Cortical laminar necrosis is selective injury to cortical layers. Its familiar imaging clue is a gyriform ribbon of intrinsic T1 hyperintensity on precontrast images, typically evident by approximately 2 weeks and most prominent around 1-3 months; it may persist longer.
It can coexist with gyriform contrast enhancement, but intrinsic T1 signal and enhancement should be assessed separately. A T1-bright ribbon does not, by itself, establish hemorrhage or calcification. Stroke Manual · Radiopaedia
Dystrophic calcification or mineralization is a later potential sequela in damaged cortex. It appears as gyriform hyperattenuation on noncontrast CT and may produce susceptibility on GRE/SWI. CT helps distinguish mineralization from blood products.
Not every late gyriform cortical hyperdensity is calcification, and the label laminar necrosis should not be applied indiscriminately to every cortical change after a full-thickness territorial infarct.
The original teaching file remains available as a read-only reference: CVA Evolution PDF.