Laminar cortical necrosis corresponds to neuronal ischemia associated with a glial reaction and a laminar deposit of lipid-rich macrophages. It occurs following cerebral hypoxia, with damage to the deep layers of the cortex [1].

Cortical laminar necrosis has been linked to a deficiency of oxygen or glucose, which can occur in anoxia, hypoglycemia, status epilepticus, ischemic stroke, and less frequently in immunosuppressive therapy and polychemotherapy [2].

When cortical laminar necrosis is seen on CT imaging, it typically appears as a gyriform linear hyperdensity in the superficial cortex, with the medial occipital lobes and perirolandic areas being the most common locations [2].

On CT, only a high, subtle cortical density is typically visible. Usually appearing after two weeks, the high cortical density peaks one to two months later and disappears after six months. Generally, cortical laminar necrosis is not easily detected on tomography, however, in the most severe cases of this pathology, far more noticeable images are visible, a situation that has been linked to a poor prognosis [3].