Subacute Infarcts

The subacute stage begins during the second week with capillary proliferation in the area of infarcted brain tissue. This neovascularity is devoid of any blood-brain barrier and intravascular contrast freely diffuses into the interstitial spaces. The serpiginous character of the gyral enhancement is quite distinctive of cerebral infarction. A focal cerebritis or encephalitis can mimic this pattern, but usually the clinical picture set apart these entities. Following contrast infusion, infarcts will typically enhanced between one to four weeks, but the enhancement can persist for up to two months.

As an infarct evolves, it becomes progressively lower in density on CT (higher in signal on T2-weighted images) and more well defined over the next few weeks, eventually approaching the density of CSF. As the mass effect resolves and the infarcted tissue is resorbed, the adjacent sulci and ventricle will enlarge. The end result is a chronic infarct with focal areas of cystic encephalomalacia and some surrounding parenchymal change due to gliosis. 

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