Specific Imaging Findings

Acute to subacute laminar necrosis (LN) on CT cannot be differentiated from brain swelling/edema and often occurs in the setting of hypoxic-ischemic changes and other lesions that lead to cerebral edema/swelling. Follow-up CT shows resolution of edema with possible local volume loss. Chronic LN demonstrates cortical hyperdensity in the affected gyri. MRI of LN in the acute to subacute setting shows reduced diffusion of the involved cortical regions, frequently with T2 hyperintensity and effacement of the sulci. Subcortical U fibers are usually affected by the edema. There is no evidence of blood products on T2*-weighted images. Associated deep gray matter changes may be present depending on the cause of the LN. Gyral enhancement on post-contrast T1WI may occur, usually in the subacute stage. Chronic LN is classically visualized as T1 hyper-intense gyri with surrounding volume loss. The hyperintensity may be even more prominent on FLAIR images while diffusion imaging is unremarkable. Cortical hypointensity is present on T2* images in some cases. Findings of LN start fading away on long follow-up studies. Encephalomalacia and gliosis of the adjacent or other areas of the brain may be present, depending on the underlying etiology.

Specific Clinical Information

LN tends to occur in the setting of hypoxic-ischemic encephal-opathy from any cause, infarction, and hypoglycemia. It is seen with seizures, posterior reversible encephalopathy syndrome (PRES), mitochondrial disorders, osmotic myelinolysis, CNS lupus, and brain injury. Extensive changes have a poor prognosis and tend to be associated with death or vegetative state.