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Glioblastoma is the most malignant glioma among all astrocytic tumors. Tumors are located subcortically and mostly grow throughout the supratentorial hemisphere of the brain. It grows infiltratively, often invading several brain lobes and deep structures, and can also spread to the contralateral hemisphere through the corpus callosum. The most common site of occurrence is the frontal lobe.
Figure 1. Glioblastoma.
A study has found that the molecular mechanisms underlying primary glioblastoma and secondary glioblastoma are different. The molecular changes in primary glioblastoma are mainly characterized by the amplification and overexpression of epidermal growth factor receptor (EGFR), while secondary glioblastoma is mainly characterized by p53 mutations.
Glioblastoma grows rapidly, with 70% to 80% of patients having a disease course of 3 to 6 months, and only 10% having a disease course exceeding 1 year. Patients with a longer course of illness may evolve from low malignancy astrocytomas. Due to rapid tumor growth, extensive brain edema, and significant symptoms of increased intracranial pressure, all patients experience headaches and vomiting. Optic disc edema can cause headaches, mental changes, limb weakness, vomiting, consciousness disorders, and speech disorders. Tumor infiltrates and destroys brain tissue, causing a series of focal symptoms. Patients have varying degrees of hemiplegia, hemiparesis, aphasia, and hemianopia. Neurological examination can detect hemiplegia, neurological damage, hemiparesis, and hemianopia. The incidence of epilepsy is less common than that of astrocytoma and oligodendroglioma, and some patients may experience epileptic seizures. Some patients exhibit mental symptoms such as apathy, dementia, and intellectual decline.
| Clinical Examination | Detail |
| Laboratory examination | Lumbar puncture often indicates increased pressure, elevated cerebrospinal fluid protein content, and increased counts. In a few cases, special staining may sometimes reveal shed tumor cells. |
| Radionuclide Examination | The positive rate of diagnosis is higher than that of astrocytoma, and the lesion shows a radioactive concentration area locally. The head X-ray plain film only shows an increase in intracranial pressure, with occasional displacement after pineal gland calcification. Cerebral angiography shows vascular compression and displacement, with about half showing pathological blood vessels. The blood vessels at the lesion site are often uneven in thickness and twisted, with some appearing as small dots or filaments. |
| CT Scan | The tumor presents as a mixed density lesion with unclear boundaries, often with high-density manifestations caused by intratumoral bleeding, but calcification is rare. Tumor necrosis and cystic changes present as low-density shadows, resulting in a polymorphic morphology. Most of the lesions are surrounded by severe brain edema, and there is no clear boundary between the tumor and brain tissue. The ventricles are often compressed, deformed, or closed, and the midline structure often shifts to the opposite side. After enhancement, some tumors show uneven enhancement, often manifested as a central low-density necrotic or cystic area with irregular circular, island shaped, or spiral enhancement shadows in the peripheral proliferative vascular area. |
| MRI Examination | The tumor appears as a low signal on T1 weighted images, while on T2 weighted images, it is a high signal tumor with unclear boundaries, which is difficult to distinguish from adjacent brain tissue and has a significant occupying effect. If there is a large necrotic area within the tumor, it shows a lower signal, and if there is bleeding, it shows a high signal. The corpus callosum is often affected, and midline structures such as the longitudinal fissure can deform, narrow, or shift. Tumors exhibit mixed signals on T2 weighted images, with high signals being the predominant feature. The significant contrast enhancement of the tumor after injection of Gd DTPA results in a clear boundary between the tumor and adjacent structures, and is more likely to occur in the deep brain, which is a characteristic manifestation. |
Glioblastoma is mainly treated with surgery, radiotherapy, chemotherapy, tumor electric field therapy, and other comprehensive treatments.
| Clinical Examination | Detail |
| Surgical treatment | Surgery should aim to remove as much tumor as possible without exacerbating neurological dysfunction. Expanding the scope of tumor resection can effectively reduce internal pressure, alleviate postoperative brain edema, and lower the incidence of neurological complications. If the tumor is located in an important functional area (language center or motor center), in order not to aggravate brain dysfunction, most can only be partially removed. For tumors located in the brainstem, basal ganglia, and thalamus, strict tumor removal can be performed under a microscope, and external decompression can be performed at the end of the surgery. |
| Radiotherapy, chemotherapy, and immunotherapy | Routine postoperative radiotherapy should be performed, and chemotherapy or immunotherapy can also be combined. Recently, literature has reported that radiation therapy is performed immediately after surgery, followed by chemotherapy every 2 months and immunotherapy, which can provide some patients with a longer period of remission. Glioblastoma has a certain degree of radiation tolerance, and for residual tumors, high-dose fractionated irradiation, tumor interstitial radiotherapy, and stereotactic radiosurgery are often used to achieve this. |
| Tumor electric field therapy | Tumor electric field therapy is a novel tumor treatment technique that uses low-intensity, medium frequency (200 kHz) alternating electric fields to act on microtubule proteins in proliferating cancer cells, interfere with tumor cell mitosis, induce apoptosis of affected cancer cells, and inhibit tumor growth. |
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