e Left posterior cerebral artery distribution infarct. Diusion-weighted MRI shows marked signal inten-sity dierence between the acute infarct and surrounding brain. DWI is sensitive for acute infarcts within 30 minutes of symptom onset and may remain abnormal for up to 2 weeks.
f Hemorrhagic conversion of a subacute infarct. Multiple areas of hemorrhage within an infarct that involves the left middle and posterior cerebral artery territories. It is due to an internal carotid artery oc-clusion in a patient whose PCA arose directly from the ICA (fetal origin).
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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 diusion-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.
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Predisposing conditions include mastoid or petrous apex infection, polycythemia, malignancy, puerperium, dehydration, oral contraceptive use, head trauma, and inherited prothrombotic disorders such as protein S deficiency. In 20% of patients, no cause is identified.
The diagnosis is made by detecting a hy-perdense venous sinus on NCCT or demon-strating nonenhancing thrombus outlined by the enhancing dural sinuswalls on CT venography or postgadolinium MRI. The initial study for the patient with suspi-cious or atypical headache should be NCCT, which can identify a dense dural sinus and exclude competing diagnoses. Find-ings are often subtle, as the venous sinus can appear dense due to technical factors or hemoconcentration. Confirmation by CT venography, MRI, and or MR venogra-phy may be necessary. The most sensitive imaging strategy often involves a combina-tion of these studies (Fig. 2.25).
◆ Venous Sinus Thrombosis and Venous Infarct
Venous sinus thrombosis (VST) should be suspected in young and middle-aged adults who present with strokelike symp-toms, unusual headache, and visual distur-bance. Elevated intracranial pressure from impaired venous outflow typically leads to nausea, vomiting, and headache. Papillede-ma may or may not be present. The most frequent, but least specific, symptom is headache, often severe and persistent and usually gradually increasing over several days. Headache onset can be abrupt and can clinically mimic acute subarachnoid hemorrhage.
While arterial occlusion or emboli cause infarcts corresponding to well-described vascular territories, venous infarcts tend to involve the cortex or deep nuclei in a nonarterial distribution and are more commonly hemorrhagic. Their location and corresponding clinical findings de-pend on which dural sinus or cortical vein is occluded.
Fig. 2.25a–fa–d Venous sinus thrombosis with venous infarct. (a,b) ~ 3 cm right posterior temporal parenchymal hemorrhage with mild surrounding vasogenic edema and local sulcal eacement. Portions of the right transverse and sagittal venous sinuses are hyperdense. (c) The contents of the right transverse and sagit-tal sinuses are isointense to brain and outlined by enhancing dural sinus walls on this postgadolinium T1-weighted MRI. The left sigmoid sinus opacies normally. (d) FLAIR images show a right posterior temporal cortical/subcortical lesion with associated surrounding edema consistent with a venous infarct. Intermedi-ate signal in the right sagittal sinus.
e,f Partial sagittal sinus thrombosis. Very-high-attenuation material in the torcular herophili and sagit-tal sinus on nonenhanced CT. Sagittal CT venogram opacies the internal cerebral veins, vein of Galen, straight sinus, and most of the sagittal sinus. A lling defect in the occipital portion of the sagittal sinus corresponds to intrasinus clot on NCCT.
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