Gbm
| Glioblastoma Multiforme | |
|---|---|
| Glioblastoma - MR coronal with contrast.jpg | |
| Synonyms | N/A |
| Pronounce | N/A |
| Specialty | N/A |
| Symptoms | Headache, nausea, vomiting, seizures, neurological deficits |
| Complications | N/A |
| Onset | Typically in adults, peak incidence at 64 years |
| Duration | Progressive |
| Types | N/A |
| Causes | Unknown, risk factors include genetic predisposition, ionizing radiation |
| Risks | N/A |
| Diagnosis | MRI, CT scan, Biopsy |
| Differential diagnosis | N/A |
| Prevention | N/A |
| Treatment | Surgery, Radiotherapy, Chemotherapy |
| Medication | N/A |
| Prognosis | Poor, median survival ~15 months |
| Frequency | 3.2 per 100,000 people per year |
| Deaths | N/A |
Overview
Glioblastoma Multiforme (GBM) is the most aggressive type of primary brain tumor in adults. It is classified as a grade IV astrocytoma by the World Health Organization (WHO). GBM is characterized by rapid growth and a tendency to infiltrate surrounding brain tissue, making it difficult to treat effectively.
Epidemiology
GBM is the most common and deadliest of malignant primary brain tumors in adults, accounting for approximately 15% of all brain tumors. The incidence of GBM is about 3.2 per 100,000 people per year. It is more common in males than females and typically occurs in older adults, with a peak incidence at around 64 years of age.
Pathophysiology
GBM arises from astrocytes, which are star-shaped glial cells in the central nervous system. The tumor is highly heterogeneous, both genetically and histologically. Common genetic alterations in GBM include mutations in the TP53 gene, amplification of the EGFR gene, and loss of heterozygosity on chromosome 10. These genetic changes lead to uncontrolled cell proliferation, resistance to apoptosis, and increased angiogenesis.
Clinical Presentation
Patients with GBM often present with symptoms related to increased intracranial pressure or focal neurological deficits. Common symptoms include:
- Headache
- Nausea and vomiting
- Seizures
- Cognitive and personality changes
- Motor weakness or sensory loss
- Visual disturbances
Diagnosis
The diagnosis of GBM is typically made using imaging studies and confirmed by histopathological examination.
Imaging
- Magnetic Resonance Imaging (MRI) is the preferred imaging modality. GBM typically appears as a ring-enhancing lesion with central necrosis and surrounding edema on contrast-enhanced MRI.
- Computed Tomography (CT) scan can also be used, especially in emergency settings, but is less sensitive than MRI.
Biopsy
A biopsy is required to obtain a definitive diagnosis. This can be done via stereotactic needle biopsy or during surgical resection.
Treatment
The treatment of GBM involves a multimodal approach:
Surgery
The goal of surgery is maximal safe resection of the tumor. Complete resection is often not possible due to the infiltrative nature of the tumor.
Radiotherapy
Postoperative radiotherapy is standard and typically involves fractionated external beam radiation.
Chemotherapy
Temozolomide is the most commonly used chemotherapeutic agent and is often administered concomitantly with radiotherapy and as adjuvant therapy.
Prognosis
The prognosis for patients with GBM is poor, with a median survival of approximately 15 months despite aggressive treatment. Factors associated with a better prognosis include younger age, higher performance status, and complete surgical resection.
Research and Future Directions
Research is ongoing to find more effective treatments for GBM. Areas of investigation include targeted therapies, immunotherapy, and novel drug delivery systems.
See Also
External Links
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Contributors: Prab R. Tumpati, MD