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 ofastrocytic 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 of microvascular and endothelial proliferation, tumoral hemorrhage, and variably sized foci of tissue necrosis (12,13). Imaging characteristics reflect the histopathologic findings as these masses are generally quite heterogeneous in appearance on MR and computed tomography (CT). Hemorrhage may be seen in up to 20% of masses and evidence of necrosis is conventionally thought of as the "imaging hallmark" of glioblastomas (14-16). Dystrophic calcification is quite uncommon, likely due to the relatively aggressive nature of the mass.
MRI demonstrates an infiltrative, intra-axial, soft tissue mass within the cerebral hemispheres that is heterogeneous in signal intensity on all pulse sequences. Although glioblastomas are quite cellular, the soft tissue components are generally heterogeneously hyperintense on the FLAIR and T2-weighted images. There is generally a large amount of surrounding vasogenic edema resulting from the proliferation of abnormal blood vessels within the mass and transudation of fluid into the interstitium through the leaky endothelium. There may also be neoplastic cells within the edematous tissue that is indistinguishable from the edema alone (17-19). In either case, this will appear as surrounding prominent hyperintensity on T2 and FLAIR and less obvious hypointensity on Tl-weighted MR images. As the corpus callosum is made up of densely packed white matter that is generally resistant to the spread of vasogenic edema, FLAIR and T2 signal abnormalities that are contiguous with the mass and extend into the corpus callosum can generally be thought of as contiguous spread of neoplasm rather than extension of vasogenic edema regardless of whether there is enhancement with gadolinium in this region of the corpus callosum or not (Fig. 2).
The vascularity and necrosis in these masses explains the presence of prior hemorrhage that may be seen in these masses. Acute hemorrhage will appear as a focus of hypointensity on T1- and T2-weighted images, subacute hemorrhage will appear hyperintense on both sequences, and remote hemorrhage may be seen as mild hyperintensity on T1 or, more likely, irregular or linear foci of hypointensity on the T2-weighted images. Turbo- or fast-spin echo acquisitions are now used routinely for conventional MRI. Unfortunately, these pulse sequences inadvertently suppress the signal loss because oflocal field inhomogeneities caused by the iron deposition at the site of remote hemorrhage. If there is a suspicion of prior hemorrhage, it is necessary to perform a T2*-weighted gradient echo acquisition with a relatively long echo time in addition to conventional MR pulse sequences to more sensitively evaluate for the presence ofprior hemorrhage. Such sequences will accentuate foci of prior hemorrhage as irregular foci of hypointensity resulting from a localized tissue gradient (hemorrhage adjacent to normal brain tissue) causing loss of signal in the tissues.
Contrast enhancement in these masses is usually quite prominent and heterogeneous in nature. The enhancement is generally more prominent peripherally as a thick, irregular rim surrounding a central area of necrosis that may occupy up to 80% of the volume of the overall mass (20). Although not uniformly present, glioblastomas classically demonstrate multi-loculated enhancement, comparable to that seen with abscess cavities. Abscess cavities would be more likely to have a thinner, more uniform rim that is hypointense on T2-weighted sequences in contrast with glioblastomas. The central cavities of abscesses are also more apt to have restricted diffusion on diffusion-weighted sequences than a glioblastoma (21,22). If these imaging findings and the clinical presentation still present a dilemma, alternative specialized studies could be employed for further preoperative evaluation.
The overwhelming majority ofglioblastomas are solitary, supratentorial, intra-axial masses that spread within the parenchyma along white-matter tracts. In less than 5% of cases, these masses may be multifocal or multicentric. Such masses are thought to arise simultaneously at several sites if the masses are clearly separated by normal appearing white matter on all pulse sequences and are not contiguous with a pial or ependymal surface. Even more commonly than AA, glioblastomas may disseminate within the CSF space along the leptomeninges, ependymal surfaces of the ventricles, and pial surfaces of the brain and/or spinal cord to cause cranial nerve symptoms, hydrocephalus, radiculopathies, and myelopathy. It is possible to identify larger deposits of neoplasm that have spread within the CSF as hyperintense to isointense nodules of tissue on FLAIR images or hypointense to isointense masses on T1-weighted images. Gadolinium enhanced T1-weighted imaging is a far more sensitive means of evaluation for leptomeningeal spread of neoplasm and will be recognized as linear or nodular enhancement along the leptomeninges or pial or ependymal surfaces. Early signs on MRI may be unexplained new hydrocephalus without evidence of infection, new linear enhancement along the ependymal surfaces of the ventricles, or enhancement along the cranial nerves in the basilar cisterns (commonly cranial nerves III, V, VII, and VIII).
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