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Current time:0:00Total duration:6:00

Video transcript

let me take you back to that time period about four to six hours after 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 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 survey a protective biological response of tissues that happens whenever it really anything sort of irritates your tissues so you know right now we're talking about something big like inflammation after 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 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 there are 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 they activate these inflammatory cells called macrophages and the macrophages come along and they 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 in inflation is well think about it this way all the brain cells that were initially dying and the inflammatory cells that were first on the scene right they all release little signals that called in for reinforcements ie 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 and he inflammatory cells and and this switch to what's called an anti inflammatory phenotype is because well a couple reasons first they don't need anymore 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 liquefaction Acronis 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 liqui fact of necrosis begins let me explain this liqui fact of 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 this cavity surrounded by normal nice solid tissue but this cavity full of sort of soft liquefied necrotic cell debris and actually I'm going to zoom out here because we want to 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 his brain and just so that we're up to speed here so we we see the ischemia and we know that resulting in brain cell death we know the damps got released then the inflammatory cells came and did their thing and then the liqui fact of 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 in 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 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 is sake step six cavity formation