The occurrence and extent of cerebral infarction is determined by three basic factors: i) site of arterial occlusion, ii) the rapidity of arterial occlusion, and iii) the presence or absence of collateral circulation.
Grossly, infarcts are usually divided into pale (non-hemorrhagic) and hemorrhagic types. Infarcts evolve over time, thus their gross appearance gives a clue to when they occurred. The temporal evolution of an infarct occurs in three stages: i) acute (1 day – 1 week) – the involved area is soft and edematous and there is a blurring of anatomic detail; ii) subacute (1 week – 1 month) – there is obvious tissue destruction and liquefactive necrosis of the involved brain; iii) chronic (>1 month) – the damaged tissue has been phagocytized and there is cavition with surrounding gliosis.
Microscopically there is also a temporal evolution of cerebral infarcts. During the earliest phase of infarction (0-48 hours) chromatolysis and swollen eosinophilic neurons are seen. Neuronal cell necrosis and an acute inflammatory response are usually seen from 24-72 hours. This response is typically followed by an influx of mononuclear cells which begin to phagocytize necrotic debris (3-5 days). From 1-2 weeks after the infarct there is vascular proliferation and reactive astrocytosis. Over time (>1 month) the necrotic tissue will be completely removed and a cystic cavity surrounded by a glial scar will be formed.