Malignant Brain Tumors
Slightly more common in men than in women, malignant brain tumors (gliomas, meningiomas, and schwannomas) have an overall incidence of 4.5 per 100,000. They cause central nervous system (CNS) changes by invading and destroying tissues and by secondary effect - mainly compression of the brain, cranial nerves, and cerebral vessels; cerebral edema; and increased intracranial pressure (lCP).
Tumors can occur at any age. In adults, incidence is highest between ages 40 and 60, and the most common tumor types are gliomas and meningiomas. They usually occur above the covering of the cerebellum (supratentorial tumors).
Most tumors in children occur before age 1 or between ages 2 and 12. The most common are astrocytomas, medulloblastomas, ependymomas, and brain stem gliomas. Brain tumors are one of the most common causes of cancer death in children.
The cause of brain tumors is unknown. Some tumors have been linked to hereditary syndromes
Signs and Symptoms
Unfortunately, high grade or aggressive tumors account for the majority of tumors at the time of discovery. Since they can occur in any part of the brain, the symptoms they cause vary according to the function of the underlying brain tissue they are invading or compressing. They may include weakness or numbness on one side, speech difficulties, personality change and cognitive problems. In addition there may be more non specific symptoms such as headache, nausea, vomiting, fatigue and seizures.
In many cases, a definitive diagnosis follows a tissue biopsy performed by stereotactic surgery. In this procedure, a head ring is affixed to the skull, and an excisional device is guided to the lesion by computed tomography scanning or magnetic resonance imaging.
Other diagnostic tools include a patient history, a neurologic assessment, skull X-rays, a brain scan, and cerebral angiography.
Specific treatments vary with the tumor's histologic type, radiosensitivity, and location. Such treatments may include surgery, radiation therapy, chemotherapy, and decompression of increased ICP (with diuretics, corticosteroids, or, possibly, ventriculoatrial or ventriculoperitoneal shunting of the CSF).
Treatment of a glioma usually consists of resection by craniotomy. Radiation therapy and chemotherapy follow resection. The combination of carmustine, lomustine, or procarbazine with radiation therapy is more effective than radiation alone.
For low-grade cystic cerebellar astrocytomas, surgical resection permits long-term survival. For other astrocytomas, treatment consists of repeated surgery, radiation therapy, and shunting of fluid from obstructed CSF pathways. Radiation therapy works best in radiosensitive astrocytomas; some astrocytomas are radioresistant.
Treatment for oligodendrogliomas and ependymomas includes surgical resection and radiation therapy. Medulloblastomas call for surgical resection and, possibly, intrathecal infusion of methotrexate or another antineoplastic drug. Meningiomas require surgical resection, including dura mater and bone. (Operative mortality may reach 10% because of large tumor size.)
For schwannomas, microsurgical technique allows complete resection of the tumor and preservation of the facial nerve. Although schwannomas are moderately radioresistant, treatment still calls for postoperative radiation therapy.
Treatment for malignant brain tumors also includes chemotherapy with nitrosoureas, which cross the blood-brain barrier and allow other chemotherapeutic drugs to go through as well. Intrathecal and intra-arterial administration maximizes drug action.
Palliative measures for gliomas, astrocytomas, oligodendrogliomas, and ependymomas include dexamethasone for cerebral edema and antacids and histamine receptor antagonists for stress ulcers. These tumors and schwannomas may also require anticonvulsants.
Treatment of brain tumors can cause several complications. Surgery can result in immediate or delayed CNS infections, with symptoms that mimic tumor progression or recurrence. If fever or rapidly progressive neurologic symptoms develop, bacterial and fungal cultures will confirm the infection.
Early delayed radiation encephalopathy may stem from temporary demyelination. Anorexia, somnolence, lethargy, and headache occur 2 to 6 weeks after the therapy but resolve spontaneously in about 6 weeks.
Late delayed radiation encephalopathy stems from brain necrosis and small-vessel occlusion. Symptoms can mimic disease advancement and may include intracranial hypertension and focal neurologic dysfunction. Both are irreversible and potentially fatal complications.
Corticosteroid therapy predisposes the patient to cushingoid symptoms and GI ulceration.
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