Anaplastic Astrocytoma

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Anaplastic astrocytomas (AA) are histologically classified as World Health Organization (WHO) grade III neoplasms. Analagous to infiltrative astrocytomas, these tumors have infiltrative margins on histology. On the other hand, they contain areas of pleomorphism and high cellularity and may demonstrate areas of necrosis and cyst formation like their higher grade counterparts. Up to 75% of AA are felt to arise from lower grade gliomas whereas the anaplastic group may also dedifferentiate into glioblastomas over time (9). The age of presentation also tends to be intermediate between these two groups, typically discovered during the fourth to fifth decades of life in patients presenting with seizures, focal neurologic deficits, or signs of increased intracranial pressure (ICP) (10). In view of the above, it should not be surprising that AA tend to have imaging findings that are intermediate between the infiltrative astrocytomas and glioblastomas.

The AA can be quite variable in location but nearly all are supratentorial and most are centered in the deep white matter and may secondarily involve the deep gray-matter structures. These masses generally have poorly defined margins and are somewhat heterogeneous in signal intensity characteristics on all MR pulse sequences, most evident on the FLAIR and T2-weighted images (Fig. 1). The amount of surrounding vasogenic edema is quite variable but more commonly relatively mild and frequently indistinguishable from the margins of the nonenhancing component of the mass. Consequently, it is difficult to determine the true extent of neoplastic cell invasion when planning complete resection by MRI. FLAIR and T2-weighted images certainly demonstrate the extent of parenchymal involvement better than the T1-weighted images but tumor cells can extend into parenchyma that is normal in signal intensity on all pulse sequences. Of the two, the FLAIR images generally make it easier to appreciate the MRI abnormality because the darkened cerebrospinal fluid (CSF) makes involvement along the pial and ependymal surfaces of the brain more obvious and resetting the gray scale makes the subcortical involvement more apparent. The T1-weighted images are generally more useful for assessing mass effect and location of the mass. The unenhanced T1-weighted images may also show small foci of mild hyperintensity related to dystrophic calcification (shortened T1-relaxation time resulting from the impact on water molecules by the calcium along the margins of the crystalline matrix) that could be misleading when assessing gadolinium enhancement. Small foci of hemorrhage that may arise de novo or may be related to a recent stereotactic biopsy procedure are commonly more obviously hyperintense on the T1-weighted images. The parenchyma that enhances with gadolinium represents the

Fig. 1. Anaplastic astrocytoma: (A) Axial T2-weighted image demonstrating large infiltrative mass in the left frontal lobe that is heterogeneously hyperintense, presumably representing the heterogeneity of the histology. (B) Large irregular nodular foci and small ill-defined patchy foci of enhancement are detected in the inferior left frontal lobe on this gadolinium-enhanced T1-weighted spin echo images.

Fig. 1. Anaplastic astrocytoma: (A) Axial T2-weighted image demonstrating large infiltrative mass in the left frontal lobe that is heterogeneously hyperintense, presumably representing the heterogeneity of the histology. (B) Large irregular nodular foci and small ill-defined patchy foci of enhancement are detected in the inferior left frontal lobe on this gadolinium-enhanced T1-weighted spin echo images.

area with the most extensive breakdown in the blood-brain barrier (BBB) and generally indicates the more aggressive component ofthe mass but clearly does not reflect the true extent of the mass. The enhancement within the masses is generally patchy or heterogeneous in nature. Ring enhancement is atypical as this is generally seen in glioblastomas with central necrosis. On the other hand, some AA may not enhance at all. One prior study demonstrated that nearly 40% of nonenhancing masses were found to be AA (8). The associated mass effect is contingent on size, location, and surrounding edema but is usually moderate in degree. Evidence of prior hemorrhage is relatively infrequent in contrast to glioblastomas. It is also important to remember that AA generally spread in a contiguous fashion along normal white-matter tracts but may also disseminate in the CSF along the pial and ependymal surfaces ifthe mass is contiguous with the ventricles or the outer surface of the brain. This is most sensitively demonstrated on gadolinium-enhanced T1 images as linear and/or nodular enhancement along the ependymal or pial surfaces of the brain and/or spinal cord or as confluent masses of varying sizes in the basilar cisterns, over the cerebral convexities, or within the spinal canal.

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