what causes heart attacks and strokes

- [voiceover] let me takeyou back to that time period, about four to six hoursafter an infarction when the blood-brain barrier was just starting to break down, because i want to talk aboutsomething that's happening

in the ischemic area of thebrain here around that time. and that something is inflammation. there's an inflammatoryreaction to the stroke going on here as well.

and just as a little reminder, an inflammatory response is sort of a protective biologicalresponse of tissues. it happens whenever really anything sort of irritates your tissues. so, you know, right now we'retalking about something big, like inflammation after a stroke. but, you know, you'd even getsome inflammation happening when, oh, i don't know, say you get

a little scratch from your kitty. so you might notice that evenif 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 aninflammatory response happening when you eat food because, technically, food is a foreign objectand 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'tactually seen this step before. but while the neurons are dying,

they release these little chemical signals called damage associatedmolecular 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 triggeran inflammatory response. so what they do is they activate these inflammatory cellscalled macrophages.

and the macrophages come along. and, a, they cause moreinflammation to happen. so they release little signals to call in all sorts of reinforcements. and, b, the macrophagesactually 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 sortof 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 cellsthat 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 morereinforcements in the area. so they stop making sortof 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 areasonable 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, theinflammatory 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 thisliquefactive necrosis thing.

so what it is, first,neutrophils in the area will start to release digestiveenzymes called hydrolases. and these hydrolases, they'llbreak down dead cells. and by doing that, what theyend 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 outwhat happens with this cavity.

and i think it's conceptually a lot easier to zoom out and look at itfrom 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 areain the brain, in this brain. and just so that we're up to speed here, so we see the ischemia,

and we know that resultedin brain cell death. we know the damps got released. then the inflammatory cellscame and did their thing. and then the liquefactive necrosis began. and now we want to knowwhat ends up happening with our necrotic cavity thatwe 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 containedby 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 somevolume to your brain since the area doesn't regenerate. so that's what happens if it'sjust 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 necrosisgets 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.