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grade astrocytomas do not induce vascularproliferation and therefore do not enhanceon CT or MRI. Oligodendrogliomas andmixed tumors comprising both astrocytesand oligodendrocytes may be histologicallybenign with modest neovascularity.
Anaplastic astrocytomas and anaplasticoligodendrogliomas are intermediate-gradeneoplasms that arise from low-grade glio-mas as a result of additional mutations intumor-suppressing genes as the preexisting tumor ages. Like high-grade gliomas, theyform blood vessels and will enhance withIV contrast administration. They are not ne-crotic, which is the pathologic hallmark ofglioblastoma. Anaplastic gliomas are typi-cally more heterogeneous than low-gradetumors on both CT and MRI (Fig. 2.31).
◆ Low- and Intermediate-Grade Glioma
Low-grade gliomas are primary CNS tu-mors, the majority of which are either as-trocytomas, oligodendrogliomas, or mixed oligoastrocytomas. They are a common cause of a first seizure in previously healthy adults. Headache and sensory or motor deficits are other presenting symptoms. In contrast to malignant gliomas, which are usually discovered in older patients, low-grade tumors frequently occur in the third and fourth decades.
On CT, a low-grade astrocytoma appearsas a nonenhancing, poorly defined, homog-enous low-density tumor. The characteristicMRI appearance is that of a diuse, non-enhancing mass, hypointense to brain onT1-weighted images and hyperintense onFLAIR and T2-weighted images. Most low-
Fig. 2.31a–fa–d Low-grade mixed oligoastrocytoma. CT shows a homogeneous low-attenuation mass involving the right frontal cortex and white matter. The mass is high in signal on T2-weighted MRI and low in signal on T1-weighted MRI, and it does not enhance after administration of MR or CT contrast material.
e,f Anaplastic oligodendroglioma. Partially calcied, partially cystic right frontal mass (CT) with scat-tered foci of enhancement on postgadolinium T1-weighted MRI.
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The emergent diagnosis of GBM andother brain tumors is often made by non-enhanced CT, which shows an irregularhypodense parenchymal mass with sur-rounding vasogenic cerebral edema. If con-trast is administered, the margins invariablyshow enhancement. MRI may be the initialstudy, especially in patients who do notpresent to an emergency department.
Once diagnosed, MRI with gadolinium andmultiplanar images is the most appropriateexamination for comprehensive preoperativeevaluation. The typical appearance is thatof a heterogenous mass within the hemi-spheric white matter, with irregular, enhanc-ing margins and central low T1 or high T2signal corresponding to necrosis. Infiltrating glioma cells have been identified well beyond the apparent margins of the primary tumor,and discontinuous foci can develop, indicat-ing migration along white matter tracts orspread via the CSF spaces (Fig. 2.32).
◆Glioblastoma
Glioblastoma multiforme (GBM) is the most common adult primary brain tumor. It is a high-grade malignancy with poor prognosis; the average survival with treat-ment is 15 months or less. Most are dis-covered in the sixth and seventh decades, and patients usually present with a slowly progressive localizable neurologic deficit, symptoms of increased intracranial pres-sure (headache, nausea, vomiting, cogni-tive impairment), or new-onset seizure. Tumor cells migrate along white matter tracts and can traverse the corpus callo-sum to involve both hemispheres (“butter-fly glioma”). Neovascularity and necrosis are defining pathologic features.
Most malignant astrocytomas are spo-radic, but certain genetic syndromes are associated with an increased incidence, including neurofibromatosis type 1 and Li-Fraumeni and Turcot syndromes.
Fig. 2.32a–f a–d Glioblastoma. (a,b) NCCT shows a 4-cm left posterior frontal cortical mass with ill-dened borders, adjacent vasogenic edema, sulcal eacement, and minimal subfalcine shift. (c) On T2-weighted MRI the mass is heterogenous with areas of cystic change. Vasogenic edema is more apparent. (d) On postgado-linium T1-weighted MRI there is heterogeneous tumor enhancement with surrounding edema and central low signal intensity change (necrosis).
e,f Glioblastoma “buttery glioma.” (e) NCCT shows a hyperdense mass that involves the genu of the corpus callosum and extends into the white matter of both frontal lobes. Large amount of associated vaso-genic edema. Thefrontal horn of the left lateral ventricle is compressed with mild enlargement of the right frontal horn and ventricular atria. (f) Postgadolinium T1-weighted MRI shows heterogenous enhancement with central low signal changes (necrosis).
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usually due to metastatic disease from an extracerebral primary site.
CNS lymphoma is characteristically hy-perdense on CT because of the high lym-phoblastic nuclear to cytoplasmic ratio.Enhancement in nonimmunocompromisedpatients is usually homogeneous, sometimesdescribed as having a “lamb’s wool” appear-ance. MRI shows one or more well-demarcat-ed, homogeneously enhancing, round or ovalmasses that are usually slightly hypointenseto white matter on T1-weighted images andof variable intensity on T2-weighted scans.
Treatment consists of steroids and chemotherapy after surgical biopsy. One feature of CNS lymphoma is that it may regress so rapidly and dramatically to ste-roid treatment that the diagnostic biopsy may be negative after as little as 24 hours. Prognosis is dependent on the grade and is usually worse in immunocompromised pa-tients (Fig. 2.33).
◆Primary CNS Lymphoma
Primary CNS lymphoma is an uncommon tumor strongly associated with HIV/AIDS and other immunocompromised condi-tions, and most are non-Hodgkin and B-cell type, with peak incidence in the fifth decade. Signs and symptoms are usually nonspecific and include focal neurologic dysfunction, seizure, and headache.
In most patients CNS lymphoma devel-ops rapidly and involves the deep cerebral nuclei or periventricular white matter. The mass is usually bulky and well demar-cated with mild to moderate surrounding cerebral edema. In immunocompromised patients, primary CNS lymphoma may be multifocal, ring-enhancing, and di-cult to distinguish from toxoplasmosis. In general, toxoplasmosis will always show ring enhancement when > 1 cm, whereas larger lymphomatous masses often, but do not necessarily, enhance homogeneously. When meningeal spread is identified, it is
Fig. 2.33a–fa–d Primary CNS lymphoma. ~ 4-cm diameter hyperdense mass centered