Figure 33-29. Giant aneurysm of the anterior cerebral artery. Left: T1-weighted MRI without gadolinium infusion. The white signal is thrombus within the anterior aspect of the aneurysm; there is some blood flow within the lesion evidenced by the darker signal. Right: Cerebral angiogram, left common carotid injection, lateral view, showing the residual flow in the posterior aspect of the aneurysm.
Figure 33-30. Left parietal arteriovenous malformation. Upper left: T2-weighted MRI shows a tangle of vessels interspersed throughout the parietal lobe. The largest of these vessels are dilated draining veins. Upper right: CT angiography demonstrates enhancement of the abnormal vessels throughout the left hemisphere. The AVM is fed primarily via branches of the left MCA. Cerebral angiography. Contrast injected into the left internal carotid artery reveals the feeding arteries (lower left) and abnormal early filling of dilated draining veins (lower right) due to blood bypassing the capillary bed.
Figure 33-31. Cerebral angiogram of a cerebral dural arteriovenous malformation. The nidus is located at the cerebral convexity (arrow). There is rapid filing of the cerebral venous system after injection of contrast into one internal carotid artery.
Figure 33-32. Cavernous malformation in the right parietal lobe. Axial T2 MRI (left) shows a round lesion which is heterogeneously hyperintense and hypointense. This appearance is due to vascular channels which are immediately adjacent to each other without interspersed normal brain tissue, containing blood products in different stages of degradation. An axial gradient echo MRI (right) shows that the lesion is hypointense, again due to blood products.
Figure 33-33. A developmental venous anomaly (DVA) and its collecting vein in the left cerebellum on a T1-weighted MRI with contrast.
Figure 33-34. Axial susceptibility-weighted MR images from a 65-year-old man with cerebral amyloid angiopathy. The left image shows innumerable cortical and subcortical microhemorrhages. The right panel shows cortical gyriform hemosiderosis, with additional cortical and subcortical microhemorrhages.
Figure 33-35. Hypertensive encephalopathy. Axial T2-FLAIR images showing fairly symmetric abnormal hyperintensity predominately in the parietooccipital lobes. The lesion affects the cortex and subcortical white matter and there is little mass effect. In severe cases, there may be hemorrhage and heterogeneous infarction in the cerebral cortex. The same imaging findings may occur in eclampsia (see also Chap. 41).
Figure 33-36. Reversible cerebral vasoconstriction syndrome. Axial (left) and sagittal (right) CT angiogram showing segmental narrowing of the middle and anterior cerebral artery branches (arrows).
Figure 33-37. Granulomatous angiitis of the brain. Cerebral arteriogram from a common carotid artery injection, lateral projection, demonstrating numerous areas of irregular narrowing (arrows) and, in some areas, contiguous slight dilatation (“beading”), particularly in the anterior cerebral artery.
Figure 33-38. Typical lesions of Susac syndrome in the central portion of the corpus callosum shown in a sagittal T-2 FLAIR MRI. These abnormal areas may show restriction of diffusion.