Figure 1: (Top Left) Axial FLAIR demonstrates a left insular infiltrative lesion involving the cortex and white matter. This anaplastic astrocytoma is fairly circumscribed, a less common characteristic in these higher grade lesions. (Top Right) ADC demonstrates no appreciable dark restricted diffusion in this lesion to suggest hypercellularity. (Bottom) Axial T1WI postcontrast shows a small round area of enhancement in the superficial insula, a feature more typical of higher grade glioma. If the T2/FLAIR hyperintensity surrounding this lesion spared the cortex, the enhancing lesion may be more easily mistaken for metastasis with surrounding vasogenic edema.
Figure 2: The medial left frontoparietal complex-appearing anaplastic astrocytoma in this patient demonstrates low T1 signal intensity (top left) and FLAIR hyperintensity (top right) with a mixed-signal hemorrhagic component at its posterolateral aspect. Black signal on the susceptibility-weighted imaging (middle left) also reflect this hemorrhage. The tumor also has a heterogeneous enhancement pattern (middle right, coronal; bottom row, sagittal) that is more typical of higher-grade adult primary brain tumors than of grade II tumors.
- Infiltrating malignant astrocytoma with ill-defined tumor margins and extensive edema
- WHO grade III
- Usually develops from malignant degeneration of low-grade astrocytoma (WHO grade II)
- Commonly dedifferentiates into glioblastoma (GBM) (~50%) within 2 years
- Focal or diffuse anaplasia, highly proliferative
- Increased cellularity and nuclear atypia; usually no necrosis or microvascular proliferation
All ages affected (fourth and fifth decades of life most common)
- Slight male gender predilection
- Median survival 2–3 years
- Better prognosis with younger age, gross total resection, absence of enhancement, KI-67 index ≤5.1%, and IDH1- or MGMT-positive genetics
- Presenting symptoms dependent on tumor location
- Seizures, headaches, behavioral changes, clinical deterioration in patients with known low-grade astrocytoma
- Treatment: resection, chemotherapy (temozolomide), radiation
- Ill-defined, infiltrating white matter mass
- Location in frontal and temporal lobes most common; brainstem and spinal cord uncommon
- Infiltrates beyond apparent imaging tumor margins
- Expansion and involvement of adjacent cortex common
- Variable enhancement
- Usually nonenhancing, but patchy or nodular enhancement may be present
- Cysts and hemorrhage are uncommon features
- Spreads along white matter tracts, but may spread via cerebrospinal fluid (CSF), leptomeninges, and ependyma
- Hypodense, ill-defined white matter mass
- Hemorrhage and calcification uncommon features
- Usually does not enhance on contrast-enhanced CT, but may show focal or patchy enhancement
- Ring enhancement suggests progression to GBM
- T1WI: isointense to hypointense
- T2WI: heterogeneously hyperintense; presence of flow voids suggests vascular proliferation and progression to GBM
- FLAIR: heterogeneously hyperintense
- DWI: usually no diffusion restriction
- T1WI+C: usually no enhancement; may show patchy or nodular enhancement
- MRS/MR perfusion: decreased NAA, increased Cho/Cr ratio, increased relative cerebral blood volume (rCBV) compared with low-grade astrocytomas, although usually less than GBMs
- Diffusion tensor imaging (DTI) may assist in surgical planning
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