This on-demand teaching session is perfect for medical professionals, particularly those interested in neurosurgery. We will be exploring the anatomy and pathology behind neurosurgery and pathology. Our highly knowledgeable speaker, William, is a penultimate year medical student at Oxford University and is here to provide you with a 12 point learning lineup to better understand the inner workings of neurosurgery. He will be using a variety of images and diagrams to make his learning points more interactive and effective. William will provide clinical relevance to the topics discussed and cover all the information you need to pass exams. He will also provide insight into niche topics so you can further your understanding of neurosurgery.
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Learning objectives

Learning objectives: 1. Identify the five layers of the scalp. 2. Identify the eight cranial bones and how they correlate to the brain lobes. 3. Understand the clinical relevance of scalp lacerations, specifically why they tend to bleed more than expected. 4. Describe the three meningeal layers and their specific functions. 5. Explain the significance of the temporon, including why its the weakest part of the skull and the artery running underneath.
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Computer generated transcript

The following transcript was generated automatically from the content and has not been checked or corrected manually.

Supped up this week. We're going to be having a look at neurosurgery with today's session focusing on any or neurosurgery. Uh speaker for today is William and he is a penultimate year medical student at Oxford University who has interested know as well as a N E and E D. Um You're a brilliant hands today and will is really good and he's got a lovely 12 point lined up for you. So um over to you will thank you, Hannah uh evening everybody. Um Thank you for the great introduction. As I said, I'm will, I'm penultimate um med student and put together this session for us today. Um Just before we start, I'm going to put in the chat. This is my first time using medal. I don't know if that's the case for the rest of you, but I'm gonna try and use the pole feature a little bit to get a little bit of interactivity going otherwise. I mean, it's half six on a, on a Wednesday. I wouldn't blame people for, for nodding off about halfway through otherwise. So, um if I throw a poll out that this is just to gauge a little bit of an idea of who's tune in, in, um, to help kind of pitch things. You know, if, if I'm facing a room of budding neurosurgeons that might make me phrase stuff a little bit differently to, if everyone's here just wanted to know, like, what do I need to know for my exams to ask them? So, a few options there, you just here because you want to pass exams, you want to know what you need to know. Are you here because you're really interested in surgery? But you don't really know what in surgery? Are you really interested in neurology or something? Neurological, whether that's surgery or otherwise or are you already, you know, nailed down? I want to be a neurosurgeon. Here we go. Um, I think I might need to answer to actually see the feedback. So I'm gonna work. I want to pass exams. There we go. That's coming up. Good spread. So, eight responses. Few budding neurosurgeons, a few budding urologist slash neurosurgeon slash neuro intensiveness. A few budding surgeons more generally and some people who just want to know what they need to pass exams. Okay. Good. Well, hopefully what's in the presentation today will have the information for all of you and a little bit extra for those who want it. Um, so if I just sort of thank you to our partners slide and then this first slides just outlining kind of what we're going to cover today. And how we're going to cover it. So the there's quite a lot of content, the intended learning objectives have multiplied a little bit from previous years. Um And that was, that kind of expansion of them was mainly done by referencing the MLA to try and make sure it's relevant to everybody. But there are points where I've got a little bit beyond the M L A or added in topics that we thought were worth knowing even if not explicitly kind of under one of those MLA headings of either presentations or or pathologies. Um unashamedly, this presentation is very visual. Okay, lots of pictures, lots of diagrams. Part of that is that's kind of how I best learn. And so how I think I can best communicate the information. Part of that is surgery is inherently very visual, right, deeply rooted in your anatomy. And I think there's a good argument to be made that neurology and neurosurgery especially are even more kind of based in, in an understanding of anatomy and the visuals of the system because it's, it's of all the systems. It's one where location is really so strongly linked to function. And that diagnostic reasoning comes down a lot too. Where can I localize the pathology? So lots of pictures, lots of diagrams. Um There'll be a little bit of sign posting towards less kind of exam important but a bit interesting content. I'm not going to go into depth into anything that niche but they might, I might mention something off hand. Um, that, that at least in my experience I've come across and think is, is worth a closer look to those that are interested. There will be a moderate amount of assumed knowledge and I'll try and state what that is when talking about the topic, but particularly some of the really core content that overlaps significantly with neurology. Some of that we will go through just to kind of cover base, but some of it I might put up a figure or one slide to sort of frame ourselves in this is the sort of knowledge I'm going to be expecting for the next few slides to make sense. Uh And then we'll take it from there. Uh And in terms of the ordering of things, I'm going to kind of work outside in and then filling the extra stuff. So, anatomically, we're going to start off with not even really the brain, we've not really got to the nervous system as such yet, but just a brief word on before we get in there. So when we get to the scalp, um it's a bit of a favorite. This if you go to theater, there's a cranial operation going on for the consultant to turn around and be like, do you know the five layers of the scalp and Handley, whoever named the five layers of the scalp clearly had the acronym in mind because it spells out scalp So we start from the outside with our skin, followed by a connective tissue. After that, you've got your upon neurosis layer, a loose areolar connective tissue layer and then the periosteum. And so there's five layers then bring you to outer surface of the skull. Um It's not just esoteric knowledge to impress the consultant in theater, little bit of clinical relevance. Um So if you get scalp lacerations, whether that's good of trauma or because you're in an operation and you've taken the scalpel to it, they tend to bleed quite a lot, quite a lot for the size of the cut that you've made. Uh, this kind of goes back to the way that the vessels are dear to those layers. So your vessels in your connective tissue layer and deer into the upper neurosis, they can't vasal constrictor so well. And so they will bleed quite a bit. And so if you've, if anyone's been in theater and so any kind of training operations going on or if you see it in the future, you're almost always notice these blue clips getting applied to the sort of skin edge, the edge of the skin flap and he's called rainy clips. They just pinch the edge and try and reduce the good loss somewhat. Um, in terms of kind of clinical pathology relevance, um, there is a there is a bit of venous drainage from these outer layers intracranially and so sort of sterile environment is important even before you got into, it sounds obvious. But even before you got into the skull because you can get some kind of seeding of infection back through the veins that connects the outside of the skull to the inside. Okay. That's what we're gonna talk about about outside the school. Now we get to the school. Um, so these eight cranial bones, these are probably quite familiar to most, if not all of you at this point, I've got eight labeled there. There's obviously the facial bones as well. That's not really what we're concerned with today. That's more of a kind of max fax direction of things. Uh and Handley the names of these map onto the lobes that we'll think about later. So starting at the front, we've got our frontal bone kind of behind the the orbits, you've got your ethmoid bone and then kind of behind and an inferior to it. You've got your sphenoid bone and then along the sides, you've got parietal uh parietal sections of the skull on the kind of superior aspect, right and left, temporal on the kind of slightly inferior aspect, right and left and at the back, your occipital bone, these are joined by sutures which in the bottom, right image, we've got labeled there corona corresponding to corona views in anatomy or in in imaging. So that kind of corona like I think corona, you're sort of like image of Jesus with his, his um his halo halo around him and that slice through their, your sagittal suture being your kind of back down the middle mohawk and then your lambdoid suture being that the, the extra one at the back that doesn't really have a radiographic viewing perspective named after it. Um And he's joined at the fontanels. So you've got your frontal fontanel or your anterior fontanel and your occipital front, anal or your posterior fontanel these clothes soon after birth. So the posterior really quite soon, 1 to 2 months and the anterior a bit more delayed. So at 99 to 18 months there, uh and those of you, anyone who's done kind of pediatrics placement already uh will have come across a bit of the significance of the anterior fontanel. Uh for example, in your Knipe, which is your newborn pediatric examination, you have a feel of the anterior fontanel just to check. It's not either bulging which could suggest something going on inside the school, but because that fontanels not yet closed is able to, to kind of press outwards or sunken, which can be a sign of kind of dehydration or low levels of of CSF okay, in terms of specific pathologies to do with the bones of the skull, I'm just gonna put a quick mention in for craniosynostosis iss very much niche, very much, not kind of exam, high yield exam knowledge. But by all accounts, if you're somewhere on placement or neurosurgery placement or kind of in theater in a center that does craniofacial craniosynostosis operations. I've never been myself, but by all accounts, they're amazing and really worth going to watch. That's just to do with the abnormal, abnormal uh fusing of a different bones. So you get abnormal suture lines and perhaps the most exam important clinical aspect of the bones in the skull is to do with this region called the Terry on. So the Terry on being you're kind of temple, kind of upper temple and back a little bit where you have this joining of four of your bones, your frontal, your parietal, your sphenoid and your temporal. And this is the weakest part of the skull is kind of relatively thin compared to the rest. And it also has a reasonably major artery, the middle meningeal artery running underneath. And so this is your kind of classic area of your stereotype vignette of someone gets trauma to the side of the temples and they end up with a tear of that middle meningeal artery and a bleed in the skull and extradural bleed. And if that term extradural is unfamiliar to you, does what we're going to get onto next is we make our way further into the school. So we've looked at the school, we've now gone just inside the skull. And from that upper right image, you can see the skin and periosteum that we talked about with the scalp. You can see the cranium, which is what we've been talking about with the bones of the skull and then inside the cranium, still before we've reached the brain, we're getting to our three meningeal layers. Now, these are the juror, the Arachnoid and the pier. These are as you'll have come across if you've done your spinal anatomy, the same way as you've got in the spinal cord where there's a slight, um where it's slightly deviates has a slight added complexity is the cranially, we have to dural layer, two layers of the jurors. So two of the outermost meningeal layer. So you can break down the juror into the periosteal juror and the meningeal juror. We'll talk about that a little bit more later on when we talk about the vasculature uh intracranially. But in short, as you can see from that image, these allow this potential space for, for venous drainage. So for blood to to flow through. Okay. So clinically what are are important clinical aspects of our meningeal layers? Well, this is just the kind of schemer going from outside to in of in black, the different layers and in red, the kind of potential spaces between them. So we've got the cranium to the juror, to the Arachnoid, to the pier in the space between the cranium and the juror is the extradural space or the epidural space. I think outside of juror between the juror and the Arachnoid, we've got the subdural space or below juror between the Arachnoid and the peer, we've got the sub Arachnoid space. So below the Arachnoid, if you, if you came to today's session, thinking, I know absolutely nothing about neurosurgery. And if you leave today's session, knowing only one topic that I talked about today, this is probably pretty much up. There is the highest yield neurosurgical topic for students to know right about your meningeal layers and identifying presentations of bleeds in one of these three spaces annexed dura bleed, subdural bleed and a sub arachnoid bleed. So, starting with the extradural what happens when we get bleeding into the extra dural space. So the stereotyped history we've already briefly covered okay. And that is head trauma typically not always but kind of stereotypically to the side of the head that terrian region leading to a tear of this medal, middle meningeal artery. Um aspects of the history that should sort of trigger off your pattern recognition of this sounds like an extra dural are perhaps an initial loss of consciousness as with any kind of significant trauma to the head. But then often a period of lucidity where they seem to recover and be okay, but then their consciousness level then declines after that. So initial insult, period of lucidity and then decline in consciousness should set off your pattern recognition for this sounds a bit like an extra dural as should you know, I don't know, cricket ball to the temple or baseball back to the side of the head thinking about that terry in area. Uh It's worth knowing what is going to look like on CT. Again, I think this is quite high yield bit of info to have to have stored away. So we've got on the right, a noncontrast ct of an extra general hemorrhage. Um the kind of three critical features of this are that it is convex. So that meaning rather than if this is the curvature of the school rather than also having that curvature, it's kind of the other way. Okay. So convex, um it's confined by the sutures. So if on that image, you, you kind of think about where the previous slide had those suture lines. So one kind of at the at the front for the corona and then at the back for the lambdoid uh lamb void, you'll see that area of bleed on the patient's kind of right. This being a CT scan. So we're looking from the feet on the right hand side doesn't cross where you can imagine those suture lines being it's confined between suture lines. That's to do with the juror itself being kind of a deer to the suture line. So if the bleeding was trying to push further round, it's like it's almost like you've got a few compartments of that potential space confined by the suture lines and typically it's hyper dense. So we're looking at a CT scan. So we're talking about density. So hyperdensity and hypodensity rather than intensity which would be an MRI and it's typically hyper dense. So coming up white compared to the surrounding uh brain parenchyma and uh CSF fluid and that's indicative of the kind of acute onset of this. This is, this is acute bleeding in the extra general space in terms of management. Well, um if it's, we'll start with, if it's small, not if it's large, if it's small, these can in some circumstances be conservatively managed, kind of watchful waiting. But if it's large, this is going to be a Crainey, that's probably a craniotomy rather than craniotomy, craniectomy and evacuation. So opening up the skull, uh sucking out blood. Hopefully, at that point there, there's some kind of uh if the bleeding has stopped at that point, you could then replace the bone flap, close up the skull, call it a day, keep an eye on it. Um There's, if this is something that, you know, if you're one of these, what are we at now? 16% of people who answer, they want to be a neurosurgeon. I really recommend you go on Twitter or youtube and look at some videos of these. They're a good one to watch and there's um some good footage online of rather than craniotomy is where you're taking off a whole portion of the skull. There's also a kind of other technique where you make two bir holes and can essentially inject saline through one of them, which will go and just push all the blood out the other one. So if you bleed was here on your head, make burr hole here. Burr hole here put in some fluid to get it to flush out. Bottom one. It's a, it's a good video to to look up if you're interested. Okay, that's our extradural hemorrhage is our next potential space is subje really in our subdural hemorrhage is or subdural hematoma as hemorrhage being the kind of acute ongoing bleeding hematoma being slightly more kind of sub acute or chronic formation of clotted blood. These are similarly precipitated by trauma, although it's it's not always a significant trauma history as with extra generals. So in an adult, it may be reasonably significant trauma in the elderly. These can be precipitated just by quite minor falls that actually often get kind of overlooked and may not even come up in the history without kind of prompting and and probing about it. Uh and in Children, the leading causes actually nonaccidental injury. This is due to the stretch and tear of the veins that are bridging from your cortex to to the the extra dural space. And so when they tear and bleed, you then get this subdural uh collection, you can sometime. So in terms of the features of the history, the signs and symptoms, again, quite a lot of overlap with extra do rules, but you're going to have this severely depressed consciousness. And that's when you get to the point that the collection is so large, you're starting to push your brain parenchyma structures significantly to the opposing side. You can see in this CT scan here that all that brain tissues being squashed quite considerably towards the the contralateral side of the bleed. And in severe instances, you might then have some papillary abnormalities due to that mass effective movement, uh impinging on cranial nerves, which we'll talk about a bit later on in very distinguishable from extradural on CT. So these aren't convex, these are concave. So that curve of the of the white bleed kind of goes the same as the curve of the skull. The color can depend a bit on the timescale. So this one here is also very hyper dense and white compared to the surrounding matter, which suggests it's quite an acute collection. But if it's a very chronic um subdural, it can actually be hypodense and so darker than the surrounding tissue. And obviously, if in the acute phase, it's white and hyperdense and in the chronic, it's black and hypodense at some point, it can be on the transition in between. And you can have a sub acute collection that looks ice a dense or very similar in color to the surrounding brain tissue. So some of them can be a bit subtler to spot than the reasonably obvious example, I've I've put in here management extremely similar, right? If large, you're going to be doing a craniotomy and evacuating that clot. If they're small, there may be a role for, for conservative management and, and watchful waiting. Ok. Onto our third space subarachnoid and this one does deviate a bit more from the previous histories again, can be caused by trauma. But as we'll see later on, when we talk about the vasculature, often a spontaneous onset of these um causes of that spontaneous onset. I've listed a few there. So Berry aneurysms A VM is arteriovenous malformations. Um and see a is cerebral amyloid angiopathy. If any of those are unfamiliar terms, we'll talk a bit more about berry aneurisms and AVMs later on the headline pattern recognition, you know, pass med question thing to be looking out for with a subarachnoid hemorrhage is this worst headache of my life, right? Thunderclap headache is the phrase we give it a sudden onset of the worst headache of their life. A little word of caution on that subarachnoid is by no means the only cause of thunderclap headache. You can list off about a dozen if not more if you, if you sit there and try. But that would be one of the stereotypical features of a supply point hemorrhage. And because of the nature of it where you're getting bleeding in the subarachnoid space, that's right next to the pier. So right next to the parenchyma of the brain, you can also get symptoms um that are associated with meningeal irritation. So that's your photophobia a bit like you seen your meningitis, we'll talk about in a bit uh and, and meninges um more broadly so stiff neck. Um that that kind of thing uh again, simply collapse and decrease consciousness due to the mass effect of the bleed on the surrounding tissue on CT. It's also going to be hyper dense in the acute phase. And this is really an acute presentation. You're not going to be seeing chronic subarachnoid hemorrhage is. So you're seeing this hyperdensity or whiteness on noncontrast CT often around the circle of Willis, which is that central portion of the scan there or in the Sylvian fissure, uh fish is out to the side. Um There's very good and I haven't included in the presentation, but I'd recommend having a look at least once at the nice flow chart diagram for managing suspected subarachnoid hemorrhage because they have these time cut offs to do with when you do the CT head. And whether you need to do further investigations that being an LP, for example, uh or whether that image is in itself sufficient to consider different diagnoses or to go ahead with with subarachnoid treatment. Um What is the treatment? What is the management? Well, in terms of management, the acute management as you got your A B C D E, but the acute management of the intracranial pathology itself, you can be controlling the ICP, the intracranial pressure. Uh and there are drugs you can give to prevent cerebral vasospasm and kind of aid perfusion uh during, during, during the the ongoing bleed is that being niMODipine calcium channel blocker, but really you're treating the underlying cause, right? So, uh if for example, this is a ruptured aneurysm, it may be that you're having to open up and do a, do a, a clipping or something like that. Okay. Very high yield topic, a lot to cover quite quickly. But there's a really nice summary of visually what is going on with the three bleeds and is 1/4 on their intracerebral hemorrhage, but the three bleeds are extradural or epidural subdural and our subarachnoid. And I think this image also really nicely illustrates why that extradural or epidural is bounded by the suture lines whereas subdural is not bounded by the future lights. Ok. Continuing with thingies. Um So we're going to talk briefly about meningitis. I'm not gonna spend a huge amount of time on this because there's a huge amount of overlap with neurology here, right? And really realistically is meningitis. A neurological pathology is a neuro surgical pathology. I probably argue it's a bit more of a neurological pathology, but it's so it's so high yield and so core to your general understanding, it's worth at least mentioning and paying attention to so meningitis, um it's the acute or chronic inflammation of the meninges that can be infectious and often we're talking about it in the context of bacterial meningitis and infectious meningitis. But strictly speaking meningitis is just any cause of inflammations. There are non infectious causes including cancers, drugs like sarcoid. I wouldn't be surprised if you can get TB meningitis. Not that I've read about it or come across it. Um, what is the presentation? And this is one that really should be hard wired in everyone's heads by the time it gets to, you know, 50 or final year or whatever exams, um, you got your two signs, you got your Kernig's sign, which is to do, which are both, they're both to do with really when you're trying to stretch the men in geez. So when you're either trying to flex at the hip, which is kind of stretching the meninges that your, your lower back. Oh, sorry. My Alexa just tried to start playing. Um and that's your Kernig's sign. You flex at the hip and the ankle will also flex. Uh And your Brzezinski sign, which is where you're flexing at the neck and you get this involuntary hip and knee flexion in a response to kind of try and minimize that stretching of the meninges. The symptoms, severe headache, fever, if infectious, not necessarily there if, if it's not infectious, next stiffness and photophobia, headache, neck stiffness, photophobia. If you see that in the stem of a question that should really be screaming out meningitis, um or at least meningeal irritation uh and the nausea and vomiting and altered mental state. People worry a lot about the rash with meningitis. And this, this idea of a non blanching rash. And yes, in the case of infection with Neisseria meningitis, the non blanching rash, a particular rash is quite specific for meningococcal sepsis with Neisseria meningitis is the cause. So, Neisseria meningitis in the bloodstream causing a septic response. Strictly speaking, you can have infectious meningitis without sepsis. You can have meningococcal sepsis without infectious meningitis, but often you get them going hand in hand, right? You have a meningea cockle meningitis which progresses to sepsis. Um And so often in a stem of a question, when you hear about this nonblanching particular rash, it will come along with headache, fever, neck stiffness, photophobia, and they're getting up infectious meningitis that has progressed to meningococcal sepsis, but just, just, just at least be aware that that those two don't necessarily come together. It's possible to have sepsis without meningitis or meningitis without the sepsis. Um Your your kind of hallmark investigation with this is gonna be CSF findings and this again, we're kind of in the realm of neurology here, not neurosurgery, but you're gonna wanna be comfortable with interpreting the CSF findings. I put it up there kind of for, for our reference, but I'm not going to go into too much depth through that, but definitely worth knowing in your neurology more broadly. Okay, let's get onto the kind of major portions of the brain. So this here is about as simpler diagram as you can get for the major portions of the brain. And so there's three that we're really looking at, we're looking at the cerebrum, which is where you have your different lobes. So we'll see in a second with your frontal, your parietal occipital, your temporal and all the functions that are associated with that. We've got the cerebellum, which is to do with our kind of motor control and motor coordination and motor learning. And then we've got the brain stem which there's a whole host of functions. But among them is kind of the path that it all comes through on its way down. Uh as well as the outflow of all your cranial nerves. This diagram and I'm gonna go reasonably quickly over the next few slides cause it's it's somewhat uh sign posting to semi assumed knowledge. This diagram I think is about the minimum you could get by with for knowing about locations within the cerebral cortex and what their function are. Okay. So what we've got there is you've got the frontal cortex, we've got the motor area, we've got the sensor area at sensory area. Sorry, we've got the primary visual cortex at the back and the occipital lobe and then we've got Vern occurs and Broca's area in their superior temporal and inferior frontal lobes respectively, uh which had to do with our speech and language control. I think that's probably, you know, that will get you 95% of the way 85% of the way to questions and, and kind of exam knowledge related to the cerebrum, the cerebral cortex. The more complicated picture looks like this. Um You can start breaking stuff down into the premotor and the somatosensory and the supplementary motor and the somatosensory association area. A bit overkill. And, and my understanding at least is the deeper you get into neuroscience, the more neuroscientists turn around and go, this isn't really that accurate. Um But just, just to be aware that it does go a bit further than just that slighter home previously. Okay. Now, three slides coming up on honing in on particular areas that I've just mentioned and their function. The first is our motor and sensor motor cortex and somatic sensory cortex. And so these kinds of diagrams are what you call, we we we s somatic mapping on the sensory side on, on, on the right. Uh And this is describing which parts of the motor area in the red and the sensory area in blue map to specific locations on the body. Okay. And handily they kind of map in quite a logical progressing way from face on the outer lateral aspects, round two arms kind of in the middle and then legs and lower body when you get to the the kind of a medial, medial portions of these two areas. Um And an understanding of this mapping is important particularly when you come to consider the vascular territories that overlay onto this. So a bit later on, we're going to talk about strokes, uh different stroke syndromes depending on which arteries are occluded. And this kind of face arm leg mapping of the motor cortex and the sensory cortex is important for thinking about cranial pathologies because you can start to piece together what are the symptoms I've got and which locations correspond to those actions or those sensations. And you can start to piece together what single locations unify, disparate symptoms. Um On the next slide, a few of our kind of extra areas. So there's been the speech center, which I've already talked about a little bit that that would be rockers up at the front and Vernick is further at the back and this diagram is showing the left side and the right side and how we don't have complete symmetry for all areas of the brain. Okay. So for the motor cortex in the sensory cortex, we've talked about already, the motor cortex is a bit more anterior, the sensory cortexes a bit more posterior. But then you've also got a left and a right and they actually have contralateral innovation. So the left motor cortex is doing the motor control of my right hand side and the right motor cortex is doing the motor control of my left hand side, but not all the areas in the brain have this kind of bilateral or redundant. Uh well, either contralateral control or redundant control. So in most people right handed or left handed in most people, the left side of your brain is what we call the dominant side. Now, that number is something like 95% of right handed people. And it's something like 70% of left handed people. So it's still most left handed people, but a few more left handed people happen to be right sized dominant. And so this diagram would be kind of flipped. Um And that again becomes important when you start to think about your stroke syndromes. And because most people will have a left hand side, controlling their speech and the right hand side controlling their spatial visualization. As we've got, we've got circle bear. If you have someone with right sided weakness and speech difficulties, you can start to think. Well, if I took out the left cortex, I'd be taking out their speech center and they're right sided motor. Whereas if they have left sided weakness, you can start to think about. Well, uh and, and spatial problems, you can start to piece that together as okay. Well, if I took out the right cortex, then that would give them their left sided weakness and their spatial visualization difficulties. Um If you think too much about the percentage is it can get complicated or what if there left handed and right side dominant. But, but by and large, it's a helpful distinction of having that for most people, the left is dealing with their speech and for most people, the right is dealing with their spatial visualization. Okay. My final cerebral cortex uh slide the other helpful system to uh or localization of function to have an awareness of before we go into all the rest of our pathologies is about the course of vision essentially and processing of visual information. So this starts at the retina, we have them traveling from the visual information traveling from the right, I'll on the right optic nerve from the left, I'll on the left optic nerve, then your medial retina images cross at the chiasm. And so at that point, you have your optic tracks where the right optic tract is no longer the right, I like the nerve was, but it's the right hand side of uh sorry, the left hand side of each eyes, visual field and the left optic tract is there going to be the right hand side of each eyes, visual field? These then radiate back to the occipital cortex where it's processed, worth getting comfortable with if you're not already. But I'm not going to labor too long on that because we have got a lot to get through. So I said a lot, they're about anatomy of cerebrum when it comes to the clinical side when it comes to lesion's. Well, the really nice thing about cerebral Asians. That sounds really weird to say the nice thing about cerebral Asians is you can really take the symptoms go okay, which systems are dealing with those things that have gone wrong and localize. Where do I think the problem is? I might not know what the problem is yet, but where is it? So you have this, where is the lesion? And then once you've identified where you think the lesion is, you can start to think about what you think the lesion is. Uh There was a really good diagram that I looked and looked and looked to try find but couldn't find it anywhere. But that essentially has different natures of medical and surgical lesion's. So stuff like your surgical save stuff, right? Vascular um infectious neoplastic or two immune and the timescales of onset for those types of lesion's. So I might have with my where I said okay, I think there's, I think there's something going on in the right cerebral cortex. But then what's the timescale is it? It did, did the symptoms come on over seconds? Did they come on over days? Did they come on over months and seconds will start to lead you to all in like something vascular going on something scheme ick. Um over days or weeks, you might be thinking well, that sounds a bit more infectious and they also have these associated symptoms of the fever. Whereas when you start to get two months and years that starts to nudge you towards a slightly slower chronic process and you might think well, is that more towards a cancer or something near plastic. So the signs and symptoms might only give you the location but the kind of timescale and associated symptoms can help with the nature of that lesion. Um So as I've given some examples, they're right. Bleeds, abscesses, malignancies, met trauma, we're going to focus on really just one or two of these. Um first being bleeds just to round out what we've talked about already. So intracerebral bleeds, which were the fourth one on that diagram I showed you a while back. They kind of are what they say in the word right there, bleeds in the cerebrum. You can break it down a bit more into intra parent time or where it's in the tissue or intraventricular when it's in the ventricles, which we'll talk about later, but essentially bleeds inside the brain tissue rather than in one of our meningeal layers. Um These are the primary or they can be secondary to some other pathology. So in a VM, uh which we'll talk about later or a cancer that then itself bleeds a kind of added, added a bit of info probably worth worth having in your, in your vault because of the uh kind of burden of care it brings on the hypertensive bleeds or the bleeds that kind of precipitated by chronic poorly controlled hypertension tend to involve these particular arteries, lenticular stria arteries which are quite deep in the brain and feed some of the deeper brain structures, the basal ganglia because those are really very narrow arteries and so are most susceptible to hypertensive damage leading to a bleed. So you're hypertensive bleeds tend to be quite deep in the brain. Whereas your blue, your interest cerebral bleeds a bit more superficially tend to be slightly different. Um etiologies. How are you managing them? Stopping the bleed? Right. Stop the bleed, relieve the pressure. Now, how you go about stopping that bleed will depend on the location. It will depend on the etiology of it. So we're not going to get into the nuts and bolts of that. Um But treating the underlying bleed and then in the way, the tents of care unit might relieving the pressure. So this could be with ICP management, we'll talk about later on, this could be with a decompressive craniectomy. So I talked before about craniotomy is where you take off a bone flat, do an operation and put the bone flat back in a decompressive craniectomy. You take off a bone flap and you leave it off so that there's more space for the brain to swell whilst it's got that bleed going on until you can get it under control and then, and then putting something in place. Okay. Let's keep moving. We've got a lot to get through and I've slowed down a bit too much abscess. Again, you're going to localize it by what function has gone wrong as well as the associated symptoms that have come along fever. You know, recent travel, they had X Y Z infection beforehand. You're gonna need source control as well as antibiotics. Okay. And this gets rapid, over and over again. Not just in your surgery but in all, in all body systems, there's no point just giving the IV antibiotics for big abscesses, you need to drain them and have source control and then the IV antibiotics to take out what's left. So again, this is going to probably be a craniotomy or this stereotactic aspiration where you're, you're kind of less invasively going in and suctioning out what you can. Um So people tumor's, this is an entire sub specialty in and of itself. So I'm not going to spend too long. Again, it's going to come back to what function's impaired. What bit of the brain does those functions? And so where could I localize this lesion and then the history? So your red flags of night sweats, weight loss, you know, family history, personal history might then point you towards a a neoplastic cause towards a tumor. And realistically nowadays, imaging to identify that um if you're a bit interested, there's some figures on here about the different subtypes uh and just to bring a bit of attention to, to because it does tend to go up and pass my questions. At least I found your, your a particular subtype which is your glioblastoma multiforme G B M uh particularly get this butterfly G B M. It's a very aggressive, fast growing tumor, really awful prognosis. Um And in some circumstances, you see this kind of butterfly sign that you can see on the on the MRI scan below there where the tumor is progressed to both hemispheres across the corpus callosum, which is joining your two hemispheres together. And so you get this kind of winged butterfly sign. Okay. Cerebrum, dumb cerebellum. Uh I think it's a bit criminal that I've only given it one slide because cerebellum is, it comes up a lot. It's very important in lots of pathologies. However, for our purposes, you can kind of crudely understand it as it's performing your motor control and your motor coordination. Um You're kind of fine tune ing of your motor control. He's got significant communication with the brain stem and then via the brain stem, the cerebrum. Um and tumor's in the area of the cerebellum a bit more common in Children than they are in adults. Whereas the reverse is true in adults in adults, you tend to see super tentorial or cerebral tumor's Children. You tend to see more infratentorial or cerebella tumor's okay. That's the cerebellum. Now, that third component, we haven't talked about the brain stem. So this is kind of the big linkage point of everything that we've talked about so far and the kind of conduit to lend the spine which has its hole in session tomorrow. Uh You can crudely cut down the brain stem into these three sections. So your midbrain, your ponds and your medulla that's going through top to bottom. A slightly more detailed view here of how the brain stem sits in orientation uh compared to the cerebellum. So this is the cerebella connections to the brain stem. There's three peduncles that it joins by superior peduncle and middle peduncle, inferior peduncle joining to the mid brain, the ponds and the medulla. Um So you can imagine that if you're, we just talked about how pediatric tumors tend to be infratentorial e near the cerebellum in this area where the cerebellum is joining the brain stem is a spot where you can see a lot of these um tumors arising. And so you're then getting mixed cerebella signs from the effect, the space occupying effect of a tumor on the cerebellum as well as brain stem signs, either of some of the descending or ascending pathways that you'll talk, talk about a bit more tomorrow in the spinal session or cranial nerve signs that we'll talk about now. So, cranial nerves again, if I want to draw your attention a few places to extremely high yield topics to learn. I A cranial nerves is definitely up there. Ok. Knowing the names of them all know the numbers of them all, knowing the rough locations of them all and definitely knowing the functions of them all. Um It's an absolute pain when you start out. Once you've gone over them, time and time again, they'll start to become more, more second nature here. We just got a bit of a view of the anatomy of what's going on just so you can appreciate the fact that these are kind of splaying out from primarily the brain stem. Although in the case of one and two higher up in the cerebrum, but 3 to 12 in the brain stem with 11 extending a bit into the spine. I'm not going to spend too long on these. I'm going to assume a fair bit of understanding and knowledge. But here is my very basic summary slide. Um with my very basic acronym, you can find different ones. You can find ruder ones, you can find whatever online but essentially linking um cranial nerve number two, the name and my crude scheme for what are they doing? So your factory is doing some of the nose work. Cranial nerves. 234 and six are doing some of your, well, 34 and six are doing your eye movements too. Is doing that your, your visual information itself, etcetera, etcetera. Um I'm not going to labor on this because it could be an entire session. It's it's going forward one too many slides. Let me just slide 35 the entire session or and of itself. But in the red arrows, I've highlighted a few that I'm going to talk about very specifically because of quite specific neurosurgical pathologies. So the first of these is gonna be cranial nerve, five, trigeminal nerve try should help you remember that there's three branches of, it's the ophthalmic branch, the maxillary branch and the mandibular branch. The neurosurgical pathology associated with the trigeminal nerve is this trigeminal neuralgia. So this is a severe stabbing pain affecting some or all of the branches. You can hear it called in some places. You'll hear it called the suicide disease because the severity of this pain is meant to be so extreme. It's now kind of understood to be often caused by chronic compression of cranial nerve five which demyelinate the nerve and can lead to this aberrant firing and severe kind of electric shock pain. And commonly, that's compression by a particular artery called the superior sarah cerebellar artery. In the bottom right image. There you can see an illustration of kind of surgical window for treatment of this. Um First line, you're gonna be treating it medically. All right, you're gonna be using new neuropathic pain agents, your carBAMazepine gabapentin, pregabalin um to attempt to get it under control when you can't, if you can identify that there is this vascular compression going on, then there is a surgical treatment of microvascular decompression where as the bottom right image shows you basically open up and put a bit of teflon in between the artery and the nerve to stop that, that vascular compression against it. That's cranial nerve five. Let's go to cranial nerve eight, which is our stimulus, cochlear nerve as the name suggests, vestibulocochlear is dealing with your vestibular systems, your balance and your hearing from the cochlea. Um the kind of neurosurgical pathology to be aware of directly relevant to this is acoustic neuromas, which you'll also see called vestibular schwannoma as confusingly same thing, different name. Now, by understanding the function of the vestibulocochlear nerve, you can start to anticipate what the symptoms might be and it's what they are. If it's dealing with hearing, you might be getting hearing loss, you might be getting tinnitus. So that kind of background background, ongoing noise on the vestibular side of things, your patient will be presenting with vertigo. So that feeling of the room spinning around them, uh kind of rotational dizziness. And if they're very large, you can start to get additional cranial nerve signs from the nearby cranial nerves. I kind of put in red here a nice little um I'd call it sort of like a pass med golden star point. But if you have patients presenting with these bilaterally, this is the main diagnostic feature of one of your neurocutaneous syndromes. So this is one of your kind of neuro system based syndromes that has more disseminated effects. And that's neurofibromatosis type two, neurofibromatosis type two diagnostic characteristic of it is these bilateral uh acoustic neuroma layers of the stipulation rollovers. What are you going to do if you find one of these as has been the case in lots of these, if it's a small lesion with minor effects. You might just have watchful waiting if it's larger, that's going to be either surgery to resect it or radio surgery to kind of try and try and shrink the size of it without having to open up a few extra kind of shoutouts for cranial nerves with surgical pathologies. Um, one is cranial nerve to the optic nerve. We'll talk about a bit later. I'm going to save that one point. We talk about aneurysms and the pituitary cranial nerve three, the ocular motor nerves that controls most of your eye movements. Uh And there's, there's a subtlety point in here that's worth knowing about which is surgical cranial nerve. Three palsy is versus medical cranial nerve, three palsies. So the top right diagram describes the slightly complex vasculature of the oculomotor initiative where you have these kind of dual blood supplies, one of which supplies um the nerve itself and one of which is supplying the sympathetic component of that nerve. And so if you have a surgical third nerve palsy, for example, due to a tumour nearby, that's squishing the whole nerve, you get a third nerve palsy where you don't have the associated movements with the ocular motor nerve, which if you can't remember, go revise. Um but with a blown people due to the failure of the sympathetic um sorry, uh sorry, failure of the parasympathetic to construct. So it dilates um with a medical third nerve palsy for example, due to diabetes, poorly controlled diabetes can give you medical third nerve palsies. You get the failure of the motion, failure of the eye movements, but typically get the parasympathetic supply sustained. And so don't get that blown people. So failure of those, I'm cranial nerve, three eye movements with a blown people should point you towards space occupying lesion is a tumor. This is an abscess. You know, our previous line of thinking rather than rather than like diabetic causes. Okay. Creon lives six abductions nerve. This uh people, people describe describe this as a false localizing sign. So, abductions nerve is moving your eyes abducting it, moving it outwards. So if you're a failure of abduction, you might think there's a cranial nerve six palsy. Um But this, this this nerve is because of its course and because of its course along the base of the skull is most susceptible to raises in intracranial pressure. Okay, do compression due to raise due to a raised ICP. And so, whilst logically, you may think okay, they've got a right sided failure of abduction. I think there may be a lesion along the course of the cranial nerve six on the right hand side that, that caution with that cause that can be a misnomer and it could actually be a sign of raised ICP. So six, no pauses should have you thinking okay. Is there a raised pressure inside the cranium seventh nerve palsies, the facial nerve? This is now controlling a lot of the musculature of the face. Um Again, we can do this division into medical and surgical. So, medically, that's then as talking about our Bell's palsy. So you get these uh post infectious unilateral paralysis of the face treated with steroids. Um Alternatively, you can have a surgical cause of that, for example, a tumor in the prostate gland which the facial nerve courses through. Again, the distinction between those two will come from the history. Has this person had a viral pro Joan. Does this person have a mass in the cheek to point you one way over the other? Okay. That is our whistlestop of cranial nerves. How are we doing for time? We're going on log, let's get a move on. So, extra bits, uh these bits didn't quite fit zone, isolate into cerebrum, cerebellum brain stem but are quite critically important. That's the pituitary sitting kind of at the front just below are frontal, frontal lobe just behind the Savina would sinus and the basal ganglia, which are those deep brain structures. So, first up the pituitary, so it sits in this bony little kind of little cup, the sell it urtica of the sphenoid. So that's the bone kind of at the front and the bottom just behind your sphenoid sinuses behind the nose, behind the the oral cavity extends down from your kind of main brain parenchyma uh from the hypothalamus via a stalk and is divided into anterior lobe and the posterior lobe. Some places you need to talk about this thin intermediate low but anterior posterior, essentially the pituitary is your big central control of hormones. And so all the endocrine systems are associated with that. We're not going to go into depth about an endocrine lecture right now. But it's worth being touched up on your endocrine knowledge because essentially dysfunction of the pituitary is likely to be presenting as derangements in one or more of these endocrine systems. Uh in terms of a bit further on the anatomy and function, certain hormones. So listed, there are secreted in the anterior pituitary and then a few, just two main ones, ADH and Oxytocin are squeezed in the posterior pituitary. So two slides here. What about when you've a few slides? Um Pituitary dysfunction, I was the function of the previous side dysfunction. On this slide, you can either have your pituitary doing too little or you can have your pituitary doing too much. So, if you have it doing too little hypopituitarism, you're going to be having a deficiency of one or more of the hormones that the pituitary controls. So that might be hypothyroidism because you've got reduced um excretion of, of TSH. It might be infertility because of decreased levels of LH and FSH. It might be diabetes insipidus because you've got decreased levels of A D H being secreted from the posterior pituitary. And so you're not retaining the fluid, you're urinating a lot. You can also have hyperpituitarism where the pituitary is aberrantly, um releasing an excess of one or more of those hormones or hormone systems. Uh And so that, that, that has in the downstream effect of any of your endocrine systems with an excess as your Your Cushing's disease. Cushing's disease being a pituitary cause of high levels of glucocorticoid, um galactorrhea from excess prolactin or acromegaly from, from excess growth hormone. For example, I've put on there, the common types of pituitary tumor that could cause one or other of these. So hypopituitarism, typically, the type of tumor is a macro adenoma hyperpituitarism. You call that functional because it's leading to excess function of functional pituitary adenoma. How are we going to deal with that? Well, again, we've got to split to medical treatment and surgical treatment. So, medical treatment is really the remit of endocrinology. Um But, but, but in in brief, you're either making use of the negative feedback system that exist in a given endo endocrine system. So for example, if you had someone with a functional pituitary, adenoma secrete in too much growth hormone. And so they had acromegaly, you can give Samata statin analogs which by negative feedback will decrease the secretion of growth hormone. Um or for some of the endocrine systems that have a degree of higher control in your sort of hypothalamus pituitary, for example, um control of dopamine over prolactin secretion, you rather negative feedback, you can just directly inhibit the secretion. So, a dopamine agonist to inhibit prolactin secretion, for example. Um but if we get to the stage where that's not working or sufficient, you might be considering surgical treatment and surgical treatment of. This is an operation that you called a trans Vinoy dull adenectomy, transsphenoidal because you're going through the sphenoid sinus as this quite good diagram illustrates. So endoscopically through your nose to the back of the nose borough, your way through the sphenoid sinus and get to the pituitary and resect the adenoma adenectomy. Uh Again, in most if not all these cases where there's a surgical option, there's also a kind of radiotherapy option to be considered too, okay. Um So at this point, I said we'd talk a bit later about cranial nerve too and the optic nerve, this is where I'm going to bring it in and talk about our bitemporal hemianopia. So on the bottom right is a diagram that I think is the most useful but a little bit complex to understand diagram to describe the propagation of information from your eyes to processing your vision. Um And from that diagram, you can see this optic chiasm, I talked about where you have the crossing fibers from the medial retina of each eye. And so if it's the medial retina that in a bit of each, either kind of nasal, nasal bit of each retina that crosses to the opposite side, that bit of retina because you're going through a lens and it's flipping are looking at the outsides of your vision. So the bits of your retina on the inside that are looking at the outer portion of vision, either side cross over at the optic chiasm to the other side. So if you have a stroke, if you have an object, you have a space occupying lesion. If you have something compressing, this optic chiasm in the middle, but not the bits that are going past it. But just the bits that are crossing over, you're going to lose the signal of the crossing fibers. So you're gonna lose the signal of the nasal or medial bits of the retina. So you're gonna lose the signal of the lateral bits of each side of your vision. So as you see on the upper right image, you're going to have that deficit on the outer edge of each eyes, visual field. And this is called a bitemporal bitemporal by being too temporal being temporal outside hemianopia because it's not left and left, which would be um well, I'm sorry, hemianopia being half and bitemporal being the outer aspects of. So this visual field defect in the top right image is a bitemporal hemianopia and that's typically due to a lesion compressing the optic chiasm. Why have I talked about that with, with pituitary or the pituitary sits just below the optic chiasm. So large pituitary tumors can compress the optic chiasm from below and cause this bitemporal hemianopia. So if we put that together with what we know already about the effects, opportunity to us, what symptoms and signs could you have people presenting with? You could have endocrine abnormalities, either hypo uh underactive endocrine systems or overactive endocrine systems. If you then got to the point of having this visual field defect where they've got a bitemporal hemianopia loss as well, that should really pointing you towards um a pituitary lesion. Just a brief word. But on, we've talked about pituitary, it's worth mentioning about hemorrhages and ski Mick or infarction damage, the pituitary. Um So this term pituitary apoplexy um is the term for that size. It is the term for either a hemorrhage or an infarction of opportunity. Very. How is this going to present? Well, it's going to present kind of partly like a pituitary tumor that we talked about, but also partly like a subarachnoid hemorrhage that we've talked about. So you're going to have that thunderclap headache because of the the the acute bleed intra intracranially is in the subarachnoid space. It is subdirectories space. Um But as well as some pituitary type signs like your bitemporal hemianopia because of the mass effect of the bleed on the optic chiasm. Uh And classically in Addisonian crisis because of the kind of endocrine derangement that that the results um slightly smaller print case of this is She Hands syndrome, which everyone's done that Hobson Gynie block or well, obscene gonna pass med rather than your block. I think I'm not sure many people have come across it in person. Um Is this postpartum pituitary necrosis often following a large post partum hemorrhage essentially because the pituitary is quite sensitive to that sudden loss of perfusion, right. So, if you have a big postpartum hemorrhage, um and that decreased perfusion and hypoperfusion of the pituitary can need to pituitary necrosis which will present a bit like a pituitary apoplexy. Um But in postpartum case is this Sheehan syndrome. When are you going to be operating? You're gonna be operating in cases where you've got visual loss? Okay. So, so if they're severe enough that you're getting this bitemporal hemianopia, that's when you're gonna be considering your transsphenoidal surgery like with your, your tumor's, if they're much milder, again, it can be managed conservatively, which is kind of the theme of the bleeds we've covered. If the bleeds very severe, you might be having to open up and do something. If the bleeds are less severe, you might be doing a bit more watchful waiting and supportive care. Okay, basal ganglia. Uh These are the deep brain structures. There are, there's one main, two main slides on this. We're not going to spend a lot of time because it can get complex and it is quite a new subspecialty of neurosurgery dealing with basal ganglia disorders. It's the realm of functional neurosurgery um because it's to do with typically movement disorders. So, Parkinson's as well as the central tremors. Um What's worth knowing is the basal ganglia? Uh is this collection of deep brain structures that primarily responsible for motor control, sort of motor learning and a bit of executive function and emotional pages. Your big headline pathologies of the basal ganglia in a neurological sense of Parkinson's disease, uh as well as the central tremors and dystonia other movement disorders. I'm going to show you two diagrams here which are quite complicated. And I think definitely we're getting two more neurology and neurosurgery. But this is a, as simple as you can make it, which is not that simple scheme of what's going wrong in Parkinson's. So, in our basal ganglia, we have our different structures labeled, who've got pertaining, labeled, got our global pallidus externals and internists. We've got our subthalamic nucleus and there's this quite complex, positive and negative feedback between them all. Um you can go through this, this activity of adding up all the negatives and seeing what's inhibiting what and what's inhibiting the excitation of this that and the other. And what you get to is that if you reduce the input from the substantia nigra, so down at the bottom there, sm if you reduce that input, then you get reduced output from the motor cortex. Once you've done all your negative feedbacks and positive feedbacks. So in Parkinson's disease, that's a deficiency of dopamine released by the substantia nigra. So deficiency of that input to the system which leads to your bradykinesia as well as your tremor associated with it. If you look at what's overactive, it's the subthalamic nucleus that's overreactive overactive as well as downstream the Globus Pallidus Internus. So there is quite a kind of new novel frontier treatment of functional neurosurgery. I say new novel, it's not that new or novel anymore. But being uh the idea is that if we could inhibit the subthalamic nucleus or inhibit the Globus Pallidus Internus, we might correct the overall output somewhere closer to normal. Uh And this is what uh either ablation or deep brain stimulation are getting out. So just go on my one summary slide of functional neurosurgery and actually Parkinson's disease, more specifically for Parkinson's. Again, this is neurology, not neurosurgery, your first line therapy and medications. So leave it open. Uh And then if that's no longer working or no longer sufficient, you've got kind of adjuncts, you can add in the dopamine agonists as well as some uh inhibitor medications. If the motor symptoms are refractory or they're intolerant to the medication, we have then got these two neurosurgical techniques to consider that being either ablation or deep brain stimulation depending on whether you're uh kind of ablating and inhibiting a structure or trying to stimulate and activate it. And for Parkinson's, this is, as I said, commonly, the subthalamic nucleus or Globus Pallidus Internus targets vary a lot depending on specific specific pathologies on the bottom, right there. What we've got is a pre DBS and post DBS attempted to draw a spinal uh spinal spiral by a patient. So on the left, on a, you can see the Parkinson's tremor is essentially so great that they can't fully form that, that inward to outward spiral. Um There's be turn on the stimulators got much better, fine motor control. Okay. That is all we're going to say about functional neurosurgery. If you're particularly interested, neurosurgery, it's a bit of a, it's one to worth worth reading up on, fair to say a bit controversial, particularly in certain places. Um But, but very interesting, very exciting. Okay. How are we doing for time? So we've taken it to just over an hour and I'm not going to lie to you. We've still got the vasculature and we've still got the CSF to go. The next bulk of slides are busier than I'm going to talk about and they're predominantly there to have a really good reference and there's a significant overlap with neurology as opposed to neurosurgery because it's to do with our circle of Willis arteries and essentially are stroke syndromes. So what happens when you block off each of those arteries? So don't be dissuaded by the business of the next 10, 15 slides. Um There's a lot there for reference. Um But I'm going to try and keep us to a good pace with it. Okay. This is what we're looking at. This is arterial supply to the cranium as well as a little bit extra. There's a lot of arteries labeled on here. And I think the ones that you need to know are the ones that are in purple, the ones that are in green. So that's what six total plus or minus one or two others. Okay. And this arterials ply, um it's not just in one end and out the other, there's kind of two connected circulation is going on anterior circulation and a posterior circulation and are anterior circulation is fed by the internal carotid artery and a posterior circulation is fed by our vertebral arteries. What I'm gonna do is I'm going to start at the bottom. I'm going to start with the posterior circulation at the bottom of anatomically and work our way up the key ones. So starting down here on the bottom, right, with a posterior inferior cerebellar artery. Now, just just before I talk about it too much, um I'd really emphasize how helpful and high yield it is to be able to visualize this image on the right in your head. Okay. And have an idea of which artery comes out of where and where the connect and what it connects up to. The helpful thing is the names. Although complicated do describe where they, what they supply and which locations. So the posterior inferior cerebellar artery is supplying the posterior inferior aspect of the cerebellum, right, as you can see from the middle figure on the bottom. And when you're able to, to have the good visualization of that, that helps with distinguishing a bit between your, see what's going to come next. In terms of superior cerebella, anterior, inferior cerebella, posterior, inferior cerebella, as well as when pieced together with an appreciation of the brain stem anatomy and the cranial nerve functions, what signs you're going to get with each stroke syndrome? Um Since I first learned it year on year, I've tried to remember the signs that go with each syndrome, the signs that go with each syndrome. And I think only very recently, it started to actually embed itself and click now that I feel comfortable linking the location and the cranial nerves to the artery rather than just a list of signs to the name of the of the syndrome. Because otherwise, it's very easy to, to mix up signs and symptoms between very similar sounding arteries or syndromes. Anyway, after that aside, so we got the posterior inferior cerebellar artery, which also feeds the lateral medulla. And so when you get occlusion of this is what we call a lateral medullary syndrome or Wollenberg syndrome is the kind of eponymous term for it. What structures it's supplying? Let's start with the posterior inferior cerebellum, cerebellum does are kind of fine motor control and a bit of coordination. And so you're cerebella signs are when you're getting a taxi, a so a taxi of your movement, having a taxi gate or a taxi a in terms of um past pointing, things like that as well as an s stag mus because of the role of the cerebellum in control in coordinating eye movements. Um And then the remaining signs you're getting with a peak or occlusion has to do with the cranial nerves. So you're getting slurred speech due to knocking out bits of the nuclear I for cranial nerves 10 and nine, you're getting facial sensory deficits as well as a vomiting vertigo, nystagmus from taking up bits of cranial nerve eight compared up to an eye ika occlusion, anterior inferior cerebella. The signs are really similar. Why are the signs really similar? Because it's supplying a lot of the similar stuff, a lot of the same structures. It's also applying the cerebellum. So you're also getting your cerebella signs of your ataxia with a bit of a nystagmus uh in there too. But in terms of the, in terms of cranial nerve signs, you're still getting the cranial nerve eight signs of your vertigo because you're taking out that, that bit of your virtue, uh the stimulus ocular cochlea nerve, you're not getting the cranial nerve nine and 10 signs, which are a bit lower down. So you're not getting the slurred speech so much, but you are getting now the facial paralysis from cranial nerve seven, which is higher up. So for the Peka, you're getting sort of a bit of nine, a bit of 10 a bit of a 10, a bit of nine, a bit of eight for the IKA, you're getting a bit of eight and a bit of seven because you're a bit higher up the brain stem. Let's go a bit higher to the superior cerebella artery. Um You might remember as being one of the main causes of trigeminal neuralgia from having this pressure on the trigeminal nerve. Um What signs are we going to be getting with that? We're going to get any ataxia still because we're still getting that cerebella dysfunction. Um And really, that's the kind of key hallmark of it ministers the a taxi a as well as a bit of a headache that comes alongside. Okay, just taking a moment to talk about the basilica artery. I've kind of said I'm working my way up and then jumped to the one in between the basilica artery is worth knowing in the context of are locked in syndrome. Okay. So, the basilica artery is that big chunky artery running all the way up up the brain stem. Um And so occlusion or insufficiency, the axillary artery can lead to quite widespread brain stem dysfunction. And that's what you're getting in your locked in syndrome. So you're getting quadriplegia where you're knocking out a lot of your descending motor control as well as a lot of your, your even above the neck, even in your face, motor control by taking out the cranial motor nerves. Um But importantly and kind of, well, quite horrifically in locked in syndrome. You're not affecting the reticular activating system, which I've not talked about today, but is, is, is a system of connections in the brain stem to, to the, to the higher structures um that's important in, in consciousness that's not getting knocked out. So typically, they've got retained consciousness and retained cognitive function but widespread um paralysis, quadriplegia that's, that's locked in syndrome as a result of the scylla artery occlusion. Let's keep working our way up. Okay. Three big cerebral arteries here. So we're gonna do the posterior cerebral, the middle cerebral and the anterior cerebral. This takes us all the way back to what lobes are there in the cerebrum and what function do they fulfill its the posterior cerebral? Sorry, I'm setting myself the wrong way. 59 uh posterior cerebral artery is the uh territory colored in blue in that diagram by and large. It's applying your occipital area. Okay. And your occipital area broadly speaking, the main function is doing is your is your visual processing and so posterior cerebral artery occlusion. The big sinus symptom to be looking out for is widespread visual deficit. Typically on one side from occlusion of say the left posterior cerebral, you get a clue, you get loss of the right side fishing or or or uh ischemia of the right sided posterior cerebral artery territory. You'd be getting left sided uh visual deficits. There's also a bit of supply to some of the deep brain structures, some of the the uh thalamic nuclei. And so, there are some additional uh kind of sensory and motor symptoms that can come alongside that. But really the visual loss is are the distinctive part of the history. Uh And the really distinctive part is that they typically have macular sparing some macular being the very center of your visual field. And that's due thought to be due in part um uh due in part to a collateral supply with the middle cerebral artery. So a classic pass med stem of a posterior sri blast, right, posterior cerebral artery occlusion would be left sided um hum on imus hemianopia. So you're using, you're losing the left side of each eye but with macular sparing. So you've got that kind of dot in the middle still, still getting filled in middle cerebral artery. These are our big common stroke syndromes. Okay. So big common one for strokes to present with is a middle cerebral artery stroke. Um and this is where the understanding of the dominant and non dominant cerebral cortices are important. So taking the typical arrangement where the left side is dominant and the right side is non dominant. A left sided middle cerebral artery stroke is going to give us our language deficits. So an aphasia, a right sided middle cerebral artery strokes or non dominant side for a spatial spatial processing is going to give a contralateral hemi neglect. So it's quite striking if you've, if you've, if anyone's come across neurological patient's, who've had a big right side is M C A stroke, you get them to close their eyes and you tap them on the right leg and you, and you ask them to say right or left, you tap them on the right leg and they say right, and you tap them on the left leg and they still say left, they've still got all the sensation, but you tap them on both legs and they'll just say right, they'll ignore the left and they'll even, they'll even be, you know, they'll, they'll talk to the people on the right more than they will on the left because they've got this, this hemi neglect of processing, especially what's going on on the left hand side. It can, it can be quite um quite surprising to see. Um now, whether left or right other symptoms that will come across with, it can be a homonymous hemianopia because you can take out the optic information before it reaches the occipital lobe. So you can take out the optic radiation before it gets there. And this typically won't have macular sparing because you've taken out the whole the whole processing of the side. So a harmonicas hemianopia with macular sparing should set off alarm bells for occipital posterior cerebral artery, her mon emus hemianopia without macular sparing should point you and will likely have other features should start pointing towards maybe this is a middle cerebral artery rather than a posterior rib lottery. Okay. And um I've put a little note in here about the lenticular streit's. This is um we're getting a little bit more small print here, but this, this is just to draw, draw attention to the idea of lacuna infarct or deep brain structure in farc's where you can get these quite widespread motor loss, widespread sensory loss or widespread mixed motor sensory loss. Um in the interest of time, I'm going to scream out of that one for the time being, but it's there for your reference to go and have a read about anterior cerebral artery. So third of our big cerebral arterial supplies, this is supplying the midline of the frontal and parietal lobes. So the yellow colored portion of that lower diagram and in a kind of inner portion of the parietal lobe and the frontal and and of the frontal lobe, as well as the kind of bulk of the very frontal frontal lobe. If you think back to the motor and sensory homunculus, i the somatosensory mapping onto their relative relative areas, you may remember that that medial portion, that midline portion was where the leg control is that whereas the lateral portions which is supplied by the middle cerebral artery are where the face and arm control uh sat. So if you've got someone with face and arm paralysis, a suspected stroke, you're thinking more middle cerebral artery. If you've got someone with a leg paralysis, um you're thinking more of a anterior cerebral artery occlusion, okay, neurosurgically. Um really strokes are by and large a medical management or a big burden of care on strokes um particularly in the modern world and, and typically managed medically, but it's worth being aware of and the different time cut offs, we do have the interventions we can do. So those being a thrombolysis window and a thrombectomy window. So thrombolysis to try and break down the clot typically older plays. Um It used to be three hours. My understanding now is now at 4.5 hours if you've excluded co existent hemorrhage or any direct contra indications to place itself thrombectomy. So not really neurosurgical but neurointerventional the sort of interventional radiology world of things going and grabbing the clot or grabbing bits of the clot and taking them out quite limited range of territories that are suitable for thrombectomy retrieval. But that has a slight slightly larger window of of less than six hours or even slightly longer if the perfusion imaging is uh suggested it suits it, getting a little small print there. So I'll leave that there for those who are kind of super interested. The last thing it's worth appreciating with the setup and the anatomy of the arterial supply is the communication between the anterior and posterior supplies between the left and right arterial supplies. So the paas to start with the posterior communicating arteries you have these bilateral is there's a right and left p calm, posterior communicating artery. And these are connecting the anterior supply fed by the internal carotid to the posterior supply fed by the verticals. The a calm, the anterior communicating artery is connecting the left and right side. At that anterior cerebral artery kind of junction, soapy calm, connecting anterior posterior p calms connecting anterior posterior Acom, connecting left to right. Um And we won't spend too much time, but it's worth thinking about kind of what this quite extensive collateral supply can mean for occlusions in different areas. For example, if you've got quite a proximal occlusion of your A C A C A, then you may actually find that the the other side is able to collaterally supply the distal branches of it so that it labeled a one and a one occlusion. You might find that your A two is actually bilaterally perfused fine because the other side can compensate. Whereas an A to occlusion on, for example, the right side, you might be knocking out everything downstream because there's no longer the opportunity for that collateral supply via the A calm. Okay. Now, the last word on on arteries um and really probably the main kind of surgical aspect of the arterial supply is two aneurysms. So, aneurysms not unique to neuro vasculature at all, but found all throughout the body that cerebral aneurysms um as elsewhere caused by local vessel wall weakness, typically a symptomatic other than the local mass effect they might have on the surrounding structures. So the anterior communicating artery sits quite near the pituitary. Uh and so also very near the optic chiasm. And so can also cause a bitemporal hemianopia. So, bitemporal hemianopia with endocrine type symptoms might be pointing you towards a pituitary tumor, for example. But a bitemporal hemianopia without pituitary like symptoms and maybe with a history that suggests some risk factors for aneurysms might point you more towards in a calm aneurysm, but having the same, you know, mass effect on that optic classes when they do become very symptomatic is when there is if they rupture, right. Uh And when they rupture, that is essentially one of our big causes of a subarachnoid hemorrhage, traumatic subarachnoid hemorrhage. But, but a lot of, a lot of them will come about from aneurysms, either unknown or kind of known, but being watched for, you know, watch, watchful waiting, then rupturing and causing a super adenoid bleed, how you're diagnosing them. Uh on CT CT uh angiography as well as more, more kind of classic angiography like imaged there. And hopefully, you can all see the kind of what we've got here is, is the angiography coming from, I think that I see a so that'll be our anterior circulation. Um and this big dark patch of a secular aneurysm filling with that that contrasted blood. Uh what I think is to my very untraded. I probably the MCH it looks like the middle, whereas the, the A C A I think is going towards the left of the screen, how we're treating aneurysms, as I said, often a symptomatic. So if it's an incidental finding may, may elect for watchful waiting with BP control to try and decrease the risk of them rupturing spontaneously. Historically, uh they'd often get clipped. So a craniotomy opening up the skull going in and placing a clip over the base or neck of the aneurysm. Uh and then snipping the aneurysms, you evacuate them of the blood, they then can't fill and, and then not, not of a concern for, for rupture but increasingly in the last, I don't know, I think decade or so ish that are getting coiled and the vascular lee. So again, this is one of our neuro interventional radiology area of treatment as opposed to surgically. Uh interestingly in the US, it's neurosurgeons who do this UK It's neuro interventional radiologists who do this. Um but endovascular coils where you're going in via the femoral a bit like in a, you know, in a cath lab in a cardiology cath lab and releasing this platinum coil in the aneurysm which causes the blood and it took lock and solidified, but it, but it's blocks off the flow into the aneurysm. And so you're, you're decreasing the risk then of, of the aneurysm rupturing and getting kind of outward flow. Okay. We're all doing very well. We're at, we're nearing the kind of the home straight of it that are a bit, a bit about veins, a bit about CSF. And then, uh, everyone can, can, can relax and stop thinking about brains anymore. Venous system. Somewhat, less, probably a fair bit less complex than our arterial system. Um, this, I think is about what you need to know when it comes to the, the venous drainage probably plus the cavernous sinuses, which I've got a view of in a minute. Um But essentially you've got, you've got your venous drainage of various structures. Be there, deep structures will be there, the cerebrum um which come together and end up ultimately draining out of the internal jugular vein. Uh I mentioned in passing earlier about the venous sinuses. So this is a closer up and I think really good view of what would be a superior sagittal sinus. Again, nice thing about neuro is they often name things by what they are or where they are so superior up at the top. Sagittal sagittal view. So this is the venous sinus that was going kind of front to back on that previous image up at the top formed by the gap, the space between our dural layers. So it's a general sinus or on the top, we have the periosteal juror on the bottom of it. We've got the meningeal juror, but still just that dural layer not getting to the Arachnoid not getting to the pier. And in that potential space in between, we have the venous flow uh slightly more complex image. I think it's a lot of the labeling is slight overkill, but you'll see the same structure as we saw on the simpler one that's superior sagittal sinus up at the top. You've got an inferior sagittal sinus a bit deeper. You've got these uh this confluence of sinuses where, where you're getting the joining and the connection of your, of your sigmoid sinus and your superior and inferior sagittal. Um The extra structure, this diagram has that it is worth knowing a thing or two about is are the cavernous sinuses. That's it a bit more anterior, a bit more inferior. So kind of at the base of the skull kind of behind the orbits a bit. Um And these, these uh these are, these are as the name suggests, sort of regions cabins sinuses uh for a lot of drainage of the frontal structures. So you're, you're ophthalmic vein. Uh So your structures up at the front of your, of your head. The clinical relevance of this is um it's a, it's a common ish site for thrombosis uh often precipitated by infection. So because it's where a few of these frontal veins track back from, for example, ophthalmic vein. If you have an infection of your orbit, say a peri orbital peri orbital cellulitis, you can get the infection tracking back into this cavernous sinus into this region of, of pull blood, which can lead to thrombosis. And if you imagine you get a thrombosis in your venous system in your head, that's gonna be causing a big backlog, which can have all sorts of when I say global sort of cranially global effects, right. So, uh the typical presentation of that would be really severe headache, um often precipitated by something like peri orbital edema. Works of the peri orbital cellulitis proptosis being your eyes kind of push, pushing outwards because of the increased pressure behind behind them and from the vida strange behind them as well as this cranial nerve six, this subdue shins nerve palsy because of um not because of the it's sensitivity to raise ICP as search. Although that, that is true that it's very sensitive to raise ICP. But because of the course of it through the cabinet sinus. So in this image, in the bottom, right, we've got the cross section of the cabinet sinus and it's not so easy to appreciate on this diagram, but the cranial nerves 34 and the two branches of five aren't sitting in the sinuses, such they're sitting sort of within a, within a sheath off to the off to the side. Whereas queen of sixes kind of right smack in the center of your sinus. And so is very sensitive to um if you get a cavernous sinus, thrombosis cranial nerve six pools, he's uh a sensitive nerve to to get a palsy. These are, these are the clots that initially when people worried about COVID vaccines, there was news articles going on about an increased rate of cabinet science from both sees with COVID vaccines, which as I understand, we won't get into that. Um Last word on vascular chair, we've talked about arteries, we talked about veins, we talked about what can go wrong with arteries. We talked about what can go wrong with veins. What goes wrong with a bit in the middle? You should be having your capillaries between your arteries and veins. If you get this abnormal connection, bypassing capillaries going straight from arteries to veins, you get this formation of an arteriovenous malformation. Again, it's neuro it is what it says in the name arteries, veins malformed. You can appreciate that. Now, rather than this intermediary of capillaries, you've got your high pressure arterial supply directly connected to your venous supply. And so the two, the two effects of this are this nidus formation. So nidus being the the bundle, the bundle of of abnormally formed vessels between the two and also a dilatations of the veins that drain that nidus okay. So nidus formation, which itself can have a mass effect and venus debilitation, which in extreme cases could have its own mass effect or could otherwise, you know, is a, is a risk factor, higher pressure flow where it shouldn't be being a risk factor for spontaneous rupture and hemorrhage. So, AVMs kind of, you know, after and alongside um aneurysms, a possible etiology of a subarachnoid. And so similarly, as with aneurysms, often a symptomatic may cause some kind of focal or global neurology with because of the mass effect. But really the kind of big symp symptoms come on when, when you get a rupture, how are they getting, how do you treat them similar to an aneurysm case? They can be endovascularly treated with kind of embolization rather than coiling embolization. Um If they're large have ruptured, you may need neurosurgical removal. So opening up the skull again, Crainey craniotomy um and find a section and a quarter ization of feeding arteries. Um Again, with the option of radiological or symptomatic kind of treatment support. Okay. With the final straight, I can see eight slides for us to go. Uh Evil done very well. We're on the last system and the last system is another um another fluid systems. We've had our blood system, their arteries or veins are AVMs. We've now got the other major fluid system which alongside the parenchyma and the blood makes up a third big component of your intracranial compartment. Talked about parenchyma, different bits of the brain. We talked about the blood arteries, veins, pms. Now going to talk about CSF. Why does the brain have this extra fluid system? Why? Why does it have the CSF fluid system? Five main points. Um One buoyancy. Okay. So the brain is buoyant in your CSF it's bathed in it all around. And I think this, this diagram quote illustrates which means it's not kind of sat, you know, with the base, uh just sat on, on your school base. Uh then at risk of, you know, compression affects effects from that contact um protection. So there's certain shock absorber effects so that any minor movement of your, of your head isn't automatically gonna be rattling your brain around inside causing, you know, concussions and contusions and coup and counter coup damage. Um It also buffers the intracranial pressure. We'll talk about that more right at the end. But alongside um vascular church, alongside the blood, alongside the parenchyma, it can buffer intracranial pressure. It helps distribute substances brain wide. So if you have certain, you know, certain electrolytes or certain transmitters that you need, that you want to maintain relatively consistent levels of distributed throughout the brain, it's sort of efficient mode of distribution as well as clearing waste. So almost in a way, you know, uh almost in August, the way that sort of lymphatics work right in that you, you get this outflow and drainage so that you can drain things off away from the brain. Um Here's the anatomy like this is really about as complex as you need to know when it comes to the CSF. Well, we'll see in the next slide a little bit about how it then loops background, you can get bogged down and worrying about the systems and things like that. But I think this really is the crux of it, knowing that you have your two lateral ventricles, you have your, which feed by your foreman, foreman of Monroe into your third ventricle, which goes down this slightly longer kind of narrow cerebral aqueduct, your fourth ventricle and then as we'll see in a second that then flows background to be reabsorbed. Um So that's, that's what's illustration on this diagram here. And, and I think this is very helpful in particular with the white arrows on the left showing that your CSF is produced quite deep at the linings of your lateral as well as I think a third ventricle also by your choroid plexus. So that's produced, there's a, there's a specialized cells producing your CSF which then flows through the system lateral to third ventricle to fourth ventricle and then out the out the systems and out the outflow around the outside of the brain to bathe it around the outside, back up to um your venous sinuses where there's then absorption into your venous system for drainage by Arachnoid granulations. So CSF produced by corot plexus flows through the ventricles out round the venous sinuses and then absorbed across by Arachnoid granulations. And so pathologies of the CSF and of the CSF system um really come under the bracket of hydrocephalus again, a subspecialty in its own, right? And we've traveled across whole ton of subspecialties in a couple of slides today. But hydrocephalus is really defined by, by an increased CSF volume. Okay, leading to typically dilation of the ventricles, they get enlarged because of this increased volume, they have to, to compensate. Um and then as this continues, you then leading to raised intracranial pressure. Um Now, hydrocephalus, you can segment into two broad categories. Communicating hydrocephalus, a noncommunicating, hydrocephalus, communicating hydrocephalus. As the name suggests, there's no blockage. So you've still got that communication all the way from chorioplexus, lateral ventricle, third, ventricle, fourth, ventricle round irrational granulations out. Um There's no physical obstruction or blockage in any of that there. But so what is going to be causing an increased CSF if there's no blockage? Well, if you decrease the outflow, if you decrease the drainage, so you get decreased absorption by Arachnoid granulations. And it's like having, I don't know a bath with the plug pulled, but you're filling the water too quickly that it can't flow out fast enough and it's just increasing and increasing and increasing. I've put a note on there about a specific subtype being normal, pressure, specific subtype of communicating hydrocephalus being normal pressure, hydrocephalus. So this typically affects the elderly idiopathic so often, you know, uncertain etiology. Um and you get a hydrocephalus, you get dilated in large ventricles um despite the pressure, not actually being raised. So normal pressure, you don't see a raised ICP. Um but you do still get this dilation of the ventricles, which then impinge on the structures that board of the ventricles, particularly the corona radiata to impart important, important for all your motor control and the stereotyped history that that will get federal a bit nicer phrasing is this. Went wacky wobbly. Okay. So this try out of urinary incontinence, the wet apraxic gait, the wobbly, I guess and the probably not the greatest choice of terminology but wacky for, for the cognitive dysfunction associated with it. Um That's our communicating, that's no blockage are noncommunicating is at least in my mind, the, the sort of more, more obvious example which is there's a blockage somewhere, okay. That could be of all, all nature's but, but commonly, you know, assist or a tumor, for example, um you get blockage and you don't get the flow, being able to continue all the way around for re absorption and there's, there's a backlog and a back pressure and so eventually get dilated. How are you managing hydrocephalus? Well, in the short term, helping it drain, right? Putting in a system to help it drain off and thus decrease the pressure. Um Short term, that might be an E V D extraventricular drain. So making a small burr hole and then popping the drain in into one of the lateral ventricles so that you can tap it off. Um In the longer term, it's going to depend on whether it's communicating or noncommunicating if it's um communicating and there's not an obvious lesion to exercise or treat too, um to reverse it, then you may have a long term shunt. So typically these RVP shunts again, neuro, the really nice thing is they say what they are. It's a ventriculoperitoneal shunt. It goes from your ventricle to your peritoneum. So it's buried burrowed underneath the skin, down, down the thorax, down to the abdomen into your peritoneal cavity where your body then absorbs it. Um They're all, there are other kind of less common infusions. So the agent ventricular atrial out of the ventricle burrows through the skin into your atrium. Um They sound crazy but, but the uh at least mine is, I think it's v patients tend to be the way to go nowadays um if noncommunicating, so if there's some kind of blockage, some obstruction, you're gonna be treating the underlying pathology. Okay. So if there's a tumor that might be a tumor reception, um or if, if that's not sufficient or if there's, there's something less easily treatable. So you can get something called a cerebral aqueduct stenosis. So you get a narrowing of the connection between the 3rd and 4th ventricle is you can um there are surgical operations to basically open up your own hole and, and re establish that flow in that connection. So for example, an E TV, to be an endoscopic third ventriculostomy. So again, it is what it says in the name, endoscopically, go to the third ventricle and making a whole uh for an alternative route for the flavor. Okay. So this is the last four slides of us today. And this also goes quite high up my list of if you don't remember many things from what has been quite a long session today. This is one of the things to take home. Um I should I not change the slide. Uh And we're starting uh this, this is also perhaps one of the topics that that's quite broadly applicable, not just surgically medically and, and you know, cross kind of intensive care as well is principles of raised intracranial pressure. Okay. I've said a few times now in offhand comments, raised ICP raised ICP without really honing in on that for, for the people who are less familiar. And so that's what this bit is for. So raised. ICP comes back to this, this doctrine called the Monroe Kelly doctrine. But if you simplify it is the skull is a fixed volume. And so if you have things in that fixed volume and you try and put more in the pressure is going to go up. But if you don't want the pressure to go up, you can offload some of the other components. So the three main components we have in the skull, our, our commerce, all the brain tissue, the blood volume and the CSF volume. Now you can't really offload the brain parenchyma. Um You can to a certain extent offload a bit of the blood volume and a bit of the CSF volume, okay. And so if your brain parenchyma, for example, starts increasing in volume and what might cause it to increase in volume, you might have a tumor growing there, then your body's going to offload some of the blood and some of the CSF volume to compensate. And initially, that might not be symptomatic, that might be okay. That might be a sufficient coping uh reactive response. But at a certain point, you're, they're no longer able to offload to kind of critical levels of blood flowing critical levels of CSF you know, there's only so much you can offload and eventually, if you're um you know, brain parenchyma volume is increasing, increasing, increasing the pressure is going to start going up okay. Your, your, your systems can't compensate. Um And that's what we then call intracranial hypertension. A bit like how hypertension is high BP. Intracranial hypertension is high pressure in the cranium. What are the symptoms of raised ICP? So, headaches and the kind of tagline that comes along with headaches. The stereotypes tagline that comes along with raised ICP headaches are that they're worse in the morning and they're worse online down okay, ocular palsies. So, cranial nerve palsy is related to the I particularly cranial nerve six, which we've talked about, we talked about how its course makes it susceptible to raise ICP. So when the pressure goes up, cranial nerve six gets compressed and you can end up with cranial nerve, six palsies. Um when it gets quite severe, you can have reduced consciousness as well as papilledema and papilledema think is a reasonably late sign of it, even though even though it often crops up in questions as you know, signs to look for. Now, I put a little kind of a footnote here on idiopathic intracranial hypertension, raised ICP typically very worrying. Um and and can be quite severe and quite nefarious pathologies underlying it, idiopathic intracranial hypertension, moderately worrying, but a bit more benign in the sense that the the main idiopathic being, we don't know that, you know, we don't know the etiology, there's no tumor, we can point to, there's no lesion, we can point to. Um but the main risk factor is obesity. Uh So actually, in fact, the main treatment for it is weight loss and, and with sufficient weight loss, you can reverse the raised ICP plus or minus a bit of help from, from uh acetaZOLAMIDE, just carbonic anhydrase inhibitor, I believe. Um But okay, what if we don't control the ICP? What if it keeps going? Well if the ICP keeps going? For example, you've got an enlarging tumor or you've got an enlarging hematoma, then you're going to start to get the brain parenchyma getting pushed out, you know, longer got blood, you can offload, you no longer got CSF, you can offload, but you're just gonna have too much pressure inside the school that's gonna be trying to find a way to, to escape and you start getting tissue pushed through areas, the tissue shouldn't be getting pushed through. And there are a few of these herniation syndromes that you can get from different bits of the brain getting pushed under or through different structures. So sub fall sign from one hemisphere of the cerebrum getting pushed underneath the fox cerebri which separates the right and left hemispheres. Um actually a compressed A C a anterior carotid and so uh anterior cerebral artery, trans tentorial herniation. So kind of from the deep brain structures in the center downwards, which can uh says has pretty horrific horrendous um prognosis, uncle herniations, you're getting the kind of hippocampal, you know, based based medial um part of the cerebrum herniating underneath the the tentorium, which which is a thin layer separating the cerebrum from the cerebellum. Uh And that, that typically presents with a third nerve palsy. So that would be one of our surgical third nerve palsies with the blown people uh as well as a contralateral hem praecis from impinges on the, on the descending fibers, which which will get talked about a bit more in tomorrow spinal session. Um I put a stress on Carnahan's phenomena if you're super interested to go and have a read, but it's very small print. Uh and one of the sort of pretty, pretty bad and keep your eye out for herniations being your tonsil er herniation or koning the kind of colloquial term where you're getting the cerebella tonsils, pushing out down through the forum and magnum compressing the brain stem as they do. And if untreated, getting you towards um uh coma and ultimately ultimately fatal, uh I've put a point on there about Cushing's reflex. So, Cushing's reflex are those symptoms that are warning you of this imminent herniation. Okay. So you get a Braddy cardio. So slowing of the heart rate, but a hypertension uh reduced respirator. So you're gonna have Braddy cardia, um reduced rest rate or Bradley or up near uh and hypertension. That's your cushing's reflex and should really be screaming at this is late, late to raised ICP and a real emergency. So our final slide, how do you actually manage raised ICP or surgically? Because that's kind of, you know, people here today, I can't leave what percent of you, but there's generally bit of a surgical inclination surgically managing raised ICP. You can do a decompressive craniectomy, which I mentioned a bit earlier on take off the bone flap and leave it off, close up the jura closet skin and give that brain some extra volume, some extra volume to expand into, that's decreasing the pressure, uh remove the mass that's causing the raised ICP if that's a tumor, if that's a hematoma, either receptor, the tumor or evacuate the hematoma. Um a medical sense, there are other agents we can use ICP lowering agents. Um medically that's are kind of osmo therapies or monotone or hypertonic saline. Um use a anti hypertensives to reduce the cerebral perfusion and reduce the blood volume. Obviously, there's a big balance to be to be struck there with the risk of hyperperfusion um as well as hyperventilation. So, if you hyperventilate a patient, they'll have a decreased CO2. And as a result, they'll have cerebral vase oh vasoconstrictions which will decrease the volume of blood and so decrease the intracranial pressure. So over ventilating patient's can lower their um there I C P um obviously to be to be weighed up with what the rest of the blood gasses doing. Okay. So thank you that we've got through a lot of slides. As I said, a lot of content to cover today. Quite a whistle stop tour broadly matched to the NL A hopefully of a lot of help to people. Um the slides I believe at least in mind studying will be made available in some form. If not, I can, I can, I can make that the case uh and very happy to stick around for a little bit and answer any questions or, or kind of comments from anyone. But hopefully, although long it's been enjoyable for you guys, uh it's been enjoyable for me to put slides together and present them. So thank you. Also a little shout out for for tomorrow's spinal session being run by by Keeley who's in the chat with us now and also, I noticed there's, there's been a feedback link put in the chat. So I know I might have missed you all as you just logged off. But please, if you hear this, get the chance to fill in the feedback, um, it is greatly appreciated. Great. Thank you so much for that session that was really thorough and extremely useful. Uh You already mentioned the feedback form is on the chat. Uh I hope everyone has a lovely evening.