Health and medicine
- What is a stroke?
- Cerebral blood supply: Part 1
- Cerebral blood supply: Part 2
- What is a stroke?
- Risk factors for stroke
- Ischemic stroke
- Hemorrhagic strokes
- Ischemic core and penumbra
- The ischemic cascade in stroke
- Blood brain barrier and vasogenic edema
- Post stroke inflammation
Post stroke inflammation
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Want to join the conversation?
- You mention how liquefactive necrosis and cyst formation follows ischemic stroke. Would liquefactive necrosis and cyst formation follow an intracerebral hemorrhagic stroke as well? Would tissue ischemia distal to the site of hemorrhage or tissue ischemia induced by blood breakdown products from the hemorrhagic blood itself cause subsequent liquefactive necrosis? Thank you(2 votes)
- Is the timeline of the blood-brain barrier breakdown, the reason why they don't give TPA past 3 hours? I thought it was just because it isn't effective after that time, but now it sounds like opening that passage might actually convert the stroke to an ischemic stroke...(1 vote)
- When an ischaemic stroke happens, the affected region of brain has an infarcted core (which will die regardless of treatment) and an ischaemic penumbra (the area around, some of which may recover if reperfused). The goal of treatment with rTPA is to get blood supply back into the penumbra so that those cells have a chance to survive. We have reasonably good evidence for doing so within 3 hours, and less convincing evidence for 4.5 hours. After this time we can't prove there's a benefit to using rTPA, which makes it hard to justify the risk of further harm to the patient.(2 votes)
- very cold body temperature. extremely cold on a very hot day?(1 vote)
- [Voiceover] Let me take you back to that time period, about four to six hours after an infarction when the blood-brain barrier was just starting to break down, because I want to talk about something that's happening in the ischemic area of the brain here around that time. And that something is inflammation. There's an inflammatory reaction to the stroke going on here as well. And just as a little reminder, an inflammatory response is sort of a protective biological response of tissues. It happens whenever really anything sort of irritates your tissues. So, you know, right now we're talking about something big, like inflammation after a stroke. But, you know, you'd even get some inflammation happening when, oh, I don't know, say you get a little scratch from your kitty. So you might notice that even if the skin isn't broken, you'd see some swelling and redness over the scratched area. And that's some inflammation happening. And you even get an inflammatory response happening when you eat food because, technically, food is a foreign object and a potential irritant. But anyway, I want to focus on this inflammation for a little bit. Let's actually follow what happens with this inflammation from the start, from the initial ischemia. And we'll do this in steps. So step one, ischemia happens, and it leads to brain cell death, right. And step two, we haven't actually seen this step before. But while the neurons are dying, they release these little chemical signals called damage associated molecular patterns or DAMPS. So as their name might suggest, they're these tiny little signals that let other cells in the area know that something bad is going on. And these DAMPS then trigger an inflammatory response. So what they do is they activate these inflammatory cells called macrophages. And the macrophages come along. And, A, they cause more inflammation to happen. So they release little signals to call in all sorts of reinforcements. And, B, the macrophages actually directly activate certain immune cells and get them involved in the inflammatory response. And I'm drawing those in in purple now. So it's this huge sort of inflammatory response that's just getting bigger and bigger. So right now you might be wondering what the point of this inflammation is. Well, think about it this way. All of the brain cells that were initially dying and the inflammatory cells that were first on the scene, right, they all released little signals that called in for reinforcements, i.e., more inflammatory cells. But once enough backup gets there, a whole bunch of them sort of switch roles to being anti-inflammatory cells. So you can see me turning these purple inflammatory cells now into green anti-inflammatory cells. And the switch to what's called an anti-inflammatory phenotype is because, well, a couple of reasons. First, they don't need any more reinforcements in the area. So they stop making sort of the inflammation worse by calling in more reinforcements. And, second, the anti-inflammatory cells end up acting as the cleanup crew. So there needed to be a reasonable number of cells there to get the cleanup job done, which actually happens through a process called liquefactive necrosis. Before I explain what that is, let me just update our little step list over here in the corner. So step three, the inflammatory cells come in. And then step four, they sort of switch over to an anti-inflammatory role. And now step five, liquefactive necrosis begins. But let me explain this liquefactive necrosis thing. So what it is, first, neutrophils in the area will start to release digestive enzymes called hydrolases. And these hydrolases, they'll break down dead cells. And by doing that, what they end up creating is this cavity surrounded by normal, nice, solid tissue, but this cavity full of sort of soft, liquified, necrotic cell debris. And actually I'm gonna zoom out here because we wanna find out what happens with this cavity. And I think it's conceptually a lot easier to zoom out and look at it from a macroscopic view. So let's zoom out a bit. So here is our guy who's been helping us learn about strokes this whole time. And here is the clot. And here is the ischemic area in the brain, in this brain. And just so that we're up to speed here, so we see the ischemia, and we know that resulted in brain cell death. We know the DAMPS got released. Then the inflammatory cells came and did their thing. And then the liquefactive necrosis began. And now we want to know what ends up happening with our necrotic cavity that we developed after our stroke. Well, it can go one of two ways usually. So if it's a small stroke and a small subsequent area of necrosis, it can be walled off. It can be sort of contained by a fibrous capsule and then sort of removed by macrophages. And notice that when macrophages remove the junk in this cavity here, you actually lose some volume to your brain since the area doesn't regenerate. So that's what happens if it's just a small necrotic area. But if you have a larger necrotic area, so let's say if you had a large stroke, then the area of necrosis gets sort of walled off again. It gets quarantined again, if you will, from the rest of the brain. And it will become a cyst, which is a cavity that's separated from the surrounding tissue. And then the cyst sort of gets cleaned up by immune system cells and just becomes a large cavity, actually just a hole in the brain that, A, unfortunately is permanent, and, B, doesn't sort of regenerate back into functional brain. So there's literally a hole that ends up staying in your brain. So just for completeness of sake, step six, cavity formation.