Intracranial hemangiopericytoma

I believe that when everyone hears that a tumor has grown in their brain, they will be very panicked, because most of the tumors growing in the brain are malignant tumors. These tumors will grow larger and larger, compressing other nerves in the brain and affecting a person's normal life. Intracranial hemangiopericytoma is a tumor that grows in the brain. So if a person suffers from intracranial hemangiopericytoma, is this disease serious?

Common clinical symptoms of intracranial hemangiopericytoma (HPC) are headache, dizziness, and compression of local brain and cranial nerves. It occurs in the anterior cranial fossa, middle cranial fossa, posterior cranial fossa, and near the falx cerebri of the parietal lobe, and is connected to the broad base of the meninges. All of them had varying degrees of edema, significant space-occupying effect, and no hydrocephalus.

The pathological findings of HPC are similar to those of meningioma, except that it is softer in texture, bright red in color, and has a rich blood supply. Light microscopy showed that the tumor tissue was rich in blood sinusoids and blood vessels with thin walls, and the sinusoids were filled with polygonal tumor cells that were diffusely arranged. The nucleus is round or slightly irregular, darkly stained, and nuclear division images are easily seen. The cytoplasm is small and may be vacuolated. There are abundant blood vessels and intercellular reticular fibers. In a few pathological cases, meningeal epithelial masses can be found, but characteristic structures of meningioma such as whorls and psammoma bodies have never been seen. Pathologically, it presents malignant manifestations.

Guthrie et al. believed that the clinical manifestations and lesion sites of HPC were similar to those of meningioma. The clinical symptoms of this group of cases were also nonspecific, and their manifestations were similar to those of meningioma. A comparison with Uttley's atypical meningioma (including angiomatous meningioma) revealed that the locations of the two were slightly different: HPC mainly occurred in the tentorium cerebellum, while atypical meningioma mainly occurred in the falx cerebri. HPC is prone to recurrence after surgery. Brunori et al. reported 9 cases in which 3 cases recurred, one of which was 15 years after the first surgery. There were 2 recurrences in this group, with the longest time from the first surgery being 7 years.

The plain scan CT of HPC shows an isodense and hyperdense lobulated mass without calcification. During CT examination, plain scan showed a lobed, non-calcified mass with mixed high and low density; there was varying degrees of edema and space-occupying effect around the tumor, which was connected to the broad base of the meninges. During enhancement, the lesion is significantly enhanced, but the low-density area inside it is not enhanced. Compressive bone resorption was observed in 2 cases in this group. HPC generally does not cause bone hyperplasia due to its invasive nature. None of the 6 cases in this group had bone hyperplasia.

It is a slightly higher signal on PDWI and a mixed signal shadow with a slightly longer T2 signal on T2WI: cystic areas and vascular flow void signal shadows can be seen within it; after the injection of contrast agent, the lesion is significantly enhanced, and an obvious "meningeal tail sign" can be seen. It is a mass with clear boundaries, attached to the dura mater and rich blood supply. The amount of intraoperative bleeding is greater than that of meningioma. The blood supply of meningioma mainly comes from the branches of the external carotid artery, while HPC is often supplied by the branches of the external carotid artery and the internal carotid artery or the vertebral artery at the same time. Angiography showed a hypervascular tumor with late arterial phase and dense staining in the capillary phase. The tumor in the middle cranial fossa showed that the main blood supply came from the branches of the external carotid artery, and partly from the branches of the internal carotid artery; the tumor in the posterior cranial fossa was mainly supplied with blood from the branches of the vertebral artery, and partly from the branches of the external carotid artery.

Macroscopically, the tumor is dark red, soft, and without a capsule. Microscopically, the tumor is composed of new blood vessels and stroma. The blood vessels vary in size, and the endothelial cells are of normal morphology. The epithelial cells undergo metaplasia and proliferate, and are irregularly arranged around the blood vessels, compressing them. The epithelial cells are round, oval or spindle-shaped, with large, darkly stained nuclei, fine chromatin, and abundant, eosinophilic cytoplasm, whereas the nuclei of malignant cells vary in size, with obvious atypia, frequent mitotic figures, and silver-stained cytoplasm. Reticular fibers can be seen scattered between cells. Clinically, the differential diagnosis should be differentiated from osteosarcoma, fibrosarcoma, synovial sarcoma, chondrosarcoma, and metastatic tumors.

Treatment method: surgical excision of the tumor bone, assisted by chemotherapy and radiotherapy. The prognosis is generally better than usual.