Figure 33-19. A. Axial diffusion-weighted MRI showing multifocal acute infarctions in the left ACA-MCA arterial border zone (watershed). B. Magnetic resonance angiography displays severe stenosis of the left internal carotid artery (arrow), just above the common carotid artery bifurcation.
Figure 33-20. Cervical artery dissections. T1 MRI with fat saturation (left) and magnetic resonance angiography (right). The upper images show bilateral internal carotid artery dissections (arrows). The lower images show a left vertebral artery dissection (arrows). The T1 hyperintensity that is shown in the left upper and lower images is due to thrombus within the false lumen of the vessel.
Figure 33-21. Moyamoya disease. Digital subtraction angiography in the coronal plane of the left common carotid artery. On the left image, there is occlusion of the left internal carotid artery near its terminus, and evidence of abnormal vascular proliferation involving the lenticulostriate vessels (arrow). The external carotid artery branches fill normally. The right image shows the same contrast injection during the early capillary phase; the characteristic “puff of smoke” is encircled.
Figure 33-22. Axial T2-FLAIR MRI of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). There is confluent symmetric abnormal hyperintensity within the periventricular white matter and internal and external capsules (left) and characteristically, also in the anterior temporal lobes (right).
Figure 33-23. Two axial T2-FLAIR images of mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS). Multifocal asymmetric areas of cortical and subcortical T2 hyperintensity are seen.
Figure 33-24. Unenhanced CT showing hypertensive hemorrhages in the putamen (A), thalamus (B), pons (C), and cerebellum (D). The thalamic hemorrhage (B) has extended into the posterior horn of the right lateral ventricle and the cerebellar hemorrhage (D) has extended into the fourth ventricle.
Figure 33-25. Diagram of the circle of Willis showing the principal sites of intracranial aneurysms. Approximately 90 percent of aneurysms arise from branches of the anterior half of the circle. The sizes of the aneurysms depicted correspond roughly to the frequency of occurrence at those sites.
Figure 33-26. Subarachnoid hemorrhage as a result of rupture of a basilar artery aneurysm. Left: Axial CT at the level of the lateral ventricles showing widespread hyperdense blood in the subarachnoid spaces and layering within the ventricles with resultant hydrocephalus. There is a blood–CSF level in the posterior horns of the lateral ventricles, typical of recent bleeding. Right: At the level of the basal cisterns, blood can be seen surrounding the brainstem, in the anterior sylvian fissures, and the anterior interhemispheric fissure. The temporal horns of the lateral ventricles are enlarged, reflecting acute hydrocephalus.
Figure 33-27. Aneurysm of the anterior communicating artery. Left: CT angiogram showing the aneurysm (arrow) arising from the branch point of the anterior communicating artery and the A1 segment; Right: Reconstructed image from CT angiogram data showing the aneurysm (arrow) in relation to the adjacent bony and vascular structures.
Figure 33-28. Vasospasm following subarachnoid hemorrhage due to rupture of an anterior communicating artery aneurysm. Sagittal CT angiography reveals multifocal narrowing of segments of the anterior cerebral artery (arrows).