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2Brain

The primary role of CT in acute strokeis to exclude hemorrhage, which contrain-dicates the use of thrombolytic agents inthose patients who present within 3 hoursof symptom onset. If readily available, dif-fusion-weighted MRI is the most sensitiveexamination for identifying early cerebral in-farction, and it can do so within 30 minutes.

Cytotoxic edema increases during the first 3 days after cerebral infarction, and on CT itappears as a well-defined area of low atten-uation involving gray and white matter. Cor-responding hyperintensity is evident on T2and FLAIR MRI sequences at this stage. Afterapproximately 2 weeks, an evolving infarctmay become less obvious on CT because of a“fogging” eect in which microhemorrhage and cellular repair lead to pseudonormal-ization of brain density. Diusion-weighted MRI signal begins to fade around 1 weekand is usually nearly normal by 2 weeks.Hemorrhagic conversionis a term that refersto spontaneous bleeding within an area ofischemic brain, most commonly in patientswith large-territory (middle cerebral or in-ternal carotid artery) infarcts (Fig. 2.23).

◆ Cerebral Infarct Due to Arterial Occlusion

Ischemic cerebral infarcts result from acute compromise of arterial blood flow to a por-tion of the brain, with consequent cellular death. The neurologic deficit resulting from the infarct depends on the vessel occluded, the location and extent of the territory it supplies, and the available collateral circu-lation. For example, a left middle cerebral artery infarct would be expected to result in aphasia as well as contralateral hemipa-resis and sensory disturbance.

The sensitivity of nonenhanced CT is limited in the first 12–24 hours after symptom onset; however, subtle signs of early infarct can be seen even within the first 3 hours. A hyperdense cerebral vessel (known as the bright basilar artery or hy-perdense middle cerebral artery) indicates thrombosis. Early parenchymal changes are due to ischemic (cytotoxic) cellular swelling and include (1) focal loss of nor-mal gray-white matter dierentiation, (2) cortical sulcal eacement, (3) poor basal ganglia definition, and (4) nonvisualization of the “insular ribbon,” which is the nor-mally dense insular cortex.

Fig. 2.23a–fa,b Early infarct with dense middle cerebral artery and insular ribbon signs. The left middle cerebral artery is abnormally dense. The left insular cortex is isodense to adjacent white matter and hypodense compared with the normal cortex.

cSubacute left middle cerebral artery territory infarct. Cytotoxic edema with homogeneous low-attenu-ation change involving both gray and white matter in the distribution of theleft lenticulostriate vessels andmiddle cerebral artery. Left hemispheric swelling with eaced lateral ventricle and minimal subfalcine shift. d Remote right middle cerebral artery territory infarct. This remote infarct is near CSF in density and is associated with volume loss and ex vacuo dilatation of the right lateral ventricle.

e Left posterior cerebral artery distribution infarct. Diusion-weighted MRI shows marked signal inten-sity dierence 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).