Evolution of cerebral infarction: edema to laminar necrosis and hemorrhagic transformation then to atrophy

Edema in the distribution of the right middle cerebral artery.  This seems more a vasogenic pattern rather than the typical cytotoxic edema involving both grey and white matter as usually seen in cerebral infarction.  This is in part explained by early cortical laminar necrosis (cortical ribbon hyperdensity due to proteinaceous material) as well as probable early petechial hemorrhage.

More substantial cortical laminar necrosis with ribbon-like hyperdensity along the entire affected cortex.  Note also more confluent hyperdensity posteriorly representing hemorrhagic transformation of the infarct (typically occuring 4 days to 4 weeks post infarct and associated with clinical deterioration including worsening of neurological deficit, headache and reduced consious state due to raised pressure).

Affected brain has become atrophic involving both grey and white matter with loss of the laminar necrosis pattern and negative mass effect.  Hemorrhagic area shows some residual hyperdensity