6 Magnetic Resonance Imaging

Chapter 6 / MRI 105 6 Magnetic Resonance Imaging Paul M. Ruggieri Summary Magnetic resonance (MR) is clearly the accepted imaging standard for the preliminary evaluation, peri-operative management, and routine longitudinal follow-up of patients with high-grade gliomas (HGG). The purpose of this chapter is to review the imaging characteristics of HGG using conventional MR imaging techniques. Whereas the newer techniques of MR diffusion, perfusion, diffusion tensor imaging, and MR spectroscopy will be included as part of this discussion of the high grade neoplasms, the detailed concepts of such studies will be discussed elsewhere in this text. Key Words: MR imaging; anaplastic astrocytoma; glioblastoma multiforme; gliosarcoma; gliomatosis cerebri; oligodendroglioma. INTRODUCTION Magnetic resonance (MR) is clearly the accepted imaging standard for the preliminary evaluation, peri-operative management, and routine longitudinal follow-up of patients with high-grade gliomas (HGG). The purpose of this chapter is to review the imaging characteristics of HGG using conventional MR imaging techniques. Whereas the newer techniques of MR diffusion, perfusion, diffusion tensor imaging, and MR spectroscopy will be included as part of this discussion of the high grade neoplasms, the detailed concepts of such studies will be discussed elsewhere in this text. In general terms, high-grade glial neoplasms are conventionally thought of as infiltrative parenchymal masses that are hyperintense on FLAIR fluid-attenuated inversion recovery (FLAIR) and T2-weighted images, hypointense on unenhanced T1-weighted images, may or may not extend into the corpus callosum, are surrounded by extensive vasogenic edema, and prominently enhance following gadolinium administration. It must be pointed out that this description is clearly just a generalization as many high-grade neoplasms clearly do not follow these “rules” and some of these characteristics may even be seen in low-grade neoplasms. The most common and obvious contradiction is the pilocytic astrocytoma in children and young adults. This is clearly a low-grade neoplasm although MR imaging demonstrates a solid soft tissue nodule that enhances strikingly following gadolinium administration. Conversely, many HGG do not enhance at all with gadolinium (1). Such contradictions would suggest that isolated MR imaging characteristics frequently do not permit a clear distinction between the different primary glial neoplasms or the histologic grades of these masses. Earlier studies demonstrated sensitivities for MRI alone ranging from 55 to 83% for grading of gliomas (2– 7). One of these studies suggested mass effect and necrosis as the most reliable predictors of From: Current Clinical Oncology: High-Grade Gliomas: Diagnosis and Treatment Edited by: G. H. Barnett © Humana Press Inc., Totowa, NJ 105 106 Part III / Ruggieri tumor grade but these generalizations are frequently contradicted. Whereas enhancement is thought to be common in higher grade masses, all such masses do not enhance and, in one study, nearly 20% of glioblastomas did not enhance (6,8). It is likely safe to state that a prominently enhancing parenchymal mass in an adult is unlikely to be a low-grade neoplasm. In practice, the primary job of imaging in the preliminary evaluation of such patients is to characterize the extent of disease and the impact on the adjacent normal brain. Limited conventional MRI features in conjunction with demographic data and the clinical presentation can help to distinguish the different neoplasms and to identify the more aggressive masses. It is still becoming increasingly common to employ specialized studies such as diffusion, perfusion, and MR spectroscopy if conventional evaluation fails to make these distinctions in patients with conflicting clinical and imaging data. Alternatively, such studies can be utilized in the follow-up of gliomas to differentiate tumor recurrence, malignant degeneration, and the sequelae of therapy if conventional MRI fails to do so. ANAPLASTIC ASTROCYTOMA 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 struc- tures. 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 Chapter 6 / MRI 107 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. 108 Part III / Ruggieri area with the most extensive breakdown in the blood–brain barrier (BBB) and generally indicates the more aggressive component of the 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 if the 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. GLIOBLASTOMA MULTIFORME Glioblastoma multiforme is classified as a WHO grade IV neoplasm and is among the most common primary intracranial neoplasms. Glioblastomas account for the majority of glial tumors, over half of astrocytic tumors, and up to 20% of all intracranial tumors (1,11). Although uncommon in the pediatric population, glioblastomas make up more than half of primary intracranial neoplasms in adults with a peak incidence during the sixth and seventh decades of life. Similar to the AA, the glioblastomas generally arise within the cerebral hemispheres and symptoms at presentation usually include headache, seizures, focal neurologic deficit, change in personality, and/or signs of increased intracranial pressure. Histologically, these masses are characterized as infiltrative masses with high cellularity, cellular pleomorphism, and increased mitotic index. These tumors are characteristically very heterogeneous with evidence

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