. But the descending tract here is it goes to muscles that control flexion. So it's supposed to control our flexors. This is supposed to control flexion muscles particularly of the upper arms. I mean the upper extremities. So your arms when you have injury that's above so say the injury starts above the red nucleus which is usually where this is going to be coming down super nuclear fibers. What happens is this causes the red nucleus to still be able to fire on its own. And so you can still flex and so what happens is these patients they un sometimes they have almost excessive flexion. And we call this posturing when a patient's like this. It's called decorticate posturing. And so sometimes that can be seen when you have a good enough compression above that red nucleus or damage above the red nucleus. So we say the first thing is they may start off with what's called decorticate posturing. 1:34:16 Then as compression gets worse and you start mashing on the brain stem, especially the midbrain, you may start damaging structures either at or below the red nucleus. As that happens, do you lose the ability to have you los the ability of flexion then and so flexion is lost and you get unopposed extension then the patient starts doing this and this is called derebrate posturing. So that's the next thing that can start to develop as the pressure continues to rise and compress further on the brain stem like an accordion. So d cerebrate. The next thing that I want you guys to remember is as we compress on the brain stem, you have different reflexes and as we compress further and further and further like an accordion, you lose these reflexes respectively. So if I compress on this one and this is going to be going to my pupil. So this is the third nerve. This is for the pupil reflex. Then I have the trigeminal nerve which co controls the corial reflex. And then I have the uh eighth nerve, I'm sorry, I'm sorry, the 10th 1:35:17 nerve, the vagus nerve, which controls your cough reflex and even the gag. What will happen is you may start to lose the pupil reflex first, right? So this may be potentially the first one to go. Then this will be the second one to go and this may be the final one to go. So it may kind of go in this order as the pro compress progression gets worse. This may be the first one and the second one and the third reflex to go. All right, that's what I want you guys to be able to remember. So if a patient comes in with central transcendtorial herniation, what I want you to remember is they may come in first with small pinpoint pupils. As it gets worse, they get mid- position and fix. They may start off with decorticate. They then progress to derebrate. They may start off with potentially having a loss of a pupil reflex, but then you lose cornal and then potentially you can lose cough and gag. And then lastly, remember sometimes if you get imaging, you can see that they can have these hemorrhages on their ponds due to complete shearing of those baselor perforators. The last type of herniation is tonsular herniation. Tonsular herniation is 1:36:17 whenever you have a tumor that's usually pretty decent size here in the cerebellum and enough that the local mass effect from that tumor is squeezing on the cerebellar tonsils enough that when the cerebellar tonsils have to go somewhere they go through the fammen magnum. And when they go through the fammen magnum guess what's the structure right here that they start mashing on? they start mashing on the medulla and the upper parts of the cervical spinal cord. So in this scenario for trans uh so tonsular herniation is the cerebellar tonsils move through the fam and magnum and then they compress the medulla. Now as you do that it's important to remember what's going to happen with that. The medulla has so much control, especially cardopulmonary control. I told you guys. And so what we think about with this one is as you lose cardopulmonary control, you can start developing features of near death. So let's say first off I 1:37:17 cause damage and destruction to the respiratory centers. This is supposed to control nerves like your intercostal nerve, your frenic nerves, all these nerves that go that control breathing. I'm going to lose this. This is actually going to end up getting destroyed. And then what happens is the patient can have apneic apnea breathing. So they don't they stop breathing at all. That's one characteristic feature that we get a little bit worried about with herniation. The next thing is I lose the control or the the the information that goes to my heart and this can start getting injured and destroyed. If this gets destroyed, I lose signals to the heart. This may start off as we talked about with a low heart rate that can then progress sometimes I've seen it into cardiac arrest. You may see hypertension that then eventually they lose all ability to regulate their their blood pressure that can progress to hypotension and again cardiac arrest. So sometimes this is how these patients unfortunately will present is they may come in with brada cardia and go into 1:38:17 cardiac arrest. They may come in with crazy high blood pressure and then all of a sudden their blood pressure tanks. The other thing you want to watch out is motor changes and if having enough compression of the medulla, guess what runs through here? Your cortical spinal tracts. And you can actually damage these enough that you especially if there's the decation point that you're compressing on. You can literally I'm not even kidding. You can end up with flaccid paralysis. And then lastly, I think the same thing goes for this is that when you notice with brain stem reflexes, again, it's the same concept. you're going to be causing damage to these. Usually the the one if you have it near the medulla, it's going to be that loss of the cough and gag reflex. So that's what you're going to potentially notice is that these patients will have a loss of their cough reflex or their gag reflex. But other potential things that could start arising is they may start having other features that start to arise. It could be completely indirect or unrelated, but they may start losing things like their coral reflex and losing things like their pupil reflex. But again, it's 1:39:17 usually going to be the cough reflex that we worry about first because again, it's very, very close proximity that where this herniation is occurring on the medulla. These may occur due to other potential pressure changes and shifts within the brain stem. But my friends, this is going to cover the herniation. There's many other features that can occur. Let's now talk about some other things that can happen as a result of a brain tumor. All right. So, next thing is if a tumor is actually pretty unfortunately very very close near the cortex, it can really really agitate the cortical neurons. And so, you have to have a cortical mass. This is very very very important. So, essentially the only way that you can truly get seizures is with a superal tumor except that superal tumor has to be very very close or pretty much at the cortex. That's where a lot of the actual control of what really initiates seizures is going to occur. So if I have a cortical mass, this creates a focus for potential things like I can have a firing here. And if this is like in the motor cortex on the left side and the 1:40:17 patient may have some tonic chronic jerking of their right side. So they could develop something like focal seizures. So that could be one potential thing is you want to watch out for like focal seizures. But the thing that we get really really concerned about is if that focal seizure starts off with them twitching their their opposite arm and all of a sudden they go into full tonic clonic seizures as a grandma seizure generalized seizure. So it may start off just this focal firing but then what happens is that continues to spread and then you get loss of awareness. You get multiple other territories that start unfortunately firing and then you can get what's called a generalized seizure. So here's what I want you to remember and this is really important when a patient comes in and they're presenting with headaches right as a potential feature and it's that classic feature of the headaches with nausea vomiting papadma those are usually key things to think patient has a high ICP right the worrisome features is do they start exhibiting signs of herniation 1:41:18 contrlateral hemiparesis only you think about subfalene contrlateral hemiparesis with the dilated pupil that's down and out and contrateral homonymous hemopia uncle herniation They start off with potentially small pinpoint pupils become mid- position. So they start decorticate go deserebrate. They lose their reflexes progressively. You think about central transcendtorial. They start off with cardio pulmonary changes. That's you're thinking about the medularary one as well the tonsular herniation. But sometimes with this they may come in with a new onset seizure. So the biggest presentation that we see in patients who have brain tumors is a new onset seizure. This is the first seizure they've ever had. Anytime that happens, it is always a structural brain lesion until proven otherwise. So it's a brain lesion until proven otherwise. Because if like let's say that the patient had a history of a seizure, right? Maybe they're not taking their medications or maybe they use drugs or something like that. There could be a lot of different 1:42:18 reasons that a patient has a seizure, but if there's a new onset seizure, no truly provoking factors, you always going to think it's a brain leion. You got to get imaging and you might find a tumor. So that's something to think about. Now the next thing is obstructive hydrophilis. I already talked about this a little bit with brain tumors. When we talked about increased intraraanial pressure, when a patient has obstructive hydrophilis, usually it can happen. You can have like, for example, if I have a tumor right here that's deep-seated and it's big enough, right? It can mash here. It may squeeze on like the third ventricle but most of the time where you see most severe hy obstructive hydrophilis oftent times than not it's going to be infrinctoral and the reason why is this is where because most of the CSF is going to start passing through here and then out into the subacoid space or down the central canal but this is where you're going to see a lot of it and so any kind of infratorial tumor medeloblasto pyocitic astroytoomas things like that they're pretty big and they mash right here onto that fourth ventricle or cerebral aqueduct If you compress this area, what's going 1:43:17 to happen? This is going to start backing up. All that CSF. If that CSF backs up, what's going to happen to these ventricles? Well, they were once this size. Now, these things are going to start ballooning up. And then this is going to cause the ventricles to become gargantuous. That's when we start getting worried about obstructive hydrophilis. Now, obstructive hydrophilis because we're impeding CSF flow. How would this potentially clinically present? Clinical presentation of this is almost often always going to be with features of increased intraranial pressure. So it's going to be your findings of increased ICP which is everything that we really spend a lot of time talking about. And I know that you probably hate me after doing all of that. But I think now you'll know if ICP is high they can present with headache, nausea, vomiting, papal edema, decreased level of consciousness, dipopia, they can present with herniation syndromes, tons of stuff. But here's the big thing. Remember I told you that the most common way that you'll see see a constructive hydrophilis is because of an infrarctoral compressing here. Who often gets infratorial tumors? Pediatric 1:44:16 patients sometimes if you have a very very very young child very young and their skull hasn't completely formed yet their fontels are still present. You know what's the problem with that is that they can move. And so sometimes in pediatric patients, this is really important to remember pediatric tumors. This can lead to something called macroephille and bulging fontineels. So this can cause their literally their skull does actually expand a little bit and it causes something called macrophille and [snorts] you can even get these things called bulging fontineels. And it looks actually a little bit like this. All right. So now from here when a patient has obstructive hydrophilis, it's a tumor that's compressing on this area and obstructing cerebral spinal fluid flow. If it happens, their ICP can go up. If their ICP goes up, they can present with all the symptoms that we talked about. But if it's in a pediatric 1:45:16 patient, this is the one that you want to remember. The enlargement of the skull and potentially the bulging of those fontels because they do have some give to them. They aren't a fibrous joint. just yet. All right, let's move on to this one over here. Vasoggenic edema. This should sound familiar. Yeah. So, if a patient has a brain tumor, what happens is they can get swelling and fluid that can really extend around this and sometimes like GBMs, GBMs can have scary amounts of like vasogenic edema and this can really occur around the tumor. What really happens is this tumor can secrete a bunch of different inflammatory chemicals. So it can secrete a bunch of different inflammatory cytoines. And when it does this, what these inflammatory cytoines do, here's the tumor. It releases that. There's vessels around this area. So there's always vessels here. These inflammatory cytoines, there's normally there's these little blue things here. You see what these are? These are called tight junctions. They're supposed to be there. So they're supposed to be tight junctions. These inflammatory chemicals, what they do is they rip apart the tight junctions. So now this guy's going to 1:46:17 come in here and let's say that I'm going to target this one right here. I'm going to destroy this tight junction. Now, as I destroy the tight junction, what do I do to the permeability here? Now, I open it up. If I open up this area, guess what's going to happen now? I'm going to allow So, let's actually bring this arrow back here a little bit. So, what happens is this guy is going to target the tight junctions. When he targets the tight junctions, he's going to cause damage to the tight junctions. They're going to open up. Now this is going to be super permeable and fluid is going to start leaking out of the bloodb brain barrier right so you have a this is naturally your bloodb brain barrier here and so what's going to happen is you cause destruction of the bloodb brain barrier and now fluid is going to start leaking out across these capillaries into the perittummeral tissue. So basically what happens with this is there is what we would say as let's write it as destruction of the blood brain barrier. if you will, there is destruction of the bloodb brain 1:47:17 barrier because you rip apart the tight junctions. Now fluid can leak out and guess what you end up getting? You end up getting period per tumoral edema. So per tumor edema. This just means that around the tumor, you're getting a lot of swelling. That's vasogenic edema. Now if I have more brain and it's associated like fluid around it, what is that doing doing to the actual Monro Kelly doctrine? I'm increasing my brain tissue and the surrounding tissue around it. So what's that going to do? It's going to increase my intracraanial pressure. So often times this will precipitate with classic findings of uh increased intraraanial pressure which again I do I need to remind you I think ah why not right? Headaches, nausea, vomiting, papa edema um dipopia right and again with this being said if it's worse worse worse enough ICP and it gets too high it can start causing herniation features. All right that's vasogenic edema. So so far we've hit the really big stuff here which is patients coming in with very high intracal pressures. An ICP crisis is the thing we get scared about. It can start off generalized and mild. What we 1:48:17 get concerned about is herniation. They can come in with a seizure. They can come in with obstructive hydrophilis. They can come in with vasogenic edema. What's another way that they may present with? All right. So, if you also have a tumor that's actually located again a little bit more within the pituitary uh region, obviously in that celotica, you get like a pituitary adenoma. So, pituitary adinomomas are kind of problematic. And the reason why is yeah not only can they cause things like potentially um headaches they also can cause things like endocrine dysfunction and usually that endocrine dysfunction is the form of prolactinium I told you prolactinomas are the most common type of really a pituitary microatinoma. So usually it has to be a pituitary microatinoma but for right now I'm just going to say we're going to call this a pituitary adenoma. Now, one of the big things about pituitary adnoism, again, we talked a lot about this in pituitary disorders in our indocrine playlist, so make sure you guys watch that for more info. But these things are pumping out a very specific type of hormone. What is that hormone that we're worried about? Well, it's pumping out prolactin, 1:49:15 usually levels that are greater than 200. And as that prolactin levels really, really go up, what does prolactin do? Well, normally it's supposed to help with breast tissue. Particularly, it's helping with milk production. That's one of the the the biggest things. But unfortunately, if that level is a little bit too high, it's higher than it should be, one of the things that can happen is that this can cause breast tissue enlargement. So one of the things that actually can do is it can lead to gynecomastia. So the patient can get gynecomastia and unfortunately it can cause inappropriate milk production. So two things can actually arise here. It can cause gynecomastia and also it can cause inappropriate unfortunately milk production. So we call this galactohea. And then the next thing here is it also can act on the what particularly the uterus and it can change the estrogen production levels and so they can actually have very funky menstrual cycles. So menstrual irregularities is another really important feature that you want to watch out for. So watch out for menstrual irregularities. 1:50:17 All right. So when a patient comes in and they present with a headache and on top of that they also are presenting with these weird endocrine features like gynecomastia, galactaria, menstrual irregularities definitely be thinking could this potentially be a pituitary adnoma. Now the other thing here is central diabetes and cypitus. So this is something that you always want to think about potentially if a patient's coming in they have polyoria, polyypipssia, hyperetriia, maybe some dehydration, you should definitely consider could this be essential diabetes and cipotus and one of the big types of tumors that is associated with this one is uh cranoparangiomas. So if a patient has that tumor, let's say that they have that tumor and it's kind of like usually around here and it's kind of around the poster pituitary. It's compressing on the pit the the stalk here. So this stalk here between the hypothalamus and the pituitary. When that happens, you lose the ability now to do what? If you're compressing on the pituitary stock, you lose that cross talk between the hypothalamus and the posterior pituitary. Now, this is an area that's supposed to be making hormone called 1:51:18 ADH. But because there's compression here, you lose that cross talk here and you lose the ability to produce ADH. If you make less ADH, ADH is supposed to go to the kidneys and act on these receptors here. What's this receptor here called? It's called the V2 receptor. It's supposed to act on the V2 receptor, send signals to cause aquaporns to be expressed. But if aquaporns are not expressed, do you reabsorb water? Well, again, less ADH. Is it going to act on this receptor? No. This interaction won't occur, right? And so this signal to that aquaporin will be gone. If I lose that, then I can't reabsorb water. And so where does the water end up going? The water ends up being lost into the urn. And so what ends up happening is I get less water being reabsorbed and I get more water ending up in the urine. When I get tons of water in the urine and less water into my bloodstream, what can happen? More water causes to dilute urine, right? But it also is going to potentially cause you to potentially 1:52:19 lose so much volume that you can become dehydrated. So it can potentially cause dehydration. So that's one of the things that we get really really concerned with. One of the things that prevents this in these patients thankfully is that not only are they losing lots of urine, polyura, they get super thirsty to try to bring back that water. So they have polyypipssia. The other thing is when this the water in the blood gets really kind of like lower potentially what this can do is it can ride that serum sodium up. And so that's one thing that we worry about is potentially a hyper nitreia. So one of the big clinical presentations to think about this is if a patient comes in with polyurea polyypsia and potentially due to the effects of polyura this is where we get concerned could they come in with complications like hyperatriia and dehydration. Now the reason this would happen is that the patient is peeing a lot so much that they're losing so much water in their actual urine and they're not getting into the bloodstream that can cause 1:53:19 hyperonetriia right but they have to drink enough water. So if there's heavy polyura with not enough drinking of water this will cause hyperetriia and it will cause dehydration. That's why that can actually happen. But again this is highly and heavily associated with which type of tumor? This is associated with cranio ferreniomas. All right. So that would cover that one. So a lot of these tumors that we've talked about, they really can increase your intraanial pressure. They can cause seizures. They can potentially cause obstructive hydrophilis, vasogenic edema. But the ones that are a little bit more unique is the pituitary adenoma and the cranial fangioma. Those can cause hyper prolactinmia. Those can potentially cause central the eye. And guess what else they can do? They can cause the next thing botmporal hemopia. All right. So next is botimporal hemopia. Now again we can see this with tumors that are usually kind of going to be within that celotica re region and then what it's going to do is it's going to be big enough that it compresses on this structure right here. What's that? So this is going to be a tumor that compression. So it's usually due to 1:54:19 compression of optic kiasma. If I have compression of the optic kiasma again there's going to be two particular tumors that are within that region that I need you guys to think about. What are they? Pituitary adenoma. Usually it's a big one. Pituitary microaddenomas. ah they don't cause as much mass effect. Pituitary macro adenomas which don't usually carry that hyperp prolactinia type effect. Those are big enough that they can actually smash on that that um optic asthma. So again you're going to see this which with with types this is going to be the pituitary adenoma. Again if we're being really really specific which we talked about in the pituitary disorders it's a macro. And the other one would be a cranio fangiomas. Little pop quiz. What was that derived from again? the remnants of Wrathy's pouch. Yes. All right. So, these are the two tumors that we get worried about. Now, when they compress on the optic asma, what's the problem with that? Let's think again. I know that this was really annoying because we talked about it over there with the uncle herniation. I'm sorry. We talked about this a little bit with uncle herniation particularly the compression 1:55:20 of the posterior cerebral artery. Now, in this one, it's a little bit different. So, we're going to follow through. Again, it' be a good kind of test. Here we have the medial fibers. They carry this information and they cross. They go to the lateral geniculate nucleus. From here they send optic radiations to the primary visual cortex. Same thing here. This is going to carry this information here. Lateral geniculate nucleus. And then where does it go? It goes to the optic radiations. If we were to just be thorough though, we add this little part on here where we have these parts of the retina which is picking up from the nasal field. These are going to come here and they're going to stay on the same side. Go to the lateral geniculate nucleus. Optic radiations. Same thing here. Stay on the same side. Lateral fibers here. letters niculate nucleus optic radiations. Where is the damage occurring? The damage is actually occurring right here. Right in this portion is getting damaged. This is the medial fibers. The medial fibers pick up visual information from which parts? So again, they pick up visual information from 1:56:20 over here. So again, if we have the eye here and we just kind of squeeze an eye right here, what is it picking it up from? It's going to be picking it up from out here. So this area is going to be the one that we get worried about this potential visual field. And then again for this portion is going to be picking it up what over here this one. So these are the ones that we're going to be losing. Now if you think about that this is your temporal visual fields. Your temporal visual fields are going to be lost. What is that called? Betoral hemianopia. All right. Now with biotmporal hemopia how will the patient usually present? they'll present with peripheral visual field cuts. All that means is if I take my fingers and I have the patient look at me and I kind of come out here on the periphery and I say, "Hey, how many fingers do you see me pointing up?" They wouldn't be able to tell me that number because they're losing that peripheral visual field. Whereas the comparison of uncle herniation causing contraateral homonymous hemopia, they would lose this 1:57:22 visual field. If I had them, if I were to try to basically cover their eye and I said, "Hey, can you see how many fingers I'm pointing up on this side?" They wouldn't be able to do it because this visual field is being affected, that medial visual field. And then if I asked them, "How many fingers am I pointing up on this side over here?" They would lose that peripheral. So they'd lose their medial and they'd lose their peripheral. That's why we call it contrlateral homous hemianopia. All right? So it's again it's on the opposite of the particular visual field but it's on that same side which is in this case we're going to say they're both on the right side. All right in this case you're losing both temporal fields. So we got that now I think we got this bmporal hemopia pituitary adenoma cranioangiomas. The last one that I want to discuss is called parin syndrome. Parin out syndrome is almost exclusively seen in a specific type of brain tumor called a pinealoma. So we see this in what's called pineal. 1:58:22 So again we're going to have this tumor here which is kind of moving downwards through the tural notch and compressing on that dorsal midbrain. As it mashes and damages the dorsal midbrain you get some potential features. So let's take a look here at the midbrain. So here's our cross-section of the midbrain. We have portions of the midbrain like you have what's called the tectum. Then you have the tegmentum and then you have the podunkils which is the cerebral podunks. Within that portion of the tectum is the superior and inferior caliculi. The tegmentum is where we have things like your pretctal nucleus and your cranial nerve 3 nuclei. What happens is that you're going to damage a couple different structures in this scenario. The first ones that get damaged are these guys in pink. These are going to get damaged and these are called your visual gaze centers. So you're going to have damage to the visual gaze center. The next thing is you're going to damage the pre-tectal nucleus. So the pretactyl nucleus is another one that gets damaged. So damage to the pretectal nuclei. And again, I'll explain what all of these kind of like do relatively to 1:59:24 the disease process in a second, but these are going to get jacked up. And then you're going to have cranial nerve three nuclei which is going to kind of be both of these which again you have the sematic fibers in black and then your parasympathetic fibers with the edinger westfall nucleus here in green. These are going to get damaged. All right. So this is going to be your cranial nerve three nuclei which includes the sematic fibers as well as what other fibers? The edinger westfall nucleus fibers. So let's think about what would happen here. Three potential presentations can occur. The first one is these patients have what's called pupil light near disassociation. Another term just to be aware of this is called an argal robertson pupil. What happens is is you have damage son of a gun to the pre-tectal nucleus. You're jacking up the pretectal nucleus. The pretectal nucleus is supposed to and very simply receive information. So let's say here it's getting information from your pupil uh pathway. we the light reflex pathway, right? It'll go to the 2:00:25 pre-tectal nucleus and that'll communicate to your Edinger Westfall nucleus which causes your pupils to constrict. That's the pupil reflex. Light will come in, you hit the eye with light, send signals down, goes to the pretinal nucleus, communicates that to both of your Edinger Westfall nucleus, goes to your pupils, your pupils constrict, and you have a direct and then a consensual response. All right? The thing that we have to remember is that's being damaged. And so whenever you do the light reflex, there will be um no pupil constriction in response to light. So you'll do light exposure and there will be no pupil response. In other words, they will not constrict. So you'll expose them to light and when you do the light there'll be no pupil response. They will not constrict. But then what you do is you you say okay look at my so you shine the light in their eyes and when you do it you're not going to get that actual constriction response but then you say okay look at my finger and when you look at your finger and you have you kind of come in 2:01:28 their eyes should be able to constrict but also they can accommodate so they'll have the near response and so they will be able to constrict with their accommodation or their near response and so when you test accommodation or their near response they will have that type of response. All right, that's really important. The reason behind this is that you have damage of the pretectal nucleus which goes to the Edinger Westfall nucleus. The accommodation or the near response is from coming from cortical pathways and they're able to bypass the dorsal portion of the midbrain and they go straight to the edger westfall nucleus and so you still have a intact near response. So you're going to have a normal near response. So a normal near response but whenever you shine light into their eyes they will not have pupilary constriction. Uh funny enough you can also see this in patients who have tertiary syphilis. I always throw syphilis in there sometimes. All right the next thing is they can have what's called convergence retraction nestagmas. Convergence retraction estagmus is again you have cortical fibers cortical bulbar fibers that come 2:02:29 down in the third nerve nucleus. What happens is this is all getting kind of compressed and this is supposed to be inhibitory fibers. So the cortical fibers are inhibitory fibers. They're supposed to inhibit the third nerve from sending signals to the muscles all the time. But now you lost the inhibitory fibers. So what's going to happen? You actually gain a loss of inhibition. So then this this puppy's like, "All right, I'm going rogue." And it becomes super stimulated. When it becomes stimulated, it sends lots of these signals to two different muscles that we really want to think about. One is it highly stimulates the superior rectus and heavily stimulates the inferior rectus. We're going to stimulate the superior rectus, the inferior rectus and we're also going to stimulate the medial medial rectus. Now watch what happens which is kind of like it's kind of cool when you think about how this works. [snorts] When you contract on the superior rectus and inferior rectus, what's it going to do? It's going to literally pull the eyeball in because you know you're not 2:03:30 going to have that. They're gonna these both these muscles are going to be opposing each other. So you won't be able to go up or down. It's literally going to jack the eyeballs back into the socket. And then the medial rectuses are are both going to contract. What's going to happen? That addu. So you get this convergence of the eyes. And I'm not even kidding, the eyeballs get sucked into the globe. Like the globes get sucked back into the socket. So it's called a convergence retraction nestagmus. And then lastly, you have destruction of the vertical gay centers. The vertical gay centers are supposed to communicate between the fourth nerve. So they're supposed to be the fourth nerve or cranial nerve four which is the tlear nerve and cranial nerve three. Both of these are supposed to be communicating with one another control your vertical gaze. But this vertical gaze center is jacked up. So you don't send signals as well appropriately to the fourth nerve and to the third nerve. And so what happens is your ability to lift the eye upwards is impaired. And so because of that the eyes actually they have a limited upward gaze and actually they 2:04:30 have they can sometimes in worst case scenarios they can sit down. We call it suns setting eyes. So one of the things that we get worried about is that if we ask them to look upwards they can't. And then on top of that not only can they not look up sometimes the eyes sit downwards and it can cause something called a suns setting eyes. So, sun setting eyes that we get kind of worried about. That was a lot for brain tumors. At this point, we've covered the patho. We've gone over the causes. We've talked about how these patients could classically present. We talked about findings of increased intraraanial pressure. We talked about how they could present with seizures, obstructive hydrophilis, vasogenic edema, indocrine dysfunctions like in hyperpolactinmia, central DI. We talked about how they could come in with loss of visual fields from both temporal visual fields or peripheral visual fields. And we talked about they can come in with limited ability to put their eyes up, how their eyes can bead inwards and get sucked back in. And on 2:05:32 top of that, sometimes they can't even have a pupil response to light, but they will upon an accommodation reflex. So now the question is is how in the heck am I supposed to determine if a patient has a brain tumor? Let's put all of these things together and go through our algorithm. All right, my friends, let's dig into this. We're going to talk about the diagnostic approach. So we spent a lot of time talking about the different types of brain tumors, primary versus secondary. Really talking about them and dividing them into superenrial, infrotentorial. We talked a lot about the classic clinical findings that we can see with these diseases. Oftentimes depending upon the location of where the tumor is determines the focal neurological deficit, the associated headaches, nausea, vomiting. Obviously those are a lot of things that we talked about. Plus, we really really dove into the complications that could be potentially possible, especially that of vasogenic edema, obstructive hydrophilis, potentially seizures if it's a cortical lesion. And there's a lot of things that we discuss. So, what I want to do is I want to take the time to say, let's put this together in a way 2:06:31 that hopefully is systematic. It's organized, and it helps you to be able to think about these clinically. So when you're on the wards and you have to evaluate a patient or if you're presented with a clinical vignette, you know how to stepwise go through this process. Let's dig into it. First thing is when a patient presents with classic findings or complications of brain tumors, you should start thinking about just in general a structural lesion of sort. So if they come in and they present with a headache that's usually worse in the morning, if they have associated nausea, if they have vomiting, if they have focal neurological deficits, a first onset seizure, new onset seizure, never had a seizure before, think structural brain lesion. Um, I think the other thing that's really important is if you do happen to pull up that that opthalmoscope and you take a look and you're like, "Oh, you look at the fundus." I know that's not always easy, but looking for evidence of papa edema is also crucial as well. So, I think those are really important complications. Often times these patients will present very very sick. 2:07:32 Um, if you have a brain tumor that's large enough, it could cause herniation symptoms. And so, watching for a fixed and dilated pupil, watching for a declining level of consciousness, watching for worsening hemiparesis or loss of sensations, breathing, cardiovascular changes. These are all really really crucial to consider. So when we think about this, whenever a patient presents with a new onset seizure, focal neural deficits, a really bad headache that's worse or it's becoming like associated with the morning headache, the nausea, the vomiting, any signs of herniation, you get a non-contrast head CT. The [clears throat] reason why we go with a non-contrast head CT first is you're trying to sus out other differentials. And what I mean by that is if I have someone coming in with a new onset seizure, if I have someone coming in with a headache, if I have them coming in with focal neural deficits, I don't know if it's a stroke, I don't know if it's a bleed, I don't know if it's a tumor, I don't know if it's something else. And so it's really, really crucial to take a look at that. Now, let's say that we do that and we end up finding, 2:08:32 hey, there is a brain mass. It's always important to categorize that as is it superal or infratorial. So one of the most common masses that we see in adults unfortunately is a glyobblastoma multififor right and this is a really really nasty type of mass. Usually what happens is when we look at this one you can see that it spans across the corpus colosum and so it crosses midline. When you take a look at this one, it's not easy to see it crossing that midline as much, but you can see here there's definitely what looks like some kind of changes in color, some hyperdensity, and you see a lot of this darkness here. This is probably the tumor and all of this around this is probably surrounding vasogenic edema. If we look at the MRI, though, we're just to say, hey, let's get an MRI to get a better look, a definitive look and get an idea of what's going on here. You can definitely see how this crosses midline, right? Lots of central necrosis, lots of this kind of hyper intensity around the 2:09:33 tumor. This is definitely classic. You see a tumor crossing midline, you definitely want to think about a GBM. All right. Now, another one is extremely common. It's probably one of the most common benign superal tumors is meningiomas. And so, this is usually extra axial. It's not usually intraarinal. Um, and it's because it's a part of the menial growth. Um, usually these can occur parasally, paraphaline. So this one is an example here that you can kind of see. This is a really solid, very hyperdense mass that's near the kind of like folks. That's a pretty common one. If I took a looked at an MRI, you can really appreciate how this is causing massive compression of the brain tissue and leading to some like just minor midline shift here. Probably causing some degree of compression. Uh, another one is an oligodendro glyoma. These are relatively rare. I wouldn't be first to think about these, but if you do see these, they can occur bifrontally. Um, and they also are just generally a pretty common frontal lobe mass. Um, so this would be something that you may see. If you take a look here, you can 2:10:34 also appreciate it here. All right. The next one is a cranoparangioma. These don't oftent times present like super easily. One of the ways that they can present that we talked about is they can present with central diabetes and cypitus. Um, cranopharreniomas are kind of one of those where they are they possible for them to cause optic kiasma compression. I'd say that's more likely with a pituitary tumor, but cranoparreniomas definitely can do such thing as well. With this one, you're definitely looking at the supercellar area. And so you can appreciate here, look at this. So here's our pituitary gland, and it's going to be right here, supercellar. So it's just above the celotica. We can appreciate a pretty good mass right there. And if we um look to the next one, a pituitary adenoma. This one's definitely sitting within the celoterica um of the sppheninoid bone and we can appreciate that all right here. This is a pretty nasty pituitary adeno and it's a pretty decent sized one. And uh one of the things you can actually see here is the sheer volume and size of this thing. It's definitely easy for this to cause some significant compression of the optic. That's where 2:11:35 you get that bmporal hemianopia um that's associated with this one as well. So we can really appreciate superenal tumors. These are the big ones that I want you guys to be thinking about. When we talk about the next one, we're talking about infratorial. So infrotenctorals but below the tentorum cerebelli. It's that kind of like dural septa that really separates the upper part of the brain superentory from the infratorium. And so we'll kind of talk about these. One of the big ones that's really important to remember is pyloitic astroytoomas. So this is kind of like a type one uh glyopblasto. And so you can see here that this is a cerebellar mass. And so when we look at these, these are usually in like a lobe um of the cerebellum. And they're pretty like cystic appearing. So you can see here a pretty nasty looking pyloitic astroytoma. Another one that they can occur is along the optic nerve. So I would remember that one as well. So these are pretty nasty ones and they definitely can cause some mass effect. So you could see some changes like atexia, some vertigo, um some changes in their overall coordination would be pretty common. And if it's pretty 2:12:31 decent, it can compress on the fourth ventricle that lead to obstructive hydrophilis. Here you can definitely appreciate with the MRI how cystic appearing this thing is. And again don't forget that these can occur along the optic nerves. You can get optic nerve glomomas. A medelblasto is a really really high yield one. This one usually occurs along the cerebellar vermis. And because of that it is very very likely to cause mass effect on the fourth ventricle. You can see just by looking at this thing you see how this is really a large mass and it's compressing and facing the fourth ventricle. That cerebral spinal fluid can't move. And guess what happens? The third ventricle gets ballooned up and then here's your lateral ventricles and the temporal horns of the lateral ventricles. These things are huge. So obstructive hydrophilis is very very common uh with this type of tumor and again you can appreciate it here with the hyperintensity that we see here especially on the T2 imaging. This is how really causing a lot of obstructive hydro. All right [clears throat] so appendimomas these are not very common but when we think about these these are kind of derived from the appendimal 2:13:26 cells. So they're going to really occur in the fourth ventricle and they can kind of kind of extrude out a little bit but they're mainly going to be a fourth ventricular mass. And so these will definitely cause obstructive hydrophilis. You can already see the temporal horns. They're pretty decent sized. You shouldn't be able to see them this big. Um, and so you can see here this mass. It's kind of encroaching. It's definitely in the fourth ventricle, but you can see it's kind of encroaching into the cerebellum causing a decent amount of mass effect. MRI, you can definitely appreciate how well defined this is inside of the fourth ventricle. Really occupying that. This is a pretty nasty one. Heangoplastoomas are not something I want you to spend a lot of time about, but I want you to think about these especially associated with the exams for von Hippolindow uh disease. So with vonipolinda this is a mutation that occurs in the von hippipolindown gene just on chromosome number three um and this is usually associated with like hemangoblastoomas which can occur in the cerebellum can occur in the retina but it's also commonly associated with renal cell 2:14:18 carcinoma and even fiochromosy which is the tumor of the adrenal medulla. So definitely something to think about with this one. So cerebellar mass is going to be what you'll have and it's very vascular highly highly vascular type of mass that you would see here in the cerebellum. All right, but you definitely want to think about this in patients who have also associated retinal heangio blastoomas, maybe a fiochromocyto and on top of that maybe maybe even a renal cell carcinoma. So that's something I would think about for this one as compared to the other ones. It's not going to be super high yield but in a classic clinical vignette and someone who's presenting with renal cell carcinoma, retinal heangoplastoomas, fiochromoscytoma uh then I would definitely be thinking about this one especially associated with von hippolindow. All right, here we can definitely appreciate the size and sheer kind of like description of the tissue surroundings with an heangioblastoma. A vestibular schwanoma I would say is really important. Remember we'll talk about this a little bit more um ent because it has an effect on balance and also on hearing particularly tonitis. Uh 2:15:14 you might get some vertigo associated with this um and so and even some deafness too, some sensory neural deafness. So it's really crucial to think about this one. But what I really want you to think about with these ones is they occur on the cerebellopontine angle. And one of the key things that we talked about is that when it's associated with a genetic condition called neurop fibromyitosis type two, it's usually bilateral. So you can appreciate here a decentsized here on the right nasty looking cerebellopontine angle mass which is likely vibroanoma. And you can appreciate a smaller one but still kind of a hyperdense sign over here on that left side around that petrus portion of the temporal bone. All right. Here we can clearly see the differences and the hyperintensities here that are showing a lot of enhancement at that cerebellopantine angle. So this is a bilateral vestibular juwanoma. Definitely think about these when you see this when you see bilateral think neurop fibromyitosis type two. All right. Now pineal not common but again something I would think about especially in a patient presenting with sunsetting eyes um which we can see we can also 2:16:14 appreciate that they can have other signs of perinode syndrome. Um and so a perinile syndrome they have that vertical gaze pausy so the sun's setting eyes and they kind of have that weird contraction retraction nestagmus as well. Um and so these are something I would think about with the perinode syndrome as well. All right. You can appreciate here kind of the pineal gland kind of sticks backwards because you should generally have you know when we think about these you'll have a portion called the um the hypothalamus and then you'll have the pituitary gland here and then you should have in this vicinity the phalamus and then over here is your pineal gland and that's going to be where this tumor is really forming and this is going to be kind of pushing dorsally and that's where you get that dorsal kind of like compression of the midbrain and that's where you see that perinaut syndrome as we can kind of see written here. All right. So, this is really kind of covering our infrarctoral masses. And I think this gives a really good picture, uh, you know, literally as to what these could look like. And I think oftent times looking at them based upon an image like a CT or an MRI, it 2:17:14 doesn't diagnose the tumor. It just gives you based upon what you've gathered from their history, what you've gathered from their physical exam, what you've gathered from other potential labs and fi and other findings, what it could possibly be. But the differential should remain the same that when you think about a superal mass you go through the list. You think about a GBM, anoma, an alodendrioma, a cranoparangioma, a pituitary adenoma. And you think about those um when you have a infrontal mass, you think about a pyocitic astroytoma, a medeloblastoma, an appendom, you think about a schwanoma, you think about a hemangioblastto and a pinealoma. Obviously depending upon the locations, the look, the overall effect of that, that's going to give you some ideas based upon these images of what it's most likely like. But I think the other thing that's really beneficial of again the non-contrast headcts is ruling out other complications. Look at this. You can appreciate when you get a pretty nasty mass. This is likely a GBM. Uh because you can kind of see it's really kind of getting close to crossing that midline around that corpus colosum. But 2:18:15 this is a tumor probably sitting right here. And you see all of this on T2, all of this kind of like hyper intensity spreading out. That's that's vasogenic edema. Uh, and so you can really really appreciate that uh on the T2 image, but really more so on that T2 flare because the T2 is going to fill up the ventricles as white too. But this one you don't see that. And so this T2 flare really shows you a lot of vasogenic edema. And vasogenic edema is really going to cause a lot of problems with headaches and midline shift which can lead to some symptoms of herniation. All right, here we can appreciate obstructive hydrophilis to the maximum. So we probably have an infrontatorial tumor um as we can kind of see and it's likely what would happen with these patients is it compresses and it faces the um fourth ventricle and then everything above that gets filled up. So you can kind of see the third ventricle is huge. Look look at these the these are like watermelons. They're lateral ventricles. They're huge. The temporal horns are really big. You can see here this ventricle is really really large in this view. So this is an appreciation of seeing how a mass can cause compression 2:19:16 on that fourth ventricle. they face it and then unfortunately we end up with a lot of uh back flow into the ventricles and sometimes if you look closely on MRIs you can even see some transependimal flow across the ventricles um and so that's a really really important thing but this is definitely classic for obstructive hydrophilis you can kind of really appreciate all of these enlargements um here's another appreciation so CT is really the best thing it's the easiest thing you can see here is a big tumor and it's compressing and it's causing all of this backflow look at the third ventricle it's gargantuous look at the lateral horn the temporal horns and lateral kind of like ventricles with the anterior horns. They're pretty big and this is definitely a sign of compression. What I wouldn't want to see and I'd be scared to see is something like this. So, this is a tumor. It's got lots and lots of surrounding edema that it's causing the uncus, you can kind of see it here, to push out over the tentorium. Um, and unfortunately that will cause compression of the midbrain. And so, you can see that there is a lot a lot of compression here. And that's nasty. That's usually a sign of uncle 2:20:12 herniation. And that can lead to a a fixed and dilated pupil in this case on the right side. They can even have some contrlateral hemiparesis and and so if you get it really bad enough it can actually smash it to the other side and you get what's called Kernan's knock syndrome where you get ips IPSal paralysis as well. So this is definitely something I would want to think about. We can also appreciate here that because of the surrounding edema it can kind of push um some of the parts the tissue on this side the right side underneath the faulks and it can actually herniate underneath the false cerebra. So we call that subfausalian herniation that can actually cause compression of the arteries of the anterior cerebral artery and you can actually get unfortunately you can get compression of those and you can start losing. So if you imagine here let's say that the tumor is here on the right side they would compress this side. Well all the nerves go to this so you could potentially start developing some symptoms of hemiparesis. Um and usually that would be unfortunately in this case it'd be on the same side. Um so they can definitely develop some ipsilateral hemiparesis due to like some 2:21:07 subfalene herniation. So that'd be that'd be pretty concerning especially of the lower limbs. All right. So we can just see and appreciate how the midline shift is significant here. Uh whenever you have a lot of mass effect like a big tumor um like a vasogenic edema, like a bleed, all of these things according to the Monroe Kelly doctrine says that if you have more blood, more brain tissue, more CSF, it's going to cause unfortunately shifting and movement of that tissue because the brain is in a fixed space which is the skull. And that's going to lead to pressure rising and unfortunately herniation. All right. So, this gives us a look at why non-contrast headct is a really good go. I showed some MRIs in there to just help you to appreciate a little bit more about what it will show us for these masses. But I think the most important thing is though although I did show you the brain MRIs in this, I want you to understand that it is the gold standard. So the purpose of an MRI is that it really gives us a contrast. Um particularly whenever you have a patient who has let's say a CT scan and it looks 2:22:07 like it could be a mass you want to see if the mass enhances uh you want to see if you get some enhancement and that usually is an indication of a lot of vascular kind of like supply to that area and some breakdown in the bloodb brain barrier and so that's really really crucial. Another thing is that when we get MRIs, it's really helpful to see if this the lesions are more like one lesion in one location or if it's scattered and it's all over the place, especially near the gray white uh junction because those are more likely to suggest metastatic lesions. So again, if I see one lesion as we showed above and it really has some ring enhancement, that would more likely suggest a primary brain tumor. Again, if it's super tentorial, then you go through the list. a GBM, an oligodendro, a meningioma, a pine, I'm sorry, a um fing cranioangioma or a pituitary adoma. If it's an infrontatory, you go medblasttoma, you go appendimoma, you go to pyocitic astrocyto, you go down the lines of a vestibular schwanoma or a pinealoma, 2:23:10 etc. Now once you have done that and you say okay I did the CT scan showed me a mass showed me maybe some complications got the MRI definitely showed some ring enhancement showed the location of the tumor gave a better look at it as we saw already then I need to figure out which one is it so we got imaging diagnosis I need tissue and that's where I would say getting a brain biopsy or doing a cranottomy with a resection would allow for us to first off help therapeutically by removing that tumor and some of the mass effect, but also it's going to be diagnostic. So here you can appreciate like a a stereotactic kind of brain biopsy where we make a small little hole and we kind of stick this needle downwards and kind of take out some pieces of that tissue. And you can also just fully do a cranottomy and resect a large portion of that tumor and again send it off to the pathologist to figure out which type of tumor it is. And that's really what you're going to be looking at is you're going to be looking at that hystopathology. This is going to fit more in the step one kind of categories. You may see some questions 2:24:10 on on your step two, but not as likely. What I want you to take away from this is really that the hystopathological diagnosis is going to be paramount to determining what type of tumor it is. So, GBMs, yes, you can make an assumption based upon the imaging for the most part, but hisystopathology would be the best way to go here because it's going to show you that pseudoalisating necrosis. As you can kind of see right here, this is a pseudopalisad necrosis. And if we stained it for the GFAP, uh, then that's definitely going to be able to show me a positive GFAP stain. All right. If I said meningioma, this one usually shows these things called samoma bodies. And so you're going to see what looks like these kind of swirls and whirls of tissue here. This is classic for um an area of what's called a meningioma. Alendricoma has the classic term kind of a fried egg appearance. And if you check for what's called a um isoccitrate dehydrogenase mutation that'll come up and they could even have some code deletions. But you can kind of see here here's the the the white of the egg and then here's the yolk of the egg. That's 2:25:12 that fried egg appearance that we look for with an oligodendricoma. Cranopharangiomas have these things called like cholesterol crystals. And so if you can kind of look here, this is a huge chunk here of where we would have these cholesterol crystals. So this would definitely be more suggestive of a cranoparangioma. But this is kind of some basic hystopathology that I would want you guys to be considering. When we think about infrarctoral masses and if we were to take and biopsy that area or resect that area again you're thinking about things with a pyocyic astroytoma. They're kind of like same same thing to a GBM. They're more just like a stage one. They'll still have that that GFAP staining, right? But when we look at these, they have these really bright rosenthol fibers that really kind of stick out here. All right. The next thing is a medulas. Medulastos are really really nasty ones because they can have drop metastases. But what we look for is the homeright rosettes. And you can kind of see this similar to the pseudopalating necrosis of this central kind of pink core with lots of cells surrounding it. This would be a homeright rosette. All right. And 2:26:13 appendimoma is again going to be a pretty uncommon one in that fourth ventricle mass. But when you look at these again, they have the pseudo rosettes and they're a very vascular one. So you can appreciate look here. Here's the vasculature. Here's the vascular vasculature. And you have these rosettes around it. All right. So, that's a pseudovvascular rosette there. All right. And angoplast are just super super vascular. When you look at these, they're highly vascular lesions. You can see here all of these red blood cells and you can see all of the tissue kind of surrounding it. Um, and so this is really going to be pretty common of a heangio blasto. Uh, the last one's a vestibular schwanoma. This one actually is kind of important when it comes to these. I think that similar to the fried egg appearance that we see with the aligodendricoma and uh the pseudopalicating necrosis with the GBM I think this is one that is worth remembering because of the Anthony A and Anthony B areas. So you can appreciate here on this kind of like whiter or let's say kind of like the lighter pink colored side there is a a tissue difference and then over here there is this kind of like more purple 2:27:14 appearance. So the dense hyperscellular environment which is this darker color is called the Anthony A bodies. And then over here this loose hypocellular kind of lighter pink color is your Anthony Bodies. And so they can have some really really important things to kind of distinguish this and that's really going to be common for vestibularomas. All right. So, we've taken a pretty good look here at understanding that when we talk about masses, you see them with imaging based upon their symptom presentation. CT is kind of the first way. Get a better look with an MRI and then get a tissue diagnosis to determine what type of primary tumor we have. When you got a tumor that is not just one but multiple all over the place and they enhance, I would be concerned again about a metastatic lesion. Could it be things like toxopplasmosis? Yes. Could you have one ringen enhancing leion? Could it be primary cus lymphoma? Yes. Could it be a brain abscess? Yes. 2:28:15 There's a lot of different things. But when you see scattered and they have an underlying history of a primary cancer, lung, breast, I think those are really really important to remember. Melanoma, renal cell carcinoma, papillary thyroid cancer, all of those things are very common for these tumors to spread. Um, and when they get into the brain, they occur everywhere. As an example, this is more characteristic of a metastatic brain cancer as compared to a primary brain cancer. I can look and point out multiple metastatic lesions that are enhancing. All right, that's more suggestive. And they really occur very commonly along that gray white junction. That's going to be important. Now, when we think about if we find this, let's say that a patient cames in, they had a new onset seizure. You get a brain CT. You find some potential lesions. You get an MRI. You say, "Oh my gosh, there's scattered lesions all over the place. This is brain metastasis. Where did it come from?" You have to go and find that. So, you probably have to pan scan them, get a CT, chest, abdomen, pelvis. I think PET CTS are pretty good as well, 2:29:17 especially if the chest, abel doesn't come back with anything. Pet CTs are pretty good. But either way, these are going to show something. So for example in this patient we got a PET CT and we can see lots of different areas of as we can appreciate here of enhancement. All right now once you've done that we should probably biopsy that area. All right because if you say that you find like a lung mass somewhere you find a breast mass somewhere a colarctal or renal mass somewhere you should probably go and biopsy that area because it's probably a primary cancer that is metastasized. So that's what I would do is I would definitely get a biopsy of that primary area to confirm and say okay this is definitely from this area and that is the likely source. It's not a primary cancer. All right. So that's a lot and I know it's a lot. So what I want you to do is okay let's say now we've gone through we say okay patient who comes in they got nuance that seizure they got focal neuro deficits worsening morning headaches with nausea vomiting maybe some papal edema they got some weird presentations I get a CT I find that there's no other causes but I see some weird like mass-like structure 2:30:18 maybe some associated complications what do I do now get a brain MRI brain MRI is going to show an enhancement it's going to show if it's a one lesion and it's going to make sure that it's actually in this particular location that may suggest maybe one primary cancer over another but you may have to get a tissue diagnosis to confirm If it's multiple scatter lesions along that gray white junction, I can think that it's metastatic. Look for the cancer somewhere else. Pan scan them, get a PET CT, find that and biopsy that area to say it's a primary cancer that metastasize. All right. When we think about treating these though, it's obviously always treating the emergencies or the urgent kind of things first. So, I think one of the big things if a patient comes in and they're herniating, uh, your first goal is not going to be, hey, let's let's let's uh let's get an MRI. No, no, no, no, no. we should definitely figure out uh how we can prevent them from herniating and unfortunately succumbing to brain death. And so oftentimes in acute scenarios like this, um I'd say it's not as common because they don't just rapidly expand as much. I'd say that's more common with 2:31:10 like a subactoid hemorrhage or a brain bleed or a stroke that has malignant cytotoxic cerebral edema, but it can happen. I've seen it a couple times with um really large brain tumors with significant amounts of vasogenic edema. You'd want to give them like hypertonic saline or manitol. Uh that's really just a temporizing measure. it's only going to help a little bit to kind of reduce some of the swelling. Um, and it's not going to be a great therapy, but it's going to be the best that you can do to kind of reduce the ICP temporarily. Um, surgical resection would be kind of barn on the the top thing because you're going to want to remove the structure that's causing a lot of this problem. And that's usually the problem with a brain tumor is that unless it's bleeding or it's causing a massive amount of obstructive hydrophilis or vasogenic edema, the osmotherapy will only help for a very, very short period of time. You have to surgically resect these, put an EVD and get them on steroids. Really so this is where I would do like a cranottomy and I would remove that tissue. That's going to be the definitive therapy. All right. Now external ventricular drain is great. 2:32:05 Like I said if you have a tumor the big things is obstru obstructive hydrophilis and vasogenic edema. Osma therapy like manitol hypertonic saline those are really really quick things but you need to get to the surgeon and say hey we needed to remove this or we need to put a drain in. Um, and the point of the drain is because if you have a tumor that's really compressing the ventricles and building up CSF, it can't flow. You're building up CSF in the the skull and it's going to cause the ICP to go up. So, I' I'd pop in an EVD. Um, that'd be the first and quickest way is where you would access this. This is usually a bedside procedure. They pop it in around the tion and they try to get that into the area of that third ventricle. Um, and then you're going to kind of pull off that fluid. Um, usually if you look here, this is a very common one when you work in a neurological ICU. They like to zero this off of the tragus, which is that's what it's representing. But it's going to help to allow for the increase in pressure inside of the ventricles to have an alternative s source to divert it somewhere else. If it's not moving down because there's some kind of mass 2:33:00 compressing here, you want to provide an alternative source and that's where it's going to drain into this bag. Um, and so that's the whole point of that is to really drain off any of this excess fluid so that the pressure because the CSF as it starts to reduce the pressure starts to go down. This would only be again another temporary thing. it would be temporary to do before I can get them to the surgery and get that actual tumor out. Corticosteroids are great, I think, initially up front. If a patient's in an ICP crisis, it's not going to be the best thing, but it's something that will help at least to reduce some of the vasogenic edema because what it does, it actually helps to reindothelialize the capillaries um and help to reduce some of that leakage um that you're getting with these kinds of problems here. All right, that vasogenicadeema is really going to be a lot of like capillary leakage, break down the bloodb brain barrier and you're going to try to help to reindothelialize that and kind of reduce that loss of fluid. All right, with obstructive hydrophilis like overall when you think about this an EVD is definitely good upfront, but long-term is what you have to say. Am I 2:33:59 surgically resecting the tumor? If you're surgically resecting the tumor, great. But let's say that you have a patient who you surgically reected it, but there's still some residual tumor or they're still having obstructive hydrophilis or they can't get a tumor removal because of the location or because the surgeon's not going to do it. You need a way to continue to divert that fluid. So, how do I do that? Well, I need a chronic CSF diversion. And so, what I'm going to do is I'm going to tap into the ventricle, but I'm going to reroute it down through the neck. I'm going to go all the way down here into the paritinium. And I'm going to do what's called a VP shunt. And when I do that, it takes a way of instead of draining it out of the body because a person can't live walking around with a pole where it's diverting fluid uh into the EVD bags. No, we have to have something where it kind of goes based upon gravity. And that's what the whole purpose of the VP shunt is is to allow for CSF when it is building up to divert down via this gravity mechanism into the paritinal cavity. And that's the whole purpose of this basogenic cerebral edema. Again, we talked about this. It 2:34:57 can cause an ICP crisis. The only thing that really helps with this is like dexamethasone. So hitting them with like usually if you really want to know 10 milligrams of dexamethasone up front and then putting them on scheduled dexamethasone after that every 6 to 8 hours will help. And eventually you'll have to taper them off that because you don't want to keep them on that forever. But that's going to help with some of the associated visogenic edema upfront that's causing some of their symptoms like ICP changes or headaches and neurological deficits. All right. So the last thing is seizures. So when a patient comes in seizing obviously if their cause is a brain tumor uh you have to treat the underlying tumor but sometimes if you can't remove that tumor uh you have to treat them and so it's really really really important that we commonly use things like levatorazz we can use things like valproate or phosphenito these are very common anti-epileptic drugs the key thing that I think is really important is that we don't give these to a patient who has a brain masses and have never had a seizure it's very controversial out there but the guidelines do suggest 2:35:56 unless the patient has had a clinical seizure, you should not be giving them anti-epileptic drugs as a prophylaxis. It's given primarily if the patient is actually having a new onset seizure clinical events. That's when this would be truly indicated, but that's again relatively controversial. So the last thing I want to talk about is when we're trying to treat these like inevitably which is kind of trying to remove the underlying source surgery is the key thing. It's just a matter of how we're going to surgically resect these. Usually cranottoies or even removing a larger portion of the actual skull like a craniactomy and trying to resect that tissue is going to be the best way to go. That's going to help to remove the tumor mass. It's going to help to be able to relieve any of any kind of like mass effect that can cause complications like vasogenic edema, midline shift with herniation, ICP changes, hydrophilis, etc. All right. Radiation therapy is something that we can do. External beam radiation therapy. I'd say that's going to be something that we would do if they have metastasis. Um, so whenever a 2:36:59 patient has diffuse metastasis, so they have a primary lung cancer and it's spread to the brain, external beam radiation therapy would probably be the way to go for that one. You can consider it after a patient has had a GBM removed, but I want you to primarily remember that it's going to be more likely to be used in metastasis that is all over the place and you can't go and pluck out each one of those metastatic lesions. So hitting him with focal beam radiation would be the best better way to go. All right. Now stereotactic radio surgery which is a type of radiation therapy is called gamma knife. It's a very localized. It's super localized. You have a bunch of gamma kind of like a bunch of radio waves and the gamma rays that are coming shooting in on one specific location. Um gamma knife surgery is a really really good one that we do with all right the other type of radiation that I want you to know it's particularly for vestibular schwanomomas is a stereotactic radius. This is essentially gamma knife. It's like a really like high localized focused area beam of radiation on a tumor, especially 2:38:00 uh vestibular schwanomomas. You can hit those with a pretty good focused area of radiation. So you can kind of see how these rays are really really highly focusing on one particular location. That would be a true benefit for something like this. We also use it a lot in trigeminal neuralgia um too to help to kind of kind of destroy where that kind of like trigeminal ganglion is at and especially near where there's compression uh where the actual vessels are. So this is a really really common one that we can use in vegetable schwanomomas and trigeminal neuralgia. A chemotherapy teemolomide is really the go-to for patients who have GBMs. Um when you have a GBM teemosomide is interesting because it plays a role with the blood brain barrier. When you think about the bloodb brain barrier here, you can appreciate that we have the vessels. So we have the endothelial cells. They have really really nice tight junctions and then on top of that you have the associated aststerytes which are helping with the formation of that bloodb brain barrier. When you have a drug like timolomide, it's not as it it has a it has a good ability to be able to cross the bloodb 2:39:00 brain barrier, but what it actually does is and especially if there's breakdown of the bloodb brain barrier, it's going to cross a lot easier. it can find a gloma and when it gets into the gloma basically what it's going to do is it's going to try to shut the DNA off. It it produces an active molecule that basically controls your DNA methylation. Uh and so you end up with a lot of these doublestranded DNA breaks which causes these cells to unfortunately go through their death process. And so that's really what teosolomi would be utilized in a patient who has a high grade GBM. So when we think about GBMs the best thing to think about upfront is do they need surgery? Okay, try to you can obviously consider resurgical resection if possible. After that, you can consider some radiation therapy if it's a very high-grade one and you can consider teemazolomide. Oftent times GBMs have a very very pro poor prognosis though. But this is what I want you to think about with that. Man, this was a lot and I really I really hope that at the end of this you feel a little bit more comfortable with brain tumors. I feel like you know what to do step by step that if you ask what's the next 2:40:00 test? What will this test show me? What will it give me? Will it actually help me in my diagnosis? Okay, if I do that, what's the next test to confirm it? I really hope that at the end of this, you feel confident with that. And also being able to decipher and differentiate between other types of disorders or between primary and metastatic. I hope that whenever you think about treatment, treat the emerging cases. Oftentimes, it comes down to surgery if you need it. In ICB crisis, temporizing measures are usually the best thing until you get to that surgery. things like osmotherapy, manitol, EVDs and steroids. Ultimately, seizures should be controlled if they're having a seizure with anti-epileptic drugs. If not, we don't really give them prophylactically. Often times with these kind of conditions, surgery is the way to go. But sometimes you may need some associated external beam radiation therapy, especially for the higher grade GBMs, but it's more beneficial for the diffuse metastasis or the primary lung cancer somewhere else. And then gamma knife was the last one that we talked about being more particular for things 2:41:00 like trigeminal neuralgia and vestibular schwanomomas. And then don't forget about the teosoline especially if they have the IDH mutation the one uh the code deletion I would definitely consider that one. It's going to be a little bit more beneficial. All right my friends I hope that you guys like this. I hope you learned a lot. I love you. I thank you guys. And as always, until next time.
