PMC4496836_01
Pretreatment imaging: Computed tomography (a) T1 magnetic resonance postcontrast (b) and fluid attenuation inversion recovery (c) showing 6 cm x 5 cm x 5 cm bilateral frontal lobe mass with internal coarse calcifications, marked enhancement, and surrounding vasogenic edema with multiple flow voids and large draining veins. There is abnormal tissue interspersed between vascular elements and large areas of cystic changes and necrosis
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F1
Computed tomography scan of the brain showed 6.1 cm x 4.8 cm x 4.9 cm mass centered over the anterior falx cerebri with moderate surrounding hypodensity and effacement of adjacent sulci [Figure 1a]. Magnetic resonance imaging (MRI) demonstrated an irregularly shaped, intra-axial mass with heterogeneous contrast enhancement that abut the anterior communicating artery (ACA) [Figure 1b]. Fluid attenuation inversion recovery imaging revealed complex patterns of hypointense tubular outlines within the lesion, suggestive of considerable vascularity within the lesion [Figure 1c].
(a) Preembolization digital subtraction angiograms of the anterior circulation performed by injection of the left internal carotid artery and right internal carotid artery demonstrating vascular pedicles emerging from the right middle cerebral artery and right anterior communicating artery (ACA) (top), and pedicles emerging from the left ACA (bottom). (b) Mid to late phase angiogram demonstrate the arteriovenous malformation nidus and the venous outflow
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Diagnostic cerebral angiogram confirmed extensive blood supply from the bilateral ACAs as well as the left middle cerebral artery (MCA) [Figure 2a] with a 2.4 cm x 1.4 cm x 2.3 cm AVM nidus and prominent venous drainages into the superior sagittal sinus [Figure 2b].
Photomicrographs of anaplastic oligodendroglioma and arteriovenous malformation (AVM) histology (a) anaplastic oligodendroglioma showing uniform cellularity, uniformly round nuclei, and perinuclear halos. This section shows classic delicate microvasculature, although microvascular proliferation was seen in other areas. Inset highlights an atypical mitotic figure of which many were identified (H and E; original magnification, x200). (b) Secondary features of oligodendroglioma include scattered microcalcifications (center of the image) and clonal nodules of heightened cellularity (right side of image) (H and E original magnification, x100). (c) Irregular large vessels of the AVM with intervening cellular oligodendroglioma (*) (H and E original magnification, x20). (d) Irregularly contoured vessels of the AVM filled with black granular embolization material. An intimal cushion is identified in one of the fibrotic vessel walls (*) (H and E original magnification, x50)
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The anaplastic oligodendroglioma exhibited archetypal histopathologic features including uniform cellularity with uniformly round nuclei set in perinuclear halos [Figure 3a]. As is common in oligodendrogliomas, microcalcifications and multiple nodules of the tumor with heightened cellularity were seen [Figure 3b]. The AVM was set within a background of anaplastic oligodendroglioma and consisted of multiple irregularly contoured vascular lumens of varying diameters including both thick-walled muscular arteries and large thin-walled veins with variable amounts of intervening parenchyma including oligodendroglioma [Figure 3c]. Irregular vessels showed intimal hyperplasia/cushions, a characteristic feature of AVMs [Figure 3d].
Immediate (a) 1 year (b) postoperative magnetic resonance imaging T1 postcontrast
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MRI at this time [Figure 4] showed no evidence of tumor recurrence.