Cystic meningiomas account for 1.7%-11.7% of all intracranial primary meningiomas, with a higher incidence in women than in men and a higher incidence in minors than in adults. They are more common in the convex and midline sagittal parietal surfaces of the brain, and the pathological types are endothelial cellular and atypical. Cystic meningioma is divided into four types according to the relationship between the parenchymal part of the tumor, the cystic part and the surrounding brain tissue: Type I: intratumoral type, the capsule is located in the center of the tumor; Type II: paratumoral type, the capsule is located at the edge of the tumor; Type III: peritumoral type, the capsule is located around the tumor and enters the surrounding adjacent brain tissue; Type IV: paratumoral type, the capsule is located at the tumor-brain junction. Type V: cerebrospinal fluid circulation disorder causes the formation of the capsule, and the capsule fluid is cerebrospinal fluid. Cystic meningioma is characterized by a combination of cystic and solid lesions on CT and MR, with enhancement of the solid part and enhancement or non-enhancement of the cyst wall. CT can well observe the location of cystic cavity, intra-tumor calcification and tumor invasion of bone, while MR can clarify the relationship between tumor parenchyma, cystic cavity and its surrounding structures. It has been suggested that cystic part formation is the result of central tumor degeneration, which is mainly caused by reduced blood supply. This is consistent with the cystic degeneration caused by insufficient blood supply in other tumors. It has been suggested that the cystic fluid component originates from tumor cells with secretory function, or from local obstruction of cerebrospinal fluid circulation around the tumor. It has also been suggested that there are multiple factors involved: degenerative changes and secretory formation of the tumor, including cystic formation, ischemic necrosis, and/or hemorrhage; others include degenerative fusion of microcysts, altered secretory properties of tumor cells, white matter edema and demyelination due to perfusion injury, and leakage of fluid from the interstitial space of vascular endothelial cells.