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centers Of great interest has been the identi cation by Cairncross and others of genetic markers in anaplastic oligodendrogliomas, and possibly low-grade ones as well (mainly on chromosomes 1p and 19q), that predict a remarkable chemoresponsivity to the PCV regimen and prolonged survival, as mentioned above For example, of 50 patients who had loss of these regions on 19p but no other genetic aberrations, the median survival was over 10 years These ndings are just being adopted into general clinical practice, and it is likely that re nements of them will be soon (see Louis et al and Reifenberger and Louis) Ependymoma (See also page 567) This tumor proves to be more complex and variable than other gliomas Correctly diagnosed by Virchow as early as 1863, its origin from ependymal cells was rst suggested by Mallory, who found the typical blepharoplasts (small, darkly staining cytoplasmic dots that are the basal bodies of the cilia as seen by electron microscopy) Two types were recognized by Bailey and Cushing: one was the ependymoma, and the other, with more malignant and invasive properties, the ependymoblastoma More recently a myxopapillomatous type, localized exclusively in the lum terminale of the spinal cord, has been identi ed (see Chap 44) Ependymomas are derived from ependymal cells ie, the cells lining the ventricles of the brain and the central canal of the spinal cord; this is the most common glioma of the spinal cord These cells have both glial and epithelial characteristics As one might expect, the tumors grow either into the ventricle or adjacent brain tissue The most common cerebral site is the fourth ventricle; less often, they occur in the lateral or third ventricles (page 567) In the spinal cord, most ependymomas originate in the lumbosacral regions, from the conus medullaris or lum terminale Grossly, those in the fourth ventricle are grayish pink, rm, cauli ower-like growths; those in the cerebrum, arising from the wall of the lateral ventricle, may be large (several centimeters in diameter), reddish gray, and softer and more clearly demarcated from adjacent tissue than astrocytomas, but they are not encapsulated The tumor cells tend to form rosettes with central lumens or, more often, circular arrangements around blood vessels (pseudorosettes) Some ependymomas, called epithelial, are densely cellular; others form papillae Some of the well-differentiated fourth ventricular tumors are probably derived from subependymal astrocytes (see later in this chapter and also Fig 31-12) Anaplastic ependymomas are identi ed by their high mitotic activity and endothelial proliferation, nuclear atypia, and necrosis The correlations between histopathologic features and clinical outcomes have not been well de ned, however Approximately 6 percent of all intracranial gliomas are ependymomas, the percentage being slightly higher in children (8 percent) About 40 percent of the infratentorial ependymomas occur in the rst decade of life, a few as early as the rst year The supratentorial ones are more evenly distributed among all age groups, but in general the age incidence is lower than that of other malignant gliomas The symptomatology depends on the location of the growth The clinical manifestations of fourth ventricular tumors are described further on in this chapter; the point to be made here is the frequent occurrence of hydrocephalus and signs of raised intracranial pressure (manifest in children by lethargy, nausea, vomiting, and papilledema) Cerebral ependymomas otherwise resemble the other gliomas in their clinical expression Seizures occur in approximately one-third of the cases.

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The imaging characteristics are rather different from those of other tumors In the CT scan one observes a well-demarcated heterogeneous hyperdense mass with fairly uniform contrast enhancement Calci cation and some degree of cystic change are common in supratentorial tumors but less so in infratentorial ones There are mixed signal characteristics on MRI, generally hypointense on T1 sequences and hyperintense on T2 An intraventricular location supports the diagnosis of ependymoma, but meningioma and a number of other tumors may be found in this location Treatment It is notable that the interval between the rst symptom and the diagnosis ranges from 4 weeks, in the most malignant types, to 7 to 8 years In a follow-up study of 101 cases in Norway, where ependymomas made up 12 percent of all primary intracranial tumors (and 32 percent of intraspinal tumors), the postoperative survival was poor Within a year, 47 percent of the patients had died, although 13 percent were alive after 10 years Doubtless the prognosis depends on the degree of anaplasia (M rk and L ken), the location of the tumor, and whether it is operable Surgical removal is supplemented by radiation therapy, particularly to address the high rate of seeding of the ventricles and spinal axis In the treatment of cerebral ependymoblastomas, antitumor drugs are often used in combination with radiation therapy Meningioma (See also page 577) This is a benign tumor, rst illustrated by Matthew Bailie in his Morbid Anatomy (1787) and rst recognized by Bright, in 1831, as originating from the dura mater or arachnoid It was analyzed from every point of view by Harvey Cushing and was the subject of one of his most important monographs Meningiomas represent about 15 percent of all primary intracranial tumors; they are more common in women than in men (2:1) and have their highest incidence in the sixth and seventh decades Some are familial There is evidence that persons who have undergone radiation therapy to the scalp or cranium are vulnerable to the development of meningiomas and that the tumors appear at an earlier age in such individuals (Rubinstein et al) There are a number of reports of a meningioma developing at the site of previous trauma, such as a fracture line, but the association is uncertain The most frequent genetic defects of meningiomas are truncating (inactivating) mutations in the neuro bromatosis 2 gene (merlin) on chromosome 22q These are present in the great majority of certain meningiomas (eg, broblastic and transitional types), but not others Merlin deletions probably also play a role in those instances in which there is a loss of the long arm of chromosome 22 In meningiomas of both the sporadic and neuro bromatosis (NF2)-associated types, other genetic defects are found, including deletions on chromosomes 1p, 6q, 9p, 10q, 14q, and 18q Meningiomas also elaborate a variety of soluble proteins, some of which (vascular endothelial growth factor) are angiogenic and relate to both the highly vascularized nature of these tumors and their prominent surrounding edema (see Lamszus for further details) Some meningiomas contain estrogen and progesterone receptors The implications of these ndings are not yet clear but may relate to the increased incidence of the tumor in women, its tendency to enlarge during pregnancy, and an association with breast cancer The precise origin of meningiomas is still not settled According to Rubinstein, they may arise from dural broblasts, but in our opinion, they are more clearly derived from arachnoidal (meningothelial) cells, in particular from those forming the arachnoid villi Since the clusters of arachnoidal cells penetrate the dura in largest number in the vicinity of venous sinuses, these are the.