Personality changes, intellectual decline, emotional lability
Seizures, headaches, nausea
Increased intracranial pressure in some patients
Neuroradiologic evidence of space-occupying lesion
About one-third of all primary intracranial neoplasms (Table 24–4) are meningiomas; a quarter are gliomas
The remainder are
Certain tumors (eg, neurofibromas, hemangioblastomas, and retinoblastomas) have a familial basis
May lead to a generalized disturbance of cerebral function and symptoms of increased intracranial pressure
Table 24–4.Primary intracranial tumors (listed by major histology grouping and by incidence within each group). ||Download (.pdf) Table 24–4. Primary intracranial tumors (listed by major histology grouping and by incidence within each group).
|Treatment and Prognosis
|Tumors of Meninges
|Originates from the dura mater or arachnoid; compresses rather than invades adjacent neural structures. Increasingly common with advancing age. Tumor size varies greatly. Symptoms vary with tumor site—eg, unilateral proptosis (sphenoidal ridge); anosmia and optic nerve compression (olfactory groove). Tumor is usually benign and readily detected by CT scanning; may lead to calcification and bone erosion visible on plain radiographs of skull.
|Treatment is surgical. Tumor may recur if removal is incomplete.
|Tumors of Neuroepithelial Origin
|Presents commonly with nonspecific complaints and increased intracranial pressure. As it grows, focal deficits develop. O6-methylguanine-DNA methyltransferase promoter methylation positivity (seen in 40% of cases) and isocitrate dehydrogenase 1/2 mutations (seen in 10% of cases) carry better prognosis.
|Course is rapidly progressive, with poor prognosis (< 20% survival at 2 years). Total surgical removal is usually not possible. Radiation therapy and temozolamide may prolong survival. Tumor treatment fields added to temozolamide after completion of radiation therapy prolong survival.
|Presentation similar to glioblastoma multiforme but course more protracted, often over several years. Cerebellar astrocytoma may have a more benign course. Isocitrate dehydrogenase 1/2 mutations (seen in a majority of cases) carry better prognosis in grade II and III tumors.
|Prognosis is variable. By the time of diagnosis, total excision is usually impossible; tumor may be radiosensitive and temozolamide is also helpful in grade II and III tumors. In cerebellar astrocytoma, total surgical removal is often possible.
|Glioma arising from the ependyma of a ventricle, especially the fourth ventricle; leads to early signs of increased intracranial pressure. Arises also from central canal of cord.
|Tumor is best treated surgically if possible. Radiation therapy may be used for residual tumor.
|Slow-growing. Usually arises in cerebral hemisphere in adults. Calcification may be visible on skull radiograph. Co-deletion of 1p/19q and isocitrate dehydrogenase 1/2 mutation required for diagnosis.
|Treatment is surgical and usually successful. Radiation and chemotherapy (temozolamide or procarbazine, lomustine, and vincristine) are used in grade II and III tumors.