Overview Glioblastoma accounts for 22.3% of neuroepithelial tumors and has been reported to account for 10.2% of intracranial tumors. It is the second most common tumor after astrocytoma. It occurs mainly in adults, especially in 30-50 years old, and is significantly more common in males than females, about 2-3:1. The age of prevalence is 40-45 years old. Glioblastoma is located in the subcortex and grows infiltratively, often invading several lobes and deep structures, and may spread to the contralateral cerebral hemisphere via the corpus callosum. The most common sites are the frontal lobe, followed by the frontal/parietal lobes and, to a lesser extent, the occipital/thalamic lobes and basal ganglia. Tumors located in the posterior cranial fossa are rare. Most of the tumors have indistinct boundaries. A few tumors are rapidly growing and cause softening and edema in the surrounding tissues, showing the phenomenon of “pseudo-envelope”, which can be mistaken for clear boundaries, but in fact, the tumors have infiltrated and grown beyond the boundaries. The tumor may invade the cortex and adhere to the dura, or may protrude into the ventricles and deep structures. The hardness of the tumor varies depending on the presence or absence of secondary changes, and the tumor is soft and hard with uneven texture. The tumor can be of various colors. The typical swelling can be seen as gray tumor, red fresh hemorrhage, purple hemorrhagic mass, yellow old hemorrhage and white interstitial hyperplasia, and the tumor can also have foci of necrosis and cystic changes of different sizes, and the fluid inside the capsule can be bloody, brown or yellow. The tumor is rich in blood flow and the surrounding brain edema is obvious. If the tumor protrudes to the brain surface and ventricles, the tumor cells may spread with the brain fluid, and some of them may metastasize to the lung, liver, bone or lymph nodes outside the brain. Clinical manifestations Because of the highly malignant tumor, the growth is fast and the course is short, most of them are within 3 months from the appearance of symptoms to the time of consultation, about 70%-80% are within 6 months. In some cases, due to tumor bleeding, the onset of the disease may be stroke-like. Occasionally, there are cases with longer duration of disease, which may be related to the malignant transformation of the tumor with the growth of the tumor after a relatively benign early stage. Due to the rapid growth of the tumor, cerebral edema is widespread and the symptoms of increased intracranial pressure are obvious, almost all patients have headache, vomiting and optic nerve papillary edema. About 33% of the patients have seizures. About 20% of patients show indifference, dementia, mental retardation and other psychiatric symptoms. The tumor infiltrates and destroys brain tissue, causing a series of focal symptoms. Patients have varying degrees of hemiparesis, hemianesthesia, aphasia and hemianopia. Patients may experience meningeal irritation due to tumor hemorrhage, and the incidence of epilepsy is less common than astrocytoma and oligodendrocytoma. CT scan: Mixed density lesions with unclear borders, most of which have high density due to intra-tumor hemorrhage but little calcification, and low density intra-tumor necrosis and cystic changes, which make the morphology polymorphic; most of the brain edema around the lesion is heavy, and the ventricles are often compressed, deformed or closed, and the midline structures are often shifted to the opposite side. Enhancement scans show non-uniform density enhancement or ring enhancement, and necrotic areas are often located within the tumor parenchyma, showing hypodense areas with irregular borders. MRI: The tumor is hyposignal on Tl plus staff image, which is not easily distinguishable from the adjacent brain tissues, and the occupancy effect is very obvious. If there is a large necrotic area in the tumor, the signal is even lower. If there is hemorrhage, it appears high signal. The corpus callosum is often involved, and midline structures such as the longitudinal fissure pool may be deformed, narrowed or displaced. The tumor has a mixed signal on T2-weighted images, with predominantly high signal and scattered low and equal signal. The very significant contrast enhancement of the tumor after Gd-DTPA injection makes a clear demarcation between the tumor and adjacent structures, and the tumor tends to occur in the deep brain. Treatment and prognosis Treatment is based on surgical resection. The principles of surgery are the same as those of astrocytoma, but it is unlikely that a true complete resection of the tumor can be achieved. If the tumor is located in the frontal lobe, the front part of the frontal lobe or the occipital lobe, the tumor can be removed together with the lobes of the brain, so that there is a larger space after surgery, which is more effective. If the tumor is located in important functional areas (language center or motor center), most of them can only be partially resected in order not to aggravate the brain dysfunction. For tumors located in brainstem, basal ganglia and thalamus, the tumor can be strictly resected under microscope and external decompression can be performed at the end of surgery. After surgery, radiotherapy, chemotherapy or immunotherapy can also be combined. Because of the high malignancy of the tumor, it is easy to recur after surgery, usually within 8 months, with an average survival time of 1 year, and individual can reach 2 years. Recently, there are reports in the literature that radiotherapy is administered immediately after surgery, and chemotherapy is administered every 2 months after radiotherapy, along with immunotherapy, which can lead to a longer remission period for some patients.