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infarction. These may be due to emboli or occlusive disease, or they can follow compression of the PCA in trauma with downward transtentorial herniation. In-volvement of the medial occipital lobe pro-duces the characteristic clinical finding of homonymous hemianopsia.

Anterior cerebral artery (ACA) infarcts are uncommonand usually occur with ICA occlusion in patients who have contralat-eral hypoplasia of the proximal ACA. ACA infarct can also follow subfalcine hernia-tion with “clipping” of the ACA under the falx cerebri. ACA infarcts appear as a region of hypodensity (CT) or hyperintensity (MR T2/FLAIR) involving the cingulate and su-perior frontal gyri.

Cerebellar and brainstem infarcts are due to emboli,vertebral artery injury, or occlusive vertebrobasilar disease. They can involve the pons, medulla, anterior inferior cerebellum, posterior inferior cerebellum, or superior cerebellum.

Watershed infarcts occur in the border-zones between arterial territories and are seen in patients with limited vascular re-serve challenged by hypotension or poor cardiac output. This may be due to ath-erosclerotic ICA or MCA disease or to vas-culopathies such as Moya Moya, in which the proximal MCAs are gradually occluded (Fig. 2.24).

◆Cerebral Infarct: Arterial Territories

The middle cerebral artery (MCA) is the most frequently involved territory in cere-bral infarction. Emboli are the most com-mon cause of occlusion and originate from atherosclerotic plaques in the common or internal carotid arteries, cardiac emboli, or infrequently venous emboli in patients with right to left cardiac shunts (patent foramen ovale). Early imaging signs in-clude hyperdense MCA on noncontrast CT, hypodense basal ganglia, “disappearing” lentiform nucleus, and loss of the normal insular ribbon. Hemorrhage, especially in the basal ganglia and cortex, is common in patients with MCA strokes and may occur 1 to 4 days after onset of infarction.

Lacunar infarctions are common, but many are clinically silent. These are due to occlusion of the small perforating and deep cerebral arterioles and are associated with increasing age and hypertension. Primary small vessel disease, rather than emboliza-tion, is the etiology, and lacunar infarcts typically involve the basal ganglia, internal capsule, thalami, and brainstem. Most are discovered incidentally. In acute small ves-sel infarct, CT findings may be subtle, but diusion-weighted MRI will usually show an area of high signal, usually less than 1 cm in diameter.

Posterior cerebral artery (PCA) in-farcts are less common than ICA or MCA

Fig. 2.24a–f a–f Arterial territories delineated by subacute to remote infarcts seen on noncontrast CT. (a) Left len-ticulostriate. (b) Left middle cerebral artery. (c) Left posterior cerebral artery. (d) Left posterior inferior cerebellar artery. (e) Left anterior cerebral artery. (f) Right frontal watershed infarct in a patient with Moya Moya disease.