1. Clinical characteristics Intracranial SFTs are mostly seen in the posterior cranial fossa, with no gender difference between men and women, and mostly in adults. Clinical symptoms vary according to the course of the tumor and the location of the tumor. Tumors occurring in the cerebral hemispheres often have headache, nausea, vomiting, convulsions and other symptoms, while those occurring in the pontocerebellar angle (CPA) often have hearing loss in the early stage. 2. Imaging characteristics Because of the diverse histological patterns and unpredictable biological behaviors of intracranial SFTs, their clinical imaging manifestations are also diverse and lack specificity, and preoperative imaging can clarify the relationship between tumor size and surrounding tissues, but it is difficult to diagnose qualitatively. The parenchyma on CT-enhanced scans generally shows mild to moderate enhancement, with a net increase in CT value of about 40-85 HU in the parenchymal portion and no enhancement in the cystic necrotic area. on MRI, it appears as predominantly low signal on T1WI and low or moderate to low mixed signal on T2WI, with inhomogeneous enhancement after enhancement, and the typical meningeal tail sign does not present. weon et al. suggested that the T2 image in MRI The “black and white interphase sign” and the characteristic of significant inhomogeneous enhancement can help the diagnosis of SFTs. 3. Pathological features Originally, intracranial SFTs were thought to originate from mesothelial cells, but recent immunohistochemical and electron microscopic observations have revealed that tumor cells of SFTs do not have mesothelial features, such as not expressing markers of mesothelial cells, and microvillous structures are not seen under electron microscopy, suggesting that SFTs are a mesenchymal tumor. Most people currently consider them to be derived from CD34-positive fibroblasts or dendritic cells in the dura mater. Gross examination reveals tumors that are usually nodular or lobulated, well-defined from the surrounding area, slightly hard in texture, fish-like in section, and grayish or gray-red in color. Microscopically, the histological features are similar to those of SFT in other parts of the body: the tumor is mainly composed of spindle-shaped cells, and the distribution of tumor cells is sparse and dense” “with no specific histological configuration”. In the sparsely cellular areas, there is an increase in collagen deposition, and in the densely cellular areas, there are abundant fissure-like or antler-like vessels in the interstitium, forming a so-called “hemangioepithelioma”-like histological conformation. The tumor cells generally have no obvious heterogeneity and nuclear division is rare. Immunophenotypic characteristics: SFTs usually express CD34 (80%-90%), CD99 (70%), Bcl-2 (30%), EMA (30%), Actin (20%), but not Desmin, CK and S-100. The positive expression rate of CD34 has been shown to correlate with tumor differentiation, and in general, CD34 expression is higher in morphologically benign areas; while in areas with significant mesenchymal changes, positive CD34 expression tends to be decreased or absent. bcl-2 is a family of apoptosis suppressor genes, and it was found that Bcl-2 is in primitive mesenchymal cells Bcl-2 is expressed in primitive mesenchymal cells and is a relatively specific marker for SFTs. The distribution of positive expression of Bcl-2 and Ki-67 is similar in character, i.e. low expression in benign regions and high expression in mesenchymal regions. In some cases, hormone receptor ER and PR can be detected, and positive expression suggests the possibility of tumor recurrence. 4. Diagnosis and differential diagnosis Combining our cases and review of related literature, the following manifestations are considered helpful for the diagnosis of intracranial SFTs: ① The tumor site is often shallow. ② The tumor shows equal or low mixed signal or high signal on T1WI, often with cystic degeneration, and low or moderate low mixed signal predominant on T2WI, with inhomogeneous enhancement after enhancement, and the typical meningeal tail sign is not presented. (3) Peritumoral edema is obvious. Pathological histological examination is still required to confirm the diagnosis of this disease. Intracranial SFTs need to be differentiated from the following tumors: (1) Fibrous meningioma: Imaging is common for fibrous meningioma because the envelope is often intact, and the presence of intra-tumoral collagen fiber vitreous changes and calcification reduces the free water content and increases the interstitial component, thus causing its low T2WI signal. Pathologically, small islands of meningioma cells and sand granules are seen in the bundles of shuttle tumor cells, and the eosinophilic-stained collagen fibers between tumor cells are less abundant than in SFTs. The tumor cells are positive for EMA, cytokeratin and S-100 protein and negative for CD34 or focally positive. (2) On MRI, hemangiopericytoma is mostly low to equal signal on T1WI, with intra-tumoral vascular flow space shadowing and high signal on T2WI. The tumor borders are clear and the surrounding edema is light, and the enhancement is obvious. The tumor cells are round, oval or short shuttle-shaped, with rare or focal eosinophil-stained collagen fibers between them. The tumor tissue is more vascular, and the vascular lumens vary in size and are branched or antler-shaped. The tumor cells are positive for wave proteins and weakly positive for CD34 in focal or small patches. (3) Nerve sheath tumor is mainly located in the pontocerebellar region, and the growth is centered on the internal auditory canal, and the enlargement of the affected internal auditory canal can be seen. The tumor envelope is clearly demarcated from the surrounding tissues, and the VII and VIII nerve bundles on the side of the tumor are thickened and connected to the mass. The nuclei of the spindle tumor cells were often arranged in a fence-like pattern or formed verocay vesicles, and there were no eosinophilic collagen fibers between the tumor cells. The tumor cells are positive for S-100 protein and may also be positive for Leu-7 and myelin basic protein. In addition, it should be differentiated from the rare meningeal sarcoma, meningeal myofibroblastoma and meningeal fibroma, which can be helped by microscopic morphological changes and immunohistochemical staining. 5.Treatment and prognosis Fkg The main treatment is complete surgical resection, supplemented by radiotherapy and chemotherapy when necessary. Radical resection is recommended to prevent tumor recurrence and metastasis. If some cases are found to be extensively infiltrated at the time of detection and cannot be treated radically and are forced to choose palliative surgical resection, adjuvant radiotherapy is required to reduce the postoperative recurrence and metastasis rates and improve long-term quality of life. To date, most studies have concluded that the morphology of SFTs is not completely indicative of prognosis, as some morphologically benign tumors often recur or metastasize, while those morphologically malignant tumors can be biologically benign, thus requiring a comprehensive assessment of the prognosis of the tumor. Those with extensive tumor infiltration or satellite foci are prone to dissemination and metastasis, all of which suggest a poor prognosis, and therefore long-term follow-up is necessary.