Is that cortical laminar necrosis or pseudolaminar necrosis? The neuroradiologists' dilemma solved!.

Abstract

This study aimed to define cortical laminar necrosis and pseudolaminar necrosis and the macroscopic, microscopic and radiological appearances. Cortical laminar necrosis is a particular sub-type of cerebral infarction where there is selective necrosis of a lamina (layer) or a few laminae of the cerebral cortex (layers 3, 5 and 6 in decreasing frequency), because of 'selective vulnerability'. Biopsy proven cases have shown that there is often no haemorrhage or calcification in the cortex to account for the pre contrast T1 hyperintensity. Proposed causes of this signal change include fat laden macrophages, mineralisation and denatured proteins and cellular components. Cortical laminar necrosis and pseudolaminar necrosis are used interchangeably in the published work on radiology. The term pseudolaminar necrosis appears to have arisen as the necrosis may not be strictly laminar. A wide range of aetiologies have been described. Gyriform cortical hyperintensity on pre contrast T1 weighted images and gyriform enhancement are the hallmarks of cortical laminar necrosis. These signal characteristics will most frequently appear in the subacute phase approximately 2 weeks post event, being most prominent at 1-3 months. T2, fluid attenuated inversion recovery (FLAIR) and susceptibility-weighted imaging (SWI) signal intensity is variable. While gyriform cortical hyperdensity and enhancement on computed tomography (CT) have been associated with cortical laminar necrosis they are not specific and have not been proven histologically. Cortical laminar necrosis and pseudolaminar necrosis are used interchangeably in the published work on radiology. Both terms appear acceptable and the terms are synonymous for describing cortical necrosis with a dominant laminar distribution. The cortical precontrast T1 hyperintensity is characteristic and should allow a confident diagnosis.