Acute Infarcts

     CT and MR scans in patients with asymptomatic bruits or TIA's are usually negative, unless they disclose abnormalities related to previous events. In patients with stroke, the earliest sign may be abnormal vascular density/signal. Acute thrombus or embolus is hyperdense on CT. Acute clot may be difficult to detect on MR, but the occluded artery should be apparent by the absence of a normal flow void. The absent flow void is easiest to see in the larger arteries at the base of the brain on T2-weighted images. It is not possible to conclusively distinguish a complete occlusion from a critical stenosis with markedly reduced flow. Subacute clot is hyperintense and is easiest to visualize in the basilar and middle cerebral arteries on T1-weighted images. One must be careful not to mistake in-flow enhancement with intraluminal clot. This phenomenon is most often observed in the end slices of a multislice set in arteries with slow flow entering the imaging volume.

      Another valuable sign of acute stroke is arterial enhancement. With slow arterial flow, the spin-echo is able to capture the intravascular signal, and the T1 shortening effect of the gadolinium renders the arteries hyperintense on T1-weighted images. Arterial enhancement is more apparent in the smaller distal branches. It will be present in up to 45% of patients during the first week. Endnote

      The first parenchymal changes observed on CT and MR reflect the cytotoxic edema affecting primarily the gray matter. It is important to remember that the CT scan may be negative for the first 24-36 hours. Massive infarctions may be visible as early as 6 hours. The MR scan is usually positive within three to four hours following a stroke. One of the earlier signs on CT is loss of the normal gray-white contrast as the edematous cortex becomes isodense to the underlying white matter. A similar phenomenon is not observed on MR because the increased water in the gray matter renders the cortex higher signal on T2-weighted images and lower signal on T1-weighted images, thereby increasing gray-white contrast. It is often easier to appreciate the increased cortical signal on proton density-weighted images. The cortical swelling is more apparent on T1-weighted scans. Cortical edema produces effacement of the sulci on both CT and MR. Endnote

      After 6-8 hours the accompanying vasogenic edema highlights the areas of brain infarction. These fluid shifts are more profound and are responsible for effacement of the ventricles and midline shifts. The mass effect increases over the first few days and becomes maximal at about five days.

      Incomplete ischemia has received special attention in the neuroradiologic literature. It results from transient interruption of the blood supply from iatrogenic causes or from an embolus that breaks up and rapidly restores perfusion to the area. The distinctive features of incomplete ischemia are early intense parenchymal enhancement and little or no arterial enhancement. If arterial enhancement is present, it disappears within 24-48 hours. The parenchymal enhancement results from a combination of reperfusion and vasomotor deregulation or vasodilatation. This "luxury of perfusion" last about 24 hours. There may be some mild brain edema during the first 24-48 hours, but the parenchymal signal changes are minimal or absent. Incomplete ischemia is associated with a good prognosis. Endnote  

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