 Let's move on to cystic circuses We know the life cycle tiniya sodium in human intestine lay eggs in the feces. They're ingested by pigs Also, they can get lost in the salads, which are uncooked. The oncospheres get hatched and penetrate the intestine and migrate into pigs muscles. If it is partially cooked meat or untreated salad that gets ingested by humans cysticers are developed from oncospheres and can involve any organ of human being as well. Most of them get lodged in muscles, but then they can go in brain, eyes, and almost everywhere. In the brain, there are four different types of presentations. What we commonly see is parent-cabin cysticerosis, but you can have them in subordinate space, intraventricular space, or it can be mixed. In the parent-cama, there are four stages which are recognized vesicular, colloidal vesicular, granular nodular, and nodular calcified. The first stage of vesicular stage is presence of cyst and scholex without enhancement. The second stage is colloidal stage where you get ring enhancement and edema. This third stage is that of granular nodular degeneration where you get decrease in enhancement, decrease in edema, and starting to get calcification. And the last stage of involution has obvious calcifications on CT scan and gradient echo images. This is the first stage where you have this 36-year-old male person with multiple T2 hyper-intense legions. Look at the vesicular stage which is not ruptured. There is no edema. There is not much enhancement. Why this patient has presented is because these two cysticerosis have ruptured and then patient presents with conversion. What you have to also notice is there is a cysticerosis in the right lateral ventricle. The next stage is when the patient presents after the cyst starts rupturing. So here is a ruptured cysticerosis, which is dark on T1, bright on T2, thin dark capsule, a small eccentric scolex. There are two daughter cysts here and a lot of edema. Gradient will show some amount of blooming of the capsule and the scolex. Next stage is granular nodular where the larvae starts getting healed. The fluid in the cyst starts disappearing. So you'll hardly see any brightness in the center. The capsule is darker and thicker in enhancement, much lesser edema. In this stage of evolution, you get calcification, no edema, sometimes little bit of Glyosis that is present. In the ventricles and in the CSS spaces, subarachnoid spaces, you get what is called as resimus type of cysticerosis, which is like cluster of grapes. The walls are thinner, the size is larger and they can cause hydrocephalus. In subarachnoid space, they can cause fluorid meningitis, arthritis, stroke and even death. Pheasta is the sequence, which is used when you have cysticerosis in subarachnoid spaces. It can be very useful when you don't see scolex on routine T2 images. So you do a submillimeter Pheasta and see scolex well, you can see capsule well and you can also see dottosis better. When it is in the subarachnoid space or in the intra ventricular space, this is in the third ventricle, you get what is called as Brun's syndrome. You get intermittent headaches, attacks here and draw attacks because of the typical location of this cysticerosis. You should not mistake cystic metastasis typically coming from musinus carcinomas of colon or stomach to cysticerosis because they also have scolex-like appearance and cystic appearance. But the scolex-like appearance, the size is much larger and the cystic appearance is also much larger. The nodule is much, much bigger. You don't require a mass spectroscopy or perfusion, but if you do one, you will see presence of lactate, alanine, succinate, which is a sugar and reduced choline. Most of them, as I said, are hyperperfused unless you are in post-extra stage where you get hyperperfusion at the periphery.